When you think of energy metabolism, most think about carbohydrates, fat, and protein.

But none of those macronutrients can actually be converted into ATP without a supporting cast of micronutrients working behind the scenes.

And the most important members of that cast are B vitamins. Their main functional role is as coenzymes, meaning they help stabilize enzymes or speed up reactions. Without B vitamins, the chemical reactions that produce energy can’t happen.

Each vitamin has a unique biochemical role. Let’s walk through it, shall we?

Note: make sure you’ve read my previous Fueling Field Notes on carbohydrate, fat, and protein metabolism to help provide context for this overview.

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If you have been following along in this study journey, you know that protein holds many roles in the body. It can serve as an energy source, but it’s not efficient. Carbohydrates and fat hold awards for supplying energy.

Protein’s real value lies in everything else it does, from building muscle and enzymes to regulating hormones and supporting immune function.

We have covered carbohydrate and fat metabolism. Now let’s look at how the body handles protein, what happens to amino acids during exercise, and why protecting protein from being used as fuel is one of the most important goals of smart endurance nutrition.

The Liver: Command Center for Amino Acid Metabolism

When we consume protein, it’s broken down into amino acids in the GI tract and absorbed into the bloodstream. From there, the liver takes the lead. It’s the primary site of amino acid metabolism and serves as a monitor and regulator of the body’s amino acid supply, directing amino acids where they are needed most.

About 20% of absorbed amino acids are processed directly by the liver. The liver uses them for two main purposes: anabolism and catabolism.

Anabolism refers to building processes. The liver takes simple molecules like amino acids and constructs complex molecules such as liver enzymes, plasma proteins like albumin, and other essential compounds. This is the constructive side of metabolism.

Catabolism refers to breakdown processes. When amino acids are in excess or when the body needs energy, the liver breaks them down into usable components. The nitrogen-containing amino group is removed and eventually converted to urea for excretion in urine. The remaining carbon skeleton can be used to produce ATP through the TCA cycle, converted to glucose through gluconeogenesis, or in some cases converted to fat and stored.

Protein Storage: Why There Is No True Reserve

Unlike carbohydrates, which are stored as glycogen in the liver and muscle, and fat, which is stored in adipose tissue, protein has no dedicated storage site. There is no reserve pool of amino acids sitting in the body waiting to be used.

The closest thing to a storage site is skeletal muscle. The body can break down muscle protein to release amino acids when needed. But this comes at a high cost.

Muscle protein breakdown impairs the muscle’s ability to function, generate force, and recover. The body goes to considerable lengths to protect skeletal muscle from being used as fuel, and this protection depends heavily on the availability of carbs and fat.

When adequate carbs and fat are consumed, they provide a protein-sparing effect.

In simple terms, when the body has enough energy from other preferred sources, it does not need to break down muscle tissue for fuel. Protein is free to do the very important things only protein can do.

When an athlete is underfueled and not meeting their caloric needs, this protection breaks down. Protein must step in to meet energy demands, and all of its other essential functions begin to suffer.

Protein as Fuel During Exercise

The body uses protein for energy during exercise through two main pathways: direct oxidation of amino acids for ATP production, and gluconeogenesis.

Amino Acid Oxidation

When muscle cells are broken down for energy during exercise, the amino acids most commonly used are the branched-chain amino acids (leucine, isoleucine, and valine), along with aspartate, asparagine, and glutamate.

Fun fact: The stress hormone cortisol stimulates muscle protein breakdown, which is why periods of high physical or psychological stress increase amino acid oxidation.

Endurance exercise is a form of short-term physiological stress, and the result is an increased oxidation of BCAA leucine in particular. The degree to which this happens depends heavily on fueling status.

When an endurance athlete exercises with low glycogen stores, such as during low-carb diets or poorly-fueled training sessions, leucine oxidation increases significantly. A higher-carb diet with near-maximal glycogen stores has the opposite effect, reducing the need to break down muscle for fuel.

Dietitian note: This is exactly why well-fueled workouts and recovery nutrition are such important priorities for endurance athletes. Every time you train underfueled, you increase the physiological stress on muscle tissue and raise the likelihood that protein is being used for energy rather than repair and adaptation. Minimizing that stress is not just about performance in the moment. It is about protecting the long-term investment you are making in your training.

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For most athletes, increasing ferritin and iron levels through diet alone isn’t going to cut it. Or, at least it’s not going to increase levels efficiently.

But the combination of dietary changes + a supplementation strategy. That’s where we can see best results.

I forgot to cover this in Part I

After publishing Part I of this series, I realized I forgot to mention how NSAID medication use can cause iron loss in athletes, so here is a quick one-off discussion because it’s worth mentioning.

Mechanisms in how NSAID meds can impact ferritin/iron levels:

Small-bowel enteropathy

Long-term NSAID use damages the small intestine directly, not just the stomach. Up to 70% of long-term users develop small intestinal inflammation, and around 30% develop erosions or ulcers.

NSAIDs damage the gut lining through two separate pathways:

• The well-known one (COX-mediated): NSAIDs work by blocking an enzyme called COX, which is how NSAIDs reduce pain and inflammation. But COX also produces protective chemicals that keep the stomach and intestinal lining healthy by maintaining its blood flow, stimulating mucus production, and helping it repair itself. When NSAIDs block COX, that protective layer weakens, leaving the gut vulnerable to acid and digestive juices.

• The less recognized one (COX-independent): NSAIDs also directly damage the energy-producing mitochondria of the intestinal cells. They essentially short-circuit the power so the cells lining the intestine can't produce enough energy to maintain themselves. When those cells weaken and die, they form gaps between them, like mortar crumbling between bricks in a wall. This makes the intestinal wall "leaky," allowing bacteria, bile acids, and digestive enzymes to seep into the deeper tissue.

Both pathways cause microscopic bleeding and inflammation along the intestinal wall. The gut is already under stress during intense exercise because blood gets diverted away from the digestive organs to the working muscles. Adding NSAIDs on top of that is essentially a double hit. The gut is already blood-deprived from exercise, and now its cells are also being poisoned from the inside. The result is more tissue damage, more microscopic bleeding, and more iron lost. Often without the athlete ever noticing any symptoms.

Impaired absorption

Beyond blood loss, NSAIDs can interfere directly with intestinal iron absorption.

They can impact your CRP (inflammatory) labs

As mentioned in Part II, when C-reactive protein is high, it can give a falsely higher ferritin lab result.

NSAIDs also lower the CRP inflammatory marker. So an athlete taking NSAIDs regularly may show a deceptively normal inflammatory panel.

Increasing dietary iron

Before we get to supplements, diet deserves its own conversation.

For reference, the Recommended Dietary Allowances are:

• 14-18 years old (male): 11 mg

• 14-18 years old (female): 15 mg

• 19-50 years old (males): 8 mg

• 19-50 years old (females): 18 mg

• 51 years old: 8 mg

• Note: Women during pregnancy require 27 mg iron/day

Heme vs. non-heme iron

Not all dietary iron behaves the same way once it hits your gut.

• Heme iron comes from animal sources, meat, poultry, and seafood, and is absorbed at roughly 15-35% efficiency.

• Non-heme iron comes from plant sources and fortified foods, and is absorbed at only about 2-20% efficiency. It is much more sensitive to what else is on your plate.

Because non-heme iron is so poorly absorbed, it’s recommended that people who eat plant-based diets eat more iron-rich foods than the RDA.

Absorption Enhancers:

• Vitamin C, eaten in the same meal as the iron source. This is the most reliable enhancer. Dosing and timing matter here. If taken hours ahead, it’s far less effective.

• Meat, poultry, or fish added to a plant-based meal, the “meat factor” boosts absorption of non-heme iron from everything else on the plate, not just its own heme iron.

• Cooking acidic, high-moisture foods in cast iron cookware.

Does cooking with cast iron really increase iron?

Yes, and it is one of the more well-documented “kitchen hack” claims out there.

A classic 1986 study tested 20 foods cooked in iron skillets versus non-iron cookware and found that 90% of foods contained more iron after cooking in cast iron. The largest effect was in acidic, high-moisture foods simmered for longer periods. Spaghetti sauce went from under 1 mg of iron to nearly 6 mg per serving when simmered in a cast iron pan.

A more recent systematic review of cast iron cookware interventions confirmed the same pattern: measurable increases in both food iron content and, in several studies, blood hemoglobin levels in populations using iron cookware regularly.

If you don’t want to use a cast iron pan, products like this Lucky Iron Fish (affiliate Amazon link) are an option too.

Absorption Inhibitors:

• Calcium from dairy, calcium-fortified foods, or supplements. The only one that blocks both heme and non-heme absorption

• Phytates, found in plant-based foods, mostly in whole grains, legumes, nuts, and bran. This is dose-dependent. The largest inhibition effect is at higher amounts.

• Polyphenols, in tea, coffee, cocoa, and red wine. Again, dose-dependent. Black tea alone can cut absorption 56-72%.

• Tannins and other compounds in tea/coffee generally, best kept an hour or more away from iron-rich meals

Iron-rich foods, and how much iron they actually provide

Here is a practical list of standard portions and iron content per USDA data.

Heme sources:

• Oysters (3 oysters): 6.9 mg

• Mussels (3 oz): 5.7 mg

• Beef liver (3 oz): ~5 mg (organ meats range widely, 1.8 to 19 mg depending on the cut)

• Sardines, canned (3 oz): 2.5 mg

• Beef (3 oz): 2.5 mg

• Clams (3 oz): 2.4 mg

• Turkey leg (3 oz): 2.0 mg

• Lamb (3 oz): 2.0 mg

• Shrimp (3 oz): 1.8 mg

Non-heme sources:

• Fortified whole grain cereal (1/2 cup): 16.2 mg

• Fortified hot wheat cereal (1 cup): 12.8 mg

• Fortified toasted oat cereal (1 cup): 9.0 mg

• Fortified bran flakes (3/4 cup): 8.4 mg

• Spinach, cooked (1 cup): 6.4 mg

• Lima beans, cooked, 1 cup: 4.9 mg

• Soybeans, cooked, 1/2 cup: 4.4 mg

• Swiss chard, cooked, 1 cup: 4.0 mg

• White beans or lentils, cooked, 1/2 cup: 3.3 mg

• Chickpeas, cooked, 1/2 cup: 2.4 mg

• Kidney beans, cooked, 1/2 cup: 2.0 mg

• Sesame seeds, 1/2 oz: 2.1 mg

• Cashews, 1 oz: 1.9 mg

• Prune juice, 1 cup: 3.0 mg

Dietitian thoughts: those fortified cereal numbers look significant next to a cup of cooked spinach. Fortification is one of the most effective yet underrated ways non-heme iron gets into the average diet.

