The thread running through this month is a statistical one, which sounds dry until you see where it bites. Four of the five things below are cases where an average says one thing and the individual moment inside it says another. A mean core temperature. A mean acceleration. A group difference between two sports. Nobody is hurt by an average. They are hurt by a peak, and most of our measurement habits are built to smooth peaks away.

1. Beyond hypothermia, in one place

The narrative review came out at the start of August, and it has been doing the rounds since. I have written about it here twice already and talked about it more than that, and the same question keeps coming back from clinicians. So here is the whole argument in one place, in order.

The paper is:

Leuci L, Melau J, Messina A, Tipton M, Carenzo L. Beyond hypothermia: mechanisms of death, rescue, and prevention in cold water immersion — a narrative review. J Appl Physiol. 2026;141(3):760–769. doi:10.1152/japplphysiol.00578.2026

The number the whole thing hangs on is this. In the United Kingdom, roughly 55% of accidental open water deaths happen within three metres of safe refuge, and two out of three of the victims were regarded as competent swimmers.

Three metres. A ladder, a gunwale, a rock. That is not a hypothermia statistic. Core cooling takes half an hour before it threatens anyone, and a competent swimmer covers three metres in seconds. Something took these people fast, and took them while they were still warm.

The review works through the four-stage model, because the sequence is the argument.

Stage 1, cold shock, 0 to 3 minutes. An involuntary gasp of two to three litres in the first seconds, then hyperventilation running two to three times resting minute ventilation for a minute or more. If the airway is under water when the gasp fires, aspiration begins there. If it is not, the hyperventilation drops PaCO₂ and takes cerebral perfusion with it, and breath-hold time collapses from around sixty seconds to a few. Motivated, experienced people cannot reliably override this in the first minute. Neither can you.

Stage 1 is also where autonomic conflict sits. Skin cooling drives sympathetic outflow hard — a systolic rise of 30 to 50 mmHg — while facial immersion triggers the trigeminal-vagal diving response. The heart gets both instructions at once. We were careful to call this plausible rather than proven, because the honest reading of the evidence is that it needs a substrate before it turns lethal. Congenital long QT affects around 1 in 2,000 people, and molecular autopsy series have found pathogenic or likely pathogenic cardiac channel mutations in roughly a third of unexplained drownings. Drowning is sometimes the first presentation of an inherited arrhythmia syndrome.

Stage 2, swimming failure, 3 to 30 minutes. Peripheral nerve conduction slows in step with tissue temperature. Muscle loses rate of force development, peak force and relaxation rate. Manual dexterity falls apart below about 15 °C finger skin temperature, and tactile sensitivity is essentially gone below 8 °C. In cold water you cross both thresholds in minutes.

This is the stage that gets missed clinically, and it is the one I keep coming back to. A person can lose the ability to grip a line, hold a gunwale, or swim three metres while their core temperature is entirely normal. Which means a victim recovered from cold water can arrive at post-mortem with a near-normal core temperature, and cold water gets written off as irrelevant to the death. It was not irrelevant. It was the whole mechanism.

Stage 3, hypothermia, beyond 30 minutes. Only here does core cooling become the main threat. Shivering peaks between 34 and 30 °C and then fails. Consciousness clouds below about 33 °C and is usually lost between 30 and 28 °C. The Osborn wave appears below 32 °C and ventricular fibrillation risk climbs below 28 °C.

The famous deep-hypothermia recoveries are real — 13.7 °C, and later 11.8 °C, with good neurological outcome after hours of arrest. They are also quoted in the wrong direction constantly. In both of those cases the cooling came before the arrest. In most cold water drownings it runs the other way: the person aspirates, arrests from hypoxia while still relatively warm, and cools afterwards.

Stage 4, circum-rescue collapse. Afterdrop is real, typically 0.5 to 1.5 °C, and it is no longer considered the main mechanism. The bigger one is mechanical. Immersion squeezes 500 to 700 mL of blood centrally. Lift a cold, cold-diuresed, relatively hypovolaemic casualty vertically out of the water and that squeeze vanishes in seconds into a vasculature that can no longer respond. Cardiac output falls off a cliff. That is the argument for horizontal extraction, and it is a much better one than afterdrop ever was.

Two things to carry from it. Fewer than 10% of drowning arrests present in a shockable rhythm — over 90% are PEA or asystole — so if you find VF, treat it as evidence that a cardiac event put the person in the water rather than the reverse, and make sure it triggers toxicology and family screening downstream. And the prevention is almost absurdly cheap: float. Sixty to ninety seconds on your back until the breathing settles. Cutaneous cold receptors adapt, the gasp passes, and you get your body back. Not because you are hardened. Because the physiology settles.

The clinical question in cold water is almost never how cold is this patient. It is which came first, the cold or the hypoxia.

2. What else I wrote

A quieter month on the page than in the field.

Norseman Report 2026 went out at the start of August. 255 starters, a fjord at around 14 °C, an open mountain, and no weather drama for once. Around ten patients, a good share of them support crew rather than athletes, which is the pattern every year and still tells the same story. The athlete is tapered, fed and watched. The crew has been awake since three, driving an unfamiliar road, thinking about somebody else all day. What worries me now is the traffic rather than the water.

Three metres from safety was the clinical version of the review, written for medics and rescue crews rather than for physiologists. It sticks to three things: the dangerous part is over before hypothermia begins, autonomic conflict is plausible and still unproven, and afterdrop has been overtaught while hydrostatic pressure loss has been undertaught. If you only read one thing I wrote this month, read that one — it is the one with the scene-side decisions in it.

I also put a run of shorter notes out on the same material, mostly on the rescue-side physiology, and they generated more conversation than the long pieces did. That is worth noticing.

And the Skagerrak. Eight swimmers, Hirtshals to Flekkerøy, roughly 120 kilometres of open sea in a straight line, an expected 50 to 70 hours nonstop. I was the research lead, with continuous core temperature logging by ingestible capsule across the whole crossing.

We called it off. After about six hours. The waves was just to high and gusting winds horrible.

I want to be careful about how I write this, because there is a version of this paragraph that turns a good decision into a failure, and that version is wrong. Stopping is not the opposite of the project. The physiology that tells you to stop is the same physiology we went out to measure, and it does not become less interesting because it argued against continuing. We have core temperature data across a long, cold, continuous exposure that nobody has instrumented in quite this way before, and the fact that it ends earlier than planned does not make the trace less useful. In some ways it makes it more useful, because the interesting part of any exposure curve is the end of it.

I am not going to put numbers here. The data is not analysed and I am not going to guess in public. But hopefully there will be a proper write-up.

3. MASHIEN: counting the impacts nobody was counting

Now to a study I am part of, and one I have wanted to write about here for a while.

MASHIEN is the MultiAgency, prospective, exploratory, non-intervention, cohort Study on Human Impact Exposure oNboard high-speed boats. The protocol is published:

Ullman J, Myers SD, Bretschneider K-T, et al. MultiAgency, prospective, exploratory, non-intervention, cohort Study on Human Impact Exposure oNboard high-speed boats (MASHIEN): protocol. BMJ Open. 2025;15(5):e090993. doi:10.1136/bmjopen-2024-090993

It runs under NATO Science and Technology Organization research task group HFM-344, and it is genuinely multinational: Sweden, the United Kingdom, Germany, the United States, France, Norway, the Netherlands, Canada and Belgium, with navies, military medical institutes, universities sitting in the same protocol. Coordinating a common data standard across that many organisations is most of the achievement.

What the problem actually is

Drive a small boat fast into a seaway and the hull leaves the water and comes back down. Every one of those landings is a vertical acceleration transmitted through a seat, a deck and a spine. Do it for an hour, and you have absorbed a number of impacts that nobody has ever counted, in a job where the transit is not the mission — it is the thing you do before the mission starts.

The injury picture is not subtle. Vertebral fractures, disc herniations, distortion injuries. Rotator cuff tears and wrist fractures from the forces going through the arms as operators brace. A systematic review found 3,312 injuries across 3,467 person-years of high-speed boat operations, which works out at roughly 1.1 injuries per operator per year. That is not an occupational hazard. That is an occupational certainty.

And it is not only the skeleton. Post-transit, operators show decreased running performance, elevated salivary cortisol and elevated creatine kinase. They arrive at the task measurably degraded, having done nothing but sit in a boat.

How it is being measured

This is the part I find elegant, and it is the reason this study belongs in a newsletter about peaks and averages.

Each boat carries a MAREC logger running three triaxial accelerometers at 600 Hz: one on the hull, and two worn by crew in kidney belts, typically the coxswain and the navigator. A slamming impact is defined as a vertical hull acceleration peak above 20 m/s² — two g. The analysis does not stop at peak magnitude — it takes rise time, vector sum, three-dimensional direction, impact duration and jerk rate, because how fast the acceleration arrives may matter as much as how big it is.

On the human side, participants log pain daily through a smartphone application: intensity on a visual analogue scale, location, modality and duration, drawn onto a body map. Professional operators aged 18 to 65, minimum two months each, target of about 192 participants for 80% power, first enrolment in August 2024 and closure planned for mid-2027. Registered as NCT05299736, ethics through the Swedish Ethics Review Authority.

The design detail that matters most: each participant is their own control. Their pain onboard is compared against their pain off duty. That single choice removes most of the confounding that has made this literature so hard to interpret — the operators who go to sea most are also the fittest, the most experienced and the most likely to under-report, and comparing them to anyone else was never going to work.

Why it matters

Because everything upstream of this has been an average, and averages are exactly the wrong tool here.

Existing exposure guidance for whole-body vibration was built for machinery — continuous, roughly stationary vibration, summarised as a dose over a shift. Slamming is not that. It is a small number of very large discrete events scattered through a transit, and a dose average smears them into a number that describes nothing anyone experienced. Two crews can come home with the same daily average and one of them has taken a single impact that fractured a vertebra.

You cannot write a sensible operational limit until you know which peaks matter — magnitude, rise time, direction, how many, in what sequence. That is what MASHIEN is built to find out. And the answer is meant to end up as guidance a coxswain can actually use, which is why the dissemination plan runs through NATO technical reports and direct stakeholder engagement rather than only through journals.

I am working on establishing the Norwegian arm of this. It sits very close to work I already care about: crews who are cold, wet, vibrated and fatigued before the job begins, and a medical system that mostly assesses them after something has already broken.

4. A model that is good at the core and poor at the fingers

To the thermometer, and a paper published in July that I have been chewing on since:

Singh M, Akerkouch L, Morrissey MC, Szymanski MR, Filep EM, Langan S, Casa DJ, Reifman J, Rubio JE. A 3-D whole-body human thermoregulatory model to simulate extreme cold stress. Sci Rep. 2026. doi:10.1038/s41598-026-57039-7

This is a three-dimensional whole-body thermoregulatory model extended to the cold end. It predicts core temperature and skin temperature at the fingertips, toes, face, hands, feet and cheeks, in air down to −40.0 °C with wind from 0.1 to 3.0 m/s. It was validated against eight cold exposure studies covering 75 subjects. There is something quietly satisfying about seeing names I mostly associate with exertional heat illness turning up on a paper about −40 °C.

The performance is where it gets interesting. Average RMSE for core temperature was around 0.2 °C. For the extremities it ran from 1.2 to 3.5 °C depending on the site — 1.6 to 2.7 °C at the fingertip, up to 3.5 °C at the toe.

Take that seriously for a moment. 0.2 °C at the core is excellent — better than a lot of field thermometry. But the core is the easy problem. It is a large, well-perfused, thermally buffered mass that changes slowly and predictably. The fingers are the hard problem, because they are small, poorly perfused, dominated by vasomotor behaviour that varies enormously between people, and capable of dropping ten degrees in the time the core moves a tenth of one.

And the fingers are where the injury is. This is the point I have made here before and will keep making. Dexterity falls apart below about 15 °C finger skin temperature and tactile sensitivity is gone below 8 °C. That is a seven-degree window between working hands and no hands, and the model’s error bar at the extremities is up to 3.5 °C. Half the window, inside the uncertainty.

So a model like this is genuinely useful for what it is good at — planning exposure durations, comparing clothing systems, running scenarios you would never get past an ethics committee. It is not yet a tool for telling an individual soldier whether their hands are about to stop working. The authors are appropriately careful about this and pitch it as informing guidelines rather than replacing measurement, which is the right pitch.

Same shape as everything else in this issue. The model is accurate about the average of the body and vague about the specific bit that fails first.

5. What the mats look like in a table

Finally, back to the tatami, where I remain the most enthusiastic white-adjacent obstacle in the room.

Preissler AAB, Clemente FM, Casal MZ, Silva RM, Silva AF, Silveira JV, Schons P. Comparison of Anthropometric and Physical Performance Profiles in Elite Judo and Jiu-Jitsu Athletes. Sports. 2026;14(5):207. doi:10.3390/sports14050207

Twenty-five elite male grapplers — twelve judoka, thirteen jiu-jitsu — tested during preparatory training on anthropometrics, handgrip, squat jump, countermovement jump, medicine ball throws and judogi-grip pull-ups. The question is whether two grappling sports with different rule sets produce different bodies.

The judoka jumped higher. Squat jump 38.71 ± 6.69 cm against 33.82 ± 4.74 cm, p = 0.045. Which is exactly what you would predict from the sport: judo is decided in explosive standing exchanges, jiu-jitsu increasingly is not.

Then the authors did the thing I want more sports science papers to do. They noticed that the judo group had been training for 13.25 ± 2.73 years against 7.85 ± 4.36 for the jiu-jitsu group — a difference far more significant than the jump, at p = 0.001 — and adjusted for it. The squat jump difference disappeared.

Nothing else separated the groups at all. At the elite end, two sports that look nothing alike from the stands produce broadly the same athlete, and the one apparent difference was five and a half extra years of training wearing a sport’s name.

I would not build a training programme on twenty-five men. But I like this paper for the discipline of it. The headline finding was sitting right there, publishable, sport-flattering and consistent with everybody’s intuition — and they checked the confounder anyway and reported that it ate their result.

The personal note is uncomfortable and useful. Both of those groups have been doing this for eight to thirteen years. I have done it for a year and a half. Whatever is different about how those bodies move is not a physiological gift I missed out on. It is time on the mat, and there is no shortcut in the table.

The thread

A drowning victim with a normal core temperature. A boat crew with an unremarkable daily vibration dose. A thermoregulatory model with an excellent mean error. Two groups of athletes with a clean statistical difference between them.

In every one of those, the summary number is defensible and the summary number is wrong about the thing that matters. The mechanism lives in the peak, the individual, the extremity, the confounder. And our instruments — statistical and physical both — are mostly built to average, because averaging is what makes noisy data tractable.

I do not have a clever resolution to that. Just a habit I would recommend: whenever someone hands you a mean, ask what the worst single moment inside it looked like. In cold water it is the first thirty seconds. In a boat it is one landing. In a pair of hands it is one finger crossing 15 °C. That is the number nobody wrote down.

Next month: the Skagerrak data, if it is ready, and something on cold and bleeding that I have been circling for a while.

This newsletter represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

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A Book, If You Want to Read On

A good deal of this issue lives in cold water, so if any of it caught your interest, I have written some short, science-based books you might enjoy.

Cold Water Swimming: A Mini Book is a friendly, short guide to enjoying cold water safely, confidently, and with a big smile. It draws on years at the Norseman Xtreme Triathlon, research with elite military swimmers, and my published work in cold-water physiology. Calm, clear, trustworthy guidance for anyone curious about stepping in.

Get Cold Water Swimming on Gumroad →

https://jmelau.gumroad.com/l/uenvfn

Thanks for reading. If something here resonated, hit me with a reply.

(The picture is from a training exercise with Redningsselskapet)

It sounds like a rhetorical question. It isn’t. The UK’s Water Incident Database recorded more than 3,100 water-related deaths between 2019 and 2023, and among accidental open-water deaths, roughly 55% occurred within three metres of safe refuge. Two out of three victims were regarded as competent swimmers.

Three metres. A ladder, the side of a boat, a rock. People who knew how to swim, dying close enough to touch the thing that would have saved them.

That is not a slow slide into hypothermia, and it is not exhaustion — a moderately intoxicated competent swimmer will usually retain enough motor function to cover three metres. Something took them out fast, and took them out while they were still warm. Answering why is the single most useful thing we know about cold water.

I’ve just co-authored a narrative review in the Journal of Applied Physiology with Laura Leuci, Luca Carenzo and Antonio Messina in Milan, and Mike Tipton in Portsmouth. We went back through the four-stage model of cold water immersion and looked hard at where the evidence actually sits. Three things came out of it that I think matter for anyone who might have to pull someone out of cold water. I’ll take them in order.

1. The dangerous part is over before hypothermia begins

Around 60% of immersion deaths in the UK occur in the first two stages — cold shock and swimming failure — without the casualty ever becoming hypothermic.

Cold shock arrives within seconds. An involuntary gasp of two to three litres, then hyperventilation running two to three times resting minute ventilation for a minute or more. If the airway is under water when the gasp fires, aspiration starts there. If it isn’t, the hyperventilation that follows drives PaCO₂ down, cerebral perfusion with it, and the casualty becomes disorientated in water they could otherwise have handled. Breath-hold time collapses from around sixty seconds to a few. Even motivated, experienced people cannot reliably override it in that first minute.

Then comes swimming failure, and this is the one that gets missed clinically. Peripheral nerve conduction slows linearly with tissue temperature. Muscle contractile function degrades — force development, peak force, relaxation rate, all of it. Manual dexterity falls off sharply once finger skin temperature drops below about 15 °C, and tactile sensitivity is essentially gone below 8 °C. In near-freezing water those thresholds are crossed in minutes.

The clinical consequence: a person can lose the ability to grip a rescue line, hold a gunwale, or swim three metres while their core temperature is still entirely normal. Which means a drowning victim recovered from cold water may present at post-mortem with a near-normal core temperature — and cold water gets written off as irrelevant to the death. It wasn’t.

2. Autonomic conflict is plausible, important, and still unproven

Cold water does something odd to the heart. Skin cooling drives sympathetic outflow — tachycardia, vasoconstriction, a systolic rise of 30–50 mmHg. Facial immersion simultaneously triggers the trigeminal-vagal diving response — bradycardia, apnoea. The heart receives both at once, and the resulting electrical instability is a candidate mechanism for sudden arrhythmic death without any core cooling at all.

The supporting evidence is real but indirect. Supraventricular arrhythmias have been documented during breath-hold submersion in healthy volunteers, and during helicopter underwater escape training in healthy military personnel. An animal model showed that simultaneous vagal and sympathetic stimulation worsened long-QT-associated ventricular arrhythmias.

