The tricky part is that peak fitness can’t be sustained indefinitely. This is especially true for elites pushing the limits of what the human body can handle. Track athletes may only do a handful of races per year depending on the event. For marathoners, it’s only one or two! The body needs cyclical variations in training and stress. You can only run the engine so hot for so long, and eventually you need a physical (and emotional) break.

What limits the length of time you can maintain peak fitness is less clear, but I imagine it is some combination of reaching a capacity of the central nervous system, hormonal disruptions, and deleterious alterations to cellular metabolism.

Josh Kerr’s recent mile world record is an exemplar case of how to peak. He put all of his eggs in one basket, and it worked. A carefully curated scientifically-informed strategy over many months allowed him to peak on a specific day in July. Later, when asked about also breaking the 1500 m world record this season (only 109 m less than the mile, so well within reach), he mentioned his the worry about “flying too close to the sun”.

The implication being the potential risk of injury from trying to maintain such an incredible form for an extended period. There is a fine line between the training load required for maximizing fitness and that producing injury, and athletes are constantly riding that line. In Kerr’s case, I assume there wasn’t many options for a world-record 1500 m race in close proximity to his 1-mile feat, because my intuition would be to attempt it ASAP so as to avoid the length of time close to the sun.

Someone who may have flown to close to the sun was Grant Fisher in 2025. After failing to medal in the 10k at the 2025 World Championships, he mentioned:

“Sometimes you reach for that gear and it’s just not there, and today it wasn’t there.”

A few days later after coming 8th in the 5k final, his legs were cooked in the final lap, and in response to reporter questions he remarked:

“Looking at now it feels like the season got a little long on me. I have been going hard for a really long time and eventually that does catch up to you. The margins are so slim now that if you’re a little bit off, a little bit tired, or not having a good day, it’s very challenging to still get a medal.”

I’m speculating here but chances are, his fitness — however you want to define it — was not appreciably different during these Championships compared to the Paris Olympics, or compared to his competitors.

Fisher was a double medalist at the Paris Olympics, getting bronze in the 5k and 10k, so lack of a medal in 2025 was a surprise. But if you look at his season building up to that point, it can start to make sense, as he alluded to.

In February 2025, he kicked off racing a 1500 m, 3k, and 5k indoors over the course of 12 days, setting world records in the latter two events. See the rest of his schedule below:

That’s a long season. Especially when you consider how hot he started (literally breaking 2 world records his first week of the year), and other factors like pretty frequent travel (he trains in Utah) to places like Jamaica, Florida, New York, Boston, Europe, and Tokyo.

In 2024, he had a similarly structured season, but only two races between mid-March and mid-June, 10 versus 13 races prior to the global championships, less travel, and importantly the Olympics in 2024 were 1.5 months earlier in the season than World Championships in 2025. You’ll notice he did the same 3k and 5k in February, but 7-8 sec slower than in 2025, meaning he wasn’t yet in tip-top shape so early.

Now, I’m definitely not saying he didn’t have a well thought out plan / training philosophy because his career speaks for itself. Also, you have to figure that at the time, doing those Grand Slam meets in 2025 was a huge financial opportunity and unwise to pass up (until the league later went bankrupt). But those meets were probably not in his best interest for peaking later on.

World Championships were in mid-September which is unusually late. Fisher was already in world-record fitness 9-months prior. While he probably had some down time afterwards, it wasn’t long until he had to prepare for those early Grand Slam meets before entering the thick of the season.

So for the better part of ~7-9 months he was more-or-less “race ready” and at or close to peak fitness, which means a long time of hard training and racing. In distance events like 5-10k, that’s a lot of weekly energetic output to sustain, especially at the speeds he has to train at to stay competitive, and likely led to not having enough gears in September.

He may have reached the sun.

Fitness

Training science and strategy has pretty much been completely democratized with the internet and social media. There’s really no secret training programs anymore and we have access to all of it. Whether it’s strength or endurance, you’ll likely see that the people at the top are doing mostly the same thing.

Maybe not exactly the same thing, but if you examine the big levers like total training volume (miles ran), time per month at each intensity zone, strength training, etc., I bet you’ll find it fairly consistent across the board. There’s a recipe that works which has been informed by over 100 years.

Athletics is like an arms race. Every athlete and coach is constantly seeking innovation or how to improve, and since there’s no real gatekeepers to training information anymore, everyone has access to the most relevant strategies. Just look how quick the rest of the world adopted the Norwegian’s training methods. Or listen to any pre-race press conference where nearly everyone says they are the fittest they’ve ever been.

Because of this, I don’t think fitness or training itself is often the deciding factor in most big events like the Olympics. Obviously there are caveats, like the 800 m in 2012 — David Rudisha was clearly on another level. Sydney McLaughlin and Tadej Pogacar also come to mind. Or it could be an athlete coming off of injury without enough time to build fitness.

But events <30 min (10k and below) are often decided by seconds or milliseconds, too small for pure fitness to be the differentiator. When the margins are that small, it’s increasingly about how well you are able to express that fitness on the day it matters.

Periodization

Periodization is how your training is structured over the short and long-term. Within any training program there are weekly, monthly, yearly, multi-year, etc. “periods” that have a specific training focus.

“Periodization is the purposeful sequencing of different training units (long-duration, medium-duration, and short-term training cycles and sessions) so that athletes can attain the desired state and planned results”

Issurin, Sports Med, 2010

Google any generic marathon or weight lifting regimen and you’ll find a periodized multi-week plan where intensity and volume change over time in effort to reach optimal fitness on the day of the event.

This is where training can get more complex, or at least it’s not as cut and dry. Anyone on social media can shout at you to do Norwegian 4x4’s because it helps VO_2max. But that’s a singular workout. There’s no context for how it fits in the broader picture.

Periodization is more art than science, IMO. There’s tons of research and theory out there, but not the kind that give you a simple answer like you might find in a study using a specific interval structure to enhance threshold or VO_2max. It’s more context dependent.

“Rather than a rigid concept, periodization could be seen as a framework within and around which a specific program can be formulated for a specific situation.”

Mujika et al., IJSPP, 2024

Now you might be thinking “well I’m not an athlete, so this doesn’t matter to me”. I would partially agree. Yes, you do not need to burn brain cells over a methodical periodization scheme if you are simply using exercise for general health, which most people are.

Even if that is the case, the concepts of periodization still can apply to anyone exercising for any reason. The goalpost just changes to whatever your equivalent of the Olympics is. Training is more fun and meaningful with goals.

If I take myself for instance, I’ve gotten into a rhythm the last 3 years with how I periodize my training. I do the Broad Street Run (10 miles) in early May, so spend the beginning of the calendar year focusing on aerobic base-building, threshold workouts, running higher mileage (for me, about 55-65/week), and strength. It works great because the weather in New England absolutely blows in the winter, and I usually have some extra Christmas calories to burn off.

I find it quite hard to do quality speed training that time of year because of 1) the frigid air, 2) the tracks/roads are often covered in snow, and 3) treadmills at Planet Fitness don’t go fast enough. But running longer distances outside is actually nice when it’s cold, and treadmills are great for threshold workouts. The short and cold days also are conducive to doing a lot of indoor aerobic training on my bike and rower, whereas in the summer I would much rather be outside.

After progressing towards and completing the 10-miler in May, the weather is usually nice again and I am sick of running higher mileage. Long runs in the heat are also just miserable. So I do some general training for a bit and then shift to more of a focus on 1-mile speed/power, which I’m pretty eager to do because it’s a new stimulus and goal. Lots of fast intervals, sprinting, and plyo’s (2-3x/week) for my hard days, and easy jogs or long bike rides on the lighter days.

As the summer winds down and I get a few mile or 5k races in, or just time-trials to test myself (I don’t have any business in an official 400 m race, but like to monitor my progress), I usually hit somewhat of a plateau and “saturate” the speed gains. That type of training is super demanding and after a few months I’m ready to shift gears, in perfect time for it to start getting cold again.

In the fall I still train daily but with a mix of stimuli and nothing overly specific. That then bleeds into the holidays where there’s not many races anyway (other than the greatest Turkey Trot of all time in Manchester, CT), and lots of social/family things to do. After that, we start over!

That’s still a “purposeful sequencing of training units to attain desired results”, just adapted towards the things I like to do. Over the course of a year, I touch on all (or most) of the relevant aspects of fitness, just for specific periods of time. It’s impossible to cram in strength, hypertrophy, speed, endurance, and power all at once, and I find shifting the focus periodically keeps me fresh and training exciting.

I should also mention that these phases complement each other. When I get done with the aerobic-dominant phase, I’m in great condition to handle 2-3 days/week of speed training. When I’m done with the speed training, the aerobic-dominant training is a breeze because the paces feel relatively slower (and the weather is cooler).

Periodization Schemes

Classic periodization methods were built around the quadrennial Olympic cycles, a long-term 4-year plan to peak at the biggest event in the world. Within that you have subdivisions of yearly (macrocycle), monthly (mesocycle), and weekly (microcycles) components that fit into the bigger picture. These schemes are traditionally linear, meaning they go from general to specific.

Where linear periodization might fail in an athletic setting is when you need to manage multiple peaks throughout a year, pertinent in sports with a long competition season. Some coaches/sport scientists promote block periodization (BP) for this purpose, which involves defined blocks of time (~7-10 days) throughout the year that are hyper focused on specific intensities and adaptations.

Below is a picture from a study on the world’s best cross-country skier — who I assume to be Johannes Klaebo — where for one year he did BP and another traditional linear periodization (TRAD). You’ll notice several 7-11 day blocks of time where he’s absolutely crushing the intensity: 5-6 high intensity training (HIT) sessions per week! But then they are offset with 3-4 weeks of only 1-2/week.

The idea being these highly concentrated HIT blocks induce a metabolic/hormonal overload, beyond what you get with a typical 1-3/week, optimizing subsequent adaptations. Instead with TRAD, the density/amount of HIT gradually increases over time into the competition phase.

While linear periodization still dominates modern athletics, there are lots of ways to skin a cat, and other strategies beyond just linear and block.

One of the more interesting periodization case studies is that of Nils van der Poel, a double gold medalist speed skater who published his training manifesto a few years back. It’s probably one of the most interesting things I’ve read related to training theory. His year was split into 4 “seasons”:

An aerobic season from ~March to July

A 10-week threshold season - threshold every single day

Specific/competition season - race pace every single day

• 5k/10k session refers to 48 (10k) or 24 (5k) laps on the ice at race pace with 1:20 rest between each

Aerobic season 2.0 (during competition season)

“After the first world cup block in December I would increase the aerobic training and substantially lower the high intensity training. This served two purposes. (1) It killed any top shape that was (if it was) stimulated during the competition block. If one keeps on training hard and with high intensity after a supercompensation to top shape, the risk of overtraining is palpable. By inhibiting the high intensity training for a couple of weeks and instead investing in more aerobic hours, the hormones settle to more salutary levels and the danger of overtraining after a supercompensation is avoided.”

-Nils van der Poel

That’s about as linear as it gets.

But I bring up block periodization because I think it could be applicable to the average person (assuming they have a decent training history already). In life our schedules tend to fluctuate and we might not have the luxury of a long-term traditional linear periodization. And if you aren’t an elite athlete, there’s not often the one big thing you need to peak for. But you might have several 7-10 day stretches with limited travel, low work stress, etc. where you can lock in and focus, so why not overload those weeks training-wise?

Moral of the story

You can have all the fitness in the world on paper, but without a proper periodization strategy you risk not being fresh on the start line and undermine your potential. In high level sports, fitness is rarely the bottleneck in producing champions, but how you are able to express that fitness when it matters (among other factors of course).

For the average person, applying periodization principles can not only make you more fit, but also keep training exciting as you reach for new goals and optimize different capacities throughout the year.

Critical speed (and for cycling/rowing: critical power) is one of the most interesting exercise metrics we have. In general, it tells us the boundary between hard but sustainable exercise intensities and very hard and unsustainable intensities.

I wrote about it more in depth in a previous article.

It basically it represents a metabolic tipping point. When you’re running slightly slower, physiology is operating in a steady state (demand for energy = supply of energy). Oxygen consumption and lactate are elevated but invariant with time. Critical speed is the fastest steady state pace our physiology can handle.

Run slightly faster than critical speed, even by just 10%, and steady state is broken. Oxygen consumption will progressively increase towards VO2max, lactate will progressively increase until volitional exhaustion, pH continues to fall with time, and so on.

Relevance for exercise research

Historically, exercise prescription in research uses % VO2max or % maximal heart rate, because we assume this normalizes the intensity across people of different fitness levels. It doesn’t!

Across the spectrum of fitness, there can be very heterogenous responses to exercising at a given percentage of VO2max, which you can see below:

There was up to a 4-fold difference in blood lactate between people exercising at the “same” intensity!

A classic study from Ed Coyle’s lab in the 80’s also showed this in highly-trained cyclists all with similar VO2max’s but different lactate thresholds. Those with a high vs low threshold could cycle at 88% VO2max for about twice as long (~70 vs ~35 min, if memory serves) with half the rise in blood lactate.

Same VO2max, different capacities. But how?

It’s because our first metabolic threshold (LT1 or VT1) and critical speed occur at different percentages of VO2max depending on our fitness, or endurance, driven by the cellular, molecular, and structural adaptations to training.

Metabolic thresholds denote distinct changes in muscle metabolism as intensity rises and can range from ~50 to 90% VO2max. These local metabolic changes determine how our cardiopulmonary system responds (pump more blood, breathe heavier), how hard something feels, and is the basis of training zones. As such, they are proxies for metabolic stability and stress that allows us to infer how long a workload can be tolerated, and the metabolic signaling responses for training adaptations.

This concept has been the source of major critiques of many training studies because if you dose the exercise as % maximal heart rate or % VO2max, the metabolic and molecular exercise responses that subsequently drive adaptations will likely differ. That is, unless all of your subjects have exactly the same VO2max, lactate threshold, and critical power (good luck with recruiting!).

One of many examples of where this becomes problematic is looking at the mechanisms underlying responders vs non-responders to physical training. Someone who responds versus not may have simply gotten a higher dose of training because the prescribed intensity was above threshold.

This is why there has been a push to prescribe exercise relative to an individuals thresholds because it normalizes the metabolic stress. In the case of moderate intensity training prescription, this would be having people train at 90% lactate threshold versus 65% VO2max or 75% maximal heart rate.

To illustrate, one recent study had people do moderate (44% maximal power output for 40min) or high intensity interval training (4x4min intervals at 80% maximal power output) for 8 weeks. Before and after they measured VO2max and critical power.