Does supplementation actually work?

Good news: once someone is identified as iron deficient, the research on supplementation is fairly consistent.

A few caveats on dose and duration matter, though.

A 2024 meta-analysis (Šmid and colleagues, Sports Medicine) pooled 13 randomized trials and found:

• Oral iron reliably increases serum ferritin, but only in people who started deficient.

• Athletes with a starting ferritin at or below 12 ng/mL saw meaningful increases.

• Athletes starting above that saw only minimal changes, regardless of dose.

• No significant effect on VO2max overall.

• Doses from 16 to 100 mg of elemental iron daily worked, but only when given for at least 6 to 8 weeks. Shorter supplementation protocols, even at high doses, did not move the needle.

A separate 2026 meta-analysis focused specifically on active women (McCarthy and colleagues) backed this up using ferrous sulfate specifically: a significant average increase of 12.61 ng/mL in ferritin and 0.42 g/dL in hemoglobin.

The biggest gains were seen in women who started more depleted (iron-deficient, non-anemic stage 2). Duration mattered more than dose, and longer durations brought smaller additional gains, basically a diminishing returns curve as stores refill.

Pengelly’s review of female athletes zeroed in on performance specifically, not just biomarkers. The real performance benefits showed up at higher doses:

• Around 100 mg of elemental iron daily, or every other day, taken for up to 8 weeks orally.

• Or parenteral (injected) administration over 8 to 10 days for more severe cases.

Lower doses in the 16-60 mg range still improved secondary markers like energy efficiency and lactate handling. They just did not move the performance needle on straight-line endurance time trials.

Key takeaway: Iron supplementation works, but on a timeline of weeks, not days. It works best in people who are meaningfully depleted rather than borderline, and the dose needs to be adequate if the goal is a performance change rather than just a biomarker change.

How much iron should you supplement with?

For athletes with low ferritin (<12 µm/L), 60–100 mg of elemental iron daily (or alternate-day) for a minimum of 6–8 weeks is the general recommendation, though the optimal dose depends on the severity of depletion and the clinical scenario.

For ferritin between 12-30 µm/L, the same 60 mg elemental iron once daily or alternate-day dosing is appropriate.

For ferritin 30–50 µg/L (suboptimal for athletes), lower doses (e.g., 30 mg/day) with dietary optimization may be adequate. But if you’re looking to speed up ferritin levels to improve athletic performance for an event, I’d go with the 60 mg elemental iron once daily.

Should I supplement daily or every other day?

I’ve seen recommendations on the internet about increase absorption by supplementing with iron every other day instead of daily. So let’s look at the research.

The physiological rationale: hepcidin rebound

The key mechanism is hepcidin, the hormone that controls iron absorption.

When a dose of ≥60 mg elemental iron is taken, hepcidin peaks at ~8 hours, remains elevated at 24 hours, but returns to baseline by 48 hours.

This elevated hepcidin effectively shutting down iron absorption for up to 48 hours after a dose. By dosing every other day, the next dose arrives after hepcidin has normalized, allowing 35–50% higher fractional absorption per dose compared with consecutive-day dosing.

This is the rationale, but what do the studies say?

Clinical Outcome Data

• A masked, placebo-controlled randomized control trial (RCT) of 150 premenopausal women with ferritin ≤30 ng/mL found parallel ferritin repletion between daily dosing for 90 days and alternate-day dosing for 180 days, with significantly fewer GI side effects in the alternate-day group.

• An RCT in 200 adults with IDA showed no significant difference in hemoglobin change between daily and alternate-day dosing at 8 weeks.

Athlete-specific evidence

An 8-week study in 31 endurance-trained runners with ferritin <50 µg/L found that daily and alternate-day oral iron produced parallel increases in serum ferritin (~19.7 µg/L increase in both groups), but the alternate-day group had far fewer severe GI complaints.

The takeaway: For athletes who tolerate daily iron without GI issues, daily dosing remains reasonable for faster repletion.Even though alternate-day dosing takes longer to replete stores, it’s the best option for athletes with gut sensitivity.

Choosing your iron supplement

This is where a lot of athletes get stuck. The supplement that works best is also, unfortunately, the one most likely to upset your stomach.

Ferrous sulfate: the gold standard

Cheap, well studied, and effective.

A 2024 clinical practice update from the American Gastroenterological Association supported ferrous sulfate as the preferred first-line oral iron formulation. Mostly because none of the fancier alternatives are quite as effective.

Their guidance:

• Dose once daily at most. More frequent dosing does not improve absorption. It just adds side effects, such as nausea, constipation, and GI discomfort.

• Consider every other day dosing if tolerance is an issue.

• Many iron supplements include Vitamin C within the supplement, so check the label. If it doesn’t, make sure to pair the supplemental iron with vitamin C to help absorption.

Dietitian Note: The ALN team has found with our athletes that NatureMade Iron (ferrous sulfate) has produced the best results raising ferritin levels. Taking 3-4x/week instead of daily has supported better gut tolerability.

A 325 mg tablet is 65 mg of elemental iron.

Ferrous bisglycinate: what an athlete-specific dosing study found

Ferrous bisglycinate is a chelated iron form (iron bound to the amino acid glycine) marketed as gentler on the gut than ferrous salts.

Most of the supporting research comes from non-athlete populations, but a 2024 study published in PM&R looked specifically at NCAA Division 1 female athletes, worth knowing about if you’re considering this formulation.

The study followed 33 Division 1 athletes (soccer and track and field) with confirmed non-anemic iron deficiency (ferritin <35 µg/L and a normal hemoglobin). Athletes self-selected into one of two dosing schedules for an 8-week course of ferrous bisglycinate at 25 mg elemental iron per dose: daily, or three times a week.

Both schedules worked. Daily dosing raised ferritin by an average of 12.88 µg/L, 3x-weekly dosing raised it by 5.17 µg/L, and statistically that gap wasn’t significant given the study’s small size.

But a more practical marker told a clearer story: 60% of the daily group crossed the 35 µg/L threshold by the end of the study, compared with only 17% of the 3x-weekly group, a difference that was statistically significant.

Side effects moved in the opposite direction. Athletes on the daily schedule reported significantly more nausea and constipation than those dosing three times a week.

The study’s limitations:

This was not a randomized trial. Athletes chose their own schedule rather than being assigned one, the sample was small (33 people at a single university), and there was no direct comparison to ferrous sulfate, just a reference to prior literature suggesting bisglycinate tends to be gentler generally. The study also found that athletes starting with ferritin <15 µg/L were unlikely to reach the 35 µg/L threshold within 8 weeks regardless of schedule. This suggests that a more severe deficiency needs a longer time frame or a higher dose than either regimen tested here.

Key takeaway: In this small athlete-specific study, daily ferrous bisglycinate got more athletes to a normal ferritin level faster, but at the cost of more GI side effects than dosing 3x/week. If tolerance is the limiting factor, 3x-weekly dosing is a reasonable compromise, just budget more time before rechecking labs.

Sucrosomial iron: the newer alternative

About a year ago, I had an athlete client (who was also a physician) tell me about a new form of iron supplement, sucrosomial iron.

Sucrosomial iron (SI) is a novel oral iron formulation where the iron particle is wrapped in a protective coating, essentially a tiny two-layer fatty membrane (similar to what surrounds a living cell), held together by a sugar-fat binder that forms an outer shell around it.

This gives unique absorption properties and excellent GI tolerability compared to conventional iron salts. The clinical trials have been promising, and it’s been studied successfully in populations often managed with IV iron: chronic kidney disease, cancer, bariatric surgery, and inflammatory bowel disease patients.

In theory, that makes absorption less dependent on hepcidin, relevant given everything in Part 2 about post-exercise hepcidin spikes blocking absorption.

There are no head-to-head comparisons to ferrous sulfate, and no dedicated trials measuring athletic performance outcomes.

Sucrosomial iron is widely available across Europe. It’s not available in the U.S. unless you order it online. It’s pricey, ~$2.40 per capsule (compared to ~$0.07/capsule of ferrous sulfate).

Typical doses range from 28–30 mg elemental iron once daily for mild deficiency, with higher doses (60 mg/day) used for moderate-to-severe IDA.

IV Iron

If oral iron genuinely is not tolerated, or ferritin has not budged after a solid trial (generally 4 to 8 weeks of consistent use), intravenous iron is a legitimate next step.

It’s increasingly used earlier in athlete populations for exactly this reason.

Competitive athletes should loop in a sports medicine practitioner here, both to rule out other causes of poor absorption and to make sure any IV protocol clears anti-doping requirements.

Iron itself is not a prohibited substance under WADA rules, but the route of administration is regulated. Intravenous infusions or injections are capped at 100 mL within any 12-hour period. Anything beyond that is prohibited unless it is part of a legitimate hospital treatment, surgical procedure, or clinical investigation.

Key takeaway: A standard IV iron infusion for repletion typically falls within that 100 mL limit, but confirm this with a sports medicine practitioner before scheduling one.

Don’t chase a high number

More is not better here.

Pushing ferritin above a sufficiency threshold does not translate into additional performance benefit. Too high a ferritin carries risks. Iron overload has been linked to oxidative stress and, in more severe cases, organ damage. The goal is repletion, not maximization.

The general upper limit of ferritin is >200 µg/L in women and >300 µg/L in men.

Where this leaves you

If you are coaching yourself or your athletes through this, here is the practical version:

• Get ferritin tested rather than guessing from symptoms alone, and read the number in the context of training load rather than the lab’s general population range.