But the same group found that concomitant vagal and adrenergic stimulation did not precipitate arrhythmias in a structurally normal rabbit heart. That is the honest state of the field: autonomic conflict appears to need a substrate — an inherited channelopathy, structural disease, or drug-induced repolarisation abnormality — before it turns lethal. Congenital long QT affects roughly 1 in 2,000. Molecular autopsy series have found pathogenic or likely pathogenic cardiac channel mutations in about a third of unexplained drownings.

I’d rather we taught it as a plausible mechanism with a named evidence gap than as established fact. It leaves no signature at autopsy. It can only ever be inferred by exclusion.

3. Afterdrop has been overtaught. Hydrostatic pressure loss has been undertaught.

Most of us were taught to fear afterdrop at rescue: cold peripheral blood returning to the core, dropping the temperature further, tipping a marginal heart into VF.

Golden’s original observation was a fall in rectal temperature when subjects moved from cold to warm water. No equivalent fall was recorded at the heart. The rectum is a slow site, not a window onto the myocardium. Later work showed an afterdrop still appears when peripheral venous return is occluded, which points to conductive equilibration between cold tissue and warmer core rather than a bolus of cold blood. The magnitude is typically 0.5–1.5 °C. In a mildly hypothermic patient, that is not going to hurt them. Near the VF threshold it might. But it is no longer the main event.

The mechanism that probably deserves the fear is mechanical. Immersion shifts something like 500–700 mL of blood centrally. Lift a cold, cold-diuresed, relatively hypovolaemic casualty vertically out of the water and that squeeze disappears in seconds, into a peripheral vasculature that is compliant and no longer vasomotor-responsive. Cardiac output falls off a cliff. That is why people collapse on the winch wire.

What this changes on scene

Extract horizontally if the lift is any distance — high-sided vessel, helicopter winch. Worth saying: a brief vertical lift over the sponson of a RIB is not what this warns against, and manoeuvring a casualty horizontal in the water to achieve it can cost you the airway.

A shockable rhythm is a red flag, not a relief. Over 90% of drowning arrests present as PEA or asystole — the expected trajectory of hypoxic arrest. VF/pVT is atypical. When you see it, defibrillate, but treat it as evidence of a primary cardiac event that put them in the water rather than one that resulted from it, and make sure it triggers toxicology, molecular autopsy and family screening downstream.

Ventilate first. Drowning is a suffocation problem. ABC, not CAB; compression-only CPR is not appropriate here.

Don’t rub the limbs in a severely hypothermic patient. Peripheral vasodilation in someone already volume-depleted by cold diuresis and the loss of hydrostatic squeeze is how you produce rewarming collapse. Insulate, handle gently, evacuate to a centre that can do extracorporeal rewarming.

Watch the thermometry. Oesophageal is the gold standard with a secured airway, though probe insertion can mechanically irritate a profoundly cold myocardium. Epitympanic thermistors are reasonable in the spontaneously breathing patient. Infrared tympanic and peripheral measurements are not.

The line I’d want people to take away

Hypothermia is real, and it is a genuine threat on prolonged immersion. But it is rarely the first threat, and in most cold-water drownings the cooling follows the arrest rather than causing it. The clinical question is almost never how cold is this patient. It is which came first, the cold or the hypoxia.

And for anyone who ends up in the water unexpectedly: don’t swim. Roll onto your back and float for sixty to ninety seconds until the breathing settles. Your clothes will help you float, not sink you. It remains one of the very few interventions in this field with real evidence behind it.

Here is the link to our new paper. I am really proud of beeing a part of it.

Leuci L, Melau J, Messina A, Tipton M, Carenzo L. Beyond hypothermia: mechanisms of death, rescue, and prevention in cold water immersion — a narrative review. J Appl Physiol. 2026. doi:10.1152/japplphysiol.00578.2026

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

A Book, If You Want to Read On

If any of it caught your interest, I have written some short, science-based book you might enjoy.

Cold Water Swimming: A Mini Book is a friendly, short guide to enjoying cold water safely, confidently, and with a big smile. It draws on years at the Norseman Xtreme Triathlon, research with elite military swimmers, and my published work in cold-water physiology. Calm, clear, trustworthy guidance for anyone curious about stepping in.

Get Cold Water Swimming on Gumroad →

This month one idea kept turning up in four different places. In a race report, in a review paper on cold water drowning, on a jiu-jitsu mat, and in a small study on warm water swimming. The idea is this. The obvious cause is usually the wrong one. The thing we assume killed someone, or hurt them, or protected them, is very often not the thing that did it.

Norseman 2026, the year the Viking Gods left us alone

This year the weather behaved. 255 athletes started, the fjord sat at around 14°C, the mountain stayed open, and the day unfolded more or less the way it looks on paper. No thunderstorms, no white out, no shortened swim.

We treated approximately ten patients. A few cardiac concerns and some minor trauma, nothing that turned into an incident. A good share of them, as always, were support crew rather than athletes. That pattern has held for years and it still says the same thing. The athlete is tapered, fed and watched over by an entire organisation. The support crew has been awake since three in the morning, driving a strange road in a strange country, thinking about somebody else all day. Then they get tired and something small happens.

What actually worries me now is not the water. It is the traffic. Support cars stopping badly on narrow Norwegian roads, with tired athletes and other traffic coming through, is the most dangerous thing on our course. Our 13 race marshals on motorbikes and the police presence made a real difference.

I wrote the full report a few days ago, including the heat plan we built for the valley and then did not need. If you want the detail, it is here.

What we were actually measuring

The part I did not write much about in that report is the research, so let me do it here.

Alongside the safety and medical work, we ran another season of blood sampling and lung function testing on our athletes. This is not a one-off study. It continues a cohort our research group has been building at Norseman over many years, and that is the whole point of it. A single race gives you a snapshot. Many years of the same measurements, on the same course, across cold years and warm years and one shortened swim, gives you something you cannot get in a laboratory. No ethics committee will ever let you design this from scratch.

The questions we keep returning to are the ones that matter on the pier at Eidfjord. What happens to the lungs after a cold swim, and who is at risk of swimming-induced pulmonary oedema. What the blood of a finisher tells us about how the heart has been loaded across a day like this. How core temperature actually behaves in a wetsuited swimmer in cold open water, which is the question that started all of this for me in 2015.

I will not put numbers here, because the data is not ready and I am not going to guess in public. But this is the work that quietly informs every call I make on race morning.

The paper: beyond hypothermia

Now the thing I am most proud of this month.

Together with Laura Leuci, Antonio Messina, Mike Tipton and Luca Carenzo, I have published a narrative review in the Journal of Applied Physiology titled Beyond hypothermia: mechanisms of death, rescue, and prevention in cold water immersion.

It is the paper I have wanted to see written for years, because it takes on a misconception that is still everywhere, including among people who should know better. Cold water does not usually kill you by making you cold.

Here is the number that should stop you. In the United Kingdom, around 55% of accidental open water deaths happen within three metres of safe refuge, and two thirds of the victims are regarded as competent swimmers. You cannot explain that with hypothermia. A competent swimmer three metres from safety does not die of core cooling. Something else got them first, and it got them fast.

The review works through the whole four-stage model of immersion, because the sequence is the point. Here it is.

Stage 1, the cold shock response, 0 to 3 minutes. An involuntary gasp of 2 to 3 litres in the first seconds, then one to three minutes of hyperventilation you cannot easily override. If your airway is under water when the gasp comes, the drowning process has already started. If it is not, the hyperventilation drops your arterial CO2 and reduces cerebral blood flow. Breath hold time falls from around 60 seconds to a few. In the UK, roughly 60% of people who die in cold water die in stage 1 or 2, without ever becoming hypothermic.

Stage 1 is also where autonomic conflict sits. Cold skin drives the sympathetic system hard while facial immersion drives the parasympathetic diving response, and the heart receives both instructions at once. We are careful to call this plausible rather than proven, and the evidence suggests it needs a pre-existing substrate to become lethal. Which brings in the channelopathies. Long QT syndrome affects around 1 in 2,000 people, and studies have found pathogenic or likely pathogenic cardiac channel mutations in roughly a third of unexplained drowning cases. Drowning may sometimes be the first presentation of an inherited arrhythmia syndrome, particularly in children and young adults.

Stage 2, swimming failure, 3 to 30 minutes. As the cold shock subsides, the limbs cool. Peripheral nerve conduction slows in step with tissue temperature, muscle loses rate of force development and peak force, and manual dexterity falls apart once finger skin temperature drops below about 15°C. Tactile sensitivity is largely gone below about 8°C. In near-freezing water you cross those thresholds within minutes, which means you can lose the ability to hold on to a rescue line before your core temperature has moved at all. This is also where swimming-induced pulmonary oedema belongs.

Stage 2 carries a forensic trap worth knowing about. A victim who drowns here may be found with a near-normal core temperature at post-mortem, which invites the conclusion that cold water played no part. It did. And one detail from this section is uncomfortably close to home: analysis of triathlon fatality data shows most deaths occur during the swim, often within the first few hundred metres. That timing fits cold shock, autonomic conflict and SIPE. It does not fit hypothermia or exhaustion.

Stage 3, hypothermia, beyond 30 minutes. Only now does core cooling become the main threat. Shivering peaks between 34 and 30°C and then fails. Consciousness clouds below about 33°C and is usually lost between 30 and 28°C. The Osborn wave appears below 32°C, and the risk of ventricular fibrillation climbs below 28°C.

The famous recoveries are real. People have been resuscitated with good neurological outcome from core temperatures of 13.7°C, and later 11.8°C, after hours of cardiac arrest. But those cases are quoted in the wrong direction all the time. Neither victim was submerged in cold open water, and in both the cooling came before the arrest. In most cold water drowning deaths it is the other way round: the person aspirates, arrests from hypoxia while still relatively warm, and cools afterwards. So the question that matters at the scene is not how cold the patient is. It is which came first, the cold or the hypoxia.

Stage 4, circum-rescue collapse. People die at the moment of rescue, and we have been teaching the wrong reason for it. Afterdrop is real but modest, typically 0.5 to 1.5°C, and is no longer considered the main mechanism. The bigger one is the abrupt loss of hydrostatic pressure. Water squeezes 500 to 700 mL of blood centrally while you are immersed. Lift someone vertically out of it, especially on a helicopter winch, and that squeeze disappears in a cold, volume-depleted body whose vessels can no longer respond. Cardiac output can fall off a cliff. This is the physiological argument behind horizontal extraction, and it is a much stronger one than afterdrop ever was.

One line I would like every emergency clinician to carry with them. Fewer than 10% of drowning cardiac arrests present in a shockable rhythm. So if you find one, that is atypical, and it should make you ask whether a primary cardiac event put the person in the water rather than the other way around.

And the prevention that follows from all of this is almost absurdly simple. Float. The RNLI Float to Live campaign works because cutaneous cold receptors adapt over the first 60 seconds or so. Anyone who can keep their airway clear of the water for 60 to 90 seconds gets their breathing back. Not because they are hardened. Because the physiology settles.

The mats

Part of what has made this summer busy is something I have not written much about here. I have been training Brazilian Jiu-Jitsu for a year and a half now, and I enjoy it more than I expected to.

I have spent twenty years being the person on the pier who knows things. On the mat I am the one getting comprehensively dismantled, several times a week, by people half my age and often half my size. A year and a half in, I am still very much near the bottom of that ladder, and it turns out that is excellent for a person. Learning something hard from the beginning sharpens your thinking in a way that reading does not.

It also hands you a new set of physiological questions, which was not the plan. So a paper by Alberto Labra and Daniel Niño-de-Rivera-García landed at exactly the right moment: a systematic review in Nortis Journal of Sports Sciences on chokes in grappling and mixed martial arts.

What struck me is how familiar the physiology felt. Most sport chokes are not chokes at all in the medical sense. They are vascular strangulations. Compress the carotid arteries and jugular veins, cerebral perfusion pressure falls below what the brain can autoregulate around, generally under 50 mmHg, and consciousness goes in less than ten seconds. Medically it looks far more like syncope than like a head injury. The rear naked choke alone accounts for 49.1% of choke finishes in UFC history, and five techniques account for 89.4% of them.

The comparison with striking is the interesting part. Repetitive head impacts have a well-established link to chronic traumatic encephalopathy. Transient strangulation, so far, does not. More surprising still, elite BJJ athletes show elevated resting global cerebral blood flow, roughly 741 mL per minute against 573 in matched controls, with well-preserved cognition despite an average of more than 3,500 choke exposures across a career. The authors discuss ischemic preconditioning as a possible explanation. A brain that has learned to tolerate brief interruptions in supply.

That is not a licence to be casual. The review is clear that cervical artery dissection and ischemic stroke are documented, sometimes after maneuvers that did not look forceful, and that in one survey 55.7% of BJJ athletes reported symptoms consistent with dissection at some point. Respiratory chokes, applied to the trachea rather than the vessels, risk structural laryngeal injury. The warning signs are the worst headache of your life, focal neurological deficits, speech or visual changes, persistent neck pain, hoarseness or difficulty swallowing.

The practical version for the mats is short. Tap early. Release immediately. And if something feels wrong in your head or your neck afterwards, do not wait it out.

A friend, a wetsuit, and warm water

The last item goes to the opposite end of the thermometer.

John Mercer at the University of Nevada, Las Vegas has published a brief report with Katsiaryna Afanasyeva and colleagues in the International Journal of Exercise Science on core temperature in triathletes swimming in warm open water, with and without a wetsuit. John is a friend, and he has raced Norseman, which means he has personally experienced the exact opposite of the conditions he studied here.

Four triathletes, two 700 m open water swims each, in water between 27.9 and 28.3°C, with core temperature logged every 15 seconds by ingestible pill. They swam faster in the wetsuit. But the change in core temperature was no different between conditions, and nobody came close to hyperthermia.

The finding I liked most is the variability. When they extrapolated each individual’s temperature trend forward to 39°C, the estimated time to reach a hyperthermic state ranged from 19 minutes to 137 minutes. Same water, same distance, same protocol, and a sevenfold spread between people. That is the argument for individual measurement, compressed into one number.

It is four participants and a short swim, and the authors say so plainly. But it is careful work on a question that matters for race rules, and I was pleased to find two of our papers among its references.

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Next: the Skagerrak

The next cold water project is a swim crossing the Skagerrak, from Denmark to Norway. Open water and a long way over. More on that soon. It starts in just a few days. .

So that was a very full summer. A quiet race that we were ready for anyway, a paper arguing that we have been blaming the wrong mechanism for decades, a year and a half of learning to tap early, and a friend measuring core temperature in water warm enough to swim in without a wetsuit.

Four different subjects, one shared lesson. Do not assume the mechanism. Measure it.

A Few Books, If You Want to Read On

A good deal of this issue lives in cold water, so if any of it caught your interest, I have written some short, science-based books you might enjoy.

Cold Water Swimming: A Mini Book is a friendly, short guide to enjoying cold water safely, confidently, and with a big smile. It draws on years at the Norseman Xtreme Triathlon, research with elite military swimmers, and my published work in cold-water physiology. Calm, clear, trustworthy guidance for anyone curious about stepping in.

Get Cold Water Swimming on Gumroad →

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Thanks for reading. If something here resonated, hit me with a reply.

I started writing reports after Norseman many years ago. To evaluate and to learn, for myself and within the team. In 2021 we had a challenging year for our race lead and our safety and medical crew. So I started making blog posts that are available to the public, in addition to my internal reports. They became surprisingly popular. So here is another one, from 2026.

If you have read the last few of these, you know the pattern. In 2023 we shut down Mt. Gausta because of thunderstorms and stopped the race at the 32 km mark, and lightning struck our racetrack in the hour after. In 2025 Fredrik and I stood in the bow of the ferry at 0420 and could not see the water, the kayaks or the mountains, and we were 20 minutes away from sending 252 people into a dark fjord in a complete white out.

This year, none of that. 255 athletes started, the weather behaved, the mountain stayed open, and the day unfolded more or less the way it looks on paper.

A quiet Norseman is a strange thing to write a report about. It is also exactly what we are working for.

The water

As always, I follow the water temperature closely in the days before the race. It changes the whole time, and it varies a lot along the swim track. I measure it several times, at several places. It seems fairly constant that the water at the starting point is about 2°C warmer than at the swim exit in Eidfjord.

On race day the fjord was around 14°C. By Norseman standards that is quite average. Not the 19°C that made it hard to call myself a cold water scientist a few years ago, and a long way from the 9.8°C that once made Jonny Hisdal and me swallow temperature sensors and swim it ourselves before deciding what to do. 14°C is a temperature we know well and are comfortable with.

But I want to be very clear about one thing, because an average year is exactly when people get careless. 14°C is still cold water. The first minute after you jump off that ferry is still the most dangerous minute of the whole race, and it has nothing to do with hypothermia. It is the cold shock response, the gasp and the racing heart, and it does not care that the number looked friendly on the morning briefing. This is why we spray the athletes with cold water on the ferry deck before they jump, and why I keep telling everyone who comes here to get into cold water at home, again and again, in the weeks before they travel. Five or six cold exposures cut that response roughly in half. It remains the single most useful thing an athlete can do to prepare for our swim, in a cold year and in an average one.

The swim went fine. So did the bike. And the valley, the first 25 km of the run where the heat can really bite, sat at around 18°C.

The heat plan we did not need

That 18°C is worth a few words, because we came into this race better prepared for heat than we have ever been.

Ahead of the race I wrote a whole piece about the heat in the valley, as part of the five-part series I published on my Substack in race week, because that stretch out of T2 lies low, is sheltered from the wind, and is run in the middle of the day. It is the part of our course where I think the risk of serious heat illness is highest. So this year we built a proper system for it, with cooling and drink stations along the first 25 km, agreements with local residents to use their garden taps, and hoses with a soft spray so we could cool athletes as they run past.

We rigged the hoses. We added staff. And then the valley gave us 18 degrees.

So the honest answer is that we did not learn very much from it, simply because it never got warm enough to test the system properly. That is not a disappointment. It is a system that is now built, staffed and ready, waiting for the year that it is needed. And that year will come.

The medical picture

People always ask if everything went well. It did.

We saw approximately ten patients through the day. Out of 255 starters, in a race like this one, that is a low number. There were no serious accidents. What we did see was mainly a few cardiac concerns and some minor trauma. Nothing that turned into a big incident.

But there is one pattern in those numbers that I keep noticing, and I want to say it out loud.

A good share of the people we treat at Norseman are not athletes. They are support crew.

Minor injuries, mostly. Nothing dramatic this year. But it is a consistent finding across many years now, and it says something about how this race actually works. The athlete is prepared, tapered, fed and watched over by a whole organisation. The support crew has been awake since three in the morning, is driving a strange road in a strange country, carrying bags up hills, standing around in the weather, and thinking about somebody else all day long. Then they get tired and something small happens.