Both groups saw increases on average, but there was a huge variation in individual responses, ranging from -5% to 25% for VO2max and +4% to +61% for critical power.

None of that is interesting by itself and aligns with other research: HIIT is a more potent stimulus, and adaptations vary a lot between people. The interesting part came from a secondary analysis where they went and determined each persons highest prescribed training intensity as a % of their baseline critical power.

Remember, training was prescribed as % of maximal power output. So if your maximal power is 300 watts, critical power is 180 watts, and got put in the MICT group (44% maximal power = 132 watts for 40 min/day), you were training at 73% of critical power. Someone else in the study could have the same maximal power but a critical power of 230 watts, which means they were training at 56% critical power, but still 44% maximal power.

If you look at the graph on the left below, you can see this exact scenario in 2 of the subjects which I circled in red.

The training-induced change in critical power was linearly related to how close the intensity was to critical power. It explained over 60% of the variance: the higher % of critical power you train at, the better your critical power gets. It makes sense, but clearly the prescription strategy of % maximal power/VO2max does not normalize the training response. Interestingly, this did not account for the variability in VO2max adaptations (figure on the right).

That was a long detour before I get into the main study I wanted to highlight. But, I wanted to drill down on the concept that critical power is a relevant metric that we could/should be anchoring training to in research studies since unlike % VO2max, it seems more capable of delivering a more homogenous training response.

Calculating critical speed

Obtaining critical speed is the most annoying part of the whole concept. It requires several (~4) maximal effort time trials between 2 and ~20 minutes to build out a speed-duration curve using mathematical modeling. As you can expect, most people don’t have time for this.

A recent study tried to streamline this and calculate critical speed from only 1 previous race performance. The authors used a pretty clever approach and I wonder why no one has thought of this before, including myself. They leveraged the classic 1979 book by the legendary Jack Daniels (RIP) titled Oxygen Power: Performance Tables for Distance Runners.

The book is the basis of the VDOT system — tables which take a recent race time and then predict performances for other distances based on the calculated VDOT value. VDOT units are conveniently quite similar to VO2max, although they aren’t the same. Consider it a running performance index that integrates the oxygen cost of running (derived from lots of lab testing) and the length of time a given % of VO2max can be sustained (also derived from lab testing).

You plug in a recent race performance, see what your VDOT is, then can see what your predicted times in other distances would be. When I do this with my own data using a recent half-marathon time of 1:15:53, the equivalent times down to the mile are quite accurate.

I was able to find a pdf online relatively easily at one point, but you can also read the brief Appendices of the book here which explain how the tables were constructed and science behind the predictions. Fortunately, there is also a convenient online calculator.

The authors condensed the original VDOT tables to 6 common distances between 1500m and the marathon (42km) in VDOT rows between 40-85 ml/kg/min (46 rows). They then calculated critical speed based on predicted race times within each VDOT value for the 1500m, 3km, and 5km distances, producing 46 critical speeds. The authors basically said “empirically these tables/times are pretty accurate, so the critical speed results should be able to apply to anyone”. In this case, “anyone” refers to those with a VDOT between 40 and 85.

Next, they did a regression of the calculated critical speed against each of the 6 race distances time columns.

The above figure/math produces 6 equations that predict critical speed based on predicted performance time from the Daniels’ tables. The result from their paper:

So, you plug a recent race performance into the equations above and get an estimate of critical speed, or more accurately, “metabolic stability”. When they had several runners run at self-selected speeds between 60-90% of the resulting value, they always achieved steady state or metabolic stability as measured by oxygen uptake. When they ran at 110% of the resulting value, all of them fatigued and had to stop running within 3.5 minutes.

While the Daniels’ tables aren’t exactly perfect, and the equations won’t give you a precision estimate of critical speed, this is a great practical tool to use in research when understanding the upper end of metabolic stability matters (per the example I provided earlier), assuming your subjects have run one of these race distances recently. At the very least it can be used as a gut check to say “we definitely don’t want you going above X mph because we know it won’t be sustainable”.

I should also say that I used the half-marathon equation from this paper a few weeks before a 10 mile race to guide some of my interval workouts. It came out to 5:36/mile pace and felt exactly what “threshold” should feel like. At my current fitness a 10 miler is run pretty much right on the nose of critical speed/metabolic stability, maybe a few percent slower, and I ran the race at an average pace of 5:40/mile. At mile 8 I tried to surge to 5:30 pace and immediately sensed impending doom / burning my final matches, so settled back in at 5:40 until a much later kick at the end. So while anecdotal the data aligned pretty well for me.

I’ll always have directionality — short intervals, long intervals, steady state, threshold, easy, max effort reps, etc. — but I usually wait until I’m done the warm up to figure out exactly what I’m going to do. Sometimes I go harder than expected, sometimes easier, but I always make sure to get it done.

It may seem haphazard but it works for me, and it helps that I live and breathe this type of stuff. So me not having a specific plan is far different than someone who isn’t an exercise physiologist. However, I am interested in hiring a coach at some point to see how I could benefit from a tad bit more structure. But for now, I haven’t seen any signs of a plateau or things going wrong.

A Blizzard

This definitely was not an ideal training week. For one we got hit with about 2 feet of snow which derailed any running on Monday and Tuesday. I also just didn’t feel great. I think the lack of sunlight is getting to me. Not sick, just a bit “lazier” than usual. The biggest sign of that was the thought of 3-4 min rowing intervals at 2000m race pace (a key workout I’ve been doing) felt repulsive the entire week. I just didn’t have the mental fortitude to do it.

I’m chalking it up to the weather and the fact the previous 2 weeks were my biggest volume weeks since early December, so the body is probably just figuring things out.

So, I decided to keep most of my hard days to right around threshold. Not quite what I wanted since the 2000m row requires more intensity and I’m trying to prioritize those 2-5min hard intervals. But, it was still enough to drive some adaptation and fitness without pushing myself to the brinks of hell.

Totals: 40.53 miles🏃 | 69.3km 🚣🏼 | 57.31 miles 🚴‍♂️ | 24 mins 🏋🏻 | (13h 14min)

• Monday

  • (AM): 65min steady bike ride at 195 W (RPE 3)

  • (PM): 60min easy row with 10 x 100m in the last 20min (RPE 2)

• Tuesday

  • (AM): Threshold intervals (rower):

    • Easy warm up

    • 16 x 90 sec / 30 sec at 260W avg.

    • 5km easy cool down (56min, RPE 5)

  • (PM): Over-unders (rower):

    • 15min warm up

    • 2 sets of 3min-3min-3min-3min / 5min recovery

      • Each 3min interval alternated just below and just above threshold. I was shooting for roughly 250 and 270 W but this was harder than expected.

    • Set 1: 243, 259, 232, 260 W | Set 2: 263, 232, 264, 238 W

    • On the second set, I started at above threshold in effort to ramp up my VO2 faster, per my previous article.

• Wednesday

  • (AM): 62min steady bike at 202 W with some 15 sec sprints at ~500+ W (RPE 3)

  • (PM): 10 mile treadmill run (RPE 4):

    • Warm up + 20 min at 6:27/mile (tempo)

    • 5 x 60 sec / 60 sec at threshold

    • 5 x 30 sec / 90 sec at 5k down towards mile pace

    • Run at 6:50/mile until I hit 10

  • (PM): Lift (RPE 5)

    • DB reverse lunges, lat pull downs, hack squats, dips

• Thursday

  • (PM): 45min easy row with 6 x 20 sec efforts (RPE 3)

  • (PM): 45 min treadmill run with 3 x 1 mile at threshold (5:52/mile)

    • This was at 9pm and I felt like shit from not eating enough.

• Friday

  • OFF 😱. The body was feeling cooked. But I made up for it Saturday.

• Saturday

  • (AM): 42min row (RPE 5)

    • 2000m warm up

    • 2 sets of 10 x 30 sec / 30 sec at around race pace. Averaged 358 W and 368 W for the first and second sets

    • 2000m cool down

  • (PM): 11 mile steady run outside (78 min, RPE 3)

    • + 3 mile treadmill jog with some 30 sec efforts at 5k pace

  • (PM): 32min row (RPE 4)

    • 1500m warm up

    • 10 x 60 sec / 60 sec at 300 W average

    • 1500m cool down

• Sunday

  • (PM): 10 mile run outside with some 20-60 sec pickups on the back half (65min, RPE 5)

  • (PM): 60 min easy bike at 180 W while watching the Millrose Games.

All in all it was a decent week. Not great. But stacking the weeks rather than specific workouts is what matters.

Exercising at intensities close to V̇O₂max places the greatest stress on oxygen delivery and utilization to yield the adaptations required to improve it.

While I am going to focus on V̇O₂max intervals here, I should mention intervals are useful beyond training for maximal capacity, like threshold and tempo reps to build the aerobic base, or the short interval approach popularized by Mihály Iglói, the legendary Hungarian coach of American runner Bob Schul.

The latter of which could involve a workout consisting of 10 x 100m - 16 x 400m - 14 x 200m - 6 x 175m - finishing with 15 x 100m; the goal of which is to get a ton of race pace volume in and focus on rhythm without crushing you metabolically.

A Bit of Background

One way to quantify the effectiveness of interval training is by measuring time spent >90% V̇O₂max. The more time you spend at a higher percentage of V̇O₂max, the greater the performance gains and improvements in physiological benchmarks like V̇O₂max and lactate threshold.

Fortunately, there’s many ways to skin a cat — meaning different variations of intensity, interval length, and recovery time.

The terms vV̇O₂max or pV̇O₂max will be mentioned often below. They refer to the velocity (v) or power output (p) that elicit V̇O₂max. There’s a few different definitions on how to calculate it, but it’s usually recorded as the final speed/power you reach before quitting a V̇O₂max test, or the highest 60sec average.

The 30/30 protocol by French researcher Véronique L. Billat found that in a single workout, trained runners accumulated 8 total minutes at V̇O₂max if they alternated running 30 sec at 100% vV̇O₂max and 30sec at 50% (they could do about 19 reps before fatiguing). Conversely, doing 1 rep at 90% for as long as possible only elicited 2min and 42 sec total time at V̇O₂max on average.

This is important because most people can only sustain their V̇O₂max during exercise for a few minutes at a time. About 4 to 6 min with lots of individual variability. Training seems to improve your tolerance to sustain it. But it’s also very stressful to do those longer, constant pace intervals at 90%+ V̇O₂max.

For perspective, my vV̇O₂max is right around my 1 mile PR. I can tell you right now I would not enjoy a workout that said: “Run at your mile PR pace as long as you can, rest 3-4 minutes, and repeat 5 times”. But I could run 400m repeats at that pace many times, enjoy it, get a great training effect, and the stress would be manageable.

In the classic Hickson study where people did 3 days / week of 6x5min intervals at 100% V̇O₂max, they had no interest in continuing to train after the 10-week study. I suspect a more varied interval structure would have facilitated longer compliance.

Billat also used another novel approach in a 2012 study where they measured V̇O₂ during two types of exercise. The first was a constant power test: subjects simply rode at 100% pV̇O₂max as long as possible. The second was a variable power test: subjects rode at 100% pV̇O₂max as long as possible, but then the researchers adjusted (reduced) the power output continuously with the goal of maintaining V̇O₂ at its maximum.

In the figure below you can see the response in 1 subject where the constant power test (dark symbols) caused exhaustion in ~8min (5min total at >95% V̇O₂max). The variable power test caused exhaustion in ~30min (26min at >95% V̇O₂max) despite a far lower average power (75% of pV̇O₂max).

It sounds paradoxical that you could decrease the workload but still keep operating at V̇O₂max. One theory involves the lag time in V̇O₂ (V̇O₂ kinetics) and metabolic processes that drive V̇O₂ upwards. Starting with a higher power output helps you reach V̇O₂max faster, and then as long as the power output remains above lactate threshold or critical power, the stimulus remains high enough to maintain a high V̇O₂.

However, this type of training is not practically relevant since people are not going to be using an oxygen analyzer during training.

Let’s look at one approach to make it more practical.

The Russian Doll Method

The impetus for writing this is a 2020 study in the International Journal of Sports Physiology and Performance, titled “Optimizing Interval Training Through Power-Output Variation Within the Work Intervals”.

I call it the Russian doll method because “power output variation within the work intervals” means doing mini intervals inside of your bigger intervals. Their goal was to take the concepts from Billat’s variable power test and apply it in trained cyclists.

Conceptually, the idea was to have cyclists do 2 workouts of 6x5min intervals at an average power output of 84% maximal aerobic power, or MAP (similar to pV̇O₂max), which in these athletes was ~400W.

The emphasis is on average because there’s many ways to arrive at a given power output. On one day they kept the pace constant, (Figure C below). The other workout varied the pace (Figure B below). Within the 5min bout, they did three 30 sec bursts at 100% MAP with everything else at 77%, resulting in an average of 84% for each interval.

The variable approach led to ~2 min more accumulated time at >90% V̇O₂max despite rating of perceived exertion (RPE) and internal training load measured via heart rate being similar.

The latter 2 points (RPE and training load, Figures B and C above), and the similar breathing rate (a great indicator of physical effort) between workouts are what’s the most relevant in terms of practical application. It suggests you can put out the same amount of effort, and average power output, but receive a larger training effect.

Physiologically, a few things may explain this. One is the V̇O₂ kinetics I mentioned earlier, which is how fast V̇O₂ rises at the start of exercise and falls at the end of exercise (or when power output changes).

If you start the interval with a hard 30 sec effort, you likely recruit more fast twitch muscle fibers and V̇O₂ gets up faster. Since V̇O₂ also has a lag time when you reduce power output (it doesn’t “turn off immediately”), you’re still reaping the benefits of operating at a higher %V̇O₂max despite less output (in this case, going from 100% to 77% maximal aerobic power).

The other thing to mention is that ventilation was slightly higher with the Russian doll method. The lungs require oxygen too, so part of the higher %V̇O₂max was due to the oxygen cost of breathing. That’s not necessarily a good thing if the lungs are “stealing” oxygen from muscles. But it only accounted for about 10% of the higher V̇O₂, so I wouldn’t be too concerned about it.

Practical Takeaways

This concept isn’t entirely new as the variability in power output during workouts is the basis of the normalized power metric, which is thought to better reflect what the body experiences internally than a simple average power.

There’s a million ways to design workouts and get more fit. This one isn’t magic. But, I do appreciate the context and purpose of the study which was to take an impractical method (the one Billat study), and test it in a scenario that any of us can do to get more bang for our buck during interval workouts.