• Treat anything under 30 as worth a conversation, especially with fatigue or flatlining performance alongside it.

• If supplementation is warranted, expect it to take 6 to 8 weeks minimum to show up in bloodwork.

• Use a dose in the 65 to 100 mg elemental iron range if the goal is a performance change rather than just a biomarker change.

• Build in the absorption basics: away from calcium and polyphenols, with vitamin C, at a frequency you can actually stick with for two months straight.

And if your ferritin comes back and the lab calls it normal while three other papers would have called it borderline, you are not imagining things. It really is the value nobody agrees on. That just means the number needs a coach’s judgment attached to it, not a rubber stamp.

TL;DR:

Diet is the first lever worth pulling. Heme iron (meat, poultry, seafood) absorbs far more reliably than non-heme iron (plants, fortified foods), and pairing non-heme sources with vitamin C matters. Cooking acidic, high-moisture foods in cast iron genuinely adds meaningful non-heme iron, too. Beyond diet, oral iron supplementation reliably raises ferritin, but the benefit depends on how depleted someone was to begin with. It takes 6 to 8 weeks minimum to show up, and performance gains specifically tend to need higher doses (around 100 mg elemental iron daily) sustained for weeks. Ferrous sulfate remains the most effective option but is also the hardest on the stomach. Sucrosomial iron and iron polymaltose complex are gentler alternatives with meaningfully weaker efficacy data, useful mainly for people who cannot tolerate ferrous sulfate at all. IV iron is a legitimate option when oral iron fails, but WADA caps IV infusions and injections at 100 mL per 12 hours. And more ferritin is not automatically better. Chasing a high number past sufficiency has no proven upside and carries real downside.

Let’s hear your thoughts!

What resonated with you? What questions do you still have? Whether you're an athlete, a coach, or a fellow RD, I want to hear your perspective. Leave a comment below and let's keep the conversation going.

Citations:

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Effect of baseline ferritin levels on post-exercise iron metabolism in male elite youth rowers. Scientific Reports. 2025.

Quick definitions:

Serum iron is the amount of iron in your blood.
Hemoglobin is the protein inside the red blood cells that uses iron to carry oxygen.
Ferritin is the protein that stores iron.
Transferrin Saturation is the percentage of carrier proteins that move iron.
Total Iron-Binding Capacity (TIBC) measures how well proteins (like transferrin) bind and carry iron in the blood.

The earliest stage of iron deficiency

It’s called iron depletion without anemia, also called latent or non-anemic iron deficiency (IDNA).

It’s the earliest stage of iron deficiency, where body iron stores are diminished (what ferritin actually reflects). But hemoglobin and serum iron remain normal because red blood cell production has not yet been compromised.

The staging framework researchers use lines up with that idea directly.

• Stage 1 (IDNA-1) is serum ferritin roughly <30 ng/mL with transferrin saturation >16%.

• Stage 2 (IDNA-2) is ferritin <20 ng/mL with transferrin saturation also dropping <16%.

• Stage 3 (IDA-3) is when hemoglobin finally drops below 12 g/mL, and you have crossed into frank anemia.

Hemoglobin is the last domino to fall, not the first. By the time it drops, you have already been running on depleted stores for a while.

IDNA is also extremely common.

A 2025 systematic review and meta-analysis (Thompson and colleagues, Pediatric Blood & Cancer) pooled data from over 17,500 collegiate athletes across 23 countries and found that roughly 23% had ferritin below 20 ng/mL, and just under 54% fell below 50 ng/mL.

In other words, between 25 and 50% of collegiate athletes are walking around with depleted iron stores at any given time.

What else to look at beyond ferritin

If ferritin is low, but hemoglobin and serum iron look normal. Here is what else to look at for a better picture of what’s going on:

Transferrin saturation (TSAT).

A TSAT <16–20% confirms restricted iron supply to tissues even when serum iron appears "normal" on a single measurement, and it’s time to focus on dietary iron and supplementation.

Note: TSAT is determined by serum iron/TIBC x 100%. In true deficiency, TIBC tends to rise as the body wants to increase transferrin production so it can scavenge whatever iron it can find. The body is so wildly smart, it’s amazing.

C-Reactive Protein (CRP)

Ferritin is an acute-phase reactant, meaning it reacts to inflammation. Whether that inflammation is from an infection, injury, or a really intense workout.

A CRP value helps confirm that the low ferritin is not being masked by inflammation (i.e., the true iron deficit may be even worse if CRP is elevated).

Complete Blood Count (CBC)

In addition to a standard CBC panel, checking a reticulocyte hemoglobin lab (CHr/Ret-He), if available, measures the amount of hemoglobin in newly produced red blood cells.

This lab is an early marker of whether the body has trouble supplying iron to make new red blood cells (iron-restricted erythropoiesis). And, before the size and volume of red blood cells decrease.

I’ll dive deeper into CRP and CBC later in this article.

Celiac serology (tTG-IgA + total IgA)

The AGA and ACG recommend testing for celiac disease in patients with unexplained iron deficiency, as celiac disease impairs iron absorption in the small intestine.

Dietary and menstrual history

Assess caloric intake, RED-S screening, iron-rich food consumption, vegetarian/vegan status, and menstrual blood loss if applicable.

Stool occult blood or GI evaluation

If iron deficiency persists despite adequate supplementation, or in male athletes or postmenopausal women without a clear cause, an endoscopy should be pursued to rule out any hidden GI bleeding.

CRP and CBC: Why It Matters for Interpreting Ferritin

I asked the question: Why do CRP and CBC labs matter in relation to ferritin? Let’s dive into this together.

C-Reactive Protein

Ferritin rises with inflammation, which can mask true iron deficiency by making stores appear adequate when they are not.

So a CRP lab will provide context to the ferritin value in two ways:

1. A low CRP (<5 mg/L): The ferritin value can be taken at face value. In this case, a low ferritin reliably reflects depleted iron stores.

2. Elevated CRP: The true iron deficit is likely worse than the ferritin suggests.

   Most standard labs would consider a CRP >10 mg/L as elevated. However, the BRINDA project that studied inflammation-adjusted ferritin cites >5 mg/L as the threshold.

A 2010 meta-analysis found that inflammation increases ferritin by approximately 30–90%. This is a big range, but basically, ferritin rises and falls with the phases of the inflammatory response.

In athletes, post-exercise inflammation (via IL-6) can temporarily raise both CRP and ferritin, so timing of blood draws relative to training matters.

CBC Indices

Standard red blood cell labs reflect iron-restricted erythropoiesis (the body has trouble supplying iron to make new red blood cells).

But they are late markers, meaning they change only after iron deficiency has persisted long enough to affect the mature red cell population (which has a ~120-day lifespan).

Standard red cell labs:

• MCV (mean corpuscular volume): Falls below 80 fL in established iron deficiency anemia, but remains normal in early/latent iron deficiency.

• MCH (mean corpuscular hemoglobin): Drops below 27 pg, paralleling MCV changes.

• RDW (red cell distribution width): Often the earliest conventional CBC abnormality. It rises above 14.5% as a mixture of normal and iron-deficient red cells emerges, even before MCV drops.

Reticulocyte Hemoglobin Content (CHr / Ret-He): The Early Detector

Reticulocyte hemoglobin content is reported as CHr or Ret-He. It measures the hemoglobin content of newly released red blood cells and is the most sensitive peripheral blood marker for detecting iron-restricted erythropoiesis before anemia develops.

The following table from a New England Journal of Medicine review summarizes how these iron-related markers behave across the spectrum of iron deficiency states:

When is a GI evaluation needed?

When you have an athlete with low ferritin, no GI symptoms, and the training load and diet are a reasonable explanation. An aggressive GI workup is not the first move.

That said, it is worth knowing where the line actually sits for further testing.

The 2020 American Gastroenterology Association (AGA) clinical practice guidelines on the GI evaluation of iron deficiency anemia lay out when investigation is warranted, though it is worth being precise about scope:

The recommendations apply once someone has crossed into iron-deficiency anemia territory (low hemoglobin, not just low ferritin).

For suspected celiac disease, the AGA recommends starting with serology instead of a small bowel biopsy.

For postmenopausal women and men with confirmed iron-deficiency anemia and no clear alternative explanation, the AGA recommends bidirectional endoscopy (upper endoscopy plus colonoscopy) to rule out a GI source, including malignancy.

For young endurance athletes and premenopausal women with IDA, the recommendation is softer and gives more room for clinical judgement. The doctor and patient can reasonably decide to hold off on GI testing and start with diet changes and iron supplementation.

If no cause of IDA is identified after endoscopy, testing for H. pylori is recommended. H. pylori impairs iron absorption independent of any bleeding it might cause.

Stay tuned for part 3 of this series as we dive into strategies to increase ferritin through diet and supplementation.

TL;DR:

Normal hemoglobin with low ferritin is its own diagnostic stage, non-anemic iron deficiency (IDNA), not a lab error. It is extremely common, affecting an estimated quarter to half of collegiate athletes depending on the cutoff used, and it can impair aerobic capacity and energy well before anemia ever shows up. Athletes are more prone to it than the general population. Beyond ferritin, transferrin saturation, soluble transferrin receptor, reticulocyte hemoglobin content, inflammation markers, and a real diet and menstrual history all add useful context. A GI workup is not the default move for isolated non-anemic depletion. It becomes relevant when the numbers do not add up, or the deficiency will not resolve with treatment.

I want to hear from you!

What resonated with you? What questions do you still have? Whether you’re an athlete, a coach, or a fellow RD, I want to hear your perspective. Leave a comment below and let’s keep the conversation going.

Citations:

Peeling P, Dawson B, Goodman C, Landers G, Trinder D. Athletic-induced iron deficiency: new insights into the role of inflammation, cytokines and hormones. European Journal of Applied Physiology. 2008;103(4):381-391.

Clénin G, Cordes M, Huber A, et al. Iron deficiency in sports, definition, influence on performance and therapy. Swiss Medical Weekly. 2015;145:w14196.