So my message to next year’s support is the same as always, and now I have numbers behind it. Look after yourselves. Eat, drink and sleep before race day. You cannot take care of your athlete if you are the one we end up treating.

The thing that actually worries me now

If the weather was not our antagonist this year, something else was, and it is the part of this report I most want people to read.

Traffic.

The traffic on our course grows every year, and it is a real challenge. This year we again had several traffic violations. The one I keep coming back to is support cars stopping badly. A car parked in the wrong place on a narrow Norwegian road, at the wrong moment, with tired athletes and other cars coming through, is genuinely dangerous. It is the kind of thing that can turn a quiet race into a very bad day in a couple of seconds.

Two things helped us a lot. We had 13 race marshals on motorbikes, and they are crucial. They see things fast, they move fast, and they are our eyes in places no car can be. And we had police present, including two police motorcycles. Having the police out on the course is extremely helpful, and I am grateful for it.

I will say it plainly to everyone who comes to Norseman with a support car. The way you drive and the way you park is a safety issue for everybody out there. Please take it as seriously as we do.

The team behind it

None of this happens by itself. Our safety and medical organisation this year was around 50 people.

We ran three medical cars following the race, each with a doctor and a paramedic or a nurse, all of them experienced people. In addition we had a paramedic car and stationary doctors at selected points along the course. And along the whole racetrack, our local Red Cross groups were present and on alert all day.

That is what a quiet race actually looks like from the inside. Fifty people spread over 226 kilometres, mostly waiting, ready for a day that never quite came. It is a strange kind of work. When it succeeds, nothing happens.

Our success is not a result of chance. It comes from preparation, from a group of very committed people, and from evaluating and improving this event year after year.

Research

We also did quite a bit of research again this year, with blood sampling and lung function testing on our athletes. This continues the work our research group has built up at Norseman over many years, and I look forward to sharing more when the data is ready.

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And finally

You can’t fight nature. Usually I write that sentence after nature has beaten us. This year I get to write it the other way around. Nature was kind, and we were ready anyway.

That is the whole point of this work. You prepare for the year with the thunderstorm, the white out and the heat, and then you accept it gracefully when you get a beautiful day instead.

If you want the physiology behind all of this, I wrote a five-part series on my Substack, Mixed Physiology, in the week before the race. It covers the first minute in the cold water, the afterdrop that catches athletes out on the bike, SIPE and the lungs, the heat in the valley, and what our research finds in the blood and the heart of a finisher. You can read the whole series on my Substack blog.

Thank you so much for taking the time to read. If you have any suggestions on how we can improve our safety and medical work, please share them with me in the comments or in a DM. I always want to hear it.

I am very happy to listen and adapt!

Jørgen Melau Safety and Medical Director, Norseman Xtreme Triathlon

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

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Part five of a short series for this year’s Norseman athletes. You will cross the line thinking the hard part is over. Your body has a different opinion. Here is what our research finds in the blood of a finisher, and why the hours after matter more than people think.

Every part of this series has carried the same quiet message. The danger is rarely where you expect it. The first minute of the swim, not the middle. The cold that catches you out on the bike, not in the fjord. The lungs. The heat down in the valley. And now the last one, the part I probably care about the most as Safety Director.

The finish line is not the finish.

I have said this in every race brief for years. Many of our medical incidents happen after the athlete has crossed the line, not during the race. An athlete who looked strong all day can fold in the half hour after they stop. And when we take blood from our finishers, which we have done now for many years together with Maria Mathiassen, Christoffer Nyborg, Martin Bonnevie-Svendsen and the rest of our research group, the numbers tell you why. A body that has just finished Norseman is not a body at rest. It is a body in the middle of an enormous repair job.

Let me show you what we actually find.

The muscles have paid a price

The first thing you see is muscle breakdown. We measure an enzyme called creatine kinase, CK, that leaks out of muscle when the muscle is damaged. In an ordinary person a normal value is under about 200. In our Norseman finishers the median was around 2450, more than ten times the top of the normal range, and some athletes are far higher than that. That is the physical cost of 226 kilometres and 5200 metres of climbing, written straight into the blood.

This matters for a very practical reason. All that broken down muscle has to be cleared by the kidneys, and the kidneys need fluid to do it. It is one more reason we push you so hard on drinking after the race, and it is why very dark urine, the colour of cola, or not being able to pass water at all, is something you must tell our medical team about. That is not a thing to sleep on.

The body thinks it is under attack

The next thing we see is inflammation. The white blood cell count jumps to levels we would normally connect with fighting an infection. The day after the race a second inflammation marker, CRP, climbs high as well. Nobody has an infection. The body is simply reacting to the damage of the race as if it were a wound, which in a way it is.

The heart, and the marker that looks like a heart attack

This is the part that gets peoples attention, and it should, but in the right way.

When somebody arrives in an emergency department with chest pain, one of the very first things measured is cardiac troponin. It is the marker of heart muscle damage, the blood test we use all over the world to diagnose a heart attack. In our most recent study, of 93 finishers, troponin rose sharply after the race. Troponin I went from a median of 3 up to around 69, more than twenty times higher, and it was still raised the next day. We also see NT-proBNP, a marker of a heart that has been working and stretching hard, climb steeply at the line.

We have also gone one step further and put an ultrasound probe on the heart itself, before the race, within a couple of hours of the finish, and then again five to ten days later. Right after the race the picture matched the blood. The hearts pumping function was clearly reduced. The squeeze we call strain, the ejection fraction, the amount of work the muscle was doing, all measurably down compared to the morning. The heart was holding its total output up mostly by beating faster, not by contracting harder, and it was doing that even though the blood pressure it had to pump against had actually dropped. In plain words, the heart muscle itself was genuinely tired, not just taking an easier ride. We sometimes call this cardiac fatigue. But here is the part I most want you to hold on to. When we scanned the same hearts again five to ten days later, every one of those measures was back to baseline. The fatigue was real, and it was temporary.

Now, read this the right way. It does not mean these athletes had heart attacks. Raised troponin after long endurance exercise is common, it is usually temporary, and in most people it settles over the following days, which is exactly what we saw. What its long term meaning is, we honestly do not fully know yet, and that is one of the things we are still studying. But here is the thing you need to understand. A perfectly healthy Norseman finisher can walk into a hospital with a troponin level that, out of context, looks like a heart attack. If the doctor treating them does not know what a race like this does to the body, that athlete can end up in a frightening and completely unnecessary cardiac workup. That is a big part of why we do this research in the first place.

The blood vessels, quietly changed

There is one more finding, quieter than the others, but the one I find most interesting.

Your blood vessels keep themselves open and healthy using a molecule called nitric oxide, which the lining of the vessel makes from an amino acid called L-arginine. After Norseman we see L-arginine drop, and we see two related molecules, ADMA and SDMA, shift in the direction that makes nitric oxide harder to produce. In plain words, the machinery that keeps your arteries relaxed and open is running down for a while after the race. And when we followed these markers out further, some of them were still not back to normal a full week later. In other groups of people, these same shifts are known as risk markers for vascular disease. In healthy athletes after a race we believe they are transient, but they tell you something simple and true. Your body is still deep in recovery long after you have showered and pulled on dry clothes.

Why I am telling you all this

I am not telling you this to scare you off the start line. Norseman is safe enough, these changes are, as far as we can tell, the normal price of an extraordinary day, and they settle. I am telling you because it explains the single most useful piece of after race advice I have.

Take the hours after the finish seriously.

When you cross that line your muscles are broken down, your heart markers are sky high, you are inflamed, dehydrated and empty, and your blood pressure control is not what it was in the morning. This is exactly the moment when people make mistakes. So do not lie straight down and fall asleep. Keep moving gently, get warm, and above all eat and drink, properly and for real, before you rest. And if anything feels wrong, chest tightness, real breathlessness, confusion, that dark urine I mentioned, then you come and find us. We would much rather see you and send you away smiling.

A word to the support crew, one more time

This is where you come in, for the last time in this series. Most of what I have just described happens in your care, not ours. It happens out at the cabins and the hotels. You are the one who has to make sure your athlete eats, drinks, gets warm and does not simply collapse into bed. Which is exactly why, as I keep saying, you have to look after yourself across this whole long day as well, so that you still have something left to give in the quiet hours after the finish, when it matters the most.

The end that is really a beginning

So that is the whole arc of a Norseman day, from the first shock of the cold fjord to the strange, humming, half-broken state your body is in at the top. The line up on Gaustatoppen feels like the end of the story. For your physiology it is the start of a new one, that plays out over the next hours and days while you sleep and eat and slowly put yourself back together.

Respect that part too. And then enjoy every second of it, because there is nothing else quite like this race, and nothing quite like how it feels to have finished it.

That is the series. Thank you for reading along. Now come to Eidfjord, and let us do this properly.

See you there.

Jørgen

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

They should.

Because here is a strange thing about one of the world’s most extreme triathlons. Many of the medical situations we deal with the whole day do not happen in the cold fjord at all. They happen many hours later, in the sun, out on the run. The same athlete that jumped off the ferry shivering in the morning can be badly overheated by the afternoon. A race everybody think of as cold is, more often than people expect, beaten by the heat.

Where the heat lives

The warm stretch is no mystery to us. It is the first 25 kilometres of the marathon, from T2 in Austbygde and inn along the valley, and then the beginning of the long climb we started to call Zombie Hill many years ago.

That stretch is a heat trap, simply because of the geography. It lies low, it is often sheltered from any wind, and you run it in the middle of the day when the temperature is at its highest. Put many hours of hard effort on top of that, add an athlete who has not been drinking enough, and you have the perfect recipe for trouble. In our own risk planning, heat illness on this section is one of the most likely medical events of the whole race. At this years Crew Race, our own dress rehearsal, the valley pushed past 30 degrees. The same people who started the day shivering were now trying to get rid of heat as fast as their skin could manage.

What heat actually does to you

The physiology is worth understanding, because it explains everything else.

Your muscles produces heat. Running makes a lot of heat, and your body gets rid of most of it in one single way, by evaporating sweat off your skin. That works fine, until two things go wrong at the same time. If the air is hot, and if you are dehydrated and can not afford to keep sweating freely, the heat does not leave fast enough, and your core temperature starts to climb.

A rising core temperature during hard exercise is normal, up to a point. Triathletes run at 39 degrees all the time, sometimes touching 40 and more. But when the core temperature get to warm and the brain starts to be affected, now you are into heat stroke, and heat stroke is a real emergency. It is one of the very few things that can kill a young, fit and healthy athlete within an hour. And here is the tricky part, an athlete with exertional heat stroke is often still sweating. That is exactly what makes it so easy to miss.

There is one more trap in this. Just like your body keeps cooling after you come out of cold water, it keeps heating after you stop running. I have swallowed a temperature sensor several times before a hard training myself, and watched my own core temperature keep rising for about ten minutes after I had stopped, because the heat I already made had to go somewhere. This is also something we have seen in several studies. So an athlete who stumbles to a halt in the valley is not safe just because he has stopped. The heat is still building inside him.

What the Crew Race showed us

So, we do not only watch this happen. We measure it.

At this years Crew Race I wired the crew up with muscle oxygen sensors, expecting them to tell me about effort. One of the signals, the amount of blood pooled in the working muscle, did something I did not expect at all. It did not follow how hard they were working. It followed the thermometer. As the run heated up into the thirties, the blood pooling in the muscle climbed steeply, because the body was busy doing its other job, opening the vessels near the skin and turning the muscle half into a radiator to get rid of heat. And at the same time their pace fell away. You could actually see it in the data, the body quietly giving up performance just to stay cool. The heat was winning, and the sensors caught it.

What we do about it, and why you must use it

Because we know exactly where the heat bites, we prepare for it.

When the forecast is warm, we set up a line of manned cooling and drink stations along those first 25 kilometres. Local people let us use their garden taps, and our crew rig up garden hoses with a soft, wide spray. You run through, we spray your head, neck and torso, and we fill your bottle. The cooling from a spray is real but it is short, this is why we have a whole string of stations and not just one. Water on the skin pulls the heat straight out of you, and keeps pulling as it evaporates.

So here is my ask to you. Use them. All of them. Even when you feel fine, and especially when you feel fine. Let us spray you, drink at every station, and do not try to save a few minutes by running past the cooling. The athlete who runs the valley proud and dry is very often the one we meet again later, in the medical tent. Cooling and drinking is not weakness. It is how you get to the mountain with something still left in you.

And a word about your own preparation. Drink before you get thirsty, and take electrolytes, not only plain water. Dress light and airy on the run. And run the valley by the temperature, not by your watch.

For the support crew

As always, the support crew is vital. You are our extra eyes out there, and in the valley you might see the first signs before we do.

You can also cool your athlete yourself, and you should. Keep a small spray or mist flask in the car, and every time you meet your runner, offer to spray the head, neck and shoulders if they want it. You do not have to use our stations. A few seconds of water on the skin in between keeps the cooling topped up, and on a hot day this makes a real difference over 25 kilometres.

Watch your athlete for the early warnings of heat illness:

• Confusion, unsteadiness, slurred speech, or behaviour that is out of character

• Nausea, a pounding headache, dizziness, or a stumbling walk

• An athlete who stops sweating, goes strangely flat and sleepy, or collapses

If you see any of this, do not wait, and do not push your athlete on. Start cooling straight away, before anything else. Get water onto them at once, over the head, neck and torso, and keep it coming. The water does not have to be ice cold to work. For much of the run you are right beside a huge lake, so use it. Lake water, bottle water, whatever is nearest and wettest, poured or sprayed over the skin, it pulls the heat straight out of the body. Any water beats standing around waiting for the perfect cold water. While you cool them, call us. Or the emergency service, if it is really bad (national emergency number is 113). Our principle on the course is simple, and I want you to remember it. Cool first, everything else second.

Both ends of the thermometer

So this is the whole shape of a Norseman day. You start it fighting the cold, shivering off a ferry into a dark fjord. And you can finish it fighting the exact opposite, overheating in a still, hot valley with a whole mountain still to climb. One body, one day, both ends of the thermometer. The athletes who respect both of them are the ones I get to meet up at the summit.

There is more Norseman physiology and research still to come. But this one mattered enough to say it plainly. Do not let the cold reputation fool you. Prepare for the heat too.

See you in Eidfjord. And enjoy it, this is a day you will remember for the rest of your life.

Jørgen

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This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

In part one I wrote about the first minute in the fjord. In part two, the cold that keeps chasing you out onto the bike. This time I want to talk about the lungs.

Most of what stops an athlete at Norseman is ordinary. Cold, fatigue, cramp, a stomach that gives up. But there is one problem that is different, because it can arrive in a young, fit, completely healthy body with almost no warning, and because pushing through it is exactly the wrong thing to do. We call it SIPE, swimming induced pulmonary edema. I have watched for it at this race for years, and our research team has published on it, so let me tell you what it is and what to do about it.

What SIPE actually is

Edema means fluid where it should not be. In SIPE, that fluid is in your lungs.

When you swim hard, especially in cold water and a tight wetsuit, fluid can leak from the small blood vessels of the lung, the pulmonary capillaries, into the alveoli, the tiny air sacs where your blood is meant to collect oxygen. Part of the lung fills with fluid instead of air. The result is exactly what you would expect if a piece of your lung stopped being available for breathing. You become short of breath far beyond what the effort should cause, you cough, and in worse cases you cough up frothy, pinkish sputum. That pink is a little blood from the leaking lung.

SIPE was first described mostly in military combat divers. We have seen a fair share of it there. But as triathlon has grown, more and more cases turn up in the triathlon medical community, and I suspect it matters in swimruns and open water swimming too. Vansbrosimningen in Sweden has several cases every year. It is still relatively rare. But it is real, it favours exactly the fit, hard-driving athletes who line up at races like ours, and left untreated it can be fatal.

What our own athletes taught us

Here is the part that made us publish.

We put together a case series of three Norseman athletes who developed SIPE, and it appeared in the journal Sports. What was striking was not that they got SIPE. It was when. All three presented not in the water, and not just after the swim, but during the last part of the bike phase, hours into the race. Shortness of breath, chest tightness, coughing up pink sputum, long after the fjord was behind them.

Stranger still, all three described the same pattern. Their breathing improved on the first big climb of the bike, and worsened on the descents. All three were treated on the spot by our medical team, none could continue, and all were sent on to a medical centre or hospital. And all three recovered well and have raced similar events since.

That timing is unusual. SIPE is normally a creature of the swim, found during it or right after. Seeing it arrive so late, and seeing it track with the uphills and downhills, is exactly the kind of thing worth writing down and sharing with researchers elsewhere. We do not fully understand it. Publishing what we saw is how the field slowly closes in on an answer.

The bigger picture: what the race does to everyone’s lungs

SIPE is the dramatic end of the story. But it turns out that the lungs of ordinary finishers, the ones who never cough up anything pink, are working hard and paying a price too.

This is where I want to credit Professor Trine Stensrud, from the Department of Sports Medicine at the Norwegian School of Sport Sciences. She has been an important part of our Norseman research group and has led the lung physiology work here. In one of our studies she measured the lung function and blood oxygen of finishers before and after the race, and the numbers are striking. Nearly half of them, 46 percent, showed exercise induced bronchoconstriction, a measurable narrowing of the airways, right after the finish. About two thirds, 65 percent, showed exercise induced arterial hypoxemia, a real drop in the oxygen saturation of the blood. For some athletes the airway narrowing was still there the following day.

These are not the same thing as SIPE. Bronchoconstriction is the airways tightening, not fluid in the air sacs. But they carry the same message, and it is why I am giving the lungs a whole issue. A long, cold, hard day like Norseman asks an enormous amount of your respiratory system, far more than most athletes realise, and it does so in nearly everyone, not only the few who end up in our medical tent. SIPE is the sharp edge of a much broader pattern of respiratory stress that Trine’s work has mapped out for us.

Why it happens, as far as we know

The honest truth is that we do not know the whole story. But the leading idea goes like this.

When you are immersed, especially in cold water, blood is pushed out of your arms and legs and pools centrally, in your chest. A tight wetsuit squeezes from the outside and adds to it. Cold makes your vessels clamp down and drives blood inward as well. Now you have more blood crowded into the vessels around the lungs, the pressure in those delicate capillaries climbs, and fluid is forced across into the air spaces. Immersion, cold, tight suit, hard effort. It is a kind of perfect storm, and the fit athlete swimming flat out in a cold fjord is standing right in the middle of it.

Risk factors, with a caution

There are some things that seem to raise the risk, and I want to give them to you honestly, because none of them are settled science. They are tendencies we and others have noticed, not a verdict.

The clearest association is with high blood pressure. Beyond that, the list of possible risk factors includes diabetes, fish oil supplements, long course triathlons, a wetsuit that is too tight, and female sex. Treat that as a list to be aware of, not a diagnosis. If you have high blood pressure in particular, it is worth a conversation with your doctor before a race like this.