Last week I used this for my 3 min rowing intervals and found it made them a bit more manageable. Instead of holding a constant ~320W, I did 15 sec at ~360W with 45 sec at 300W (ballpark) each minute which landed me right at a 320 average for each rep. The main thing I noticed was that it kept the workout stimulating and the 45 sec at 300W felt almost like a recovery. Three minutes starts to feel very long when you do it 8 times in a row at hard effort, so anything to spice up the process helps in my opinion.

Next time you have long intervals on the schedule, adding a couple 20-30 sec bursts in the middle of it may optimize the training effect, and more importantly, make it more tolerable (fun?).

I have some lofty goals for 2026. In 2025 I saw big improvements in nearly every running distance from 400m to 10 miles and want to keep the momentum going and capitalize on the increased fitness. I’m also turning 30 this year, so my window for optimizing the shorter and faster events (which I’m more fond of) is closing slowly.

First goal: The 2000m Row

A 2km row test is one of the hardest things I’ve ever done. It’s like an acid bath. I wrote about all things rowing in a previous article here.

I like rowing for many reasons. For one, successful performance requires a unique blend of endurance, strength, and power. It’s also full-body exercise. From a general health standpoint, the benefits are obvious. I also enjoy how you can upload performances to the Concept2 website and see where you stack up among the population because their ergometers are so widely used.

A few weeks ago I was running VO2max tests for a research study and opportunistically hopped on the erg to test myself when we had some down time.

I was pleased by the results. Since the 2000m row is essentially a VO2max test (i.e., the 6-8min duration makes success heavily reliant on VO2max), I thought I might as well go through a training block and re-test both VO2max and 2000m performance in 8-10 weeks.

I’m long overdue for a proper 2000m test. My last one was in February of 2024 in a time of 6:44 (339 watt average). There’s a really good VO2max prediction equation based on the average power output during a 2000m test:

VO2max (ml/min) = 10.96 * average 2km power output + 1168

That estimates my 2024 VO2max at 4,883.44 ml/min. Thats pretty spot on to what I tested at on the treadmill at that time. But I’ve since done a lot of rowing volume and as you can see in the picture, improved my VO2max by 400 ml/min, giving me hope I can probably rip a solid PR.

But it’s better than blind hope. If I flip the equation around since I know my current VO2max of 5,191.87, I can predict the power output and thus 2km time:

Power = (5,191.87 − 1168) / 10.96 = 367.141 watts. That’s a 6:33 2000m which I would be thrilled about. I’m hoping to get close to 6:30 after this 8-10 week training block (lofty but possible). It makes me sick thinking about holding that pace for 6.5min.

So how will I train for it?

My current training plan

Throughout the year running will probably again be my primary exercise modality because I’d rather be outside than sit on the erg. But since I don’t have a major race planned until May (I’ll do some 5-10k’s before then), and the weather sucks in New England this time of year, it’s a good time for indoor rowing.

Big picture wise, the next 8 weeks or so will be:

• ~50 miles a week of base-building for running where I keep the majority of work below threshold (~5:45/mile).

• 3 hard rowing interval sessions

• 2-3 days of lifting:

  • 30min each. Focus is 2 heavy lower and upper body exercises each with plyo’s, core and calisthenics mixed in

• Fill in the rest of the time with easy/steady cycling or rowing, which brings me to 12-14 hours per week.

I’m saving all my hard efforts for the rower, but still want to build a good running base for when I start to train for a 10mile race in May.

My hope with this is to share my thoughts about training philosophy, spur some good conversations and feedback, and maybe even give you all some ideas for how to train if you need them. Below is the weekly breakdown for the past 3 weeks, and then I’ll post weekly updates until I re-test.

January 5th - January 11th

This week was rough so I’ll keep it short. I was working 12-14hr days and could only train for ~60min late at night.

Totals: 50.52 miles🏃 | 28.7km 🚣🏼 | 2.25 miles 🚴‍♂️ | 26 mins 🏋🏻 | (8h 27min)

January 12th - January 19th

Schedule was still a bit off but got some good work in on the back half of the week.

Totals: 49.24 miles🏃 | 61.5km 🚣🏼 | 25.06 miles 🚴‍♂️ | 43 mins 🏋🏻 | (12h 20min)

• Monday

  • PM (run): 9.5 miles steady with some strides (76min, RPE 3)

• Tuesday

  • PM (row): 5 sets of:

    • 60sec / 60sec at 276 to 313W; 40sec / 60sec at 300 to 330W; 20sec / 60sec at 371 to 405W (60min RPE 3-4)

• Wednesday

  • PM (run): 8.9 miles steady (63min, RPE 3)

  • PM (row): 3 x 3min / 3min at 305 to 310W; 4 x 90sec / 90sec at 321 to 325W (50min RPE 5)

• Thursday

  • PM (run + lift):

    • 60min run with tempo intervals: 1 x 15min at 6:31/mile / 4min jog; 2 x 10min at 6:22/mile / 3min jog (RPE 4)

    • Leg press, RDL’s, shoulder press, rear delt fly, deep reverse lunges

  • PM (row): 7km easy at 156W (31min RPE 2)

• Friday

  • AM (bike): 80min steady at 207W (RPE 3)

  • PM (run): 8 miles with 7 x 1km at sub-threshold/threshold (3:45 to 3:36) (56 min RPE 4)

• Saturday

  • PM (run + lift):

    • 4 x 8:00 / 2:00 tempo intervals at 6:40 to 6:18/mile (65min RPE 4)

    • DB bench, DB row, lat pull downs, tricep pushdown

  • PM (row): 30min easy + 6 x 30sec / 2:00 at ~350W (45min RPE 3)

• Sunday

  • AM (row): 15min easy (RPE 2)

  • PM (row): 3km at 220W, 8 x 500m / 2:00 at 307 to 330W, 2km at 222W

  • PM (run): 5.4 miles easy (42min, RPE 2)

January 19th - January 25th

Totals: 50.20 miles🏃 | 54.7km 🚣🏼 | 66 miles 🚴‍♂️ | 54 mins 🏋🏻 (14hr 31min)

• Monday

  • AM (bike): 64 min. endurance bike ride at 210W (RPE 3/10)

  • PM (run + lift): 5 steady miles in 33:43 + 5 x 60” / 60” at threshold and 3% incline (45min, RPE 4)

    • Dips, leg press, push ups, leg raises, machine back row (RPE 4)

• Tuesday

  • AM (row): 8 x 2:30 / 2:30 at 305 to 317W. 1st 4 reps constant pace, last 4 reps included 2 x 15sec micro intervals within the 2:30 (61’, RPE 5-6)

  • PM (run): 50 min treadmill run 4 sets of 60” - 45” - 30” at 10k to 5k (5:42-5:15/mile) pace with 30” jog between each rep. (RPE 4)

• Wednesday

  • AM (run): 40 min easy run with strides (RPE 3)

  • PM (run): 36 min easy run (RPE 3)

  • PM (bike): 45 min steady at 200W with 6 x 30” pickups at 250W (RPE 3)

• Thursday

  • AM (run + lift):

    • 10’ at 6:31/mile / 2:30 jog; 7’ at 5:49/mile / 3min jog; 5’ at 5:39/mile / 3min jog; 3 x 4min / 2min at 5:39/mile (62 min, RPE 4-5)

    • Single leg RDL, DB split squats, DB incline bench, DB row, SL leg press

  • PM (row): 2 x 6min / 2min at 230 and 242W; 3 x 45” / 2:15 at 364 to 404W; 3 x 30” / 2:30 at 441 to 483W (45 min, RPE 4)

• Friday

  • AM (bike): 60 min steady ride at 200W with 20” pickups every 5 minutes at 360 to 410W

  • PM (run): 50 min easy progression run plus 7 x 60” tempo pickups

• Saturday

  • PM (row): 4 x 3km / 2min aerobic (180, 190, 200, 210W) + 10 x 20” / 40” at 310 to 382W) (66 min RPE 3)

  • PM (run): 3 sets: 10min / 1min - 3min / 2min (10min reps at 6:27, 6:22, 6:15/mile; 3min reps at 5:52, 5:46, 5:39/mile) (68min, RPE 4)

• Sunday

  • PM (row): 5 x 3min / 3min at 315-320W with 2 x 15” micro intervals within each rep + 5 x 1min / 1min at 330W (67min, RPE 7)

    • This was hell for some reason

  • PM (bike): Easy 45min bike at 170W

Some people might ask how I have the time for this. My general answer would be that most people have at least 2 hours of free time per day even if you work full time. So I just choose to spend 1.5-2 of those hours training. Different strokes for different folks. I also don’t have kids yet which helps, but sometimes I do have to workout at odd hours like 8-9pm because that’s the only time I could manage. I also recognize I likely won’t have the time to train this much forever, so I’m trying to capitalize on it now.

Another question might be how I have the energy (something that puzzles my mom). 1) I eat a lot. 2) I have been training for a long time and building up to the point where I can handle 12-14+ hours per week.

See you next Sunday 🫡. I’m also on Strava so give me a follow.

That’s partly because my close circle of friends and family—who ask me the most questions—think that because I have a PhD in 1 health-related area, I obviously must know everything about health.

The last month alone included skin cancer treatments, shoulder arthroscopy rehab, swelling from Lyme disease, and specific food molecules that reduce dementia.

“I don’t know” followed nearly all of them. But they often create a learning opportunity, like stumbling on two studies (here and here) showing nicotinamide (a B vitamin) may help skin cancer prevention.

Blood donations

Recently, I was asked whether donating blood would influence a VO2max test in 2 weeks. Off the top of my head, I knew the health/safety risk was minimal, but that blood donations do acutely (within 1-3 days) reduce VO2max pretty substantially.

What I didn’t know was how long those negative effects linger around for.

I am not trying to persuade people not to donate blood. But it’s not an entirely innocuous process if you care about aerobic performance in the short-term. Basically, I wouldn’t recommend an endurance athlete donate blood in-season.

A standard blood donation is 1 pint (480 mL) and 10% of what you have circulating in your body. You can also specifically donate red blood cells (Power Red donation), plasma, or platelets only.

Blood and exercise capacity

Aerobic performance requires delivering oxygen to muscle and blood is our delivery driver.

The table below is part of a resource I’m working on characterizing physiologic traits distinguishing elite athletes from normal people. Blue text indicates values for men and pink for women, both in absolute (total liters or grams) or relative (per kg of bodyweight) units.

Blood volume simply means the total amount of blood in the system and is made up of the differing portions like red blood cells and plasma (the yellow part you see after spinning a tube of blood in a centrifuge). Clearly, the amount of total blood, plasma, red cells, and hemoglobin are much higher in athletes.

Red cells contain hemoglobin which carries oxygen. The total amount of hemoglobin (in grams) is directly related to exercise capacity. This is why people blood dope and train at altitude.

Plasma is important for thermoregulation, and one of the primary adaptations to heat acclimation is plasma volume expansion. The expansion of plasma volume with training is why relative hemoglobin values (in grams per deciliter of blood volume) are similar in athletes and the general population despite much higher total hemoglobin and red blood cells.

What happens when you lose a pint of blood?

Blood is 40-50% red blood cells and 50-60% plasma (1% platelets and white blood cells). Losing a pint is enough to make you a little dizzy, reduce blood pressure and how much blood the heart pumps, which raises heart rate to compensate. If that happens, it resolves quickly.

The specific losses

We have about 5 million red blood cells per microliter of blood, meaning donations remove a couple trillion red cells. Total hemoglobin decreases by about 8% (men) to 13% (women) and hemoglobin concentration (g/dL or g/L) by a similar amount. The blood bag also steals about 250mg of iron, which can be substantial, particularly in females (~75% of their total iron stores vs 25% in men).

The replenishment process

Plasma starts replenishing ASAP. The body does an “auto-transfusion” where fluid within the tissues gets pushed out into the bloodstream. This dilutes the blood a bit and reduces hematocrit progressively for 2-4 days before it eventually starts to increase back to normal.

It emphasizes the body’s priority of restoring total blood volume, even if it is a bit diluted and might “dehydrate” the cells within tissues transiently.

Red cells, hemoglobin, and iron take a bit longer.

In one study, it took people 60 to 170 days for hemoglobin concentration to return to what it was pre-donation, depending on baseline iron status and supplementation.

In an analysis of >1 million Finnish blood donors it took men 200, and women 300 days for hemoglobin to recover, which was influenced by age and blood donation frequency. The latter point is interesting. It could either mean the body is adapting to frequent blood loss by up regulating the replenishment process, or that some intrinsic (genetic or otherwise) phenomenon allows faster recovery, and the people that recover faster are more likely to become frequent donors.

Keep in mind the above figure is averages, and there is some individual variability here. See below the changes in total hemoglobin and hemoglobin concentration from a study in pre-menopausal women, where the black lines are the averages and the grey are individual subjects.

What about iron?

After all, protecting against iron deficiency is the reason that you can’t donate blood more than every 2 months or so (in the US and Canada, but longer in other countries).

Many blood biomarkers are used to evaluate iron status, like ferritin, transferrin, transferrin saturation, total iron binding capacity (TIBC), soluble transferrin receptor (sTFR), and hepcidin. This link has a good basic overview.

Iron is a component of heme proteins and is what binds oxygen within hemoglobin. Heme proteins are also found in mitochondrial enzymes like cytochrome c oxidase, and very important for energy production, metabolic health, and endurance.

Most of the research around iron and exercise performance understandably focuses on oxygen transport via circulating hemoglobin. I’m very curious about whether low iron status influences mitochondrial training adaptations given its role in oxygen transport in mitochondria.

Most bodily iron (two-thirds) is stored in red cells. Erythropoiesis — the creation of new red cells — is the biggest iron consumer. We create ~200 billion new red cells every day which requires ~23 mg of iron. When we’re doing high loads of endurance training, or spending time at altitude, that demand is much higher and it’s critical to have adequate iron levels to support it.

For this reason it’s very common for research studies investigating altitude adaptation, and athletes at altitude camps, to provide iron tablets to ensure the subjects/athletes have enough “fuel” to support erythropoiesis. However, iron is also poorly absorbed by our intestines. Taking it with vitamin C assists with that a bit.

A great example is a study of young, otherwise healthy, but slightly iron deficient women, where the effects of endurance training on VO2max were blunted. But if those women supplement with iron daily, VO2max increases twice as much.