Thompson AA, et al. The global prevalence of iron deficiency in collegiate athletes: a systematic review and meta-analysis. Pediatric Blood & Cancer. 2025.

Barney DE Jr, Ippolito JR, Berryman CE, Hennigar SR. Running increases hepcidin and decreases dietary iron absorption. Journal of Nutrition. 2022;152:2039-2047.

Ko CW, Siddique SM, Patel A, Harris A, Sultan S, Altayar O, Falck-Ytter Y. AGA clinical practice guidelines on the gastrointestinal evaluation of iron deficiency anemia. Gastroenterology. 2020;159:1085-1094.

Auerbach M, DeLoughery TG, Tirnauer JS. Iron deficiency in adults. JAMA. 2025.

Hamdeh S, Micic D, Hanauer S. Review article: drug-induced small bowel injury. Alimentary Pharmacology & Therapeutics. 2021.

ter Steege RW, Kolkman JJ. Review article: the pathophysiology and management of gastrointestinal symptoms during physical exercise, and the role of splanchnic blood flow. Alimentary Pharmacology & Therapeutics. 2012.

Bjarnason I, Scarpignato C, Holmgren E, et al. Mechanisms of damage to the gastrointestinal tract from nonsteroidal anti-inflammatory drugs. Gastroenterology. 2018.

Stewart JG, Ahlquist DA, McGill DB, et al. Gastrointestinal blood loss and anemia in runners. Annals of Internal Medicine. 1984;100:843-845.

Stoffel NU, Cepeda-Lopez AC, Cervantes-Gracia K, et al. The effects of reducing chronic inflammation in overweight women on serum hepcidin and iron absorption with and without supplemental ascorbic acid. British Journal of Nutrition. 2021;126(6):877-884.

Nolte S, Malhan D, Klemmer A, et al. Training in normobaric hypoxia induces hematological changes that affect iron metabolism and immunity. Scientific Reports. 2025;15:17757.

Garvican-Lewis LA, Vuong VL, Govus AD, et al. Iron insufficiency diminishes the erythropoietic response to moderate altitude exposure. Journal of Applied Physiology. 2019;127:1569-1578

Iron sits underneath almost everything that makes endurance training work: oxygen transport, the electron transport chain, the enzymes that let your muscles actually use the oxygen you are hauling around.

A low ferritin doesn’t just leave you tired. You’re training with the engine detuned. So let’s get into what the research actually says about iron status and ferritin levels in endurance athletes.

Why iron is a performance issue, not just a lab value

Iron deficiency is common among endurance athletes, and it’s not a minor footnote.

Estimates range from about 15-60% in female athletes depending on the population and the cutoff used, with male athletes affected considerably less often, typically up to 30%.

Menstrual losses account for much of that gap. Women with normal, healthy menstrual cycles can lose around 10 mg of iron per cycle. This is why female athletes have a higher recommended dietary intake than males (18 mg per day versus 8 mg per day).

A 2024 systematic review from Pengelly and colleagues, pulling together 23 studies and nearly 700 female athletes, found that iron deficiency reduced endurance performance by 3-4% compared to iron-sufficient athletes, and that treating deficient athletes with supplemental iron improved endurance performance by 2-20% and maximal aerobic capacity by 6-15%. Those are not trivial numbers for athletes.

The mechanism is straightforward once you follow it through.

A ferritin test measures the amount of ferritin in your blood. Ferritin is a protein that stores iron inside your cells.

Low iron stores impair the oxidative enzymes and cytochromes in the electron transport chain, which limits how efficiently your muscles convert oxygen into ATP. That happens even before hemoglobin drops, which is exactly why ferritin (a marker of stored iron, not just circulating iron) has become the biomarker everyone leans on.

And exactly why the disagreement over what counts as an “optimal” ferritin level is such a practical problem.

The ferritin nobody agrees on

Here is the tour of disagreement.

The World Health Organization has historically used 15 ng/mL as the threshold to flag iron deficiency in the general population.

A 2022 study of blood donors of reproductive age argued that 25 ng/mL was a more physiologically accurate cutoff, based on the point at which iron absorption begins to ramp up.

In 2025, an expert consensus group published in Lancet Haematology recommended a considerably higher threshold of 50 ng/mL for clinical management of iron deficiency.

A newer study takes a different approach. Published in early 2026 by Kodger, El-Khoury, and Yurtsever in the Journal of Applied Laboratory Medicine, it skipped the debate over which cutoff is correct, and instead they measured ferritin in a group of women confirmed to be genuinely iron sufficient, ages 18 to 40, with normal blood counts and normal iron levels across the board. That group's ferritin had a median of 59.5 ng/mL, with a normal range spanning roughly 20 to 133 ng/mL.

The researchers also tracked the point where hemoglobin stopped climbing as ferritin rose. In other words, the point past which more stored iron stopped producing any additional benefit. That point landed around 25 ng/mL, and it’s the number they ultimately adopted as their own clinical cutoff.

So depending on which paper you grabbed off the shelf, “deficient” could mean anything from <15 to <50 ng/mL. And that is before you even get to sports science.

Researchers routinely debate that athletes need a higher bar because training can increase iron turnover and losses.

Several exercise-specific mechanisms drive iron depletion in athletes:

• Iron is lost through sweat and, in some cases, exercise-induced hematuria (blood in urine).

• Foot strike hemolysis - the repetitive, forceful impact of running can destroy the red blood cells inside the small blood vessels of the feet.

• Gastrointestinal microbleeding - Exercise-related gut ischemia (reduced blood flow) can cause hidden GI blood loss.

• Hepcidin-driven absorption blocks after hard sessions - Prolonged exercise can trigger the release of interleukin-6, a protein that upregulates hepcidin. Hepcidin is the master iron-regulatory hormone, leading to a 36% reduction in dietary iron absorption post-workout.

The sports nutrition literature generally treats anything below 30-35 ng/mL as a red flag in athletes.

However, researchers openly acknowledge there is “little consensus” on exactly where to draw that line for trained populations.

The dietitian team at Alex Larson Nutrition we see best results from our athletes with ferritin levels >50 ng/mL.

Checking ferritin annually is ideal. However, if ferritin levels are sub-optimal, re-checking in 3-6 months is recommended.

Stages of Iron Deficiency

In the Pengelly et al. 2024 systematic review, they staged out the severity scale for iron deficiency:

Stage 1 (non-anemic deficiency): ferritin has dropped <30 ng/mL, but transferrin saturation is still normal. Transferrin saturation measures how much of the iron-carrying protein in your blood is actually loaded with iron.

So at this stage, your stored iron is starting to run low, but there's still enough iron circulating and being delivered around the body that nothing else is affected yet.

Stage 2: ferritin drops further, <20 ng/mL, and transferrin saturation drops, too. So it's not just storage that's low anymore. The iron actually being transported in the blood is restricted. Still no anemia at this point, but it’s a more advanced stage than stage 1.

Stage 3: hemoglobin itself finally drops <12 g/dL. This is anemia, the point at which the shortage is severe enough that the body can't make enough functional red blood cells.

None of this article is meant to be a knock on the research and the scientific community.

Ferritin is a genuinely hard biomarker to pin down, partly because it’s also an acute phase inflammatory protein, so a hard training block or recent illness can nudge it around independent of your actual iron stores.

But in practice, it means the number on your lab report needs context, not just a pass/fail stamp. If you are training seriously and sitting in the 20s or low 30s with symptoms (unexplained fatigue, flatlining paces, restless legs), it is worth addressing even if the lab flags it as “within range.”

Stay tuned for part 2 of this series as we dive more into lab values beyond ferritin.

TL;DR:

“Normal” ferritin levels are not standardized. Published thresholds range from 15 to 50 ng/mL depending on the source. Sports science generally sets the bar even higher (around 30) than general medicine, because athletes lose and turn over iron faster. The ALN team sees best results from athletes with ferritin >50 ng/mL.

I want to hear from you!

What resonated with you? What questions do you still have? Whether you're an athlete, a coach, or a fellow RD, I want to hear your perspective. Leave a comment below and let's keep the conversation going.

Citations:

1. Pengelly M, Pumpa K, Pyne DB, Etxebarria N. Iron deficiency, supplementation, and sports performance in female athletes: A systematic review. Journal of Sport and Health Science. 2025;14:101009.

2. Addo OY, Mei Z, Hod EA, et al. Physiologically based serum ferritin thresholds for iron deficiency in women of reproductive age who are blood donors. Blood Advances. 2022;6:3661-3665.

3. Benson AE, Lo JO, Achebe MO, et al. Management of iron deficiency in children, adults, and pregnant individuals: evidence-based and expert consensus recommendations. Lancet Haematology. 2025;12:e376-e388.

4. Kodger J, El-Khoury J, Yurtsever N. Reevaluating Ferritin Reference Intervals: Defining Limits Based on Iron-Sufficient Population Studies, Clinical Relevance, and Healthcare Efficiency. Journal of Applied Laboratory Medicine. 2026;11:193-196.

5. Clenin G, Cordes M, Huber A, et al. Iron deficiency in sports, definition, influence on performance and therapy. Swiss Medical Weekly. 2015;145:w14196.

6. McKay AKA, Sim M, Moretti D, et al. Methodological considerations for investigating iron status and regulation in exercise and sport science studies. International Journal of Sport Nutrition and Exercise Metabolism. 2022;32:359-370.

So I got curious about the science behind the claims, and down the research rabbit hole I went.

What is actually in the shot?

Broccoli sprout juice, lemon, and sugar. Why broccoli sprout juice?

Broccoli, kale, cabbage, and mustard all contain a group of plant compounds called glucosinolates. When you chew or crush these vegetables, an enzyme in the plant turns those glucosinolates into a different compound called an isothiocyanate, or ITC for short.

The most studied ITC is called sulforaphane. Almost every study I mentioned in this article is measuring sulforaphane, even when the product in question is marketed as an ITC product.

Isothiocyanates work differently than antioxidants. At first, they act like a small irritant inside your cells. They use up a bit of your glutathione, which is one of the body’s own antioxidants, and this creates a small burst of stress. That stress flips on a pathway called Nrf2. Nrf2’s job is to tell your cells to build more of their own antioxidant defenses.