The other thing to know is that SIPE tends to recur under the same conditions. If it has happened to you once, it can happen again.

What I need you to do

This is the part that matters most, so I will keep it plain.

If your breathing becomes far worse than your effort can explain, if you are coughing for no good reason, or if you cough up anything pink or frothy, take it seriously at once. Do not tell yourself you are just unfit or having a bad day. Stop. If you are still in the water, get out immediately and keep warm. Then get to us, to our medical team, or to any health care professional. SIPE usually settles within about a day, on its own or with medicine, but it can be dangerous, and it is never worth racing through.

One more thing, for those of you swimming or training with a partner. Mild SIPE is easy to wave away as your buddy just being a little out of shape. If someone next to you is breathless for no reason that makes sense, think of this, and get them looked at.

For the medics reading

Some of you reading this are clinicians, so a few quick words. Assess the athlete as you normally would, but reach for a pulse oximeter early, because a low reading is one of your best first clues. Give oxygen if you have it. Listen for crackles at the lung bases. If you are an advanced provider carrying portable ultrasound, look for vertical B-lines, the wet lung sign. And if you have seen a case of your own, you are welcome to get in touch. The more cases we can compare, the closer we get.

Where this goes

That is three parts of the same story now. The first minute, the cold that follows you onto the bike, and the lungs. Different systems, one theme. The water asks more of your body than it looks like it does, and the smart athlete respects that. There is more Norseman physiology and research still to come over the next few days.

If you want the full case series, it is open access in the journal Sports.

https://www.mdpi.com/2075-4663/7/6/137

See you in Eidfjord.

Jørgen

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

A Book, If You Want to Read On

If any of it caught your interest, I have written some short, science-based book you might enjoy.

Cold Water Swimming: A Mini Book is a friendly, short guide to enjoying cold water safely, confidently, and with a big smile. It draws on years at the Norseman Xtreme Triathlon, research with elite military swimmers, and my published work in cold-water physiology. Calm, clear, trustworthy guidance for anyone curious about stepping in.

Get Cold Water Swimming on Gumroad →

Photo by Morten Sivertsen

When you come out of the fjord at Norseman, the first two people you meet are me and our race director, Fredrik.

You will not climb a ladder or haul yourself onto a pier. The swim finishes on a small beach, and you wade the last few strokes and steps out of the water and up onto the sand, toward T1 and your waiting support crew. Right there at the waterline, Fredrik and I are standing. We greet every single athlete as they come out. To you it probably looks like a welcome, two familiar faces and a few words after a hard swim, and it is that.

But it is also the first real medical assessment of your race, and it is one of the most important few seconds of the whole day.

To understand why we care so much about that exact moment, you have to know something that surprises most people. The swim does not stop being dangerous when you reach the beach. For many athletes, the coldest their body will get all day is not in the water at all. It comes later, out on the bike, around twenty minutes after they left the fjord.

That effect has a name. Afterdrop.

Why you keep cooling after you stop

Afterdrop is the continued fall of core temperature after you leave the cold. It sounds like it should be impossible. You are out of the water, usually into warmer air, so surely you can only warm up from here. But two things keep pulling heat out of your core after you exit.

The first is simple physics. During the swim your body protects its core by clamping down the blood flow to your skin and limbs, building a cold outer shell around a warm middle. That shell does not vanish when you get out. Heat keeps flowing, by plain conduction, from the warm core outward into the cold muscle and fat and skin, and it goes on doing that until the gradient evens out. The core pays to warm the shell.

The second is circulation, and this is the one that matters most in a triathlon. In the water you are working, and moving muscles keep some blood flowing through the cold limbs. The moment you stop swimming, wade out, and stand still while your support crew works on you, those vessels begin to open again. Cold, stagnant blood that was sitting in your arms and legs washes back toward the middle of you. That returning blood is colder than your core, and when it arrives, core temperature drops further. Stopping is part of the mechanism. The athlete who exits and stands still cools more than the one who keeps the engine running.

What our own data shows

This is not theory to me. It is something we have measured at Norseman.

In our studies, using ingestible temperature sensors that log core temperature continuously from inside the gut, we have followed athletes right through the swim and out the other side. We have done this on more than 100 athletes during the years. The sensors show it plainly. Core temperature kept falling after the athletes had already left the water, and on average it reached its lowest point about twenty minutes after they came out.

Twenty minutes!

Think about where you are twenty minutes after the swim at Norseman. You are not on the beach, and you are not standing in T1. You are already well out on the bike, climbing away from Eidfjord, feeling good and picking up speed, while somewhere underneath all of that your core temperature is quietly bottoming out. The swim was over. The cooling was not.

That finding changed how I think about the swim exit. The beach is not the finish line of the cold. It is the start of the part nobody watches.

Back to the beach

So now you understand what Fredrik and I are really doing standing on that sand.

As you come up out of the water and past us, we are watching every single one of you. Not casually. In those few seconds we are reading a lot. Who is moving well and who is not. Who is clear-eyed and who looks confused. Who is shivering hard, who is coughing or fighting for breath in a way that worries me, who simply looks too cold. It is the earliest point at which we can catch an athlete heading for trouble, whether that is a body still cooling toward afterdrop or a set of lungs that did not like the swim.

Most of you we send on with a smile, and that is the whole point. A quick, trained look at the waterline lets us find the few who need us before afterdrop and fatigue make things worse further up the road. It is a welcome and it is a checkpoint at the same time, and after twenty years I would not give up those few seconds with each of you for anything.

How to handle T1

So treat T1 as a cold problem, because for your body that is what it is.

Plan it for a cold, clumsy version of yourself. Your fingers will not work the way they do at home. Zips, buckles, gels, and helmet straps all get harder. Lay everything out so it is simple, and rehearse it with your support crew until it needs no thinking.

This is where a good support crew earns the trip.

Be your athlete’s hands, keep them calm, have the warm clothes ready, and get them moving.

And keep moving is the real instruction. Do not sit down and settle in. The bike is your best heater, so get onto it and let the work of pedalling turn your own muscles back into a furnace. Dress for the cold you feel now, not the warmth you hope for later, because the first part of the ride up onto the mountain is exposed and cold, and because your core is still falling toward its coldest point while you ride. That lowest moment arrives out on the road, not in transition, so the warm layer you put on in T1 is doing its most important work twenty minutes after you leave it. Get some warm fluid and a little food in early. Expect to shiver, and do not panic about it. Shivering is your body doing its job.

One honest warning. If an athlete comes out of the water confused, unable to function, slurring, or has stopped shivering while still clearly cold, that is not ordinary afterdrop and it is not for the support crew to manage alone. That is when you find one of us. That is what Fredrik and I are on the beach for.

More to come

This is only one piece of what we see and measure at Norseman. Over the next few days I will keep going, with more of the physiology and the research that comes out of this race. There is a great deal of it, and much of it started right there on the beach, with a temperature sensor in an athlete and a question we could not answer any other way.

See you in Eidfjord.

Jørgen

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

A Book, If You Want to Read On

If any of it caught your interest, I have written some short, science-based book you might enjoy.

Cold Water Swimming: A Mini Book is a friendly, short guide to enjoying cold water safely, confidently, and with a big smile. It draws on years at the Norseman Xtreme Triathlon, research with elite military swimmers, and my published work in cold-water physiology. Calm, clear, trustworthy guidance for anyone curious about stepping in.

Get Cold Water Swimming on Gumroad →

Every July, my inbox fills up.

The messages come from all over the world, and underneath the different words they ask the same thing. The water. What about the water. How do I prepare for jumping four meters off a ferry in the dark into a Norwegian fjord and swimming 3.8 km through it. I have been the Safety Director at the Norseman Xtreme Triathlon since 2005, and I did my PhD on exactly this, on what cold water does to the core temperature of triathletes swimming it. So let me answer the question properly, for everyone racing this year, in one place.

First, the reassuring part. In more than twenty years and thousands of swimmers, the fjord is not where we lose people. The water is survivable, the swim is survivable, and if you respect it and prepare for it, you will most likely have one of the best swims of your life. But respect is the operative word. The cold is not something to out-tough. It is something to understand.

What the water actually does to you

There are two separate problems in cold water, and people mix them up all the time.

The first problem hits in the first minute. It is the cold shock response, and it has nothing to do with getting cold. It is your skin, not your core, reacting to the sudden drop in temperature. You gasp, and that first gasp can pull in two to three liters of air in a single second. Your breathing rate jumps. Your heart rate spikes. And underneath it, cold on the face can trigger a second, opposite reflex that tells the heart to slow down at the very moment the shock is telling it to speed up. In a few unlucky people, including people with perfectly healthy hearts, that collision is what actually kills in cold water, not hypothermia. If your face is in the water during that first gasp, you can also inhale it. This is the genuinely dangerous window of the whole swim, and it is over in about a minute. Almost nobody gets hypothermic in the first minute. But the first minute is where the trouble is, which is why the entire Norseman start is built around it. I will come back to that.

The second problem is the slow one, the one my PhD was actually about. Your core temperature falls, but it falls slowly, and in a good wetsuit it falls a lot more slowly than people fear. Our data on Norseman athletes showed that a wetsuited swimmer in roughly 10°C water does not plunge into hypothermia over the swim distance. The body defends its core well. The cold you feel on your skin is real, but it is not the same as your core actually dropping. Knowing that difference is half of staying calm out there.

So the two things to prepare are almost opposite. Blunt the cold shock so the first minute does not own you. And insulate the core so the long swim stays comfortable.

The single most useful thing you can do now

Adapt to the cold. It is the one intervention that changes everything, and it cannot be bought or faked in the last week.

The cold shock response is trainable, and it trains fast. A handful of cold water immersions, even short ones, measurably blunts the gasp and the heart rate spike. The research here is clear and it is one of the most reliable effects in all of cold physiology. Somewhere between five and ten cold exposures and the response is roughly halved. That is the difference between a controlled first minute and a panicked one.

You do not need a fjord to do this. A cold shower, a cold bath, the sea, a lake, whatever cold water you can get into safely and repeatedly in the weeks before you travel. Get your face wet, because the face is where a lot of the shock is triggered. Practise slowing your breathing while the cold is telling you to gasp. Never do this alone, and never do it anywhere you cannot easily get out. But do it. If you take one thing from this whole piece, it is this paragraph.

Gear, and the rule you already know

You know this rule because I say it every year. Do not try anything new on race day.

That applies to the swim as much as the nutrition. Your wetsuit, your neoprene cap, whether you wear a second cap, gloves, socks, a swim skin underneath, all of it should be tested in cold water before you get to Eidfjord. Not tested in a warm pool. Tested in cold, open water, ideally more than once. A wetsuit that felt fine in September at home can feel different in a cold fjord at dawn with adrenaline running. Find that out at home, not at the start.

A well fitting wetsuit is the biggest single piece of insulation you have, so it has to fit. Too loose and it flushes cold water through on every stroke, which defeats the point. Too tight around the chest and neck and you add to a breathing problem I will come to in a moment. Neoprene caps and gloves are allowed within the race rules and they help, particularly for the hands and head, which is where a lot of people feel the cold most. But test them, because they change your feel for the water.

Race morning: the ferry, the spray, and the jump

Start with the obvious thing people still get wrong. Get warm before you get cold. The ferry leaves the pier at Eidfjord in the dark, around four in the morning, and the car deck is cold. A raised core temperature going in buys you margin, so stay dressed until late, move, keep the blood warm, and do not spend an hour shivering in a wetsuit before we have even left the pier.

Now the part that matters most. The Norseman start is, on paper, close to the worst possible cold water entry I could design. Dark, cold, a four meter jump, 250 people going at once, adrenaline at the ceiling. That is exactly why we spray you with cold water on the deck before you jump. It is not theatre and it is not a wake up ritual. It is the most useful minute of safety we can give you. Standing on deck, the cold hits your face and neck, the gasp comes, your breathing quickens, and then within twenty or thirty seconds it settles. We have just fired your cold shock response once, in a safe place, while you are still standing on a boat. The next hit, when you actually go into the fjord a minute later, is much smaller. So when we spray you, lean into it. Get your face and neck properly wet. Let that first shock happen on deck, not in the water.

On any other cold water, my advice is always the same: do not jump, walk in, and splash your face first. At Norseman you cannot walk in, so the deck spray is your walk in. And when you do jump, the one thing I really need you to avoid is going in face first while holding your breath. Cold on the face plus a breath hold plus the shock of entry is the worst combination I know of for the heart. Go in feet first, let yourself surface, and expect the gasp. It is coming and it is normal. Get your breathing back under control before you ask anything of yourself, and only then start to build into the swim. Those first calm strokes cost you almost nothing on a swim of an hour or more, and they are the cheapest safety insurance in the sport.

If you want the full physiology of why that first minute is the dangerous one, and why a gasp reflex and a diving reflex arriving together can stop a healthy heart, I wrote it up separately in The First Sixty Seconds.

The one thing I need you to know about your breathing

There is a condition we study closely at Norseman called swimming induced pulmonary edema, SIPE. It is fluid building up in the lungs during a swim, and cold water, hard effort, and an overly tight wetsuit all raise the risk. It is not rare in races like this and it is one of the things my medical team watches for most carefully.

You do not need to fear it, but you do need to recognize it. If you find yourself unexpectedly short of breath in the water, coughing, wheezing, or bringing up frothy or pink tinged sputum, that is not you being unfit and it is not something to swim through. Roll onto your back, signal, and get to a kayak or boat. Raise your arm. Our people are there for exactly this, all along the swim, and there is no medal worth ignoring those symptoms for. Loosening the wetsuit around the neck and chest and not swimming beyond your control both reduce the risk in the first place.

When you come out

The swim is not over when you exit the water. Your core temperature can keep falling for a while after you get out, as cold blood from the limbs returns to the middle. We call it afterdrop, and it is why T1 at Norseman can feel colder than the swim did. Plan your transition for a cold, clumsy body. Warm clothes for the first part of the bike, a plan your support crew has rehearsed, fingers that will not work zips the way they usually do. Get moving, generate heat, and let the bike warm you back up.

None of this is meant to frighten you. The opposite. The fjord at dawn is one of the most beautiful things you will ever swim through, and the vast majority of you will love it. Prepare for the cold honestly, respect the first minute, get in cold water before you come, and you will be ready.

See you on the pier.

Jørgen

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

A Few Books, If You Want to Read On

A good deal of this issue lives in cold water, so if any of it caught your interest, I have written some short, science-based books you might enjoy.

Cold Water Swimming: A Mini Book is a friendly, short guide to enjoying cold water safely, confidently, and with a big smile. It draws on years at the Norseman Xtreme Triathlon, research with elite military swimmers, and my published work in cold-water physiology. Calm, clear, trustworthy guidance for anyone curious about stepping in.

Get Cold Water Swimming on Gumroad →

Then the marathon starts and the problem flips. The first 25 km run through the valley, and the valley is usually hot. By the time the athletes reach the foot of the long climb we named Zombie Hill years ago, the grind up toward Gaustatoppen, a lot of them are already overcooked. Not cold. Overheated, walking as often as running, and the name suits the faces. At this year’s Crew Race the valley sat above 30°C. The same athletes who started the day shivering in the fjord were now shedding heat as fast as their skin could manage.

What an overheating body needs is simple, and it is close to the opposite of what most people reach for. Not a chair and a cold drink. Water onto the skin and around it, as cold as we can make it, over as much surface as possible, and fast. Cool first. Everything else second.

That gap, between what feels right and what actually moves heat, is the subject of this issue. When it comes to a hot body, intuition is a poor thermodynamicist. You are reading this as clinicians and medics, so let me skip the throat clearing and go to the physics, because the rest falls out of it.

The only lever that really matters in the heat

A body exchanges heat with the world in four ways: radiation, convection, conduction, and evaporation. On a cool day the first three do most of the work for free. On a hot day they quietly betray you. As air and surface temperatures climb toward skin temperature, the gradient that lets you dump heat by radiation and convection shrinks, and once ambient temperature exceeds skin temperature those routes reverse and start delivering heat into you.

That leaves evaporation. Every gram of sweat that evaporates carries off roughly 0.6 kcal, about 2.4 kJ, of heat. This is the dominant lever in the heat, and it is worth saying plainly to a clinical audience because it reframes almost every piece of summer advice: sweat that drips off the chin does nothing. Only sweat that turns to vapour cools. The body also drives heat to the surface by opening skin blood flow, and in the glabrous skin of the palms, soles, and face, the arteriovenous anastomoses act as purpose built radiators, shunting warm blood straight to the surface. Hold those two facts, evaporation and surface blood flow, and the rest of this issue is really just applied bookkeeping.

The fastest way to cool a hot human

When a body is genuinely overheating, the single most effective intervention is cold water immersion. It is the standard of care for exertional heat stroke for a reason: water pulls heat out of skin far faster than air, and immersion recruits an enormous surface area at once. Cooling rates comfortably beat 0.15°C per minute and can run quicker with cold, stirred water, which is why the field mantra is cool first, transport second. Lowering core temperature below roughly 39°C within the first half hour is what changes outcomes, and that clock starts at collapse, not at the hospital door.

When a tub is not available, you build the same effect out of parts, in rough order of power. Cold water over the skin with air moving across it. Ice or cold packs to the neck, face, and those glabrous radiators at the palms and soles. Cold fluid or ice slurry taken internally, which cools from the inside and buys you thermal headroom. None of these individually matches immersion, but stacked together they are a serviceable substitute. The hierarchy is the useful part to carry: surface water and airflow first, targeted cold to high flow skin next, internal cooling alongside.

Ice water will not put you into shock

Every summer the same warning recirculates on social media: drink ice water when you are overheated and you can send your body into shock. It makes a good cautionary tale. It is, for practical purposes, a myth. When people do faint after cold water on a hot day, the culprit is almost always what was already going wrong, dehydration, heat exhaustion, an underlying condition, rather than the temperature of the drink itself. In healthy people the genuine downsides are minor and familiar: gulp a large volume of very cold water very fast and you may earn some gastric discomfort or a bout of brain freeze. Sip rather than chug and even that goes away.

There is one nuance worth keeping in the back of your mind, because it connects to the next section. Cold in the mouth and stomach slightly suppresses the sweat response. In dry heat, where evaporation is doing the heavy lifting, that is a small mark against a very cold drink. In practice the direct heat sink of the cold fluid usually wins, which is exactly why ice slurry ingestion is an evidence based cooling strategy rather than a hazard. The myth has it backwards. Cold water is mostly a tool, not a threat.

The paradox worth knowing: a hot drink can cool you

Here is the one that makes people at dinner put their glass down. Under the right conditions, a hot drink lowers your heat storage more than a cold one.