When we lose that 250mg of iron from a blood donation, our body kickstarts erythropoiesis to get red cells back to normal. As you now know, that consumes a lot of iron which causes levels to fall.

Whether you have low or high iron levels to start — as measured by serum ferritin — it will likely take longer than ~170 days for ferritin to return to normal if you don’t supplement with iron. If you do supplement, thats shortened to ~80 days.

Back to the original question

Fortunately, VO2max and performance are recovered much faster than hemoglobin or ferritin, but still can take quite a bit of time depending your viewpoint and the importance of aerobic capacity in your daily life.

Remember that oxygen delivery from heart-to-muscle is a key determinant of high-intensity performance, and oxygen delivery depends on the heart’s pumping capacity and arterial oxygen levels.

What the research shows

The first issue is that initial loss of blood volume that takes 2-4 days to recover. The heart pumps less blood irrespective of any changes to hemoglobin or iron levels, and that causes a performance hit.

One study put untrained people through 6 weeks of training that increased their cardiac output and VO2max by 10%. Then, they withdrew ~380 mL of blood and it completely reversed cardiac output and VO2max back to baseline levels. For some this was even less blood removed than with a standard donation, and it basically erased 6 weeks of training adaptations, for at least a couple days.

But they measured VO2max within days after phlebotomy. Do the negative effects last longer?

A 2015 study on 20 men shows a recovery period of 15 days, with similar effects for 3km time-trial performance.

Two years later they did the same study in women and VO2max was still lower than baseline 28 days later. There wasn’t a statistical difference between day 28 and day 0, but if you just look at Figure A below, I would argue that’s not quite recovered. 3km performance did however return to normal by day 28.

And if you thought it couldn’t get worse, the most recent study on the topic in 2024 found even after 12 weeks, VO2max in pre-menopausal women was still not back to baseline. Although, it suffered from a small sample size and the fact some of the women could have been classified as iron deficient throughout the study.

Why the sex difference?

Two main reasons. 1) Blood donations take an absolute amount of blood (~500mL). Since men are bigger with more blood volume, losing 500 mL is relatively less of reduction than it is for women. 2) Pre-menopausal women lose extra blood monthly via menstruation, creating a further stress on the system and delaying recovery.

What you can do

The easiest way to avoid all of this is to not donate blood (don’t tell the Red Cross).

I’m mostly joking, but for endurance athletes in-season (potentially all the time), or anyone training for a demanding event in the upcoming months, it’s probably your best bet. Especially since endurance athletes already can struggle with low iron.

However, lack of blood donations could severely impact medical care, so let’s not suggest that for the masses.

What you can do is get your iron levels checked (i.e., ferritin). High iron status to start gives you a way better recovery trajectory. The other would be iron supplementation following the donation. Those with adequate ferritin + daily iron for 6 months after donating restore hemoglobin and iron stores twice as quickly.

Final thoughts

If there’s any topics you’d like to see me cover next, drop a comment below. I’m always keen for new ideas.

“No one knows what it means, but it’s provocative, it gets the people going” - Will Ferrell

I’ve been measuring oxygen consumption (V̇O₂) on various people continually since 2018. Everywhere from the basement of UConn’s Gampel Pavilion to a US Army lab at one of the highest altitudes in the United States. When you’re a physiologist and human performance scientist, it’s just something you do because V̇O₂ is a critical part of human biology.

Recently, maximal V̇O₂ (V̇O₂max) has surged in popularity. From where I sit, the renewed interest is driven by health/medicine influencers with big platforms, and that some metabolic analyzers are now cheap (we’ll save their accuracy for another day).

And then they talk about it. A lot. And a lot of them don’t really know what it means, but it’s apparently provocative.

The increased awareness is a win, because it is a relevant health metric, perhaps even a vital sign. We know that higher V̇O₂max or aerobic fitness is associated with lower risk of death and disease, and that type of language is good for views.

These studies started popping up in the 1980’s and every one of them has shown the same thing. And the effects aren’t small. In the latest iteration, for people in their 50’s, 1 out of every 3 (33%) in the lowest fitness bracket (bottom 20%) died within ~10 years. In the highest fitness bracket (top 3%), the death rate reduced to 5%.

But why is that the case?

Dumb data

In The Book of Why, Judea Pearl goes deep into the science of cause-and-effect, or causality. This matters because when you understand what truly causes something, you can intervene and change the outcome.

But often we see relationships that look causal and aren’t. The classic example is ice cream sales and crime. Both rise in summer, but eating ice cream doesn’t cause crime. They’re associated because they share an underlying driver: warm weather.

Associations can point toward causality, but they’re not enough to prove it.

This confusion bleeds into the health space frequently. Think about age and mitochondrial function or muscle mass. Does older age actually cause these things to get lower? Or because older people are more inactive?

If it’s the latter, an NAD+ supplement won’t fix it.

Big Data

Massive data sets (like the UK Biobank) let researchers test thousands of associations between lifestyle, biology, and disease. This drives medical discovery, but the data are mostly observational, so they tell us what is linked, not why.

As Judea Pearl put it:

“I hope to convince you that data are profoundly dumb. Data can tell you that the people who took a medicine recovered faster than those who did not take it, but they cannot tell you why. Maybe those who took the medicine did so because they could afford it and would have recovered just as fast without it.”

V̇O₂max and longevity - is the data dumb?

The impressive statistics between V̇O₂max and longevity are still just associations.

In these observational studies, low V̇O₂max might reflect cancer or COPD preventing adequate exercise. Is low V̇O₂max causing death? Or is disease causing both?

If a stage 4 cancer patient had a V̇O₂max of 75 ml/kg/min, would they have survived?

The data are too dumb to tell you!

So what about V̇O₂max mechanistically makes it relevant to health? Saying “because it reduces your risk of death” isn’t enough. Yes that’s true, but it’s an association. Fortunately we can anchor this concept to deeper insights.

Evolution

Oxygen wasn't always present in Earth’s atmosphere. It’s thought to have increased above zero ~2.5 billion years ago, eventually increasing to the present-day value of 150 mmHg.

Before oxygen, there was a bunch of single-celled organisms: bacteria, some algae and fungi. They used glycolysis or anaerobic metabolism to produce energy, which I’ve talked about a ton in other blogs as it relates to exercise.

Humans are multi-cellular; we have many cells (muscle, immune, neurons, etc.) all with specialized jobs. This makes us biologically complex: the degree of organization, specialization, and coordination inside a living system. Simply put, we have much more “going on” than a single-cell bacteria.

As oxygen rose on Earth, biological complexity was unlocked. The figure above shows that as oxygen rose, the number of cell types rose with it: roughly one new cell type for every ~2 mmHg increase in atmospheric oxygen.

Energy and entropy

Entropy is a measure of randomness or disorder in a system. In life things naturally trend toward disorder (like DNA errors with aging) and we are always fighting this drift. Everything is working against us.

The only way to mitigate entropy is to put energy into the system. Your room gets messy unless you clean it. The body can’t maintain the organized cellular processes that keep us alive without energy input (food).

Unfortunately, we can’t destroy entropy, and every time we break down food for energy to do work, like contract a muscle, we produce some entropy. The irony.

Entropy of the body + the environment must increase (>0) for any process to occur. The important piece is “+ the environment”. This means we can decrease entropy internally as long as we raise entropy in the environment even more. We can literally have our cake and eat it too.

Living systems are dependent on outside energy fluxes to maintain their organization and dissipate energy gradients to carry out self-organizing processes. - Lauren Koch and Steven Britton, 2022

We do it by exporting high-entropy metabolic byproducts from inside to outside the body, such as heat and CO₂. When metabolism is fired up during exercise, we hyperventilate (breathe CO₂ into the environment) and sweat (evaporate heat into the environment). Humans are notoriously inefficient: about 80% of the chemical energy for useful work (walking, lifting) is “lost” as heat. We’re walking radiators.

Oxygen-dependent biology

As oxygen accumulated on Earth, organisms developed increasingly complex mitochondria, the machinery of aerobic metabolism and our internal entropy pump.

We consume low-entropy food and O₂, break down their high-energy chemical bonds, strip off electrons and send them to the mitochondria, release free energy to do work, and dump the waste (heat and CO₂).

Example: A pile of firewood is low-entropy, the ash + smoke are high entropy.

Aerobic metabolism is essentially a multi-step energy-transfer machine.

Oxygen’s physical and chemical properties make it an exceptional electron acceptor. It has one of the strongest electron affinities in biology, second only to fluorine. In the electron transport chain, oxygen is the final electron acceptor. When electrons reach oxygen, they react to form water. CO₂ is produced earlier as carbon atoms are oxidized and then exhaled. Heat is released at every metabolic step.

Oxygen is like a vacuum that sucks in electrons. It’s a powerful driving force that releases large amounts of free energy each time electrons move toward it. Species that evolved to use oxygen efficiently could generate far more energy, support more specialized cells, complex tissues, and larger, more capable organisms.

At the same time, aerobic metabolism is entropy export machine. Without the ability to export entropy we’d become fatally disordered within minutes. Running a 5k, for example, would kill you either from heat stroke (can’t dump metabolic heat) or respiratory acidosis (can’t breathe off CO₂).

Oxygen fueled biological complexity by enabling a highly efficient energy-transfer process paired with powerful entropy-export mechanisms.

Back to V̇O₂max and health

If we believe that excess entropy accumulation in the body is bad by promoting internal disorder, it makes perfect sense.

V̇O₂max is the highest rate at which we can bring in oxygen from the air and use it as the final electron acceptor in mitochondria. You could also define it as our maximal ability to produce energy and export entropy.

It reflects the maximum possible:

• electron flux down the electron transport chain

• free-energy release

• heat production

• entropy export to the environment

One study in humans has quantified this using state-of-the-art heat measurements (metabolic production and export to the environment) during exercise to quantify the flow of entropy.

Older age, low fitness, and presence of disease (diabetes in this case) all produce greater entropy accumulation during stress (exercise). V̇O₂max was negatively related to entropy accumulation (higher V̇O₂max = lower entropy accumulation).

Earlier I mentioned humans have “more going on” than a single-celled bacteria due to our biological complexity driven by aerobic metabolism. We perform complex movement, can think with our big brains, are more resilient against stressors, live longer, and so on.

In a similar way, but on a less drastic scale, someone with a high V̇O₂max has more going on. They can produce and export more energy, building a more resilient biological system and keep internal entropy low. Inflammation is kept lower, antioxidant status is more robust, recovery from surgery is enhanced, and of course there is protection from many diseases.

Learning from rats

Lauren Koch and Steven Britton are two scientists who developed many of the concepts I talked about above regarding evolution, entropy, and what not. It’s called the "Energy Transfer Hypothesis” and they wanted to test it by artificial breeding rats based on their fitness.

Their idea was to understand the bottleneck of human chronic disease, and what causes it. Chronic diseases are complex diseases, meaning they don’t have 1 specific cause. There’s not a single “type 2 diabetes gene”. The disease is influenced by many different genes and many different environmental factors (nutrition, exercise, etc.).

It is hard to replicate these diseases accurately in animal models to test new treatments. Scientists can administer chemicals or mutate or delete 1 or more genes that reliably produce type 2 diabetes, but it is unlikely that is representative of the condition humans experience.

Since low fitness seems to be a common underlying factor, why not test that?

Fitness is the common bottleneck of chronic disease

In the mid 1990’s they had a bunch of rats run on a treadmill at continually increasing speeds until they fatigued. The 13 males and females who ran the furthest (high-capacity runners) were paired to have children. They did the same for those who ran the shortest (low-capacity runners).

And they kept doing it. The rat children do the exercise test at 11 weeks old, the high and low fitness ones mate with each other, rinse and repeat. Currently, they have produced about 40 generations of high and low capacity running rats.

The figure below shows running performance from the 1st to 40th generation. Over that time, performance has increased 400% in the high-capacity runners (purple) and was unchanged (or even decreased) in the low-capacity runners (green). The difference between groups at generation 40 is about 700%.

This is strictly the effect of inheritance because these rats did no exercise training. It’s their intrinsic fitness. If fitness wasn’t relevant to health, those traits wouldn’t have been passed down. So what do they look like from a health standpoint as opposed to running performance?

By any health metric you can imagine, the high-capacity runners win. For starters, they live 30-50% longer and lifespan is directly related to V̇O₂max.

They have better vascular health, lower blood pressure, less inflammation, less weight gain, improved electrical function of the heart, improved antioxidant status, lower blood sugar, insulin, triglycerides, visceral fat, etc. I could go on and on. They’ve even tested more obscure things like alcohol-induced liver damage, which was less in HCR’s.

What does all of this mean?

First of all, if you’re still here, I appreciate it.

My point was to illustrate why V̇O₂max is critical from a mechanistic standpoint. It’s our inherited capacity to transport O₂ from mouth-to-muscle cell, move electrons, export entropy, and stay organized against the natural drift toward disorder.

Maintaining a high level of fitness should be center stage in any healthcare plan. It represents our energy transfer capacity which underlies the mechanism of every chronic disease. Aerobic fitness isn’t just associated with health, it’s baked into the operating system of complex life.

If you’re a clinician, I think knowing the human limits in the back of your head helps give you a better grasp on interpreting a patient’s values. It also helps you stay grounded when you’re presented with atypical but not life threatening numbers.

If you’re a scientist, it can serve as a great teaching tool and help you develop innovative research questions. They’re also good for impressing people at a social gathering.

Here are some fun ones:

• The highest heart rate ever recorded is about 600 (for a brief period of time).

• The human body can go at least 382 days without food (he was obese to start).

• How much blood has a human heart ever pumped in 1 minute (cardiac output)? 42.3 liters in a Swedish endurance athlete, double the normal adult during max exercise.

• The highest VO2max ever is 96.7, more than double a college-aged male.

• The highest human sweat rate ever is 5.73 liters of sweat per hour (1.5 gallons), well over 3x most normal values.

• The maximal amount of calories we can digest and absorb per day to fuel activity indefinitely is ~5,000 calories (maybe up to 7,000 calories). It’s our gut’s limit.

Now let’s dive into the heat.

Normal and abnormal body core temperature

Everyone finds out 98.6°F is a normal temperature at rest after getting a thermometer stuck in our ear enough times. The threshold for heat stroke (the worst of the heat illnesses that can cause death) is said to occur when body temperature goes above 104°F. And I’m talking actual body core temperature, not measured in your ear, but with a wired thermometer stuck a few centimeters up your backside.

Five degrees (~99 to 104°F) is not a lot of wiggle room between normalcy and potential death! It’s one reason why thermoregulation is so fascinating.