So instead of adding outside antioxidants like vitamin C, isothiocyanates may nudge your body into making more of its own. It is a genuinely interesting idea. It is also, so far, still just an idea. Nobody has shown yet that this actually makes people perform better in real exercise.

The Research Behind the Lactate Claim

The Nomio ads claim that in clinical studies, ITCs showed a 12% reduction in blood lactate during submaximal training tests.

Let’s dive into the claim.

The first human study is from Flockhart and colleagues in 2023, published in the journal Redox Biology. Nine healthy people trained hard for seven days. Half the time they drank a broccoli sprout beverage 2x/day, and half the time they drank a placebo, in random order.

On the broccoli sprout days, their lactate was lower during exercise, they showed less oxidative stress, they could exercise longer before hitting exhaustion, and they had fewer overnight blood sugar crashes. Interestingly, their VO2max and their mitochondria did not change. So whatever caused the lower lactate, it was not simply that people got fitter or grew more mitochondria.

The researchers could not explain why it happened.

Limitations: This was also a very small study, just nine people. And the article was transparent in sharing that two of the authors, Filip Larsen and Michaela Sundqvist, are co-founders and owners of the company that would go on to sell this exact product. They also hold a patent on using ITCs compounds to improve exercise performance.

The 12% reduction in blood lactate claim most likely comes from a 2025 study, published by Vinge and colleagues.

This one is only posted online as a preprint, which means it has not yet been peer reviewed, the process where other scientists check a study before it gets published in a journal.

Fifteen people drank a single dose of kale sprout extract, either a smaller amount or a larger amount, or a placebo, then rode a stationary bike three hours later.

With the smaller dose, their lactate was about 0.4 mmol per liter lower than on placebo, at a work rate close to their lactate threshold. That is a small, but real difference. Their blood sugar was also a bit higher after the sprout drink than after the placebo.

There was no difference in how hard the effort felt, their blood pressure, or their heart rate. And again, nobody knows why the lactate went down.

Limitations: This study was single-blind, meaning only the participants did not know which drink they were getting, not the full double blind gold standard. The two senior researchers here are again Larsen and Sundqvist, the same two who own a stake in the product.

This does not mean the studies are fake, or that the results are wrong. However, a small pile of evidence, entirely from people with a financial stake in the outcome, topped off with a headline number that is still not peer reviewed, is exactly the situation where you want someone else to check the work before you believe it.

What About Muscle Soreness and Recovery?

The other Nomio claim is a recovery benefit. That ITCs protect muscles during intense exercise through activating the Nfr2 system.

There’s not a lot of evidence, but let’s dig into what we have to go off of:

The one human study here with no financial conflict of interest at all comes from Komine and colleagues in 2021. Sixteen young men took a sulforaphane supplement for two weeks around a bout of arm exercise designed to make their muscles sore.

The group taking sulforaphane had less soreness, better range of motion, and lower markers of cell stress than the control group. This is a small study without its own placebo group, but it is genuinely independent, and it points in a positive direction.

The animal research is more consistent than the human research. A 2025 mouse study by Ruhee and colleagues found that a single dose of sulforaphane, given before an exhausting treadmill run, reduced inflammation and protected muscle function.

The Cesanelli and colleagues 2026 study is one that did not support the recovery story at all.

This was a double-blind placebo study. They gave 15 people two weeks of high-dose broccoli powder before a muscle-damaging arm workout.

There was no difference between the groups in strength, muscle damage markers in the blood, range of motion, or muscle appearance on ultrasound.

So they found that broccoli supplementation did not help people recover faster.

Should you spend your money on a broccoli shot?

When it comes to supplements, it’s all about weighing the benefits and the risks.

I don’t see any health risks to taking it, as the ingredients of broccoli sprout juice, lemon, and sugar seem harmless for healthy adults. Assuming you don’t have an allergy to any of these ingredients.

Broccoli sprout extracts, particularly in higher doses, have been known to cause mild GI side effects (bloating and gas). Individual tolerance may vary.

The product does say it’s not suitable for children, pregnant or breastfeeding women, and the recommended maximum intake is 2 shots per day and not to exceed 150 shots per year.

Spending your money on this product, based on where the evidence stands to date, that’s completely up to you. My goal for this article is not to influence you. It’s to help you make a more informed decision.

I’d love to hear your thoughts on this product, especially if you’ve tried it! What does it taste like?

References

Cesanelli, L., Thomas, R., Mickevičius, M., Sniečkus, A., Mickevičienė, D., Venckūnas, T., Stasiulis, A., & Kamandulis, S. (2026). Short-term effects of broccoli-derived glucoraphanin on recovery from eccentric muscle damage: A double blind randomized crossover study. Nutrients, 18(4), 710. https://doi.org/10.3390/nu18040710

Fahey, J. W., Moreno, D. A., Licciardi, P., Grassi, F., Karagiannis, T. C., & Mazarakis, N. (2025). Editorial: Sulforaphane and isothiocyanates in health. Frontiers in Nutrition, 12, 1558025. https://doi.org/10.3389/fnut.2025.1558025

Flockhart, M., Nilsson, L. C., Tillqvist, E. N., Vinge, F., Millbert, F., Lännerström, J., Nilsson, P. H., Samyn, D., Apró, W., Sundqvist, M. L., & Larsen, F. J. (2023). Glucosinolate-rich broccoli sprouts protect against oxidative stress and improve adaptations to intense exercise training. Redox Biology, 67, 102873. https://doi.org/10.1016/j.redox.2023.102873

Gonzalez, D. E., Dickerson, B. L., Roberts, B. M., Kurtz, J. A., Waldman, H. S., Gonzalez, A. M., McAllister, M. J., Heileson, J. L., Bloomer, R. J., Arent, S. M., Candow, D. G., Stout, J. R., Hecht, K. A., Campbell, B., Kerksick, C. M., Kalman, D., Antonio, J., & Kreider, R. B. (2026). International Society of Sports Nutrition position stand: Effects of dietary antioxidants on exercise and sports performance. Journal of the International Society of Sports Nutrition, 23(1), 2629828. https://doi.org/10.1080/15502783.2026.2629828

Komine, S., Miura, I., Miyashita, N., Oh, S., Tokinoya, K., Shoda, J., & Ohmori, H. (2021). Effect of a sulforaphane supplement on muscle soreness and damage induced by eccentric exercise in young adults: A pilot study. Physiological Reports, 9(24), e15130. https://doi.org/10.14814/phy2.15130

Ruhee, R. T., & Suzuki, K. (2024). The immunomodulatory effects of sulforaphane in exercise-induced inflammation and oxidative stress: A prospective nutraceutical. International Journal of Molecular Sciences, 25(3), 1790. https://doi.org/10.3390/ijms25031790

Ruhee, R. T., Ma, S., & Suzuki, K. (2025). Effects of sulforaphane treatment on skeletal muscle from exhaustive exercise-induced inflammation and oxidative stress through the Nrf2/HO-1 signaling pathway. Antioxidants, 14(2), 210. https://doi.org/10.3390/antiox14020210

Vinge, F., Tillqvist, E., Horwath, O., Apró, W., Larsen, F. J., & Sundqvist, M. L. (2025). A glucosinolate-rich beverage lowers blood lactate concentrations during submaximal exercise [Preprint]. bioRxiv. https://doi.org/10.1101/2025.04.15.648889

Welcome to Fueling Field Notes, where I’m documenting my journey to preparing for the CSSD (Certified Specialist in Sports Dietetics) exam. These posts are equal parts study notes, science breakdowns, and practical takeaways from the field.

Similar to my last Fueling Field Note, we are in the weeds of metabolism. It’s complex, but hopefully it helps explain some common misconceptions that athletes have about “fat-burning”.

How Fat Is Used as Fuel

Most fat digestion occurs in the small intestine, where bile salts and digestive enzymes break large fat molecules into smaller components so they can enter the intestinal cells and eventually enter the bloodstream.

Transporting fats into the blood is a slow process. Once digested and absorbed, fats circulate and are stored in the body primarily as triglycerides. The main storage sites are adipose tissue (body fat), the liver, and muscle. A small amount also circulates in the blood at all times.

Before fat can be used as fuel, it has to be removed from storage and transported to where it is needed. This happens through two key processes.

1. Lipolysis is the breakdown of triglycerides into glycerol and three fatty acids. The fatty acids are released from adipose storage into the bloodstream, where they travel to working tissues, like muscle. Once inside the muscle cell, they are taken up into the mitochondria for aerobic metabolism.

2. Before entering the TCA/Kreb’s cycle, fatty acids enter a process called beta-oxidation. Beta-oxidation involves four chemical steps that progressively remove two-carbon segments from the fatty acid chain, converting them into acetyl-CoA. Acetyl-CoA then enters the TCA/Kreb’s cycle to produce ATP. The beta-oxidation process also generates electron carriers (FADH2 and NADH) that feed into the electron transport chain, contributing to additional ATP production.

This process is highly productive, but takes time to get going. During moderate-intensity, steady-state exercise, it may take 10-20 minutes for fat oxidation to reach its maximal rate.

It is also worth noting that fat does not enter the muscle cell by simple diffusion the way many people assume.

Research has shown that fatty acids are actively transported across the muscle membrane and into the mitochondria via specific transport proteins. This transport system ramps up during exercise, but takes longer to activate than carbohydrate metabolism, which is part of why fat oxidation is slower to reach full speed at the start of exercise or with sudden increases in intensity.

Fat Is an Excellent Energy Source, With a Catch

Fat provides a high yield of ATP, making it an incredibly efficient energy source over the long term. The complete metabolism of a single fatty acid, such as palmitate, for example, produces approximately 113 ATP, compared to the 32 ATP produced from one glucose molecule through aerobic metabolism.

However, as I mentioned, fat metabolism is a complex, relatively slow process. It requires more oxygen per unit of energy produced compared to carbohydrate, and it cannot keep up with the energy demands of high-intensity exercise.