The mechanism is elegant. Thermoreceptors in the mouth and, more importantly, in the abdomen sense the warm bolus and report a larger thermal load than the drink actually delivers. The sudomotor response overshoots. You sweat out considerably more than the modest heat the drink added. If that extra sweat evaporates, the books close in the negative and you end up slightly cooler than you started. Bain and Jay showed exactly this in the laboratory with hot versus cold fluids during exercise.

But read the condition again, because it is doing all the work: if the extra sweat evaporates. Put the same person in humid air, or under clothing that traps moisture, and the bonus sweat simply runs off or sits on the skin. Now you have paid the heat cost of the drink and collected none of the cooling. So the hot drink trick is a real, measurable effect in dry heat with exposed skin, and a bad idea in a sauna or under a raincoat. It is less a life hack than a clean demonstration of the principle that evaporation, not the temperature of what you swallow, is what decides the outcome.

Two smaller puzzles: sleep and why some of us cope better

The same physics explains why tropical nights are miserable. Sleep onset depends on a fall in core temperature of roughly half a degree to a degree, achieved by dumping heat through the skin of the hands and feet. A hot bedroom blocks that fall and fragments sleep, cutting into slow wave and REM. The counterintuitive fix, well supported in the literature, is a warm, not cold, shower an hour or two before bed. It floods the distal skin with blood, and the enhanced heat loss that follows drops core temperature and speeds sleep onset. Beyond that it is unglamorous: a cool room around 16 to 19°C, moving air, light bedding, feet out from under the duvet.

As for why some people wilt in heat while others barely notice it, most of the variance is not mysterious. Acclimatization is the big, trainable one: ten to fourteen days of heat exposure expands plasma volume, lowers the sweating threshold, raises sweat output, and drops both heart rate and core temperature at a given workload. Aerobic fitness buys some of the same. Morphology matters too, since a larger mass with more insulating fat stores heat and sheds it slowly, while a smaller body with more surface area per kilogram dumps it faster. Age blunts sweating and skin blood flow. And a good deal of what gets filed under sex differences turns out, on closer inspection, to be body size and shape rather than sex itself.

The through-line

None of this is really a collection of tricks. It is one idea wearing different clothes. The body is a heat engine obeying a short list of rules, and evaporation and surface blood flow sit at the top of that list. When a piece of summer advice sounds surprising, the fastest way to test it is to ask what it does to those two things. Hot drink, ice water, warm bath before bed, the answers stop being paradoxes and start being arithmetic.

That is the same discipline I keep coming back to, in the cold fjord and in the heat. Do not trust the feeling. Check it against the physics.

Stay cool. Or warm. Whichever the day is asking of you.

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

A Few Books, If You Want to Read On

A good deal of this issue lives in cold water, so if any of it caught your interest, I have written some short, science-based books you might enjoy.

Cold Water Swimming: A Mini Book is a friendly, short guide to enjoying cold water safely, confidently, and with a big smile. It draws on years at the Norseman Xtreme Triathlon, research with elite military swimmers, and my published work in cold-water physiology. Calm, clear, trustworthy guidance for anyone curious about stepping in.

Get Cold Water Swimming on Gumroad →

This month, the thermometer would not sit still.

On one side of it, cold water, because Norseman is now only four weeks away and my head is already in the fjord. On the other side, real heat, because Norway are on a World Cup run in the warmth of North America, and heat has suddenly become the most interesting problem in Norwegian sport. Two opposite ends of the same instrument, and the same human body caught in the middle. Let me take you through the month.

The fjord, four weeks out

In four weeks I will be standing on the pier at Eidfjord again for the Norseman Xtreme Triathlon, watching the water and making the same call I have made for twenty years. Every year, race directors from many different races, ask me for our cutoff temperature. They want a number. A line on a thermometer that says safe above, dangerous below.

We do not have one. And that is deliberate.

A fixed number feels safe. But it can create false safety. 14.1°C is not automatically fine, and 13.9°C is not automatically a disaster. The swim decision is the sum of many things: air temperature, wind, current, expected time in the water, and above all whether you have a rescue and medical crew that can actually pull people out.

This one is personal. Back in 2015, days before the race, we measured 9.8°C in the fjord. The literature had no good answer for what that water would do to a wetsuited swimmer, so Jonny Hisdal and I swallowed ingestible temperature sensors and swam it ourselves before making the call. We shortened the swim that year. The data later proved it was the right decision, and that swim became the start of my PhD. So when someone asks for our number, I tell them the truth. Do not copy the number. Copy the system behind it.

What heart rate hides: muscle oxygen

The tool I have been most excited about this month sits a little deeper in the body. Muscle oxygen.

For years we have used heart rate to judge how hard someone is working. Heart rate is useful, but it is a whole-body average. It tells you how hard the heart is beating, not what is actually happening inside a working muscle. Two athletes with the same heart rate can have very different things going on in the tissue.

Muscle oxygen sensors change that. They use near-infrared light, a technique called NIRS, shone gently through the skin and into the muscle just below. Oxygenated and deoxygenated blood absorb that light differently, so the sensor can read, second by second, how much oxygen is arriving in the muscle and how much is being used. The number it produces, muscle oxygen saturation or SmO2, is a live window into the balance between supply and demand right where the work is being done.

Why does that help? Because it shows the moment a muscle starts to run out of headroom, often before the athlete feels it and before heart rate reflects it. You can see when a muscle tips from comfortable into trouble, how quickly it recovers between efforts, and how blood flow shifts under stress. For pacing, for interval design, and for understanding fatigue, it sits much closer to the real event than heart rate alone.

I am building two studies around it. One puts the sensor on the latissimus dorsi of open-water swimmers, to watch how blood flow to the working muscle tracks with how fast the body is cooling. The other moves onto the Brazilian Jiu-Jitsu mats, where I train, to see what really happens to a body in close combat. Grappling is a strange and beautiful laboratory. The heart says one thing, and the muscle very often says another.

One race, both ends: the Norseman Crew Race

I did not have to travel far this month to find both ends of the thermometer in a single day. I found them in one race.

Every year, the team that puts on the Norseman Xtreme Triathlon races the whole course themselves first, a dress rehearsal we call the Crew Race. It is the full Norseman: a 3.8 km swim in the cold Hardangerfjord after jumping off the ferry at Eidfjord, 180 km on the bike climbing up onto the Hardangervidda plateau past Dyranut, and a 42 km marathon grinding up toward Gaustatoppen. You start in near-freezing water and, several hours later, you are running in the heat. From very cold water to a very hot run, in one continuous effort.

That range is exactly why it makes such a good natural laboratory, the kind you cannot build indoors. So this year we put muscle oxygen sensors on the crew and lined them up, on a single clock, with heart rate, pace, altitude and temperature.

Then came the real work. Collecting the data is easy. Cleaning it is the job. Hours went into aligning clocks, hunting artifacts, and deciding what to trust before any of it meant anything.

The reward was a picture you rarely get to see. The detail I keep returning to appeared in the heat of the marathon. The total blood volume in the working muscle, what the sensor reads as tHb, climbed as the athlete warmed up. Read simply, the body was pushing more blood toward the surface to shed heat, turning the muscle partly into a radiator. Cold water at the start, a body dumping heat at the end, and one sensor quietly catching the whole swing.

Advice for a football team in the heat

Now the hot end of the thermometer.

Norway are back at the World Cup after 28 years, and as I write this they have just beaten Ivory Coast to reach the Round of 16, with Brazil next. Wonderful for Norwegian football. But the tournament is being played through a North American summer, and heat, not the opposition, may turn out to be the hardest thing to beat. More than a third of the matches are at high risk of dangerous heat, and some could be played at a wet-bulb globe temperature above 28°C, the level at which players’ unions argue a match should be postponed. Norwegians are not built, and not usually trained, for that.

So if the national team asked me, a temperature physiologist, what to do, here is what I would tell them.

First, and most important, acclimatize. Heat acclimation is the single most powerful thing you can do, and it cannot be faked in a day. Ten to fourteen days of training in the heat teaches the body to expand its blood volume, to sweat earlier and more efficiently, and to hold a lower core temperature and heart rate at the same workload. If the players are already living and training in the heat between matches, they are banking exactly this adaptation. Protect it.

Second, cool down before you play. Lowering core temperature before kickoff buys thermal headroom for the ninety minutes to come. Ice slurry to drink, cooling vests, and cold towels in the final half hour before the whistle all work, and they are cheap.

Third, use every break to cool again. FIFA now mandates cooling breaks when it is hot. Treat them as tactical, not as a rest. Iced towels on the neck and face, more ice slurry, shade, and a cooling vest at half time. Do not waste them.

Fourth, make hydration individual. Every player sweats at a different rate, so weigh them before and after training, learn each man’s losses, and replace fluid and salt to match. Not too little, which invites heat illness, and not too much, which carries its own risk.

And finally, measure. This is the part I cannot resist. The same ingestible temperature sensors we swallow before a cold fjord swim work just as well in the heat. Let a few players train with them, learn how their core temperature actually behaves under match load, and then individualize everything above from real data rather than a rule of thumb. In the cold or in the heat, the principle is identical. Do not guess. Measure.

Next stop, the Skagerrak

And the next cold-water project is already on the horizon. A crossing of the Skagerrak, from Denmark to Norway, is coming up. Open water, a long way over, and about as far from a warm football stadium as you can get. More on that when it is closer.

So that was the month. A near-freezing fjord four weeks out, a Crew Race that ran from cold water to a hot marathon, a football team sweating through a World Cup, and a stretch of cold sea still waiting on the other side. Both ends of the thermometer, one body, one question. How does a human hold its temperature where it needs to be, and how do we measure that in a way we can believe?

More soon, once the data has earned it.

Stay warm. Or cool. Whichever the day demands.

A Few Books, If You Want to Read On

A good deal of this issue lives in cold water, so if any of it caught your interest, I have written some short, science-based books you might enjoy.

Cold Water Swimming: A Mini Book is a friendly, short guide to enjoying cold water safely, confidently, and with a big smile. It draws on years at the Norseman Xtreme Triathlon, research with elite military swimmers, and my published work in cold-water physiology. Calm, clear, trustworthy guidance for anyone curious about stepping in.

Get Cold Water Swimming on Gumroad →

This newsletter represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog! You can enjoy all my newsletters for free, and I promise to keep it that way.

If you find this interesting and want to support my work, consider selecting the paid option.

Thanks for reading. If something here resonated, hit me with a reply.

This piece is about the kit I carry specifically for hypothermia prevention, and the reasoning behind each item. I want to be clear from the start that this is a scenario-specific loadout. It is built for this event, this terrain, and this weather. In another type of work I would very probably choose otherwise, and I will return to that at the end. And obviously, we carry much other medical gear. This article just covers hypothermia-specific gear.

The most likely scenario: trauma-induced hypothermia

When I plan the kit, the casualty I am planning for most is not the swimmer pulled blue from the fjord. It is the rider who goes down hard on the bike leg, or the runner who falls on technical ground. Trauma is the highest-probability mechanism across a long day on bikes and exposed roads, and trauma brings its own cold problem with it.

Trauma-induced hypothermia is not the same animal as the cold you get from sitting still on a mountain. It is a secondary hypothermia driven by the injury itself. Hemorrhage and shock reduce perfusion and metabolic heat production; the body’s thermoregulation is blunted, clothing gets cut away, blood and water leave the patient wet, and any fluids we give can pull the core temperature down further. The result is that a casualty can lose heat fast even in conditions that would never threaten an uninjured person.

This is dangerous even though the numbers on the thermometer say otherwise. In trauma, hypothermia is one corner of the lethal triad, together with acidosis and coagulopathy, each of which influence the others. Cold directly impairs the enzymatic clotting and platelet function, so a hypothermic trauma patient bleeds more, which worsen shock, which worsen the cold. Some clinicians now describe a diamond rather than a triad, adding hypocalcaemia, but the principle is unchanged. Even mild drops matter. A core temperature below roughly 36 degrees is already clinically significant in a bleeding patient, and mortality climbs steeply as the core temperature falls further. There is no place for more cooling here. For the injured casualty the doctrine is simple and aggressive: stop the heat loss early, before it ever becomes a problem to treat.

So the first job of my kit is to let me wrap an injured person quickly and completely, on the spot, before evacuation even begins.

When the clock turns: accidental hypothermia

The second scenario is the one created by time. A long wait at the point of injury, or a long and slow evacuation across difficult ground, can tip a casualty, or even a stopped but uninjured athlete, into accidental hypothermia. This is the primary, environmental kind, and the Norseman course is built to produce it: cold-water swimmers, lean and glycogen-depleted competitors with very little insulation of their own, wet clothing, wind on the high sections, and weather that can turn on the climb to Gaustatoppen with little warning. An athlete who was generating plenty of heat while moving can cool alarmingly fast the moment they stop.

Soon, the patient will depend entirely on us to stop further loss. A casualty waiting forty minutes for a stretcher carry in the wind is a very different problem from one I can package and move in two minutes, and my kit has to cover both.

The kit, and the logic behind it

Whatever the mechanism, the physics of heat loss are the same. A person on the ground loses heat by radiation, convection, evaporation, respiration, and, above all when they are lying down, by conduction into the cold surface beneath them. My kit is organised around attacking those pathways in order, and the single most important principle is this: insulate from the ground first. A casualty lying on cold rock or wet grass will keep losing heat no matter how well you cover the top of them.

My default, go-to setup is two items: a windproof insulated casualty wrap and an inflatable insulating ground mat. The wrap I use is a Jerven blanket, a multi-use insulated cover I can deploy in seconds to build a casualty burrito: it stops convective and radiative loss, blocks the wind, and keeps rain and spindrift off. Underneath goes the air mat, a Therm-a-Rest NeoAir Xlite, as the conductive barrier, lifting the patient off the ground with a high warmth-to-weight ratio for its packed size. For a controlled scene and a reasonably short evacuation, this pairing is light, fast, and more than enough. It is what I reach for first.

When the situation gets worse, in bad weather, or with a long wait at the point of injury, or a long evacuation, I escalate to a heavier system: an insulated synthetic sleeping bag with an overbag that boosts it for the cold. The bag I carry is a Halite Recce Synth 3, a synthetic-filled bag (ClimaShield Apex under a Pertex shell) rated to roughly minus four for comfort, with a comfort limit near minus eleven. The choice of synthetic over down is deliberate and central. Norseman casualties and Norseman weather are wet, and down collapses and stops insulating when it is soaked, whereas synthetic fill keeps most of its loft and warmth when damp. Over the top goes an overbag, in my case a Halite Overbag Pro, which adds in the order of fourteen degrees and turns a three-season bag into something I would trust for a genuinely cold, prolonged hold. This is the kit for the casualty who is going to be with me for hours rather than minutes.

The last variable is the terrain of the evacuation itself, and this is where I change the mat rather than the bag. For an evacuation over rough ground I swap the inflatable for a closed-cell foam mat, a Mammut Bamse. The air mat is an outstanding piece of kit, but an inflatable is vulnerable to puncture. On a stretcher carry across boulders and scree, a single sharp edge can deflate it, and a deflated mat means the patient is back on the cold ground with the conductive pathway wide open again. Closed-cell foam cannot puncture and cannot fail, and it goes on insulating no matter how roughly the carry goes. I accept the extra bulk because reliability is the whole point at that stage.

It also goes by the story that I also carry a tent as a shelter when necessary. I use both a one-man tent (Nortent Vern 1) and a two-man tent (Hilleberg Nammatj 2). I choose depending on the pack size, current conditions, and weather forecast. When using for casualties, I use both without an inner-tent, as the shelter option is what I am after. So I unclip the inner tent before race day.

So the full logic is a ladder. The insulated wrap over the air mat (Jerven and NeoAir Xlite) for the fast, controlled case. The synthetic bag and overbag (Halite Recce Synth 3 and Overbag Pro) when cold and time stack up against me. The foam mat (Mammut Bamse) in place of the inflatable whenever the ground we have to cross would threaten an air mattress.

One scenario, one kit

I want to repeat what I opened with, because it is easy to read a gear list as a universal recommendation, and this is not one. This setup is chosen only for this scenario: a defined event, well-known terrain, a supported evacuation chain, and the specific wet, cold, maritime-to-alpine conditions of the Norseman course. Every item is a deliberate answer to those particular constraints.

In another type of work, the answers would change. A different climate, evacuation distance, weight budget, mission length, or casualty profile would all push me toward different equipment. The kit is for this specific mission, not the other way around. What I would keep in any setting is the reasoning: identify the most likely casualty, respect the cold as part of almost every trauma picture, insulate from the ground first, and build a ladder you can climb as the situation gets worse.

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies mentioned in this text.

Ten Years of Norseman Science

When Jonny Hisdal and I stood on the pier at Eidfjord in 2015, measuring the fjord at 9.8 °C three days before race day, we were not starting a research program. We were trying to figure out whether to send 250 athletes into that water at four in the morning.

Then Jonny said: “Jørgen, you should do a PhD on this.”

Ten years later, the Norseman research group has produced more than twenty peer-reviewed papers and grown three PhDs. We have shown that cold-water swimming has a clock: triathletes hold their core temperature for the first 30 minutes in 10 °C water, but the danger zone opens past about two hours. We described late-presenting swimming-induced pulmonary edema, where symptoms declare on the bike rather than in the water. We measured what happens when Norwegian Naval Special Forces recruits swim 10 km in 5 °C: large drops in grip, dexterity, and reaction time. We traced how the race rearranges blood chemistry, lung function, and vascular tone for days afterwards.

That work now sits behind the scientific rationale for World Triathlon’s water-temperature limits, in NATO HFM-aligned cold-weather operations literature, and in the safety protocols Norseman itself runs every August.

None of it happened alone. Jonny Hisdal, Trine Stensrud, Julie Stang, Maria Mathiassen, Mike Tipton, Christoffer Nyborg, Martin Bonnevie-Svendsen, William Morton, and many others built it with me. Hundreds of athletes and soldiers trusted us with their bodies and their data.

The next chapter is FAM100, one hundred days in the high Arctic. Same questions, harder environment. The through-line is the same: find a hard place, measure what happens to the human body, and translate it into something that helps the people who have to be there.

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A Visit to London Air Ambulance

I came across this photo again the other morning, coffee in hand, and it stopped me for a moment. It’s easy to forget what you’ve actually done, and how it stacks up against the people you quietly measure yourself against. So let me tell you a short story about that.

Never underestimate yourself. You are probably far better than you realize.

This picture is Dr. Ben and me, caught between missions at London Air Ambulance. A few years back I spent some time there, flying, watching, and learning from the best in the business.

London Air Ambulance is arguably one of the most famous and most capable air ambulance services in the world. Trauma calls, all day long, on some of the most demanding jobs imaginable. Lifesaving procedures under pressure are simply what they do.