Where did the 104°F (40°C) threshold come from?

It came from studies in rats where 104.7°F was the lowest core temperature after exercise that resulted in death within 24 hours (when left untreated).

Serious cell and organ damage starts to occur above this level, which can become irreversible above ~109°F. Proteins break down and can’t return to form, cell membranes get destroyed, etc. Think about frying an egg. Once the yolk and whites solidify, there’s no going back.

Thousands of observations on heat stroke patients by medical professionals also show that they are almost always >104°F, giving the value validity for sure, despite originating from rats. But there are caveats because it isn’t a magical threshold.

On two occasions during my PhD my core temperature went above 104 while exercising in the lab. It was kind of an accident, but I felt fine, which makes me think it has probably happened outside the lab too during intense summer training sessions.

I also worked on projects at the Falmouth Road Race where I was mainly in charge of measuring core temperature in runners. I encountered numerous people in the 104-106 range who were also fine (tired and hot for sure, but without heat stroke symptoms). But I sent them into the medical tent anyway because that was our policy.

The “zone of potential danger”

So from those experiences alone, going above 104°F clearly isn’t a death sentence, but it’s not trivial either because it definitely is physiologically taxing. I like to say that heat stroke always occurs >104°F, but not everyone >104°F will have heat stroke.

Going above 104°F places you in a zone of potential danger, not guaranteed danger, because it’s how long you’re above that temperature that matters. Scientists calculate a value for this called “degree-minutes”.

For example: Using the 104 threshold, a core temperature of 108°F for 5 minutes would be 20 degree-minutes. (108 - 104 = 4°F | 4°F x 5-minutes = 20.)

In the original rat study, 80+ degree-minutes was guaranteed death. 80 degree-minutes equates to 108°F for 20 minutes, 106°F for 37 minutes, or 116°F for 7.5 minutes. Keep that last number in mind.

Even though I just mentioned a bunch of nuance, using 104°F as a general medical treatment threshold is a good idea. It’s not really effective to say “start treating someone for heat stroke when they have spent somewhere between 7 and 26 minutes above 104°F”. It’s better to be safe than sorry.

Pushing Limits

You can’t do a study determining body temperature limits because people would have to die. That’s why labs have ethical restrictions. Ours was 104°F in grad school, but many around the world are less than that, making it obviously difficult to study heat stroke in any type of controlled way in humans.

This is where you need observational data and case studies. Hospitals and emergency rooms are a great place for this. You can also find people who are voluntarily putting themselves at risk for heat stroke, like endurance athletes.

The man who accidentally cooked himself

At 8:30pm on July 10, 1980, a 52-year old fella from Atlanta was admitted to the emergency room with a core temperature similar to that of steak cooked rare. Ironically, he was in fact cooking at the time of the incident:

“For most of the day, he had remained inside cooking over a hot stove. He had consumed 1 to 2 pints of vodka, his usual amount. Until resuscitation began, the last activity the patient recalled was turning off the oven and lying down to rest. He performed no daily exercise, had no adult history of significant fevers, thyroid disease, or recurrent infections, and he was not maintained on any daily medication.” - Slovis et al., Annals of Emergency Medicine, 1982

When the paramedics measured his temperature at the scene, it maxed out their device, which couldn’t handle a reading >107.6°F. It’s unclear how long he was unconscious while at home, but they subsequently transported him to hospital and tried to cool him on the way.

After 25-minutes at the hospital, his rectal temperature was recorded at 115.7°F. After 1 hour they were able to cool him down to 104°F, and after 2 hours to a nice chilly 101°F. Let’s be very conservative and say he hit 115.7°F about 5-minutes before EMS arrived, they spent 5-minutes evaluating him, and it was a 5-minute drive to the hospital.

That’s at least 50-minutes at 115.7°F, plus another 35-minutes above 104°F as they were cooling him. If I assume his temperature dropped 2°F every 5-minutes, it adds up to roughly 700 degree-minutes. Remember that 80 degree-minutes essentially guaranteed death in all of the rats.

He was hospitalized for 24 days, battled multi-organ failure and internal bleeding, but miraculously survived. To my knowledge this is the highest core temperature an alive human has ever experienced.

After withstanding 2 pints of vodka per day, I wouldn’t put anything past this guy, and makes me wonder if he has any unique heat-resistant genetics.

In close second, there was a 23-year old kid who got pulled over with a ton of meth (somewhere over 1 gram) and swallowed it all (~100 street doses) before running away. That landed him a core temperature of 113°F and rhabdomyolysis (toxic muscle breakdown). He too, survived, with aggressive treatment.

So, 116°F is our top end. But, keep in mind both of these people certainly would have died had they not gone to the hospital, which begs the question of how hot you can get and survive without any medical intervention?

Pretty damn hot.

Runners who voluntarily cook themselves

The highest recorded core temperature in a person who survived without any medical intervention is 41.9°C (107.4°F). This was during the classic University of California-Santa Barbara marathon field studies. The person was actually the guy who wrote the article linked in the previous sentence.

That temperature without heat illness symptoms is rare, but not a fluke. One guy reached 107.1°F during a half-marathon in Singapore, and core temperatures between 104 and 106.7°F were reported in several cyclists at the road cycling world championships. The 3 people reaching 105°F and above all won medals.

To wrap it all up, there’s not one specific temperature that is fatal across the board. The zone of potential danger starts at about 104°F for all of us, but after that it depends on how hot for how long, and things like genetics and how fit you are.

These cases are certainly outliers, and people have died from heat stroke at lower core temperatures, so it shouldn’t be taken lightly. But if you’re working in an emergency room or with elite athletes in a medical context, these help put in perspective what the actual limits can be.

They were playing friendly matches against Mexico in Hartford, and would train in our environmental chamber to prepare for the Tokyo heat in the morning.

I was just a cog in the wheel, but it was an awesome experience to work with them.

Check out the cool video that got produced:

Heat Training for Tokyo - NBC Connecticut

He came mainly to interview my advisor, Dr. Douglas Casa, but my buddy Dave Martin and I also put him through a VO2max test and some exercise in the heat so he could see how his body responded to exercising in extreme conditions.

He’s a phenomenal writer and you can read the article here:

What a Heat Wave Does to Your Body - The Human Body is a Remarkable Effective Cooling Machine, But it Has a Limit

There’s also a YouTube video a podcast episode where he interviews Doug Casa.

MYOS MD makes a nutritional supplement for humans (and animals) called Fortetropin, an egg yolk extract that acts as a myostatin inhibitor to improve muscle growth.

They have a series where they interview various experts and I was fortunate enough to have the chance to take part.

Check out the 30-min conversation:

Performance Under Pressure: Muscle Health Insights from Military and Sports Science

It didn’t take long for endurance sports to pick up on it for its performance enhancing effects.

Lately, there has been renewed interest and a rebranding you’ll hear called “heat training”, partly due to new research showing it can have altitude-like effects on red blood cells.

My friend Rachael Woodruff who works with professional runners in Colorado asked me to write on article on heat training which you can find here:

Issue 51 - Heat Training For Runners - Sean Langan, PhD, Explains What Runners Need To Know About The Heat

It’s meant to be an easy-to-understand and practical guide to heat training, specifically geared towards runners.

Training is a cyclical process of exercise, fatigue, recovery, and competition performance. When balanced appropriately, training improves performance. An imbalance of excess training without proper recovery augments fatigue and reduces performance, and can take a long time to overcome.

Read more here: Overtraining: Pushing the Boundaries of Physical Activity.

It’s hard to talk about exercise without talking about the heart. Exercise is mostly beneficial for the heart, but there are some caveats that are good to be aware of, particularly regarding cardiac arrest.

Check out one of the short articles I did for them titled “The Irony of Exercise and Sudden Cardiac Arrest”.

1. Pushing the absolute limits of human performance using science

2. Paying athletes what they deserve.

3. Leveling the playing field because sports are not 100% clean anyway.

4. Giving athletes freedom to choose what to do with their body.

Due to all of the doping stories in my lifetime, most notably cycling and baseball, people like me have always wondered what would happen if we just make everything legal. The biggest bottleneck to that is money. Someone has to pay for it. And they have to pay enough to draw in actual athletes, because you could pump me up with all the EPO or testosterone in the world and I’m not breaking a world record.

The Enhanced Games can do this because they’re financially backed by serious investors and venture capitalists like Peter Thiel. They have big money.

My First Viewpoint on the Enhanced Games

If I put my scientist hat on, I think it has the potential to produce some great human performance science. There’s really no great research on what most of these drugs actually do in the context of elite athletes because they’re not publicly volunteering to be studied, for obvious reasons.

With more PED research we may find out that some banned drugs don’t actually give a competitive advantage. I think this is true for many substances on the banned list. Many of them are banned simply on theoretical grounds or from animal studies. Understanding what actually works and what doesn't is important for several reasons. It improves our health/safety/medicine/performance knowledge, reduces costs (don’t have to test as many things), and could reduce unnecessary bans for truly unintended doping violations.

“Critical research in anti-doping organizations is critical for improving their governance. The lack of critical research in this area is a significant shortcoming” - Fabien Ohl (in this article)

Take trimetazidine for example, a heart disease drug that improves the heart’s use of glucose for energy when the tissue becomes hypoxic (lack of oxygen). A Russian figure skater got popped for it during the Olympics. However, there’s no evidence, even theoretical plausibility, that this would help a figure skater. Ben Levine, a renowned sports cardiologist, and other medical experts supported this view which you can read here and here. Did she intentionally take it? Was she forced by a coach? Did she have intent to cheat? Who knows.

But who cares if it doesn't actually work? The fundamental concept of the anti-doping code is to protect the value of the sport, integrity of the sport, and health of athletes. So if they find a substance that to our knowledge does not enhance performance or pose health risk, the rationale for a violation is not quite strong.

Trimetazidine was involved in doping violations of 23 Chinese swimmers in 2021, an American swimmer in 2018, a marathon runner in 2022, and a tennis player in 2024. Many of them had the decision reversed due to contaminated supplements. While they should have been more rigorous about their supplements, WADA should have more background knowledge before adding something to the banned list to avoid unnecessary bans, and also establish critical threshold limits for all prohibited substances. The latter of which was the topic of articles in 2012 and 2023.

Research is also critical for safety reasons. People are still doping and will continue to do so until the end of time. With rigorous medical research on PED’s, we will get a better understanding of their risk profile, not only right now, but also lifelong effects.

Ironically, if they publish their work, anti-doping agencies will actually benefit because no one else has this kind of information, besides maybe the historic East German doping program. A tangential effect of could even be skewing people away from doping that otherwise would opt to cheat if they see documentation of how these things affect elite athletes, instead of anecdotes.

So, perhaps selfishly, because I am interested in the science behind PED’s, I think there are some positives since it serves as a vehicle to answer these questions. I’m also operating under the assumption that they are indeed using advanced medical screening to ensure athlete safety and it’s not just “pump them up with all the drugs we can and hope for the best”.

Also, for reference, I nearly landed a job with these people as a scientist. Nearly everyone I met with was great but my final interview with the co-founder was very strange to say the least, and I didn't get it. I only bring that up because it would seemingly give me a good reason to shit on the whole thing.

My Other Viewpoint

At the same time, I do like the idea of a “natural” competition, which the Olympics, for instance, claims to be. Not everyone will be willing, or wants to, use PED’s, even if they work with the best doctors in the world that make it as safe as possible. So there certainly should be a competition that does not involve doping where athletes know that they are on the start line with other natural athletes.

I also simply love watching the Olympics, World Championships, Diamond League, etc.

And at the end of the day, rules are rules, and the International Olympic Committee (IOC) has the right to want their sport to be clean. Also, it must be absolutely gutting to miss out on the moment of an Olympic medal only to find out later the people who won were doping.

In my fantasy world I’d like to clone all of these best athletes in the world and have two competitions, one doped and one natural.

Where I think the Enhanced Games could be severely flawed is by not getting enough good athletes on the start line. Like I said before, you can’t just dope any random person to a world record. They need innate talent and physical ability. With Fred Kerley, they certainly stepped up in this aspect. But they need more.

In track events, you often see the best performances when athletes are competing. It’s much harder to break a world record doing a solo time trial than when you are neck-and-neck or chasing someone and actually racing.

We saw this in the women’s 400m at the 2025 World Championships when Sydney McLaughlin-Levrone ran the second fastest time in history. The two women behind her also ran the best races of their lives, which I doubt would have happened otherwise. The men’s 800m final at the 2012 Olympics was another great example where David Rudisha obliterated the world record and dragged everyone else behind him to their personal bests or national records.

Competition brings out the best in athletes, so for these world records to fall, the Enhanced Games needs more than just PED’s.

Doping Issues in Track/Running

I’m a realist at heart, and the fact is that many athletes are doping at the Olympics and other reportedly “clean” events. Look at Kenyan distance running. I’m not saying every Kenyan is cheating, but they clearly have a serious doping issue. Over 100 athletes are currently ineligible to compete for doping violations.

Let’s view it from their standpoint. Kenya is naturally a distance running hotbed and many of their athletes already have the innate talent and training environment to compete at the top level clean. Winning a major marathon pays a good bit, enough to make you rich back in Kenya. The prize money can be life changing.

Economically, Kenyan’s aren’t as well-off as us in the USA or other more developed countries. Taking EPO is almost a no-brainer as a means to get paid. As long as they collect a check, what should they care if they cheated? It’s not like it’s a criminal offense. The worst that happens is they are disliked by the running purists and banned from future events.

I’m not saying it’s right or wrong, it just is what it is.

Since I don’t want to pick on only Kenya and distance running, let’s look at the history of the men’s 100m sprint which is mainly USA and Jamaica. Currently, there are 11 men who make up the top-10 100 meter times in history. Among them, only 4 (Usain Bolt, Kishane Thompson, Oblique Seville, Trayvon Bromell) have made it through their career without any doping violations, whether that’s a whereabouts failure or a failed test.

You can’t deny it’s a historically dirty event.

“Olympic movement stakeholders must change their idealistic view of the fight against doping, recognize its limitations and uncertainties, and accept its complexity. This cultural change must be implemented in sports organizations to think about anti-doping beyond the binary opposition between cheats and clean athletes.” - Fabien Ohl (in this article)

So you can’t look down on Fred Kerley for joining the Enhanced Games without having the same energy towards those other athletes in the top 10. There’s also several world records that still stand today because it was prior to the anti-doping revolution and they were never caught. WADA wasn’t formed until 1999! I recommend the book “Faust Gold” about the East German doping program. Or, just take a look at the women’s world record holder in the 800m and tell me if you think she was clean.