This is why carbohydrate remains the dominant and preferred fuel for performance, particularly at moderate-to-high intensities.

Ketones: When Carbohydrate Gets Too Low

When carbohydrate intake is very low, whether from deliberate restriction or prolonged starvation, the body must find alternative sources of acetyl-CoA. It turns increasingly to fatty acids and amino acids (aka: breaking down muscle) to fill the gap.

As more fatty acids are broken down, they accumulate because of a low supply of oxaloacetate, a molecule needed to process acetyl-CoA through the TCA cycle. When acetyl-CoA builds up faster than it can be processed, the liver converts it into ketone bodies.

Ketones become an important alternative fuel for the brain when glucose is scarce, since fatty acids cannot cross the blood-brain barrier directly.

In the first 2-3 days of severe carbohydrate and calorie restriction, the body produces glucose from alternative sources, including lactate and amino acids released from muscle tissue.

As restriction continues, metabolic adaptations shift further. Glucose is made primarily from glycerol released during fat breakdown, and ketones take over as the primary fuel for the brain. After approximately six weeks of starvation, around 70% of the brain’s energy comes from ketones.

A higher protein intake during periods of restriction may help reduce muscle loss, though it does not eliminate it.

Curious about the science behind exogenous ketones and performance? Check out my Endurance Eats podcast episode #23 with Dr. Jonathan Little.

Listen on Apple, Spotify, Amazon, YouTube

Why Does Fat Metabolism Decrease as Exercise Intensity Increases?

If fat produces so much ATP, why does the body rely on it less as exercise gets harder?

There are three key reasons.

1. Higher-intensity exercise recruits more fast-twitch muscle fibers. These fibers are designed for power and speed, and they rely primarily on anaerobic glycolysis. They have a relatively limited capacity to oxidize fat.

2. Anaerobic glycolysis produces lactate, which is known to inhibit the ability of the plasma protein albumin to transport fatty acids through the bloodstream. As a result, fatty acids essentially get held up in fat cells rather than being delivered to working muscle.

3. At higher exercise intensities, blood flow is redirected heavily toward working muscle. Less blood flow through adipose tissue means fewer fatty acids are being picked up and circulated for use as fuel.

The result of all three of these factors is that as intensity increases, the body shifts progressively away from fat and toward carbohydrate as its primary fuel source.

This is not a flaw in your physiology. It is a design feature. Carbohydrate is a more efficient fuel at higher intensities, producing more ATP per liter of oxygen consumed, which is exactly what the body needs when demands are high.

What About During Long, Steady-State Exercise?

Duration changes the equation.

Even at moderate intensities where carbohydrate starts as the dominant fuel, fat oxidation increases over time as glycogen stores are gradually depleted.

Research tracking fuel use during four hours of cycling at moderate intensity found that carbohydrate dominated in the first two hours, accounting for roughly 63% of energy production, with fat making up the remaining 37%. By hours two to four, fat oxidation had increased, contributing a larger share of energy, with circulating free fatty acids becoming the primary fat source as intramuscular fat stores were depleted.

Here is where it gets critical for endurance athletes: this shift toward fat doesn’t mean you no longer need carbohydrates in the later hours of a long effort. It means your body is being forced to rely more heavily on fat because carbohydrate availability is declining. That is a very different thing.

Fat oxidation can keep you moving at lower intensities, but it cannot sustain the moderate-to-higher intensity efforts that performance requires. As glycogen drops and blood glucose falls, pace slows, perceived effort rises, and the ability to respond to surges, climbs, or race demands diminishes. This is what bonking actually is at a physiological level.

The practical takeaway is the opposite of what the fat burning narrative often suggests.

The fact that fat oxidation increases during prolonged exercise is not a reason to skip carbohydrate intake. It’s exactly the reason to keep fueling with carbohydrate throughout a long effort, to maintain blood glucose, protect glycogen stores for as long as possible, and preserve your ability to work at intensities that fat alone cannot support.

Even at zone 2 efforts, athletes who underfuel their “easy-effort, long-duration workouts” end up bonking and feeling depleted the rest of the day. Even the easy efforts require fuel.

Do You Have to Burn Fat to Lose Fat?

Read more

A simple Google search revealed all sorts of media coverage of the Tour de France and talks about lactate gels. Is Tadej using these new gels? There’s a lot of speculation.

A research group called From Lab to Field (FLF, led by sports scientist Aitor Viribay), created a product called ExoLactate. A gel that supplies 40 grams of carbohydrates and 5 grams of lactate. They claim a 3% increase in power output for highly trained athletes.

So let’s talk about what lactate actually does in the body, what the research says about eating it for performance, and whether you should be dropping big $$$ on this new trend.

Wait, isn’t lactate bad?

For a long time, lactate got blamed for muscle burn, fatigue, and the reason you couldn’t hold pace on that last climb.

If you read my last Fueling Field Notes post on how bodies power our muscles, or listened to episode #43 of my Endurance Eats podcast. You know that it’s the buildup of hydrogen ions, which are acidic and produced alongside lactate, that causes that muscle burn.

UC Berkley exercise physiologist George Brooks spent decades building the case for the “lactate shuttle”, the idea that lactate isn’t metabolic trash. It’s fuel.

During exercise, trained athletes derive approximately one-third of their carbohydrate energy from blood lactate. An exogenous lactate infusion will increase lactate oxidation while producing a glycogen-sparing effect in exercising muscle.12

This provides the theoretical basis for supplementing lactate as a fuel source during endurance events.

What the Research Shows

The current evidence for lactate gels as an ergogenic supplement is weak and inconsistent, despite a compelling physiological rationale.

There are two proposed reasons lactate supplementation could help performance:

• As a direct fuel source. It’s absorbed in the gut and either oxidized directly by muscle or converted to glucose in the liver.3

• As a buffer. Lactate metabolism consumes hydrogen ions, which could theoretically blunt the acidosis that contributes to fatigue.4

Neither mechanism has translated cleanly into a performance benefit in controlled trials. Here’s a summary:

• A meta-analysis of 189 studies on buffering supplements found sodium bicarbonate produced a clear, positive effect on performance. But only 7 of those studies involved lactate, and bicarbonate significantly outperformed it.5

• A randomized, placebo-controlled trial of lactate before a 40-km cycling time trial found no improvement in performance and no change in acid-base measures, although riders did report feeling like they were working less hard.6

• Trials of magnesium lactate and calcium lactate found no improvement in 20-km time trial performance.7

• One small study did find a benefit: acute calcium lactate raised blood bicarbonate and improved time-to-exhaustion by 17%. But that was in a short, supramaximal (aka: very hard) effort, nothing like an endurance event.8

What Does The Lactate Gel Do?

According to FLF’s launch webinar, the right dose of lactate is 10-25 grams per hour.

By fueling with different types of carbohydrates (aka: glucose and fructose) that use completely different transport pathways, athlete can increase their absorption to 90+ grams of carbs per hour.

Lactate has a similar effect, serving as a fuel source that takes a separate transport pathway. The result is that, with two types of carbohydrates and lactate, athletes can have the benefits of three different fuel sources for performance.

The other potential advantage is that lactate is absorbed directly from the intestines into the bloodstream, so the energy can be used much faster (potentially within 5 minutes) compared to glucose and fructose (15-30 minutes).

According to Viribay, during low-to-moderate intense workouts, the exogenous lactate will reduce reliance on carbohydrates and promote fat burning. For higher-intensity exercise, when there is limited oxygen available, lactate will promote carb burning and inhibit fat burning.

Can Viribay prove this in data? We shall see. Rumor has it that they have a scientific paper under review.

This whole situation feels similar to the ketone craze, where one study said they were the next best thing in performance and ketone companies exploded with wild marketing claims. Then all follow-up studies said there was no performance benefit. But we shall see!

Practical Concerns

Reports are saying that Tour riders using these lactate gels, they are consuming 4 gels per hour. This is 160 g carbs and 20 g of lactate. This volume of fuel requires epic gut training to tolerate this.

The ExoLactate gels are expected to retail at €5. The Santa Madre lactate gels are currently listed at €9 each (~$10 USD).

Why haven’t we used lactate as a fuel source sooner? It has been highly unpalatable and difficult for the gut to tolerate. However, Viribay and the FTF team have reportedly solved this to make it digestible and palatable.

Should you buy them?

For now, save your money. Let’s keep an eye on this one. It’s genuinely interesting science, but I think we’re majoring in the minors here.

I’m waiting for the FLF data to be published and follow-up research studies to prove results can be replicated. Based on what they’ve shared so far, the gains are marginal.

Let’s keep a healthy skepticism with buzzy new trends and just continue to enjoy watching the Tour de France and Tour de France Femmes.

I’d love to hear from you.

Do the fueling strategies of elite athletes influence you and your fueling/nutrition decisions?

TL;DR

Lactate is a legitimate fuel source, and the physiology behind it is sound in theory. But the actual performance evidence so far for supplemental lactate is weak, mixed, and mostly negative across the trials that exist. Any real benefit is likely marginal at best; the gels are pricey. For now, let’s watch the space, but don’t spend your fueling budget here yet.

Welcome to Fueling Field Notes, where I’m documenting my journey to preparing for the CSSD (Certified Specialist in Sports Dietetics) exam. These posts are equal parts study notes, science breakdowns, and practical takeaways from the field.

This Field Note is a big one. It’s long, and we’re in the weeds. But it also provides fascinating context for how our bodies fuel performance. I actually really enjoyed writing this so much more than I did in my 2007 biochemistry class.

The body needs a continuous supply of energy to function, move, and perform. But it doesn’t run directly on the food you eat. It runs on a molecule called adenosine triphosphate, or ATP.

Think of ATP as the body’s universal energy currency.

Every cell in your body uses it, from your brain to your heart to your skeletal muscle.

For today’s study notes, we’re going to focus on how skeletal muscle uses ATP to produce force and power during exercise.

How ATP Works

ATP releases energy through a rapid chemical reaction. When the body needs energy, ATP is broken down into adenosine diphosphate (ADP) and an inorganic phosphate (Pi), releasing energy in the process.