Back when I was working air ambulance in Norway, a lucky few of us got the chance to ride along for a handful of shifts in London. It meant a great deal to us, because in our own service we don’t see major trauma every day. Their professionalism and the sheer pace of it left a real impression on me, and so did the British humour. Those shifts turned out to be one of the most valuable learning experiences of my career, something I’ll carry for life.

A few months later, one of the London doctors came north to visit my station in Tromsø. He followed me and the crew for a whole week, out on missions across northern Norway.

And he was, frankly, astonished by what we did.

Here’s the thing. London Air Ambulance handles enormous volumes of trauma, but Tromsø does a great many other things. During that week we responded to avalanches. We flew daring mountain rescues, including one where I was hanging on a rope beneath the helicopter. We flew at night, something they don’t do in London. We turned out to road traffic accidents where we were the only unit on scene for the first fifteen minutes. We reached a mother giving birth on a remote island with no hospital, no doctor, and no ambulance anywhere nearby. And we did all of it in scenery that looks nothing like London.

So don’t spend your time measuring yourself against everyone else. We run different missions because we operate in different contexts.

London Air Ambulance is still, in my opinion, the best of the best. But we hold our own up here too.

Same Temperature, Different Damage

We’ve long assumed men and women recover from exertional heat stroke the same way. A study out of Ft. Moore says we assumed wrong.

Goodwin and colleagues reviewed 62 EHS cases. The women reached the same recorded core temperatures as the men, yet showed lower peak creatinine and creatine kinase, the markers we lean on to gauge kidney and muscle damage. They also spent roughly half as long in hospital.

Here’s the part that sticks with me: in 91% of the women, cooling had already started before anyone took a temperature. Their true peak was almost certainly higher than the chart says. So the gap in organ damage is probably wider than the numbers suggest, not narrower.

Two honest caveats. The CK difference mostly tracks body size, not sex. And only ten women were studied. This is a signal, not a verdict. But the signal matters. Our return-to-duty criteria and clinical reference ranges were built on male data. Apply them blindly to women and we risk discharging too early, or holding too long. Sex-specific recovery protocols aren’t a nicety. They’re patient safety.

Worth your fifteen minutes.

Goodwin KC, Giersch GEW, Murray TA, DeGroot DW, Charkoudian N. Sex differences in biomarkers of end-organ damage following exertional heat stroke in humans. J Appl Physiol. 2024;137:1434–1445. Open access.

Twenty Minutes, a Beer, and a Napkin

A few months ago I was in Malta for Medicine in the Mediterranean, the conference hosted by the College of Remote and Offshore Medicine Foundation (CoROM). The whole gathering is built around one unglamorous idea: medicine in the places most people would rather not go. Remote. Offshore. Cold. A long way from the nearest hospital.

I was there to give a lecture on operations in cold weather.

And yes, the program was full of fascinating talks, the kind you scribble notes through and chase down afterwards. But if I’m honest, the lectures are not what I love most about a good conference. It’s everything that happens between the sessions. The corridor conversations. The questions you only think to ask once someone is standing in front of you.

The picture above is one of those moments.

It’s a napkin. On it, a world-class expert in diving medicine, Vishwanath Rajan, is walking me through rebreather physics: the breathing loop, where the gas travels, and where the CO₂ has to go. We got talking about something close to my own work: how cold and prolonged exposure reshape a diver’s physiology, and what that means when you can’t simply surface and warm up.

Twenty minutes. One beer. One napkin. And I came away having learned more than I would have from days of reading.

That is exactly why I keep showing up. Put me in a room full of people who are the best in the world at what they do, and let me wander, listen, ask, and, apparently, collect napkins. It energizes me in a way little else does.

So thank you, CoROM, for building a room like that.

A Few Books, If You Want to Read On

A good deal of this issue lives in cold water, so if any of it caught your interest, I have written some short, science-based books you might enjoy.

Cold Water Swimming: A Mini Book is a friendly, short guide to enjoying cold water safely, confidently, and with a big smile. It draws on years at the Norseman Xtreme Triathlon, research with elite military swimmers, and my published work in cold-water physiology. Calm, clear, trustworthy guidance for anyone curious about stepping in.

Get Cold Water Swimming on Gumroad →

This newsletter represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog! You can enjoy all my newsletters for free, and I promise to keep it that way.

If you find this interesting and want to support my work, consider selecting the paid option.

Thanks for reading. If something here resonated, hit reply. The corridor conversation is the best part.

His answer was a simple 2x2 he calls the Longevity x Universality matrix. He sorts techniques along two axes. Longevity asks how long a technique keeps working once everyone understands it. Universality asks whether it holds up across different rulesets and body types, or only in one narrow context. Plot those two against each other and every technique lands in one of four quadrants. The flashy stuff that wins for a season and then dies. The specialist systems that only work under one set of rules. The tricks that depend entirely on surprising someone who does not know better. And, in the top corner, the techniques that work across every context and have kept working for decades.

It is a clean piece of thinking. But that was not the part that stopped me.

The part that stopped me was a single line near the middle:

“People often conflate the ‘fundamentals’ with the basics, but they couldn’t be more wrong. Unlike basics, which are stages of learning you pass through, fundamentals are techniques that work across all rule sets and body types and have worked for a really long time.”

I read that and felt slightly caught out. Because a few months ago I wrote a post on this very Substack called “Don’t Forget the Basics.” And I think I used the wrong word.

The word I got slightly wrong

My post argued that the most common mistake new medics make is drifting away from the basics. They finish a demanding course, their heads full of drugs and devices and advanced procedures, and they reach for the impressive intervention while the foundational steps get rushed or skipped. I stand by every word of that.

But “basics” was lazy shorthand, and The Lost Creonte put his finger on exactly why. “Basics” implies a stage. Something you do at the start, then leave behind once you have earned the right to do the interesting things. That framing is the whole problem. It is precisely the belief that gets people hurt.

What I was really describing were fundamentals. Not a phase you graduate from, but the small set of skills that work in every environment, hold up under every kind of pressure, and have kept working for as long as the job has existed. In his matrix, they sit in Quadrant 1: long-term and universal. They are not where you begin and then move on. They are where you keep returning, for your entire career.

That single relabel changes how you train. You do not “cover” a fundamental once and tick it off. You own it, refine it, and come back to it again and again, the same way the best grapplers keep drilling positions that every white belt can already name.

The day I learned this the hard way

I have told this story before, but it reads differently through the matrix.

Several years ago I was invited to teach prehospital emergency procedures to a Special Forces group. I walked in with confidence. I was an experienced rescue paramedic and I genuinely thought I had something new to show them. Within a few hours I was humbled.

These operators were exceptional, but not in the way I had braced for. There were no exotic interventions, no clever clinical party tricks. They were exceptional because they had mastered the fundamentals to a degree I had not anticipated. Their patient assessments were methodical and calm. Their hemorrhage control was fast, clean, and correct every single time. Their airway management was not flashy. It was simply right.

Put that in The Lost Creonte’s language and it is obvious what I was watching. These were people who had stopped chasing the lower three quadrants entirely. No fragile tricks that only work on someone who does not know better. No specialist gadget that shines in one narrow scenario and fails everywhere else. No technique that wins by surprise and then collapses the moment the situation turns unfamiliar. Just relentless, almost monastic investment in the handful of skills that work everywhere, every time. It maps almost perfectly to a quote a Norwegian commander gave the newspaper VG when asked what makes their operators so effective: not the high-tech gear, but the fact that they are exceptionally skilled at the basic skills, trained without mercy.

I adjusted my approach, taught with a lot more humility, and left having learned far more than I came to give.

The same four quadrants, in medicine

The reason the matrix travels so well is that medicine has its own version of every quadrant, and new clinicians are pulled toward exactly the wrong ones.

The fragile tricks are the maneuvers that only work on a cooperative patient in an ideal position, and fall apart the moment reality intrudes. The information advantages are the newest drug or device or protocol that feels cutting-edge precisely because few people have it yet. There is real value in keeping up with these, but their edge fades the moment they become standard, and they are worthless if your foundation is shaky underneath them. The specialist systems are the genuinely useful skills that only apply in one setting, worth learning if that is your world, dangerous if they become your whole identity.

And then Quadrant 1. In prehospital medicine that means a systematic patient assessment, scene safety, a clear and structured handover, airway positioning before reaching for any advanced device, correct tourniquet placement, and recognising deterioration early. None of it photographs well. All of it is what separates a good clinician from a great one, because the great ones execute these correctly regardless of what else is on fire around them.

These are not beginner tasks you outgrow. They are the techniques you return to for thirty years.

What the science actually says

This is not just a nice metaphor borrowed from a combat sport. The research has been pointing the same direction for decades.

It starts with K. Anders Ericsson, whose work on deliberate practice showed that simply accumulating experience does not, on its own, make anyone better. What matters is how you practise, not how long. Focused, intentional repetition of specific skills, with feedback, beats years of going through the motions. Ericsson argued that the goal in medicine should not be reaching an “adequate” level but reproducibly superior performance in the skills that matter most (Ericsson, Academic Medicine, 2004). A study in BMC Medical Education later found that students’ clinical skill results correlated with deliberate practice behaviours like planning and sustained concentration, across every year group (Moulaert et al., 2011).

But why do fundamentals specifically survive when everything else degrades? Two findings explain it.

The first is about how experts see. In the classic chess studies by Chase and Simon, masters could glance at a board for a few seconds and reconstruct it almost perfectly, while novices could not. The masters were not remembering harder. They had stored tens of thousands of recognisable patterns, or “chunks,” in long-term memory, so a complex scene resolved instantly into something familiar (Chase and Simon, Cognitive Psychology, 1973). This is what Patricia Benner described in her nursing framework “From Novice to Expert” (1984): the expert does not do more than the novice, but reads the situation faster and acts with greater precision. The expert sees what matters. The novice reaches for complexity as a substitute for clarity.

The second is about what happens under stress. When cognitive load spikes, the deliberate, effortful parts of the brain are the first to falter. What carries you through is automaticity, the state where a skill has been practised so thoroughly it runs almost without conscious supervision (Poldrack et al., Journal of Neuroscience, 2005). This is exactly why the basics break down first in a crisis. If your patient assessment is not deeply habitual, it gets compressed or skipped the moment things go wrong. The fix is to overlearn: train a skill beyond the point of first competence until it is automatic. Overlearning measurably improves how well a skill survives, especially under pressure (Driskell, Willis and Copper, Journal of Applied Psychology, 1992). The honest caveat, which the same literature is clear about, is that overlearning fades without occasional refreshing, and that spacing your practice over time beats cramming it. So fundamentals are not a one-time conquest. They are a standing appointment.

And the payoff is not theoretical. Tactical Combat Casualty Care was never built around exotic interventions. It was built around the systematic mastery of a small number of high-impact skills, mainly hemorrhage control and airway management. Combat fatality rates fell from 19.1 percent in World War II to 9.4 percent in Iraq and Afghanistan (Puryear et al., StatPearls, 2022). Not because the right people had better gadgets. Because the right people had mastered the right fundamentals, and trained them relentlessly.

So, an honest question

Here is what The Lost Creonte’s little 2x2 really gave me. A cleaner word for something I already believed, and a sharper way to defend it. The best people in any demanding field are not the ones with the most techniques. They are the ones who have decided, deliberately, where to spend their finite hours, and who keep returning to the universal, durable core long after everyone else has wandered off chasing the new thing.

So I will leave you where I left my last post, with the word corrected.

When did you last actually audit your fundamentals? Not perform them in the rush of a busy shift, but stop and ask honestly: is my assessment systematic every single time? Is my airway management as clean as it could be? Do I communicate clearly under pressure, or do I just assume I do?

The great ones are not built differently. They have simply committed to mastering what most people take for granted, and they never stop refining it.

That is available to all of us.

So, how are your fundamentals, really?

References

• Chase WG, Simon HA. Perception in chess. Cognitive Psychology. 1973;4(1):55-81.

• Driskell JE, Willis RP, Copper C. Effect of overlearning on retention. Journal of Applied Psychology. 1992;77(5):615-622.

• Ericsson KA. Deliberate practice and the acquisition and maintenance of expert performance in medicine and related domains. Academic Medicine. 2004;79(10 Suppl):S70-81.

• Moulaert V et al. The role of deliberate practice in the acquisition of clinical skills. BMC Medical Education. 2011;11:101.

• Poldrack RA et al. The neural correlates of motor skill automaticity. Journal of Neuroscience. 2005;25(22):5356-5364.

• Puryear B, Roarty J, Knight C. EMS Tactical Combat Casualty Care. StatPearls. Updated October 2022.

• Benner P. From Novice to Expert: Excellence and Power in Clinical Nursing Practice. Prentice Hall Health, 1984.

Inspired by “Why some jiu-jitsu techniques are worth your 10,000 hours and others aren’t worth 10” by The Lost Creonte BJJ, and building on my own earlier post, “Don’t Forget the Basics.”

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

But here you are, soaked and shivering on Gaustatoppen, having just swum 3.8 km in 14-degree water, biked 180 km over more than 5000 meters of climbing, and run a marathon to a mountaintop in 6-degree air temperature. You feel, relatively speaking, fine. So what is actually going on inside your heart, and should we be worried?

That is the question our research group has been chasing, and our latest paper, on which I am a co-author, was just published in BMJ Open Sport & Exercise Medicine. It is one more piece of the puzzle.

What troponins are, and why clinicians care

Cardiac troponins are small proteins that live inside the muscle cells of your heart. They are part of the machinery that lets the heart contract. Normally they stay neatly tucked inside those cells, and the amount circulating in your blood is vanishingly small. When heart muscle is injured, most famously during a heart attack, those proteins leak out and show up in a blood test.

That is why troponins are the workhorse of cardiac diagnostics. If you arrive at the hospital with chest pain, a troponin test is one of the first things ordered. Modern high-sensitivity assays can pick up tiny amounts. Above a certain threshold, paired with the right symptoms or ECG findings, troponin elevation is one of the criteria used to diagnose myocardial infarction.

There are two main flavors clinicians measure: cardiac troponin I (cTnI) and cardiac troponin T (cTnT). They behave slightly differently in the bloodstream, and that difference turns out to matter.

The athlete paradox

Here is where it gets interesting. Over the last decade or so it has become clear that troponin also rises after hard endurance exercise in apparently healthy people. Marathons, ultras, long bike races, triathlons: researchers keep finding the same thing. Run far enough, hard enough, and your troponin goes up.

For a long time this was waved away as a benign quirk of the exercising heart. But more recent work has complicated that story. A large study of long-distance walkers found that participants with elevated cTnI after the event had a meaningfully higher risk of cardiac events and death over the following years. Another group showed that cyclists with hidden coronary artery disease had bigger, longer-lasting troponin elevations the day after racing than cyclists with clean arteries.

So we have a paradox. Most athletes with post-race troponin elevation are perfectly fine. A small minority may be telling us something important about their hearts. The clinical question is: how do you tell them apart? Right now, we cannot, reliably.

Why Norseman is the right place to ask

If you want to understand what extreme endurance exercise does to the heart, you need extreme endurance exercise. Norseman delivers. The cold water start. The brutal bike profile. The marathon that ends with 1880 meters of climbing for the top finishers. Race times that stretch from 10 to nearly 18 hours. Few sporting events combine duration, intensity, altitude and cold exposure quite like this one.

That makes Norseman a kind of open-air physiology lab. We can ask what happens at the edges of what the human body can tolerate, in real conditions, in real athletes, not in a climate chamber.

What we did, and what we found

We collected blood from 93 athletes at three timepoints: a day or two before the race, within an hour of finishing, and roughly 15 hours later. We measured both cTnI and cTnT, and we calculated the ratio between them, because emerging evidence suggests that ratio may carry more information than either marker alone.

The pattern was striking. At baseline, almost everyone was well within the normal range. Immediately after the race, cTnI had risen more than twentyfold and cTnT roughly sevenfold. Nearly every participant was above the threshold a cardiologist would use to call myocardial injury. The cTnI/cTnT ratio also climbed sharply.

A day later, most values were on their way back down. For most athletes, this looked like a transient, physiological response, the heart’s version of the muscle soreness in your legs. But not everyone followed the script. Three participants actually had higher cTnI the day after than immediately after finishing. Fourteen had a rising cTnI/cTnT ratio into the next day.

The most dramatic case was an athlete who had previously been diagnosed with coronary artery disease and had undergone bypass surgery. He completed the race without symptoms, but his post-race numbers were extraordinary: cTnI of 24,242 ng/L, hundreds of times the upper reference limit, and a cTnI/cTnT ratio many times higher than what a typical athlete in our cohort showed, climbing further the day after the race rather than falling. At six-year follow-up, he was still healthy, with no cardiac events since the race. What that means, we genuinely do not know yet. But it is exactly the kind of signal worth chasing.

What this changes, and what it does not

For the average athlete, the message is reassuring. The cTnI/cTnT ratio in our cohort behaved like a physiological response: up sharply, then back down. We do not see the pattern that severe heart muscle necrosis would produce.

But the ratio is interesting. It separated our outliers from the pack in a way that the absolute troponin numbers alone did not. If future studies confirm it, the cTnI/cTnT ratio could become a useful tool: a way to look at a post-race blood draw and triage who needs further investigation and who can be reassured.

We are not there yet. This study is descriptive. It cannot prove that elevated ratios predict disease. That requires longer follow-up and bigger cohorts. But it is a step.

A few words on the research group

The Norseman Research Group was founded in 2015 after Jonny Hisdal and I were worried about a particularly cold swim. I was the safety director at the race then, and I still am. The research group started as the home of my PhD work and has since grown to roughly twenty studies and three completed PhDs, with several ongoing and upcoming projects.

We have looked at thermoregulation in cold water, pulmonary function and swimming-induced pulmonary edema, cardiac responses to extreme endurance, and increasingly, the connections between them. The work has been a collaboration across Oslo University Hospital, Akershus University Hospital, the University of Oslo, the Jebsen Centre for Cardiac Biomarkers, the Norwegian Armed Forces Medical Services, and a long list of clinicians, scientists and athletes who keep showing up to draw blood, gather data and ask better questions.

Norseman has always been a race that pushes people past what they thought was possible. It turns out it is also a place where we keep learning something new about what the human body actually does out there. More to come.

The full paper is open access: Bonnevie-Svendsen M, et al. Cardiac troponin patterns in athletes completing Norseman Xtreme Triathlon. BMJ Open Sport & Exercise Medicine 2026;12:e002810. DOI: 10.1136/bmjsem-2025-002810

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I have written a book on Cold Water Swimming.

I wrote it because I think everyone deserves calm, trustworthy guidance before they get in cold water. The cold is worth experiencing. But it deserves your respect.