Why This is a Good Move for Fred Kerley

First of all, I’m a big fan Fred Kerley fan, so maybe I’m biased. He’s one of the best sprinters in the world. World Champion, 1x Olympic silver, 1x Olympic bronze, and one of the fastest 100m times ever. He’s also only one of 3 athletes to ever run the 100m in <10 seconds, the 200m in <20 seconds, and the 400m in <44 seconds. However, he’s 30 years old and sprinting is a young man’s game.

The next big global stage in sprinting is the 2027 World’s in Beijing and the 2028 LA Olympics, when he would be 33. Of course there will be other races in 2026 like the Diamond League, but that doesn’t carry near the same status as the World and Olympic Championships.

33 is not old, but in sprinting you’re pushing retirement. A gold medal in LA would make him the oldest 100m champion in history. While advances in training, nutrition, technology, and medicine have allowed certain athletes to extend their careers longer than expected, the odds simply are not in your favor as a sprinter.

The move to the Enhanced Games gives Kerley a chance to capitalize on his physical prime and focus on running the fastest 100m of all-time. Currently, he is provisionally suspended for whereabouts failures, which is when you miss 3 drug tests for not being where you said you would. Active elite athletes are put into a registered testing pool (RTP) and have to provide anti-doping authorities their schedules in the event they are selected to be drug tested (see picture below).

If you miss 3 tests in 12 months, you are subject to a 1-2 year ban:

This doesn’t mean you actually doped, but while he is contesting the decision and has not claimed to have taken anything illegal, the chances he competes in any standard races next year are slim. Kerley has also had some legal issues in the last year, and the culmination of these events have likely reduced his stock as an athlete in terms of sponsorships and sources of income.

It’s all about the Benjamin’s

Historically, track and field athletes are criminally underpaid. Many athletes go into debt to be able to compete, or have to fit their training in around full time jobs until they hopefully run fast enough one day to secure a shoe deal.

A select few big time athletes (Noah Lyles, Sha’carri Richardson, etc.) will make big money through private sponsorship deals and other ventures, but they still aren’t even in the same zip code as the NBA, NFL, or MLB. In boxing, Canelo Alvarez allegedly made as much as $150 million for his recent fight with Terrence Crawford. Even the lowest paid people in the NBA make at least ~$1.2 million per year (league minimum).

NBA ref’s even make more than most track athletes, and veteran ref’s allegedly can earn up to $30,000 per game in the NBA finals, almost as much as an Olympic gold medalist.

Prize money for Olympic gold varies by country. In the US you receive $37,500. That’s a slap in the face. The IOC had a revenue surplus of over $1 billion in 2024, and the US Olympic committee about $100 million (keep in mind 2024 was an Olympic year, too). The NBA and NFL were at about $10-20 billion. So one issue is where the money to pay the athletes will come from. Since there’s so many athletes in a large country like the U.S., it’s not realistic for a governing body to support them all.

Grand Slam Track tried to fix this in 2025, offering relatively big prize money for their unique event which drew in some of the biggest athletes in the world. But after a major investor pulled out, the athletes still haven’t collected a check.

So, financially, it’s literally a no-brainer for Kerley. With everything else going on it is hard to imagine him making any considerable money as a track athlete anywhere else. As their biggest athlete to date, I guarantee he signed a nice contract, plus appearance fees, and the potential for $1,000,000 if he breaks the 100m world record. There’s also something like a $500,000 prize pot for event winners.

“Unless they start paying athletes properly, people will put themselves first. The sport can't survive on outdated pay models. Athletes carry the product, but in the old system they're underpaid and overregulated. We're building something where they're supported, compensated, and protected.” - Fred Kerley

I can’t imagine he breaks the world record but who knows. It’s important to say that it wouldn’t be the first time people have set out to achieve an “artificial” world record. Nike tried it twice with the sub-2 hour marathon and sub-4 minute women’s mile. So, having events using illegal strategies to produce a world’s best time is not new.

However, I should mention that as recently as last week, Kerley vehemently stated on a podcast he is not taking any PED’s and doesn’t plan to. So he might just be treating it as another event to compete in, like how some athletes competed in Grand Slam Track.

The only argument against him doing it is basically just one based on morals/ethics. The vibe I get from tried and true track fans is that he is tainting the sport and his legacy. They seem to take pride in the fact they do it for the love of sport despite getting paid terribly. And I think that is great because sport is not just about money. But it’s also a bit self-righteous to think other people should be willing to go broke in order to keep a certain image for the sport.

If anything, the Enhanced Games is a far better option than people secretly doping and competing in clean events, because that is certainly still going on.

I personally see it as a smart business move and Kerley capitalizing on a rare opportunity, regardless of your opinion on the whole ordeal. What will be more interesting is to see who follows him. I imagine the downstream effects will be other bigger athletes joining him, which will eventually put pressure on traditional athletics bodies to improve the sport and pay athletes more. It can’t survive on the self-righteous philosophy if there are other ways to make far more money running.

Sean Langan has his PhD in exercise physiology. He is interested in how exercise training rewires our biology and harnessing the intersection of human physiology, technology, research, and coaching/training to improve human performance.

A track reporter recently sounded shocked during an interview with Donovan Brazier (USA and World Champ in the 800m) when he said he wasn’t taking it, hinting at the fact he could shave some time by having it on board pre-race. It’s unclear if Brazier has since dabbled with it, but I don’t suspect he takes training advice from the media.

Don’t get me wrong, bicarbonate can be effective. It’s a tried and true legal supplement for those acidifying events in the 2-6 minute range that has been around for ages (it’s baking soda). At the same time, it’s not magic and can have side effects. A bit later I’ll get into why Maurten’s innovations have transformed the supplement, but first let’s understand sodium bicarbonate and how it works.

A Little Chemistry

Sodium is a positively charged molecule (Na+) and bicarbonate is negatively charged (HCO3-). The reason they're combined is because these electrically charged molecules can’t exist alone and be stable; solutions need to be electrically neutral. If you just put bicarbonate by itself in water, it would react with positively charged molecules like hydrogen (H+) to form something else. I’m not a chemist but you can ask one if you need more clarity.

Any positively charged molecule could theoretically be paired with bicarbonate (potassium, magnesium, etc.), but sodium is usually used for safety reasons since it is well-tolerated and we have a ton of it in the blood and extracellular fluid.

When sodium bicarbonate encounters an acid (or heat), either in your stomach or when you’re baking a cake, it dissociates into its individual parts often ending up with carbon dioxide and water. As a gas, the carbon dioxide helps your bread “rise” but can cause gnarly gastrointestinal (GI) discomfort when you take it as a supplement. The doses used are higher than the amount of acid in the stomach causing some of the bicarbonate to be absorbed by the intestine and enter the bloodstream.

Bicarb is a buffering agent, and a buffer helps resist changes to pH. Various metabolic reactions and certain foods are constantly causing things attempt to change our pH, which likes to stay at a neutral ~7.4. Bicarb specifically buffers (mitigates) the acidity that builds up in muscles during intense exercise, and it also might limit the increase in extracellular potassium. The acidity, as I recently wrote about, plays a role in muscle fatigue, as does elevated potassium, so modulating these systems is likely beneficial.

Performance Enhancement

Metabolic effects as a buffering agent

The first bicarb study was done in 1931 at the Harvard Fatigue Laboratory where they gave one guy (one of the authors) either 10 grams of sodium bicarbonate (alkalizing), or 15 grams of ammonium chloride (acidifying). In today’s standards it would never get published, but at the time it was novel, showing that starting exercise with a little alkalosis benefited endurance performance.

Since then the studies have thankfully gotten more rigorous with bicarbonate being tested in many different sports and activities. The International Society of Sports Nutrition put out a consensus document in 2021 that reviewed well over 100 bicarb studies. The weight of the evidence clearly suggests it improves performance on the order of ~1-3% during time trials (how fast you can cover a specified distance).

I’ll note that three percent is generous. That’s equivalent to a professional female 800m runner shaving her time from 1:58 to 1:54 at the drop of a hat. It is likely that the more fit you are, the less benefit, because it’s hard to further improve an already high-functioning human body with a supplement. Many of the studies did include highly-trained people, but not necessarily elite athletes, and there is a difference.

Marginal gains are relevant to athletes

Competitive endurance races are often decided by hundredths of seconds. In rowing, performance enhancements of 0.3% may give a real-life competitive advantage. I believe it, because the 2016 Olympic gold was won by 0.007 seconds (see picture below). Just this week, only 0.02 seconds separated gold from silver in the men’s 1500m world championship (0.009%).

Let’s assume Jake Wightman, who finished second in the 1500m race, does not use bicarb (I don’t know if he does or not). Based on the available data, I’m confident enough in the probability bicarb would give at least a 0.01% advantage (enough to win). Now, everyone responds differently to everything, and winning a 1500m race is not entirely dependent on who buffers acidity the best. But if it were me, I’d probably wish I had at least experimented with it.

Can bicarb enhance training adaptations?

There’s also benefits for repeated bout exercise (interval training), resistance training, and perhaps how we adapt to training. Bicarb is classically used pre-race and not as a daily supplement. It’s not like creatine where if we take it every day we store more in our muscles for later use, but there could be something to the idea of taking it before all of your training sessions to further enhance training adaptations.

An 8 week study in females found it improved lactate threshold and VO2max. A 6 week study in males saw improved peak power output. I don’t think it’s necessarily due to direct effects of bicarb. What is more likely is that by going harder/faster during training, you get a greater physiological stimulus to improve fitness. We need more studies but I’m definitely interested in the concept.

Overall, it’s a clear performance enhancer, particularly between events ~30 seconds to ~10 minutes. The sweet spot is right in the 2-6 minute range (800m and 1500m run, 2000m row).

I once saw an influencer promoting it during his 2 hour 50 minute marathon. That was the first red flag. Metabolically speaking, marathons are low intensity. Nobody can maintain a high intensity, acidifying pace for 3 hours. Then he said it was to buffer his lactate. That’s how you really know he didn’t know what he was saying, because lactate unanimously gets higher when you’re on bicarbonate.

Other non-traditional effects

Hydration

Sodium bicarbonate has been used under various settings for hydration purposes, mainly because sodium is the primary electrolyte involved in fluid balance. One area is cardiology patients undergoing coronary angiography, or any imaging procedure requiring infusion of a contrast dye. These dye’s can cause acute kidney injury called contrast-induced nephropathy and pre-operative hydration is key. It’s often recoverable but ~10% of cases lead to kidney failure. Several meta-analyses show it does reduce the risk of kidney injury, but not mortality, and is likely not better than sodium chloride (table salt).

For athletes, it could be a 2-for-1 strategy given the metabolic + hydration effects. It defended against dehydration in rowers by maintaining plasma volume, and slightly reduced urine volume while increasing plasma volume compared to water, suggesting a benefit. Although, you can get similar effects with regular salt without the gut issues.

Exercise in the heat

Exercise-induced acidity and increased body temperature can cause an increased drive to hyperventilate, which is uncomfortable. A recent study found that during 1 hour of moderate cycling in the heat, taking bicarbonate versus table salt reduced perceived effort and hyperventilation. Body temperature, heart rate, blood pressure, and brain blood flow were all similar between the two groups. These effects were pretty small and the exercise was very light, but it’s an interesting concept showing that bicarbonate could at least have a benefit for reducing effort during longer exercise.

Dosing Protocols

How much bicarbonate you should take is based on your body weight, and most of the research convenes on a dose of 0.3 milligrams per kilogram of your body weight. Higher doses don’t seem to have a bigger effect. As far as timing, it should be 1-3 hours before your event/training. Working out the exact time might take some experimentation. There doesn't seem to be any additional benefit to combining it with caffeine or creatine, but it’s smart to have some carbohydrates alongside it to reduce the potential for gut issues. The capsule form seems to be better than mixing baking soda in your water for gut symptoms as well.

Maurten’s bicarb system

Maurten’s product is a 2-part system comprising sodium bicarbonate tablets and a carbohydrate hydrogel. The hydrogel is the real innovation and has also been responsible for the dramatic increase in carbohydrate intake in endurance sports.

The main issue with bicarbonate as I’ve mentioned earlier is the gut irritation that comes from it interacting with acid and producing excess carbon dioxide. At best you get a bit bloated and burp. At worst, you shit yourself halfway through an 800m race on TV.

Companies have long tried to create products that bypass the GI issues. We know bicarb is very effective, and legal, but nobody wants to endure those unpleasant side effects. One product was a topical lotion that went on the skin, attempting to transdermally deliver sodium bicarbonate. I actually worked on a study that tested this product. From my experience in the lab, and several published studies, that strategy simply does not work.

The hydrogel technology is a much more clever innovation. It is made of alginate, a polymer from seaweed used in oral drug delivery and other medical applications. The gel can be designed to form in areas of low pH, like the stomach, which essentially encapsulates the bicarbonate (and carbohydrate) within the gel until it reaches the intestine. Therefore, you don’t get the excess carbon dioxide production in the stomach that causes GI distress when bicarbonate interacts with acid. It also bypasses stomach issues encountered with high carbohydrate intake.

This is probably one of the biggest advances in sport nutrition, or endurance sports in general, besides maybe super shoes, in a long time.

Sean Langan has his PhD in exercise physiology. He is interested in how exercise training rewires our biology and harnessing the intersection of human physiology, technology, research, and coaching to improve human performance.

“That is what you call trying to run through a sea of lactic acid” - commentator at the UK Athletics Championships as an athlete fell at the finish line of the 800m

Going “lactic” is common parlance for athletes and coaches. It’s that feeling of, well, pain and genuine discomfort. In an effort to run a fast 400, 800, and 1 mile this summer I have been frequently encountering this pain in training. Last weekend I dove head first in the sea of lactic acid during this workout:

• 4 sets of: 600m (1min rest) - 400m (1.5min rest) - 200m (5min rest)

Fatigue comes in many forms. The reason you want to stop during a maximal 800m run is a much different feeling than what makes you want to stop a marathon. We’re focusing on the short-duration pain.

Fatigue: when you lose the ability to produce as much force as you had been.

What’s causing it?

There are several contributing factors, but metabolic acidosis is certainly in the lineup. Before we get into it, a quick note on lactate and lactic acid.

Lactate and Lactic Acid

Lactic acid is the historical villain for causing metabolic acidosis and fatigue. However, it may not even exist in the body in relevant amounts (lactate and lactic acid are different molecules).