ATP → ADP + Pi + energy

That chemical reaction produces about 7 calories of free energy, and it happens fast. During exercise, especially high-intensity exercise, ATP breaks down at a very rapid rate.

Here’s the catch: your muscles can only store a small amount of ATP at any given time. Enough for roughly 1-2 seconds of maximal effort. So the body must continuously rebuild ATP from ADP at essentially the same rate it’s being used.

ADP + Pi + energy → ATP

If ATP cannot be replenished fast enough, muscle function deteriorates. This is one of the underlying mechanisms behind fatigue.

Three Ways the Body Rebuilds ATP

The body has three mechanisms for resynthesizing ATP. Each has its own advantages depending on the intensity and duration of the activity.

All 3 energy mechanisms are “on” all the time. They work in parallel with each other. But, in certain situations, one of the mechanisms may be “turned up” more than the other two because each has its own advantages.

We will cover each in detail, but here is a quick overview:

Creatine phosphate hydrolysis is ideal for very short, very intense, anaerobic efforts lasting roughly 5-10 seconds.

Anaerobic glycolysis uses carbohydrate stored in the muscle or circulating in the bloodstream to produce ATP without oxygen. Also used in more intense, higher-effort efforts.

Oxidative phosphorylation is the aerobic system, using carbohydrates, fat, and protein to produce large amounts of ATP over longer durations.

The Creatine Phosphate Energy System

ATP is not the only high-energy phosphate stored in muscle.

Creatine phosphate (CrP), also called phosphocreatine (PCr), is stored in muscle fibers at concentrations 3-4x greater than ATP. Like ATP, it does not require oxygen to produce energy.

When the body needs to rapidly rebuild ATP, CrP donates its phosphate group to ADP, instantly regenerating ATP. The enzyme creatine kinase facilitates this reaction.

ADP + CrP → ATP + creatine

This system can produce ATP faster than any other mechanism, which is why it powers the most explosive, high-intensity efforts.

The tradeoff is that it is very short-lived. CrP stores are depleted within approximately 5 to 10 seconds of maximal effort and require several minutes of recovery to be fully restored.

How do our creatine phosphate stores recover?

CrP recovery depends on aerobic metabolism. Creatine molecules use energy from ATP produced aerobically in the mitochondria to convert back to creatine phosphate.

This is why after a short-duration, high-intensity effort, athletes are out of breath. The body must temporarily increase oxygen intake and aerobic metabolism to meet the high need to restore creatine phosphate.

(*Geeking out over here with how cool the body is).

Dietitian note: This is exactly why creatine supplementation is relevant for endurance athletes, not just strength athletes. Topping off muscle creatine stores supports those explosive high-intensity moments that show up in endurance racing and training, like sprinting to the finish line, powering over a steep climb, or surging away from the pack.

The major food sources of creatine are beef and fish.

The body can also synthesize some creatine on its own when adequate amounts of the amino acids arginine, glycine, and methionine are available, which is one more reason solid overall protein intake matters.

I have numerous creatine articles written here on Substack. Make sure to check them out!

Anaerobic Glycolysis Energy System

Glycolysis is the breakdown of carbohydrates for energy. The “anaerobic” part means it happens without oxygen.

All forms of carbohydrates consumed are converted to and used as glucose or stored as glycogen for future use. (For an overview on carb basics, read here)

For clarification:

Glycolysis involves the breakdown of glucose through a series of chemical steps to reform ADP into ATP.

Glycogenolysis involves the breakdown of glycogen.

Here is what happens in simple terms:

Glucose is broken down through a series of many chemical reactions in the sarcoplasm, producing a small but rapid yield of ATP.

The end product of this process is pyruvate.

What happens to pyruvate depends on how hard you are working.

At lower intensities, pyruvate moves into the mitochondria and enters the aerobic energy system, where it can be used to produce much larger amounts of ATP.

At higher intensities, when the aerobic system cannot keep up with the energy demand, pyruvate is converted into lactate. Lactate often gets a bad reputation, but it is not the villain it has been made out to be.

Lactate is actually a useful fuel that can be shuttled to other tissues and used for energy.

The problem is not lactate itself but the accumulation of hydrogen ions that occurs alongside it, which contributes to the burning sensation and fatigue associated with high-intensity efforts.

Anaerobic glycolysis is the next fastest option for energy behind the creatine phosphate system. It can usually sustain high-intensity efforts for about 30 seconds to 2 minutes.

This is why carbohydrate availability matters so much for high-intensity endurance efforts. When muscle glycogen stores are low, the anaerobic glycolysis system loses its primary fuel source, and performance at higher intensities suffers quickly.

This is one of the foundational reasons why carbohydrate intake before, during, and after hard training sessions is not optional for endurance athletes pushing intensity.

Check out my podcast, Endurance Eats episode #43 with Dr. Jeff Stout, where we talk about how supplements like beta-alanine and sodium bicarb can help buffer those hydrogen ions.

Listen on Apple, Spotify, Amazon, YouTube

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Welcome to Fueling Field Notes, where I’m documenting my journey to preparing for the CSSD (Certified Specialist in Sports Dietetics) exam. These posts are equal parts study notes, science breakdowns, and practical takeaways from the field.

Before we get into how muscles use fuel, let’s take a quick look at the structure of the muscle itself. This context will make reviewing energy systems much easier to understand when we get there.

Muscle Fibers

Muscles are made up of long, cylindrical cells called muscle fibers. Each fiber is essentially one very long muscle cell, and a single muscle contains thousands of them bundled together.

Surrounding each muscle fiber is the sarcolemma, which acts as the outer boundary of the muscle cell. It controls what enters and exits, and plays a key role in conducting the electrical signals that trigger contraction.

Sarcoplasm

Inside each muscle fiber is a thick, gel-like fluid called sarcoplasm. Think of it as the working environment inside the cell. It contains everything the muscle needs to function, including:

• Nuclei, which control cell activity and protein synthesis.

• Mitochondria, the energy-producing organelles responsible for generating ATP. You may have heard them called the powerhouse of the cell, and in muscle tissue, that description is especially fitting given how much energy muscles demand during exercise.

• Myoglobin, a protein that stores oxygen inside the muscle cell and gives the muscle its characteristic red color. It works similarly to hemoglobin in the blood, but its job is to hold oxygen in reserve within the muscle itself.

• Myofibrils, the contractile units of the muscle fiber. Each fiber contains approximately 500 myofibrils, and these are what actually move when a muscle contracts.

Dietitian note: The mitochondria are exactly why aerobic capacity matters so much for endurance athletes. More mitochondria and better functioning mitochondria mean a greater ability to produce ATP efficiently using oxygen. One of the key adaptations we want from endurance training is an increase in mitochondrial density within muscle fibers.

Energy Stored in the Sarcoplasm

The sarcoplasm also serves as a storage site for the muscle’s fuel supply:

• Glycogen is the stored form of carbohydrate and a primary fuel source during exercise.

• Triglycerides, the stored form of fat, serve as a fuel source, particularly during lower-intensity and longer-duration activity.

• Phosphocreatine (PCr), a rapidly available energy source used to regenerate ATP during short, high-intensity efforts.

• ATP (adenosine triphosphate) is the body’s direct energy currency. Every energy-requiring process in the cell runs on ATP.

• Free amino acids. The sarcoplasm also contains a small pool of free amino acids. While amino acids are not a primary fuel source, they can contribute to energy production during prolonged exercise when carbohydrate stores are running low.

Next week’s article is going to walk through how these fuel sources power muscle for performance.

Myofibrils and the Contractile Proteins

Each myofibril is made up of overlapping thin protein filaments (called actin) and thick protein filaments (called myosin) arranged in a repeating pattern. These filaments interacting is what allows muscles to contract and generate force.

The sarcomere is the basic functional unit of the myofibril and the actual site where muscle contraction happens.

Within each sarcomere, myosin binds to actin and pulls, shortening the sarcomere and producing force.

When thousands of sarcomeres fire simultaneously, you get visible muscle movement. Every contraction requires ATP (aka: energy), which is why energy availability is so directly tied to how well your muscles perform.

Wrapped around the myofibrils is a network of connecting, bag-like, membranous tubules called sarcoplasmic reticulum. They store calcium and release it when the muscle needs to contract. When the contraction signal stops, the calcium gets pumped back in, and the muscle relaxes.

T-tubules are narrow channels that carry the contraction signal from the surface of the muscle fiber deep into its interior, making sure the entire fiber contracts at once rather than just the outer edges.

Fiber Types

There are different types of muscle fibers based on their contraction speed and metabolic characteristics.

Muscle fibers are extremely adaptable. However, the distribution of muscle fiber types is genetically determined and not easily altered. The training program will impact the metabolic potential of the muscle, regardless of the proportion of fiber types.

Read more

Defining a Calorie

Let’s start with the basics, because even the word “calorie” is more complicated than it looks.

Scientists measure energy using a unit called the joule. But a joule is tiny, so in practice we use kilojoules (kJ), which are 1,000 joules grouped together.

In nutrition, we use calories instead. A calorie (lowercase c) measures the heat required to raise the temperature of 1 gram of water by 1 degree Celsius. Like the joule, it’s also a very small unit, which is why you’ll never see it on a food label.

What you do see on a food label is the kilocalorie (kcal), sometimes written as Calorie with an uppercase C. One kilocalorie equals 1,000 calories, and it represents the heat required to raise 1 kilogram of water by 1 degree Celsius. This is the unit the nutrition world actually runs on.

For the sake of conversion: 1 kcal equals 4.184 kJ.

For the rest of Fueling Field Notes, when I say calorie, I mean kilocalorie. That’s the standard in sports nutrition, and it’s what’s on your food label.

How do we measure the energy content of food?

The thermal energy of the food is directly measured by a process called direct calorimetry. This analysis of food involves a device called a bomb calorimeter. The “bomb” is a metal container in which the food sample is burned in a pressurized, pure oxygen atmosphere. It’s surrounded by an insulated water bath. As the food sample burns, temperature changes in the surrounding water bath are recorded to determine the thermal energy of the food.