Get it here: Cold Water Swimming — A Mini Book

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

A new study just came out that I want to share, partly because it’s good work and partly because the first author, Tuva Steinberg, is a colleague in the Norwegian Armed Forces. This paper is part of her PhD, and it does something we don’t see often enough in cold-injury research: it asks the soldiers themselves what happened, and listens carefully to the answer.

The paper is Steinberg et al. (2026), “Causes and Consequences of Freezing Cold Injuries in the Norwegian Armed Forces from the Soldier’s Perspective — A Qualitative Study,” published open-access in Int. J. Environ. Res. Public Health.

What the study did

Tuva and her co-authors interviewed sixteen soldiers. Eight women and eight men, mostly young, all with a verified grade 2 freezing cold injury (FCI) sustained during service. Participants were recruited through the Norwegian Armed Forces Health Registry, the interviews were semi-structured, and the analysis followed conventional qualitative content analysis. Saturation was reached at fourteen interviews; two more were done to be sure.

Three big themes came out of the material: the causes of FCI, the consequences, and the role of military culture.

Causes: it’s almost never just “the cold”

The most striking finding for me is how rarely FCI is caused by cold alone. It’s a pile-up. Soldiers described long ski marches at −30 to −40 °C, but the freezing fingers tended to arrive when several things stacked on top of each other: exhaustion, dehydration (”we were so tired and dehydrated that even melting snow for drinking water became a challenge”), missing or ill-fitting kit, and the simple operational reality that you cannot rack a rifle in thick mittens.

That last point is a real paradox. The official guidance is to keep gloves on. But weapon handling, tent buttons, fine tasks under time pressure — these often force gloves off, especially when the unit is rushed. One participant put it bluntly: “I knew removing gloves was against guidelines, but tight time constraints made me take risks to complete the task.” Another, who had practiced weapon handling with mittens during recruit training, noted that the practice tapered off afterwards — exactly when the field exposure ramped up.

A third thread is the absence of systematic reporting. Some leaders were excellent; one participant credited a superior for ensuring the report was filed. Others were told, more or less, to walk it off. The paper makes the point that without consistent documentation, lessons don’t get learned at the unit level.

Consequences: long after the boots come off

Eleven of the sixteen participants still had symptoms at the time of the interview, on average 4.5 years after the injury. Chronic pain, numbness, cold hypersensitivity, fingers that ache when handling raw chicken or scraping ice off a windshield. A few were discharged from the military because of the injury. One described moving into indoor work as a computer scientist because outdoor jobs were no longer realistic: “Due to my cold and sensitive fingers, I cannot work outdoors.”

That stuck with me. We tend to count FCI as a winter-exercise mishap and move on. The paper documents that for many soldiers it becomes a quiet, lifelong constraint on what kind of work they can do and how they live their weekends. The Norwegian governmental injury compensation system estimates a 5–20% lifelong disability for FCI, and yet, as the authors note, soldiers who sustain FCI during conscription are typically excluded from continued service and ineligible for compensation. That combination quietly encourages people not to report.

The piece I think is most important: culture

This is where the paper earns its keep. Tuva and her co-authors describe military culture not as a vague backdrop but as an active risk factor. Strict discipline, hierarchy, and a strong norm of toughness can suppress exactly the behaviours that prevent FCI: speaking up, slowing down, putting gloves back on, asking for a warm-up break.

Several participants described being afraid to look like “the weak link.” One, ordered into a plank position on ice without gloves despite an existing injury, did it anyway: “I was strictly told to go down, down. So, I didn’t dare do anything else.” Another, whose unit was ordered to remove their hats because a comrade had forgotten his, ended up with FCI on an earlobe, and afterwards had to wear a beanie instead of a beret, which itself became a visible marker of “weakness.” The authors connect this to the familiar military mindset of “suck it up and drive on,” and to the harder truth that values which make a unit effective in combat can also silence health complaints in training.

What the paper recommends

The implications are practical and not particularly exotic. Develop standardized diagnostic criteria for FCI (right now diagnosis depends a lot on the attending physician at the local ward). Build systematic reporting into cold-weather exercises so lessons travel beyond the platoon. Keep training soldiers in handling weapons with mittens, and keep doing it after recruit training, not just during. And, hardest but most important, work on the cultural side: make early reporting normal and unstigmatized, so soldiers can protect themselves without feeling like they’ve failed the group.

Norway sees roughly 120–150 new FCI cases per year in the NAF. The kit and the doctrine are mostly in place. What this study suggests is that the remaining gains are less about better gloves and more about how we talk to each other in the cold.

This paper is well worth a read!

The full paper is open access here: https://doi.org/10.3390/ijerph23040444. Worth a read — and a thanks to Tuva for the work she’s putting into this PhD.

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I have written a book on Cold Water Swimming.

I wrote it because I think everyone deserves calm, trustworthy guidance before they get in cold water. The cold is worth experiencing. But it deserves your respect.

Get it here: Cold Water Swimming — A Mini Book

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

As Safety Director and Research Lead at Norseman, I’ve spent more than a decade watching this race from inside the operation — at the swim start, at Stavsro, on the mountain.

If you’ve ever stood at the Stavsro checkpoint and watched athletes shuffle in just under the cut-off, you know the Black Shirt isn’t really decided on Mount Gaustatoppen. It’s decided much earlier — somewhere out on the bike, often before anyone realises it. We’ve talked about this for years inside the Norseman team: the race within the race, the 160 athletes who get to climb to 1,850 metres, and the difficult call of telling a tired athlete at Zombie Hill that the math no longer works.

A bachelor’s thesis from Manuel Miethke landed on my desk recently, and it’s the first piece of work I’ve seen that actually puts numbers on this intuition. Manuel built two things: a probabilistic model that estimates an athlete’s Black Shirt probability at every timing point, and an interactive dashboard that turns that model into something a coach or athlete can actually use. I want to share what he found, because I think a lot of you in the Norseman community will recognise your own race in the data.

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The dataset

Manuel pulled official timing data from six editions of the race — 2018, 2019, 2021, 2022, 2024, and 2025 — extracting it directly from the live timing platform via the JSON endpoints behind it. He had to skip 2020 (cancelled) and 2023 (timing system inconsistencies, confirmed with the organisers). What remained is rich: more than 35 timing stations per race across the swim, bike, and run, giving a near-continuous picture of how each athlete progresses.

He enriched this with weather data and a course profile, then trained an XGBoost classifier to predict, at any given split, whether an athlete would ultimately end up with a Black Shirt or not.

I’ll admit a personal bias here: I do most of my own research statistics in Python, and it’s also the language I reach for whenever I want to poke at a dataset for myself. So seeing a pipeline built end-to-end in Python — JSON scraping, pandas wrangling, XGBoost modelling, SHAP for interpretation, Streamlit for the front end — felt instantly familiar. It’s also what makes the work reproducible. Anyone with our raw timing data and a Python install could, in principle, retrace Manuel’s steps.

What the model actually learned

The headline number is good — an AUC-ROC of 0.975 on the test set. But the more interesting part is when the model becomes confident. Accuracy passes 90% already during the early bike leg. By the time athletes are on the run, the prediction is essentially settled. This matches what our team has long suspected: the Norseman Race Director told Manuel during evaluation that experienced organisers can usually call the Black Shirt finishers around kilometre 36 of the bike. The model agrees.

Manuel ran a SHAP analysis to open the box, and the dominant signal turned out to be position-based — relative split rank and absolute split rank carry the most weight. Pacing variables and cumulative time matter, but in a secondary way, mostly through how they shift your rank. Wind, temperature, and elevation showed surprisingly small direct contributions. That doesn’t mean weather doesn’t matter — it clearly does — but its effect is mediated through how it changes athletes’ positions relative to each other. The model captures that indirectly.

Three findings worth sitting with

First, the bike is where the race separates. Across every edition Manuel analysed, swim differences between Top 10, Black Shirt, and White Shirt finishers were small and overlapping. The bike leg is where the field stretches out, with the run continuing the separation up to the cut-off. We’ve intuited this for years, but it’s the first time I’ve seen it quantified across high-resolution split data from multiple editions.

Second, Black Shirt finishers don’t dominate early — they hold position. Looking at rank progression, many successful athletes were not leading after the swim. They moved up gradually, or simply maintained their place, while White Shirt finishers and DNFs tended to drift backward early and never recover. This reframes the Black Shirt as less about heroics and more about avoiding catastrophic slowdowns at the wrong moment.

Third, there’s an empirical “frontier” near 13:51h. Manuel constructed this from the actual times of the 160th finisher in past editions, and our own organisers’ rule-of-thumb (13:45–13:50h for the cut-off arrival) lines up with it almost exactly. The frontier becomes the spine of the dashboard — a benchmark against which an athlete’s current pace can be assessed in real time.

The dashboard

The model is one artefact; the dashboard is the other. Built in Streamlit with Plotly, it’s organised into four pages: an overview of the field, pacing and course analysis, model predictions, and a Tools page for “what-if” planning.

Two tools stand out. The empirical pace planner lets athletes build a race plan grounded in what’s actually been done at Norseman — swim, transitions, bike, run — and adjust it for their own strengths. Out comes a personalised split table you could literally tape to your bike. The What Are The Odds module is the in-race counterpart: enter your current distance and elapsed time, and it shows your model-based Black Shirt probability, the empirical share of similar past athletes who made it, and the bike speed or run pace required to still reach Stavsro before 13:51h. If the required pace becomes implausible (faster than 5:30/km on the run, for example), the tool flags it as theoretical rather than achievable.

How well does it hold up?

Manuel evaluated the dashboard with nine experts — elite triathletes, coaches, our Race Director, and triathlon data analysts. The reception was strongly positive across all nine of his design principles. The “what-if” scenario tool was the most-praised feature. The most consistent critique was about onboarding: some charts need clearer interpretive guidance before they sing on their own.

He’s honest about the limits. The frontier time is built on only two editions, so it should be read as an empirical approximation, not a universal law. The dataset has no athlete-level information on training, equipment, nutrition, body composition, or experience — variables we know matter enormously. The expert panel skewed toward strong athletes, so feedback from those racing closer to the cut-off (where the dashboard arguably matters most) is underrepresented.

What I take from it

For me, the most exciting part isn’t the model accuracy — it’s that we now have a tool that talks about Norseman performance in the same language athletes already use: splits, paces, position, time-to-cut-off. The next obvious step is live race integration. Imagine a support crew at Geilo seeing not just elapsed time, but a probability that updates as their athlete moves through the field. Manuel discusses exactly this in his future work, alongside extending the framework to other XTRI events and finally pairing the timing data with proper athlete surveys.

If you’ve finished a Norseman, this thesis will tell you, in retrospect, exactly when your race was decided. If you’re preparing for one, it gives you the first quantitative reference point I’ve seen for how to pace toward 160th place — and not a finish-line minute later.

Manuel’s work is a real contribution to how we think about this race. I’ll be watching closely as iteration two takes shape.

You can read the full thesis here: https://doi.org/10.13140/RG.2.2.35740.24966

I have written a book on Cold Water Swimming.

I wrote it because I think everyone deserves calm, trustworthy guidance before they get in cold water. The cold is worth experiencing. But it deserves your respect.

Get it here: Cold Water Swimming — A Mini Book

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

On Friday, Emilie Mass Dalhaug defended her PhD thesis at the Norwegian School of Sport Sciences. I had a small part in the wider research project around it — temperature regulation and the lab work behind temperature measurements — and I want to use this post to do two things: congratulate Emilie publicly, and explain why the project she completed is more interesting than its quiet title suggests.

The thesis is called Strong Mama: What happens when pregnant athletes push beyond conventional exercise guidelines? It’s the largest study to date of fetal responses to high-intensity exercise and heavy lifting in pregnant elite and recreational athletes. And the answer it gives — carefully, with all the right caveats — is that the pregnant athletes were fine, the babies were fine, and the conservative advice they had been given for decades may need rewriting.

A question that’s been hard to answer

For most of modern medicine, the standing advice to pregnant women has been: keep moving, but keep it moderate. Walk, swim, do prenatal yoga, hit 150 minutes a week of moderate activity, and don’t do anything that gets your heart rate too high or makes you lift anything heavy.

It’s reasonable advice on paper. It’s also frustrating advice if you came into pregnancy as a national-team athlete, a competitive CrossFitter, or simply someone who has trained five days a week for twenty years. “Take it easy” is not an individualized prescription. It’s a default — built more on caution than on evidence — and the evidence base for whether high-intensity intervals, heavy lifting, and high training volume are actually unsafe in well-trained pregnant women has, until recently, been thin.

The classic worries are physiological and intuitive. Hard exercise sends blood to working muscles; could that steal blood from the placenta? Heavy lifting raises intra-abdominal pressure; could that hurt the baby? Hard sustained effort raises core body temperature; could maternal hyperthermia harm the fetus, particularly above the 39°C threshold often cited as a safety ceiling? Lying on your back to bench press compresses the vena cava in late pregnancy; is that dangerous?

None of these were silly questions. They just hadn’t been properly tested in the population most affected by them — pregnant women who actually train hard.

What Strong Mama did

The Strong Mama project recruited 60 pregnant athletes — 10 elite (national-team or comparable level) and 50 highly active recreational athletes — and brought them into the lab in their third trimester. Each woman came in for two visits.

On day one, after baseline measurements and a baseline ultrasound to confirm the fetus was healthy, she ran a 5×5-minute high-intensity interval session on a treadmill, targeting 17 on the Borg perceived-exertion scale (a “very hard” effort) and 90% of estimated maximum heart rate. Between every interval there was a four-minute pause, during which an obstetrician–gynecologist did a focused ultrasound: fetal heart rate, blood flow in the umbilical artery, blood flow in the uterine artery.

A day or two later she came back for the same interval session on a stationary bike, followed by a heavy strength-training protocol: three sets of eight repetitions, with one repetition in reserve, in sumo deadlift, bench press, and incline bench press. Ultrasound again, before and after each exercise.

In parallel, all 60 women filled in a detailed questionnaire late in pregnancy and sat down for an interview six weeks postpartum. That captured the things lab measurements miss: how much they actually trained during pregnancy, how the pregnancy went, how the birth went, how the baby was doing.

My contribution sat at the boundary of that lab work. Heat is one of the classical theoretical risks of hard exercise in pregnancy, and the worry — that maternal core temperature might cross 39°C and stress the fetus — has shaped guidelines for years. We needed to know whether that worry held up in the actual population we were studying. So a parallel sub-study, Cool Mama, was built into the project to measure it.

Cool Mama: does pregnancy actually overheat?

Cool Mama (Brevik-Persson et al., Journal of Exercise Science & Fitness, 2024) compared 15 pregnant athletes from the Strong Mama cohort with 15 non-pregnant athletic controls, all running the same high-intensity interval protocol in a 20°C lab. Continuous core body temperature was measured by rectal probe, skin temperature by sensors at eight body sites, and fluid loss by careful before-and-after weighing.

The result was, I admit, slightly counter-intuitive: the pregnant athletes did not get dangerously hot. None of them crossed the 39°C threshold. The highest core temperature recorded in any pregnant participant was 38.76°C — and the highest in the non-pregnant control group was actually higher, at 39.56°C. The pregnant women started cooler, rose less, sweated more, had higher skin temperature, and rated themselves as feeling cooler than the controls.

In other words, pregnancy looks like it enhances thermoregulation rather than compromising it. Higher blood volume, lower vascular tone, more efficient heat dissipation through the skin, more sweat — the body is, if anything, better at shedding heat in late pregnancy than out of it. That’s a real finding, and it directly addresses one of the load-bearing reasons the conservative guidelines exist.

It does not mean pregnant women can train hard in any environment — running intervals at 35°C in direct sun is a different story, and the study makes that clear. But it does mean the hyperthermia concern, in normal indoor conditions, is much smaller than the guidelines have implicitly assumed.

What the fetus did during all that effort

Back to the main thesis. Across the running protocol, fetal heart rate stayed mostly inside the normal range of 110–160 beats per minute, with the average rising modestly across intervals. There were a small number of episodes that crossed the lines: six cases of prolonged fetal bradycardia (heart rate under 110 bpm for at least three minutes) during running, and a handful of fetal tachycardia episodes (above 180 bpm) during both running and cycling.

Every one of these triggered immediate exercise termination. And every one of them resolved on its own — the bradycardia cases all returned to normal within eight minutes of stopping. None went anywhere clinically dangerous. Notably, the running protocol produced bradycardia and the cycling protocol did not.

Heavy lifting produced calmer responses. Fetal heart rate stayed inside the normal range across sumo deadlifts, bench press, and incline bench press, with small statistically detectable rises after deadlift and incline bench press but nothing approaching pathology. Even the supine bench press — the one most theorists worry about, because of vena cava compression — was tolerated well by mother and fetus alike. One participant did get classic vena cava symptoms, but the fetus stayed stable and the umbilical artery flow even improved slightly.

Plain-English translation: the fetus occasionally complained, never seriously, and always recovered.

Pregnancy and birth

The prospective side of the project is just as striking. The elite athletes trained an average of 11.6 hours per week during pregnancy. The recreational athletes trained 7.0 hours per week. Both numbers are far above what current guidelines advise.

Despite that — or, more provocatively, alongside that — the outcomes were good. The preterm birth rate in this cohort was 1.6%, well below the Norwegian national average of around 5.8%. There were no babies born under 2500 grams. Most women had spontaneous vaginal deliveries at term. Apgar scores were generally high. Almost all the women who wanted to, resumed exercise within six weeks of giving birth.

Complications did occur, but mostly in the elite group: two cases of gestational diabetes and two cases of gestational hypertension among the ten elite athletes. None among the fifty recreational athletes. The thesis is appropriately careful here — sample sizes are small, and elite athletes are not immune to obstetric complications just because they’re fit — but it is hard to look at this dataset and conclude that high training volume is bad for healthy, well-trained pregnant women.

What this means in practice

Caveats first. Sixty women is not the world. This was a third-trimester snapshot, not a longitudinal study from conception to birth. The participants were healthy, screened, monitored, and supported by an OBGYN on every test day. Long-term effects on the children are not yet known. None of this is a license for any pregnant woman, anywhere, to start doing maximum-effort intervals tomorrow.

But that isn’t really the question Strong Mama was asked to answer. The question was: should well-trained pregnant athletes really be told to drop their training to “moderate” levels, when there’s no evidence this is necessary and a great deal of clinical experience that they don’t want to? Together with the broader literature, the Strong Mama findings suggest the answer is no — that high-intensity intervals, heavy resistance training, and high overall training volume are tolerated well by mother and fetus when training is individualized, well-paced, and accompanied by regular prenatal follow-up.