The debate is (or was) even more heated if you ask whether lactate/lactic acid causes fatigue. Lactate and acidosis tend to increase at the same time during fatiguing exercise, but correlation is not causality. You could even easily make the opposite interpretation, that lactate is increasing in an effort to prevent fatigue, as George Brooks would say.

Most people agree now that lactate does not cause fatigue. It is a remarkable carbohydrate molecule used for many, many things in the body. Without even getting into complex biochemistry, there are 2 very simple observations illustrating that lactate itself does not cause fatigue:

1. Lactate keeps increasing or stays elevated several minutes after exercise while your ability to produce force has recovered. Say you run maximally for 400 meters. Lactate will get pretty high. After 60 seconds you go again as hard as you can. Lactate is still high or even maximal, but I guarantee you’ll run the second 400 faster than if you hadn’t taken any rest. So there’s a disconnect between the ability to produce force and lactate levels.

2. When you take sodium-bicarbonate, high-intensity performance is improved while lactate goes higher than it would normally.

From previous blogs you’ll know that during high-intensity exercise we use mainly carbs for fuel. During this process each sugar molecule goes through a series of steps that produces energy along the way, and ultimately ends up with something called pyruvate. At this point, pyruvate is at fork in the road.

If the exercise is somewhat sustainable, it takes a longer, more scenic route that produces a bunch more energy. If intensity is really high (a maximal 800) and we’re demanding energy very fast (more than we can replenish), there’s no time for the scenic option and it takes a shortcut that gives us quick energy. That second option is getting converted into lactate, but it’s not sustainable.

One of the main benefits of the pyruvate-to-lactate conversion is producing NAD+, which keeps the sugar-breakdown process in full swing. Lactate can subsequently be used to produce energy itself in other muscle fibers, be sent to the liver to produce glucose, and other complex biochemical things.

But, to be clear, we’re always making lactate. You have a small amount in your blood right now. Most of the time we make use of it directly for energy and also converting it back into glucose. During intense exercise it starts to accumulate, and we produce more than we can dispose of. It’s really just a byproduct of carbohydrate breakdown. High intensity = high carb breakdown = high lactate. So we have this connection between exercise intensity and lactate, but where’s the acid?

Exercise Acidosis

Acidity is measured with the 0-14 pH scale. At rest, human blood pH is about 7.4 and can decrease as low as 6.9 during maximal rowing. In running and cycling the values can get down to about 7. Within human muscle cells, resting pH is about 7.1, with values as low as 6.3 (rowing) to 6.6 (running and cycling) after maximal exercise.

The further we go above a sustainable exercise intensity, the more acidic we get, and the more muscle function is impaired. With that being said, other things besides low pH contribute to fatigue, and from the previous sentence it’s hard to say acidosis explicitly causes fatigue (remember the lactate correlation is not causation example). But let’s look at how the acidity comes about and what its effects are.

One reason rowing (and carrying heavy groceries) feels so challenging is because the pH of our arms gets lower than the legs. Part of that is because the upper body has more fast-twitch muscle which is more prone to acidity. Rowers and 800m runners have more fast-twitch muscle than marathoners and can induce more acidity, but they also have ~50% or more greater capacity to buffer the acidity as a result of their specific training adaptations.

Continuing with our 800 meter run example, within seconds of the gun going off both anaerobic and aerobic metabolism kick into high gear. The metabolic reactions where we breakdown ATP (the energy currency of the body), phosphocreatine (PCr), and glycogen produce energy and cause changes in ions with positive and negative charges (stay with me now).

When you add up all of the positively and negatively charged molecules, you get the strong ion difference (SID). Lactate is negatively charged and goes up A LOT, but sodium for example is positively charged and also goes up. Potassium is positively charged but goes down. During intense exercise if you add all of these up the SID becomes negative (white circles in the figure above).

But, the body likes to remain neutral with these electrical charges floating around. To counteract all this negativity, hydrogen (H+, positive) increases to balance things out through the same metabolic reactions. pH stands for potential hydrogen, and increasing H+ decreases pH and vice versa.

How might this acidosis influence fatigue/performance?

One way is by inhibiting carbohydrate metabolism. When you give people an oral dose of ammonium chloride, which causes acidosis, then have them exercise, the activity of enzymes involved in breaking down carbs decreases and they use less glycogen. In that same study subjects also ventilated much more at the same intensity which (in my experiences) contributes to higher perceived effort.

Another is by directly interfering with the process of muscle contraction. On a cellular level the hydrogen gets inside the muscle machinery and interferes with calcium, which has important role in how we produce force.

In the picture below, scientists took out a piece of quadriceps muscle and measured how much power the individual muscle fibers could produce. They also looked at how fast the fibers could contract. They did this in the presence of increasing amounts of acidity. In each group, from left to right is the maximal power or velocity at muscle pH levels of 7.0, 6.8, 6.6, and 6.2. As acidity goes up, muscle power and velocity goes down. The top row is fast twitch fibers and the bottom row is slow twitch fibers.

If you looked at the figure closely you’d see that pH wasn't the only thing they manipulated. Inorganic phosphate (Pi), another byproduct of muscle contraction was also increased as the pH went down because that’s what happens in actual exercise.

A study in humans exercising tried to see which one (pH or Pi) was more important by having people do 60 maximal muscle contractions over 5 minutes, rest for 5 minutes, then do it again. It was designed this way because pH would still be decreased (H+ still elevated) at the start of the second bout, but Pi returns to normal quickly.

In the study they were able to measure how much force the muscle itself had the capacity to produce by delivering an electrical stimulation to activate the muscle. But since the subjects were also maximally contracting their muscles, they could determine the voluntary muscle activation, which tells us how much effort they were able to muster from the brain to the muscle.

Basically, both of them matter and were directly related to reduced force production during both exercise bouts. But acidity specifically reduced voluntary muscle activation, indicating “central fatigue”. So the low pH is also sending a signal to the brain that makes us not want to contract our muscles as hard. Makes sense. It hurts!

To summarize, acidity 1) impairs carbohydrate metabolism, 2) interferes with muscle contraction, and 3) tells our brain to ease off.

Are there any benefits to acidity?

Of course! What fun would it be if everything was so cut and dry. When our blood gets acidic, it helps us dump oxygen off of hemoglobin in red blood cells. This is good for exercise when we are trying to get oxygen from the air, into the blood, and ultimately into our muscles for energy.

About 20 years ago a Petri dish study on rat muscle fibers suggested that acidity helped resist fatigue, showing that acidic conditions helped the muscle remain more excitable and willing/ready to contract. It had to do with counteracting the negative effects of potassium accumulation on muscle fatigue. I don’t think their data was wrong, it’s just the applicability to exercising humans which is hard to tease out.

Clearly, the science of fatigue can be complicated, but at the end of the day we have great tools to manage it regardless of the cause, primarily hard training specific to the demands of an event. Stay tuned for my next article where I’ll go into supplement strategies that might provide an extra edge.

Some sources

Buffering capacity of deproteinized human vastus lateralis muscle. J Appl Physiol. 1985. (this study compares muscle fiber type and buffer capacity in rowers, 800m runners, and marathon runners).

Effect of induced metabolic acidosis on human skeletal muscle metabolism during exercise. Am J Physiol. 1999. (this study induced acidosis with ammonium chloride and looked at carbohydrate metabolism)

Cumulative effects of H⁺ and P_i on force and power of skeletal muscle fibres from young and older adults. J Physiol. 2025 (this study looked at power and velocity on muscle fibers during acidic conditions)

On the role of skeletal muscle acidosis and inorganic phosphates as determinants of central and peripheral fatigue: A ³¹ P-MRS study. J Physiol. 2022. (this is the Pi versus acidity study)

Lactic acid--the latest performance-enhancing drug. Science. 2004 (this short article covers the more complex article suggesting acidity prevents fatigue)

Sean Langan has his PhD in exercise physiology. He is interested in how exercise training rewires our biology and harnessing the intersection of human physiology, technology, research, and coaching to improve human performance.

But how does it actually decrease in a physiological sense? What’s going on under the hood?

The Heart’s Nervous System

Two types of nerves innervate the heart, sympathetic (the gas pedal; increases heart rate) and parasympathetic (the brakes, decreases heart rate, also known as vagal nerves). These nerves are like two dimmer switches controlling the same light and we are constantly toggling between sympathetic or parasympathetic predominance.

When we exercise or are stressed (physically, emotionally, mentally), the sympathetic switch ramps up and the parasympathetic switch turns down. Actually, when we first start running the parasympathetic switch turns down before the sympathetic one turns up, referred to as parasympathetic withdrawal.

But what is controlling the switches?

Our brain does its fair share. Some of these nerves have a direct path from the brain to the heart. Just thinking about exercise will increase heart rate (pre-race jitters). This is also why mental or emotional stress alter heart rate (up or down), and can cause fainting which is often due to the so-called vaso-vagal response (vaso = dilate blood vessels, vagal = decreased heart rate).

The nerves can also go in the reverse direction, from the heart to the brain. The heart can sense low oxygen or increased pressure, for example, relays that information upstairs, then the brain sends signals back that increase or decrease heart rate.

But what are the signals?!

They’re basically electrical currents that zoom down the nerves at incredible speeds, as quick as 11.5 meters per second (26 mph) in one study and 16.4 meters per second in another. When you consider how close your heart is to your brain, it’s easy to see realize how quick these effects can happen (milliseconds).

When these currents reach their destination (the heart, and others), they release chemicals. The parasympathetic nerves release acetylcholine which slows heart rate. Drugs like atropine block acetylcholine and increase heart rate. Sympathetic nerves release norepinephrine (also known as noradrenaline) which increases heart rate. Beta-blocker drugs block norepinephrine and decrease heart rate.

Sympathetic nerve activity is important to ramp ourselves up during exercise, but other than that we want more input from the parasympathetic side. Excess sympathetic activity is notable in many disease states.

The Effect of Training

A lower RHR as we get more fit can be explained by 2-3 things.

1. Higher stroke volume

2. Increased parasympathetic activity (also known as vagal tone)

3. Decreased intrinsic heart rate

Number 1 is pretty easy. If a heart pumps more blood per heart beat you simply don’t need as many beats. But that’s not necessarily why it decreases.

Number 2 is probably the most accepted mechanism. Those nerves in the brain sending signals to the heart are literally more active (more electricity). Most people measure this with the [imperfect] heart rate variability measure. Higher HRV usually means higher parasympathetic activity. In my opinion, resting HR is mostly just as useful as resting HRV, but nonetheless it is a decent marker.

A good way to illustrate this is a study in dogs, who are often used in invasive cardiovascular research because of a better relationship to humans than mice/rats. After 3 months of training, resting and exercising heart rate decreased substantially as expected, compared to non-exercisers. They repeated the same heart rate tests but administered drugs to block both types of nerves in the heart, and this time there was no difference between groups, meaning that the reductions in heart rate were solely due to enhanced parasympathetic nerve activity. Studies in humans after 8 months of training, and comparing athletes to non-athletes, find similar results.

Number 3 is a bit contentious. We have an intrinsic heart rate set by the sinoatrial (SA) node. Everyone’s heart has one and this sets our heart rate at 100 beats per minute. It’s our built in pacemaker. If I took your heart out of your chest it would still beat 100 times per minute.

You might then wonder why you’re resting heart rate isn’t simply 100 bpm. Weird.

It’s because the parasympathetic nerve activity and acetylcholine overrides the pacemaker. Fortunately we don’t have to take your heart out of your chest to test your intrinsic heart rate. That’s why the study I mentioned above used drugs to block the heart’s nervous system. When you remove that input, the heart rate you get is presumably due to the pacemaker, and it’s pretty much exactly 100 bpm.

Some scientists think getting more fit decreases the intrinsic heart rate below 100, and they have data to back it up. Runners, rowers, and cyclists all seem to have a slower pacemaker. These were not training studies though where they measured them before and after they “became athletes”. They were snapshots in time of highly fit athletes and regular people of a similar age.

This is an important point because it means you can’t rule out a potential genetic component. It could also mean that training might cause your pacemaker to slow, but only after years of high volume, high intensity training that athlete’s do and wouldn’t be captured in an exercise study of only a few weeks/months. How the pacemaker actually slows down is a whole other topic. It might involve metabolic changes in ion channels within the heart, which is hard to directly measure in humans and a bit complex.

Physiology is Rarely Binary

You can read about the debate between the two mechanisms here. Parasympathetic activity without a doubt increases with exercise training and contributes to a lower RHR. But, years of hard training may also eventually slow your built-in pacemaker. There seems to be a genetic influence on RHR as well which is linked to atrial fibrillation (lower RHR, higher a-fib risk). Lifelong endurance athletes are known to be at risk for a-fib. There’s no data yet to suggest their low RHR is a reason for why they get a-fib, but understanding the mechanisms of decreased heart rate might be helpful for developing prevention strategies or treatments.

Some References

Immediate and sustained increases in the activity of vagal preganglionic neurons during exercise and after exercise training. Cardiovascular Research, 2023.

Exercise training-induced bradycardia: evidence for enhanced parasympathetic regulation without changes in intrinsic sinoatrial node function. Journal of Applied Physiology, 2015.

Exercise training reduces resting heart rate via downregulation of the funny channel HCN4. Nature communications, 2014.

Sean Langan has his PhD in exercise physiology. He is interested in how exercise training rewires our biology and harnessing the intersection of human physiology, technology, research, and coaching to improve human performance.

“We grow, mostly, by dying” - a psychiatrist in Boston

Scientists have been interested in the aging process for quite some time and some argue aging itself a disease. As one of the biggest risk factors for many diseases, curing, or delaying it would be a big win.

But that would mean we need a good way to measure it, and is there something we can use other than the calendar?

A recent review article published in Physiological Reviews covers to current state of aging biomarkers, from DNA methylation clocks to grip strength.

Hallmarks of Aging

The Hallmarks of Aging are what defines aging on a cellular level. They have 3 criteria:

1. They change (go up or down) as you get chronologically older

2. When you over-activate them, aging is accelerated

3. When you block or reverse them, aging slows down

Understanding these mechanisms will, in theory, allow for a blood test to provide our “biological age”, or the age of our insides. It would be really cool to know that, because then we can test and re-test to see what interventions potentially slow down aging, if any.

It would be a phenomenal research tool because we could test something (drugs, exercise) and not have to wait several years to record mortality rates to see if worked.

Epigenetics & Molecular Clocks

Epigenetics is the study of how your genes are expressed, and lifestyle influences it a lot. This is good news. Even with a less favorable set of genes, you aren’t doomed.