The Atwater Factors

The calorie values you see assigned to macronutrients:

Carbohydrates: 4 calories/gram

Protein: 4 calories/gram

Fats: 9 calories/gram

Alcohol: 7 calories/gram

These are known as the Atwater general factors, named after an American chemist who developed them over 100 years ago.

Atwater measured how much energy food releases when burned in a bomb calorimeter, and recognized that the human body doesn’t absorb everything it consumes. So he adjusted the raw combustion values to account for digestive losses. The result was a practical set of values that could be applied to any food to estimate its available energy.

Here’s how he arrived at the final numbers:

Raw combustion values from the bomb calorimeter:

Carbohydrates: 4.1 calories/gram, protein: 5.6 calories/gram, fat: 9.4 calories/gram.

After adjusting for digestive losses, the values were rounded to the familiar numbers we use today.

Carbohydrates: 4 calories/gram

Protein: 4 calories/gram

Fat: 9 calories/gram

Note: The reason protein drops from 5.6 to 4 calories per gram is that protein contains nitrogen, and the body cannot fully burn nitrogen for energy the way it does carbon and hydrogen. Instead, nitrogen is excreted as urea in the urine, which represents energy that leaves the body unused.

The Coefficient of Digestibility

The coefficient of digestibility is the percentage of a food that is actually absorbed and used by the body after digestion.

Individual foods can vary.

Highly processed and refined foods tend to have higher digestibility, meaning more of their energy is absorbed. Whole foods with more fiber and complex food matrices tend to have lower digestibility, meaning some energy passes through without being absorbed.

This is also why, mid-exercise, it’s ideal to select foods/fuel sources with higher digestibility so we can access all the energy it has to offer to support performance. To the processed-food police on the internet, it’s not broccoli that’s getting athletes across the finish line.

Measuring Energy Out

There are a variety of ways we can measure the amount of energy we expend. But it’s difficult. Even the most accurate measurement techniques have limited use with athletes because of their impracticality.

Here are just a couple of methods used in research:

Direct calorimetry measures the heat the body produces directly.

Remember the bomb calorimeter? The same principle applies here, except instead of burning food, a person sits inside a thermally insulated chamber, and the heat they release is measured. It’s the most accurate method we have, but also the most impractical. You’re essentially asking someone to sit in a very sophisticated box. Useful for research, not useful in the field.

Indirect calorimetry is the more practical option and the gold standard for measuring energy expenditure. Instead of measuring heat directly, it measures oxygen consumption and carbon dioxide production.

The logic behind it: The body burns fuel to produce energy, and that process requires oxygen and produces carbon dioxide. By measuring how much oxygen you consume and how much carbon dioxide you exhale, we can calculate how much energy your body is using.

Components of Energy Expenditure:

Energy is needed for various bodily processes, such as basal functions (proprioceptive and conscious movements), digestion, absorption, metabolism, food storage, and expended energy during exercise.

Resting Metabolic Rate (RMR)

Refers to the energy needed to perform normal daily body functions, aka: the energy needed to keep our body functioning even if you rested all day long.

RMR has become a more popular measurement, and it’s influenced by age, sex, body composition (height, weight, muscle mass), thyroid hormones, and genetic factors.

RMR seems to decrease with age (2-3% every decade). Men generally have a higher RMR than women because of their larger body size and greater muscle mass.

Estimating RMR

RMR is often calculated using a formula/prediction calculator to provide estimates.

Read more

Protein Basics

All proteins are made up of amino acids and are bound by peptide bonds. Once connected, they are called peptides.

Dipeptide refers to two amino acids

Tripeptide is three amino acids

And polypeptides are four or more. Most proteins are polypeptides that combine up to 300 amino acids.

Amino acids contain carbon, hydrogen, oxygen, and nitrogen. The nitrogen is what distinguishes protein from other nutrients. The basic chemical structure will contain an NH2 (amino) group and a COOH (carboxyl) group.

Differences in chemical structure will play a critical role in the functions of the proteins created.

20 different amino acids are commonly found in proteins.

Humans can synthesize 11 types of amino acids, making them dispensable (non-essential).

Dispensable (non-essential) amino acids:

• Alanine

• Arginine*

• Asparagine

• Aspartate

• Cysteine*

• Glutamate

• Glutamine*

• Glycine*

• Proline*

• Serine*

• Tyrosine*

The other 9 are indispensable (essential) amino acids, meaning the body can’t manufacture them and must get them through the diet.

Indispensable (essential) amino acids:

• Histidine

• Isoleucine (BCAA)

• Leucine (BCAA)

• Valine (BCAA)

• Lysine

• Methionine

• Phenylalanine

• Threonine

• Tryptophan

*Conditionally Essential Amino Acids

This 3rd category of amino acids is interesting. In abnormal circumstances, such as when the body is under physiological stress. The demand for these amino acids is higher than what the body can produce on its own. Think: intense exercise, injuries, illness, surgery.

Glutamine and arginine are two conditionally essential amino acids. They get a lot of attention in the supplement world, often marketed to athletes, particularly around recovery and performance.

For glutamine, studies in healthy adults that combine supplementation with resistance training showed no added benefit for muscle strength or fat-free mass compared to placebo.

For arginine, despite its role in nitric oxide production and theoretical blood flow benefits, research has not shown a meaningful impact on muscle protein synthesis or anabolic response after exercise when sufficient essential amino acids are already being consumed.

Consensus: The science doesn’t support the hype, especially for healthy athletes eating adequate protein.

Protein Roles

Let’s walk through the list:

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The good news is that the data on creatine safety exists, and it is now massive.

A 2026 analysis reviewed 684 randomized controlled trials on creatine, covering more than 12,800 participants. The researchers specifically looked at whet…

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Here is my best attempt to explain lipids vs fats in an easy-to-understand way. Happy to answer any questions to clarify!

Lipids are a broader group of biomolecules. They’re insoluble in water and include a variety of substances such as fats, oils, waxes, phospholipids, lipoproteins, and sterols. In medicine, lipids are known as the large fat-containing components in the blood.

Fat refers to a type of lipid. In nutrition, fat is often referred to as the energy-containing nutrient found in food. Fat is also used to describe a storage site for fats (adipose tissue).

Different Types of Lipids:

Triacylglycerols (or triglycerides)

These are the most abundant dietary lipids consumed.

They are composed of a 3-carbon glycerol backbone esterified with three fatty acids. Triglycerides vary in their fatty acid composition.

Fatty acids are the fundamental building blocks of fat.

Triglycerides found in food contain a combination of saturated, monounsaturated, and polyunsaturated fatty acids. When carbohydrates are consumed in excess, they are stored mostly as triglycerides in adipose tissue.

The nature of the fatty acids in a triglyceride will influence the temperature at which the fat will melt.

For example, coconut oil contains 92% saturated fat, 6% monounsaturated fat, and 2% polyunsaturated fat. This explains why it stays solid at room temperature.

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A 2025 review in the Journal of the International Society of Sports Nutrition collected what we now know a…

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Nutrient Breakdown

Sports nutrition recommendations are built upon basic nutrition guidelines. Let’s star…

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A little context about this exam:

Is the CSSD credential required for me as a dietitian?

No. It’s a bonus credential. Many professional and collegiate sports teams prefer a dietitian with CSSD on their staff.

ALN’s dietitian Mary has had her CSSD cre…

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That is starting to change.

A 2026 narrative review in the Journal of the International Society of Sports Nutrition pulled together th…

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Race day is done.

But here’s what the research makes very clear: your body still has a lot of work to do.

What the Research Looked At

A 2021 study published in the Journal of Strength and Conditioning Research (Bernat-Adell et al.) followed 86 recreational marathon runners to track exactly what happens inside the body in the days after a race.

Researchers drew blood at six time points: 24 hours before the race (baseline), immediately after finishing, and then at 24, 48, 96, and 144 hours post-race. That’s up to 6 days of follow-up.

They tracked four biomarkers:

• Creatine kinase (CK) — a marker of acute muscle damage

• Lactate dehydrogenase (LDH) — a broader marker of tissue damage

• High-sensitivity troponin T (hs-TnT) — a marker of cardiac stress

• C-reactive protein (CRP) — a marker of systemic inflammation

Think of these four markers as your body's damage report. Under normal circumstances, they sit quietly within a healthy baseline range.

After a marathon? They tell a very different story.

The Data: What Actually Happens

Muscle Damage Peaks and Stays Elevated for Days

CK, the primary marker of muscle damage, didn’t peak immediately after the race. It peaked at 24 hours post-finish and remained significantly elevated through 96 hours (4 days). It didn’t normalize until 144 hours, or 6 full days after the race.

LDH followed a similar pattern, staying significantly elevated across all measured time points and not returning to baseline until 192 hours (8 days post-race).

To put that in plain terms: your muscles are still in an active state of damage and repair for nearly a week after you finish. Not recovering from damage. Still in it.

Inflammation Hangs Around Longer Than You’d Expect

CRP, the inflammation marker, told perhaps the most striking story. It peaked at 24 hours post-race and began to decline, but remained significantly elevated at every single time point measured, including 192 hours post-race.

Eight days later. Still inflamed.

This isn’t a sign that something went wrong. It’s a sign of how significant the physiological demand of endurance racing actually is. Your immune system is actively managing the aftermath of what you asked your body to do.

Your Heart Is Under Stress Too

Troponin T, a marker typically associated with cardiac stress, spiked dramatically immediately after the race. In this study, it averaged nearly 9x the pre-race baseline value. It normalized within 96 hours, but the spike itself is a meaningful signal.

To be clear: this doesn’t mean athletes are having heart attacks.

Research suggests that this rise of troponin is a physiological response to endurance exercise, not a sign of permanent cardiac damage in healthy athletes. But it does underscore that the cardiovascular system takes a real hit on race day, and deserves the same recovery respect as your legs.

What This Means for Endurance Athletes

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A 2023 study published in the International Journal of Sport Nutrition and Exercise Metabolism looked at exactly that.

And the findings are interesting, especially if an athlete has ever experimented with reducing carbohydrates during a training blo…

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