The thesis ends where good science ends: by asking for more research, particularly on long-term outcomes for the children, on the physiology of repeated bradycardia episodes, and on practical questions like the Valsalva maneuver during heavy lifts. But the direction of travel is clear. Future guidelines should differentiate between the general pregnant population and pregnant athletes — and the differentiation should be based on physiology, not on a default of caution.

A modest part of a project worth being proud of

My role in all of this was small. Temperature work, lab measurements, a co-authorship on Cool Mama, helping make sure the conditions in which the data was collected were clean enough that the data meant something. The hard intellectual work — designing the protocols, running the testing, analyzing it, writing the papers, defending the thesis — belongs to Emilie and her supervisors and her team. I’m a tiny part of a larger effort.

But this is what good research looks like. A clearly stated question. A team with the right mix of obstetricians, sport scientists, and physiologists. Careful protocols. Real data. Sceptical co-authors. Honest discussion of limitations. Findings that don’t just confirm what people already believed.

Huge congratulations to Dr. Emilie Mass Dalhaug — and to Lene Annette Hagen Haakstad, Kari Bø, Wendy Brown, Birgitte Sanda, and the whole Strong Mama team. The pregnancy training rulebook may genuinely need rewriting, and you’ve moved it.

The three Strong Mama papers are open access:

• Dalhaug et al., “Is fetal well-being jeopardised during high-intensity interval training?” — BMJ Open Sport & Exercise Medicine, 2025.

• Dalhaug et al., “Pushing limits: the acute effects of a heavy-load resistance protocol and supine exercise on fetal well-being” — BMJ Open Sport & Exercise Medicine, 2025.

• Dalhaug et al., “Exceeding the guidelines: A descriptive study of exercise, pregnancy, maternal and neonatal health outcomes in elite and recreational athletes” — BMC Pregnancy and Childbirth, 2025.

And the temperature paper:

• Brevik-Persson et al., “Cool mama: Temperature regulation during high-intensity interval running in pregnant elite and recreational athletes” — Journal of Exercise Science & Fitness, 2024.

This blog post represents my personal views and does not necessarily reflect the opinions of my employer or any organizations. I have no affiliations with any companies relevant to this.

I’d love for you to join my Substack blog!

If you find this interesting and want to support my work, consider selecting the monthly paid option.

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But before any of that reaches you in published form, there was a stage to stand on first. I’m just back from Raleigh, North Carolina, where I lectured at SOMA 2026 — and that’s where this issue begins.

SOMA 2026 — A Summary

About SOMA

SOMA — the Special Operations Medical Association — holds its annual scientific assembly in Raleigh, North Carolina each spring. It is the leading international forum for special operations medicine, bringing together SOF medics, physicians, surgeons, researchers, and operators from the United States and partner nations. The program spans Tactical Combat Casualty Care, Prolonged Field Care, austere and remote medicine, mass casualty response, and operational lessons learned from current and recent conflicts. I attended SOMA 2026 and lectured on the Norwegian FAM100 exercise and an Arctic case for PFC and EVAC. The notes below summarise my three main takeaways from the week.

1. Arctic capability is a knowledge problem, not a gear problem

There is significant international interest in how the Nordic countries operate in the cold, and a clear willingness to invest in equipment, sensors, and new technology to “conquer” the Arctic. That interest is welcome, and we should continue to engage with it. But the conversations I had at SOMA only confirmed what I already believed: gear is the smaller part of the answer. Knowledge and training are the larger part. Our comparative advantage is not what we carry — it is what our soldiers and medics know, and how often they have done it cold, tired, and in the dark. Any partnership or capability development we engage in should reflect that order of priority.

2. PFC means very different things to different units. Our case sits on the austere end of the spectrum

The range of PFC capability presented at SOMA is enormous. Some nations and units are setting up for PFC with resources and footprint that look closer to a forward Role 2 than to a patrol. Others are operating with far less. The scenario most relevant to us — a four-soldier patrol, one medic, everything carried on the medic’s back, no medevac, long evacuation including prolonged field care, in the Arctic — sits on the leaner end of that spectrum. SOMA was a useful confirmation that we are not designing for an exotic edge case. We are designing for our actual operational reality, and we should keep planning, training, and equipping from that baseline rather than from someone else’s.

3. The most valuable part of SOMA happens outside the lecture halls

The formal program was strong. The corridor conversations were stronger. Over coffee, over late dinners, in the small rooms where people compare notes after the lights have come up — that is where most of my learning happened. I met many people who are much smarter than me, and I came home better for it.

This community operates without using names, which is part of its effectiveness. But the medics, surgeons, team leaders, and researchers I spoke with at SOMA 2026 should know that their time and openness meant a great deal to me. I appreciate it deeply, and I came home a better professional for it.

A Paper, Two Authors, and a Coffee in Raleigh

There are moments at a conference that feel scripted. At SOMA, somewhere between a coffee refill and the next session, I’m sitting with Bart van Herwijnen and Colin Smart when an email lands on their laptops at the same time. Their paper has just gone live in BMJ Military Health. We read the abstract on a phone, the three of us hunched over the screen.

The title is the kind of thing that makes you smile: “Hypothermia as a risk factor for injury outcome: are we really serious?” It’s a question, but it’s not really a question.

Their argument is sharp and, for those of us working in cold-weather operational medicine, overdue. We’ve spent two decades getting very good at haemorrhage control. Tourniquets, junctional devices, blood products forward — the trajectory is genuinely impressive. Hypothermia, the cold half of the lethal triad, has not moved. Incidence is roughly where it was. The kit has barely evolved. Foil blankets still appear in casualty bags as if they were doing meaningful work, which, against the four mechanisms of heat loss — conduction, convection, evaporation, radiation — they largely are not.

With Europe’s strategic centre of gravity shifting north and east, and prolonged field care becoming the realistic planning assumption rather than the edge case, this gap is no longer academic. A casualty in a Norwegian winter, moving through three national medical chains before reaching surgery, is exactly the scenario the current system is least equipped for.

The paper offers two practical anchors. The 4Cs — Consider, Conserve, Create, Continue — give providers a thinking framework at the point of care. The Hypothermia Emergency Response Approach 7 (HERA-7) gives a structured model for packaging, insulation, and rewarming through the evacuation chain. Around these, the authors push for things that should already exist: a common NATO staging system, measurable insulation standards rather than marketing claims, and equipment actually designed for the cold rather than repurposed from temperate kit.

This could have a meaningful impact on hypothermia management. If the 4Cs and HERA-7 are adopted across allied doctrine, we may finally see the kind of standardisation in cold-casualty care that haemorrhage control has enjoyed for a generation — with the same downstream effect on survival.

I closed the phone, finished the coffee, and went back into the next session thinking that some of the most important work in our field is the work that finally names a problem we’ve been quietly tolerating.

Read the paper → Hypothermia as a risk factor for injury outcome: are we really serious? — BMJ Military Health

Coffee in Valletta, Lungs in Cold Water

Some of the best conversations in this field happen sideways from the actual programme. Malta, February, Medicine in the Mediterranean — I’d just come off the stage after a lecture on cold-weather operations, the kind where the questions afterwards are more interesting than the slides, and someone introduces me to Harrison Steins. We end up at a small table with two coffees, and within about ninety seconds it’s clear we’re both fascinated by the same odd, awkward, undertaught condition: swimming-induced pulmonary edema. SIPE.

If you don’t work around open water, SIPE may not mean much. If you do, you’ve almost certainly seen it and possibly called it something else. A healthy swimmer — often young, often fit — surfaces gasping. Cough. Dyspnea. Sometimes pink froth at the lips. No aspiration, no near-drowning, no underlying cardiac history. The lungs have simply filled, with the glottis closed, while the person was doing something they’ve done a hundred times before.

Harrison’s scoping review, just published in Wilderness & Environmental Medicine, is the cleanest synthesis I’ve read on the subject. He pulls together the pathophysiology — central blood pooling from immersion, cold-induced peripheral vasoconstriction, exercise-driven cardiac output, and the resulting rise in pulmonary capillary pressure that pushes fluid across the alveolar membrane — and walks through how SIPE actually presents in the field rather than how a textbook might describe it. He’s deliberate about the population at risk: not just triathletes and open-water racers, but combat swimmers, divers, and any service member in cold water with a load and a heart rate.

The clinical core of the review is diagnostics in resource-limited settings. SpO₂ and auscultation, on their own, miss too much. Handheld lung ultrasound — B-lines, a few minutes of scanning — emerges as the field-ready tool that can actually distinguish SIPE from drowning, exertional dyspnea, or early ARDS, and do it on a beach, a deck, or a rib boat. Management is largely supportive: removal from immersion, oxygen, upright positioning, observation. Most cases resolve within 24–48 hours. A minority don’t, and those are the ones we need to catch early.

This could have a meaningful impact on how SIPE is recognised and managed in austere and operational environments. The combination of a clear pathophysiologic frame, a practical diagnostic pathway built around POCUS, and a population-aware view that explicitly includes military swimmers gives providers something they can actually carry into the field — not just into a seminar room.

I think about that Malta coffee occasionally. Two people from very different systems, agreeing that the most useful work in our corner of medicine is often the work that takes a half-known phenomenon and makes it teachable. Harrison’s review does exactly that.

Read the paper → Swimming-Induced Pulmonary Edema: A Scoping Review — Wilderness & Environmental Medicine

Slow Down. Make the Coffee Yourself.

As you’ve probably figured out by now — I love coffee. Properly love it. The ritual, the smell, the quiet four minutes of paying attention to something that asks nothing of you except a steady pour.

If you’ve never ground your own beans and brewed a V60 by hand, you’re missing one of the cheapest, most quietly enjoyable parts of a morning. Kettle on. Beans out of the bag. That first crack of the grinder, and suddenly the whole kitchen smells like something good is about to happen. Pre-ground coffee smells fine. Freshly ground coffee smells alive — sweet, oily, warm, sometimes a bit fruity, sometimes like dark chocolate and toast. The kind of smell that makes you stop checking your phone for a second.

I bring the ritual with me. I have a small travel set — hand grinder, dripper, filters — that lives in my pack on exercise. There’s something quietly funny about pulling it out in a cold tent or a cabin somewhere far north, while colleagues are reaching for instant. The grinder cranks, the smell hits the canvas, and suddenly everyone wants to know what I’m doing. By the time the bloom rises off the grounds, I’ve usually got an audience.

Then the slow circles. Water finding its way through. Four minutes where nothing is asked of you. What you get back is a cup that tastes like the bean it actually is — and a small, repeatable bit of calm that travels anywhere you do.

Buy a grinder. Buy a V60. Or similar. Take it with you.

When the Cold Bites Back: What Norwegian Soldiers Told Us About Frostbite

A new study just landed in the International Journal of Environmental Research and Public Health that I think anyone interested in Arctic operations, military health, or simply the human cost of cold should read. I’m especially pleased to share it because the lead author, Tuva Steinberg, is a great colleague of mine in the Norwegian Armed Forces and a PhD candidate now in the home stretch of her doctorate. This article is one of the cornerstones of that doctoral work, and it shows.

Tuva and her co-authors — Mona Anita Kiil, Arne Johan Norheim, and Trine Stub at UiT The Arctic University of Norway and NAFKAM — set out to do something the FCI literature has been missing: actually listen to the soldiers. Most cold-injury research is physiological or epidemiological. This one is qualitative. Sixteen Norwegian soldiers (eight men, eight women, mean age 27) who had sustained a grade 2 freezing cold injury during service sat down for in-depth, semi-structured interviews. The team then worked through the transcripts using systematic content analysis. Three themes emerged.

1. FCI is rarely “just” the cold

The soldiers described injuries that grew out of a tangle of parallel events: extreme temperatures (down to −37 °C and −40 °C in some cases), exhaustion, dehydration, lack of food, ill-fitting or missing equipment, and the unforgiving tempo of field exercises. As one participant put it, after days in the cold “you stop noticing or caring for yourself.” Another developed FCI on his fingers while standing isolated outside in a storm awaiting a COVID-19 test, feverish and wearing the warmest gloves he had.

2. Equipment use is a paradox

Time and again, soldiers removed their gloves for tasks that demanded dexterity — handling weapons, putting up tents, fastening buttons — because mittens made precise work impossible. Officers told them never to take the gloves off. Reality forced them to. Combine that with poor-fitting kit and time pressure, and you have a reliable recipe for frostbitten fingers.

3. Military culture is part of the etiology

This is perhaps the most uncomfortable finding. Strict discipline, hierarchy, and a “suck it up” ethos discouraged soldiers from reporting symptoms early or pushing back on orders. One soldier got FCI on his ear because his unit was ordered to remove their hats in solidarity with a comrade who had forgotten his. Others described feeling embarrassed, weak, or disloyal for raising concerns — even when they had medical exemptions. Reporting and follow-up after cold-weather exercises was inconsistent at best.

The consequences are not minor

Eleven of the sixteen participants reported long-term sequelae years later: chronic pain, numbness, cold hypersensitivity, altered career paths (one chose indoor IT work because outdoor jobs are no longer possible), and in two cases medical discharge from service. Norway sees roughly 120–150 new FCI cases each year, and Norwegian compensation estimates put the lifelong disability burden at 5–20%. Yet soldiers injured during conscription are typically excluded from further service and ineligible for compensation — a gap that almost certainly contributes to underreporting.

What to do about it

The authors are clear: develop standardised diagnostic criteria for FCI, build systematic reporting and follow-up into cold-weather operations, train soldiers to actually use their clothing systems under operational stress, and — crucially — shift the cultural norms so that reporting cold injuries is not treated as weakness. Brief cold-acclimatisation sessions, the literature now suggests, do not produce meaningful protective adaptation. Prevention has to be structural and cultural, not just physiological.

For an organisation like ours, with NATO obligations in the High North and a conscription system that brings in thousands of young Norwegians with limited cold-weather experience each year, this is essential reading. Congratulations, Tuva — looking forward to the defence.

Steinberg, T., Kiil, M.A., Norheim, A.J., & Stub, T. (2026). Causes and Consequences of Freezing Cold Injuries in the Norwegian Armed Forces from the Soldier’s Perspective — A Qualitative Study. Int. J. Environ. Res. Public Health, 23, 444. doi.org/10.3390/ijerph23040444

A Small Book About Cold Water

If the cold-weather thread running through this issue piqued your interest, I have something for you. My new mini-book, Cold Water Swimming — A Mini Book, is out now.

It’s a friendly, short, science-based guide to enjoying cold water safely, confidently, and with a big smile. Cold water isn’t just about discomfort — it’s about understanding your body, respecting the environment, and discovering something deeply rewarding. The book draws on years of real-world experience at the Norseman Xtreme Triathlon, research with elite military swimmers, and my published scientific work in cold-water physiology. Calm, clear, trustworthy guidance for anyone curious about stepping in.

Get Cold Water Swimming on Gumroad →

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It’s 4:30 in the morning on a ferry in a Norwegian fjord. The air is cool, the water is somewhere between 10 and 15°C, and a few hundred triathletes are pulling on wetsuits in the half-dark. Some are silent. Some are laughing too loudly. A few are clearly trying not to throw up. In about thirty minutes, they will jump off the side of this boat and start swimming.

For the last twenty years, my job has been to make sure they come back out.

Since 2005 I’ve led the Safety and Medical team at the Norseman Xtreme Triathlon — a race that begins exactly that way and ends, many hours later, on top of a mountain. Standing on that ferry, year after year, I started collecting questions I couldn’t answer well enough. Athletes asked them. Coaches asked them. Journalists asked them. Doctors asked them.

How dangerous is the cold, really? When is it too cold? Who is most at risk? Does my core temperature actually drop, or does it just feel that way? What is “afterdrop,” and should I be worried about it? Does a wetsuit basically solve the problem? And — almost always — what on earth is happening to my hands?

At some point I realized I couldn’t keep guessing. So I went and did a PhD on it.

We studied triathletes in cold open water. We followed Norwegian Naval Special Forces recruits swimming long distances in near-freezing seas. We measured core temperature, skin temperature, dexterity, reaction time, strength, biomarkers, and performance in real athletes racing at Norseman. We watched what the body actually does — not what we assume it does.

That work, plus two decades of standing by the water before sunrise, became a book: Swimming in Cold Water — Understanding Your Body, Staying Safe, and Enjoying the Experience.

I want to share three things I learned that surprised me, because they keep coming up — and because they tell you something about why I think this book is worth your time.

1. People cool very differently — and the difference is bigger than you think. Two swimmers of similar size, fitness, and experience can spend the same time in the same water and come out in completely different physiological states. One is fine. The other is on the edge of trouble. The reassuring averages you read online (”you can stay in for X minutes at Y degrees”) hide enormous individual variation. The real skill isn’t memorizing numbers — it’s learning to read your own body.

2. The first two minutes are the dangerous ones, and it isn’t hypothermia. When people think about cold-water risk, they usually think about hypothermia. But hypothermia is slow. The acute danger lives in the first couple of minutes: the involuntary gasp, the hyperventilation, the sharp rise in heart rate and blood pressure, and — for some people — what we call autonomic conflict, where the heart receives contradictory signals at exactly the wrong moment. This happens to fit, experienced people too. Understanding it is, in my view, the single most useful thing a cold-water swimmer can do.

3. A wetsuit is wonderful. It is not magic. Wetsuits buy you time and comfort, and I’m grateful every time I see one zipped up correctly on race morning. But a poorly fitted suit flushes water through and can actually accelerate cooling. Hands, feet, and head stay vulnerable. You can absolutely become hypothermic in a wetsuit. You can absolutely have an afterdrop in a wetsuit. The suit is a tool, not a guarantee.

There’s a lot more in the book — chapters on cold shock, on afterdrop, on why your hands stop working before you notice anything else is wrong, on adaptation (yes, you really can get used to it, within limits), on who should be extra careful, on what hypothermia actually feels like from the inside, and on practical first aid when something goes wrong. I’ve tried to keep it grounded in evidence but also human: there are stories, there is some Norseman folklore, and there is the occasional joke, because cold water is serious but it doesn’t have to be grim.

I didn’t write this for elite athletes or for physiologists. I wrote it for the recreational cold-water swimmer, the curious triathlete, the open-water adventurer, and anyone who has stood at the edge of a cold lake or sea and thought, I’d love to do this — but I’d like to do it intelligently.

Cold water is one of the most rewarding things I know. It clears your head. It changes your day. For some of us it changes the shape of a year. But it also deserves respect, because biology does not negotiate. My hope is that this book gives you the understanding to enjoy it more, and the knowledge to come home safely every single time.

If that sounds like your kind of thing, the book is here: Svimming in Cold Water

I’d love to hear from you in the comments. What’s your cold-water story — what pulled you in, and what scared you the first time? I read everything.

See you in the water.

— Jørgen