Genes are like a light in your room with a dimmer switch. Increased expression makes it brighter, decreased expression makes it darker. A gene in our quadriceps might control how big our muscle gets. Turning the switch up = you get jacked. Exercise, and many other things, leads to “tags” being put on a gene that controls its expression, and in this case, its size.

An interesting study had people do endurance training of only 1 leg for three months. Afterwards, the trained leg had gene expression changes in over 4,000 genes versus the leg that did nothing. Scientists at Joslin Diabetes Center have shown these exercise effects are transmitted to your children. Other things like smoking induce epigenetic changes in a negative direction.

Epigenetic aging clocks (like DNAgem PhenoAge, GrimAge) first came about in 2013 and claim to report biological age, and they are continually being refined/improved.

These clocks are complex mathematical models using DNA methylation (a type of epigenetic “tag”), or other molecules to predict biological age. I won’t pretend to give you a detailed breakdown because the modeling behind it goes over my head.

To date there’s still a lot of uncertainty and they haven’t been completely validated. Some have shown promise, and the science is really interesting, but we aren’t yet at the point where we can use these with confidence, such as to determine age-reversal or age-acceleration.

There’s also no standardization between the available molecular clocks on the market, so they’re all measuring things slightly differently. One study tested 6 different clocks on the same blood samples and some of the predictions were 9 years apart.

Another issue is that they aren’t tissue-specific because they use blood samples. One might catch something beneficial in the blood reflecting liver or muscle health and say you’re biologically young but be overlooking an aging-related issue in your brain that is more difficult to detect in blood samples.

There’s also clinical aging clocks that use blood biomarkers measured in a typical doctor’s visit, but applying complex modeling to predict biological age. These seem more practical for the masses in my opinion, and may be pretty accurate.

From Cellular to Functional Hallmarks of Aging

Ultimately, cellular aging changes are often reflected in functional measures that are much easier to measure and also track very well with the aging process.

What I like about the Functional Hallmarks is that we relate to them better, and they’re what actually matters. Easily getting up out of a chair, the ability to jog, climb stairs, carry heavy groceries, be attentive in a conversation, etc., are all relevant activities that improve quality of life and require adequate performance in the Functional Hallmarks.

When you improve function, the cellular stuff follows along, like the 1-leg exercise study I mentioned. However, in the reverse direction, we aren’t as certain that these biological aging clocks directly translate to improved function.

Another advantage is that we have hundreds, probably thousands of studies showing how physical function changes over the lifespan, from people that are extremely sick to elite athletes and the best “age-ers” among us. This is critical because we have benchmarks to compare ourselves to, unlike the ambiguous molecular clocks.

Bortz and Bortz wrote a short article in 1996 about this topic, titled “How Fast Do We Age? Exercise Performance Over Time as a Biomarker” in the Journal of Gerontology.

By using Master’s athletes as a model population, they analyzed the change in world records over time (35 to 70 years of age) as an indicator of aging. Master’s athletes continue training hard well into old age, so any fall in exercise performance or physical capacity is likely due to aging per se rather than reduced activity.

“Athletic endeavor involves most of the major body systems. By observing the rate of change of records with age, it is proposed that no subtending cellular organ or system function can deteriorate at a rate faster than the exercise performance, or that function would become rate-limiting. Athletic records thereby constitute a possible biomarker of aging.”

They found about a 0.5% per year decline in performance across various events, as well as V̇O₂max. Interestingly, that number corresponds well to the age-related reductions in several cellular processes like DNA repair, cell division of skin fibroblasts, telomere length, nail growth, flow-mediated deflation, maximum heart rate, appendicular bone calcium, and more.

The coherence of performance and the cellular responses suggests monitoring performance can tell us how fast we’re aging.

DIY Aging Biomarkers

We can test the Functional Hallmarks quite easily. For research purposes, the high-tech measurement methods are common place in any human research center I’ve ever worked in, many of which offer reasonably priced pay-for-services for the general public. However, for little cost, you can measure nearly all of them on your own. Here’s how:

1. Brain health. Online cognition tools, such as this one developed by the University of Oxford, can be useful. I’m not saying this should replace seeing a medical specialist, but there are many of these types of validated tests out there.

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2. Neuromuscular function. The ability to sit down to the floor and stand back up (sit to stand test) does the trick (video from the study), as does testing your balance which is related to dementia risk and easily testable in your living room with the Balance Error Scoring System.

   The sit-to-stand test is actually quite challenging. I can’t do it — and while I don’t think it that reflects poor aging because it’s only one of many tests, it’s a good one to strive for since we have data on it. Also, it’s pretty easy to see how the ability to do it would be beneficial in your later years.

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3. Muscle strength and power. The 30 second chair stand test is the simplest—see the link for instructions and scoring. But if you have a good score, don’t stop there. Focus on steadily improving any leg-dominant exercise in the weight room (leg press, squat, deadlift). The more weight you can push in the gym, the easier the chair test will be. For the upper body, I like pull-ups and push-ups.

   For muscle power: vertical jump or a stair climb test. Put some chalk on your hand, jump as high as you can and touch the wall, then measure the height. I personally like the stair climb test, which is just how quick you can get up a set of stairs. There’s validated tests out there (4 stars, 10 stairs, etc.), but really you just need to find something that’s 10-20 stairs, give a hard effort, and always try to beat your score.

   A bit more technical/advanced, but the reverse medicine ball throw is also great, full-body movement and can be measured easily on a football field with a friend.

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4. Cardiorespiratory fitness. The Cooper Run Test. Find a track, warm up, and run as far as you can in 12 minutes. Plug the distance into this calculator and you have a good VO2max estimate.

   • There is also plenty of data on performance for various distances across the lifespan for sports like rowing, running, and cycling. I really like the Concept2 machines for this purpose because if you create an account on their site, you can record an effort, rank it online, and compare to others around the world.

   • Many people use it, so you can see which percentile you fall in for various distances and then aim to shoot as high as possible for your age group, or even younger age groups. If you’re above the 50th percentile for the age group a decade younger, I’d say you’re aging pretty well.

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5. Body composition. Waist circumference (tape measure) relates to metabolic and cardiovascular health. With skin fold calipers (cheap on Amazon) you can also measure body fat percentage with the help of a friend (how to video, and calculator for the results).

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6. Bone density. I can’t help with a DIY test here. This would require a DEXA scan, which may run you anywhere from $75-200. But, it’s worth it!

Using the DIY biomarkers

After the age of 30-40, strength and VO2max will, on average, start declining at about 1-2% per year. So, to put this into practice you should record your data over time and see if you’re delaying the expected average decline. I suggest setting goals to see if you’re on track: if you want to be able to carry 30lb of groceries in each hand when you’re 70, you should be able to comfortably carry ~80lb per hand when you’re 40.

What I Think Are Reasonable Strength and Endurance Standards

The table below can be used as aging biomarkers for aerobic fitness, in Cooper Run Test terms. These distances roughly correspond to VO2max data from this study, with the lower end of the range corresponding to the fitness needed to cut your mortality risk in half compared to someone with the lowest fitness levels in the study (sedentary).

I personally believe everyone could run 1.5+ miles in 12 minutes (8:00/mile) well into their later years with consistent training (assuming no physical limitations).

For strength, let’s use a 5-rep hex bar deadlift since it’s pretty low risk, hits all the relevant lower body musculature, and works your grip strength. 1-rep max efforts aren’t necessary for 99% of people and are low on the risk-reward equation.

The table below is a general guideline initially based on myself (175-180 lb). I’m almost 30 and 1.8x bodyweight is 315 lb. Assuming a strength loss of 1% per year, if I make it to 70 I should be able to deadlift 190lb 5 times, which is 1.1x my bodyweight. Both of which in my mind are completely reasonable. Obviously my bodyweight may change by then and it may require an adjustment.

The main point is that if you’re on track to deadlift your bodyweight by the time you’re 70, you will be above and beyond the required strength needed for activities of daily living. You’ll be thriving and avoiding frailty, which is the common issue I see with older adults.

With All That Said, Physical Performance Doesn't Prevent Aging

I wanted to make a final note that while I am a big advocate for fitness, hard training, and overall physical activity, even the most fit people still succumb to aging. You age better for sure, but it still happens. However, how you perform physically is a phenomenal indicator of the aging process. As of now, in my opinion, it is just a good a surrogate as the molecular level aging clocks, but I am definitely looking forward to see the science advance in that area.

Sean Langan has his PhD in exercise physiology. He is interested in how exercise training rewires our biology and harnessing the intersection of human physiology, technology, research, and coaching to improve human performance. Please contact if there are any topics you’d want to see covered next.

What worked for me is, you gotta do something. You ever meet somebody that don’t do nothing? They don’t do nothing! - Joey Diaz

Many of us are in pursuit, or are pondering the idea, of doing something new. Sports, writing, construction, speaking, teaching, relationships, video games, anything. It’s pretty much what life is about, and it’s all relative to the individual.

Achieving that thing requires putting yourself out there and doing it. You can read about it, talk about it, think about it, but the people who take the risk and do it usually come out on top.

In my line of work, reading is necessary and a staple in my weekly routine. You have to stay up to date on what people are doing in your field because it helps you generate new innovative ideas. Fortunately, I also enjoy it.

Reading things completely outside of your field also has a tangential benefit. Azra Raza wrote a phenomenal book on cancer called The First Cell. In it, you’ll find quotes of poetry, science fiction, and a host of seemingly unrelated literature that she is able to synthesize and tie it back to cancer in a way that I honestly wish I had the brain power to do.

I’m pretty “well-read”, which I’ve found is very helpful in life. By simply knowing more things you can relate to more people you encounter and have more meaningful conversations. But, I think doing may be more important in developing most skillsets.

What do I mean by the power of “doing”?

The obvious cases are people who work in trades—plumbing, construction, painting, etc. Do you want the plumber who read 1,000 plumbing books or the one with 20 years of work experience?

Similarly, you could read all of the theory on strength and endurance training but still have no idea how to coach someone because you’ve never done it. You’ve never trained yourself or coached anyone. An experienced coach might not have all of their science correct when explaining things, but they sure do make people faster.

I did my Ph.D. in exercise physiology, focusing on thermoregulation research in humans—measuring body temperatures during physically stressful scenarios, drawing blood, validating new technology, seeing how we adapt to the heat, etc. Prior to arriving, I spent a ton of time diving deep on thermoregulation science because I did not want to show up and look like an idiot.

I developed a good knowledge base for sure, but the rate at which I learned (learning rate = knowledge / time) by actually doing the studies I was previously reading about was way faster. Now, when I answer someone’s questions or discuss the topic, most of the knowledge I draw upon is from the thousands of observations by just being in the lab for far too many hours.

I was doing it, not just reading about it.

Often times it is the things that you don’t realize but are just inadvertently diffusing into your brain. I remember explaining to someone how high body temperature gets during exercise, or how much sweat you might lose in 2 hours of running in the heat, and they seemed shocked. “How do you know that?” or “Are you sure?”. I don’t need to go cite a research study to know the answer, it’s just something you pick up on by doing the work.

A Humbling Experience

Several years ago now a fella reached out to me to train him. He was a relatively seasoned marathon runner, in his mid-40s with several performances just over 3 hours and couldn’t break the barrier. He felt like he plateau’d and thought more strength and speed might help, which is more in my wheel house. Ultimately his primary goal was still to run a faster marathon.

I have never run or trained for a marathon, but since I train far more seriously than I probably should (for shorter distances), and know a bit about high performance physiology, I’ve developed an understanding of the demands of running quite well. However, I should mention I do not come from a running background and picked this stuff up in my early to mid 20s.

As far as the marathon goes specifically, most of my knowledge at the time was through reading science and coaching information and communicating with people in that world.

Anyway, I thought it would be a good experience to work with this guy. I saw a lot of potential, and at the end of the day he wasn’t an elite runner so the stakes weren’t high. The first few months were great. A lot of focused speed work, 5k-10k races, and specific strength training sessions. Most of this was novel for him which led to a bunch of quick adaptations. Although, this type of training tends to be more painful, so I can’t say he enjoyed it more than longer runs at slower paces.

I remember building up to a marathon and ~4-6 weeks out (I can’t remember the exact time) he asked me: “When are we going to do a long run?”. Long runs (~16-22 miles) are a staple for marathoners.

Most of the longer sessions I prescribed were based on time, around 80-90 minutes, and were used as easier runs to build mileage and time on the feet while we focused on speed. I was so focused on the speed aspect—which, don’t get me wrong, is critical for marathon performance—that I honestly neglected the fact this guy was 4-6 weeks from a marathon and hadn’t run over ~14-16 miles in the last few months.

I played it off, but felt like an idiot.

If I had experience doing a marathon, that wouldn’t have slipped my mind. In fact, the main reason I don’t run marathons because I hate long runs (the most I’ve done in one shot is 14 miles, twice). I know that they are critical to running marathons well, and if I did a marathon, I’d want to run it well, so then my conclusion is that I just won’t do it.

Since my personal experience and training has been for more middle-distance and up to 5k and as far as 10 mile races, my mind was constantly in that mode. I think that, my personal disdain for long runs, and lack of personal marathon experience, led to a suboptimal coaching strategy.

To be fair (to myself), after that conversation he knocked out some 16-18 milers and if memory serves he was stoked about his marathon performance. So it’s not like he was completely unprepared, he ran his fastest time in several years. But I couldn’t help but think that with a better plan, and more experience on my part of doing, he could have smoked the 3 hour barrier.

Besides the more intimate experience you get with whatever goal you’re after, I find that one of the best benefits of doing is that the failures are quite visceral. The screw ups are inevitable, and they stick with you—most likely more than if you misinterpreted a sentence in a book—which in my experience is a great way to make sure it never happens again.

People value and respect experience. The only way to get it, is to do it. Put yourself out there, try things, and see what happens.

Action produces information, even if it’s the wrong action. The wrong action at least gives you better insights for your next action.

“We cement ourselves where we are because we don’t think the next action is the right one. It doesn’t matter. Take the tiniest step in any direction then correct course. Do this over and over again until you get where you want to go.” - Tyler Bruno

*I have no idea who Tyler Bruno is, but I have a screenshot these ideas and the above quote he wrote in my phone. If you know him send this to him.

Sean Langan has his PhD in exercise physiology. He is interested in how exercise training rewires our biology and harnessing the intersection of human physiology, technology, research, and coaching to improve human performance. Please contact if there are any topics you’d want to see covered next.