Iron deficiency affects as many as one in three female runners and one in ten male runners. That's not just about diet — running itself sets off at least three independent mechanisms that draw down iron stores.
Yes, through at least three independent mechanisms
Regular running, especially endurance running, can genuinely lower ferritin — independent of diet. This happens not through one, but through at least three overlapping mechanisms: foot-strike hemolysis (red blood cells destroyed by the impact of the foot hitting the ground), minor gastrointestinal microbleeding linked to exertion, and a rise in hepcidin — a hormone that temporarily blocks iron absorption from the gut after intense training.
Foot-strike hemolysis is a phenomenon in which the repeated, forceful impact of the foot on the ground during running mechanically damages red blood cells passing through blood vessels in the foot. Iron released from the breaking-down erythrocytes is largely recovered by the body, but the recovery process isn't fully efficient — with daily or near-daily training, the cumulative iron loss over time becomes real, even though any single episode has little significance on its own.
In parallel, prolonged, intense physical exertion increases intestinal permeability and can lead to small, subclinical gastrointestinal microbleeds — a side effect of reduced splanchnic blood flow during running, as blood is redirected to working muscles. Individually, these episodes are usually undetectable without specialized testing, but in runners training regularly over months and years, they can add up to a meaningful, chronic iron loss.
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The third mechanism, now considered the most important, involves hepcidin — a peptide hormone produced by the liver that regulates iron absorption from the gut and its release from stores. Intense, prolonged physical exertion triggers an inflammatory response in which interleukin-6 (IL-6) — a pro-inflammatory cytokine released in large amounts by working muscles — plays a key role. IL-6 directly stimulates the liver to increase hepcidin production within a few hours of training.
Elevated hepcidin blocks ferroportin — the protein that transports iron from intestinal cells into the blood — which temporarily limits absorption of dietary iron consumed in the hours following intense training, regardless of how much iron the diet provides. In athletes training almost daily, these windows of reduced absorption can recur often enough to genuinely make it harder to maintain adequate iron stores.
A Prolonged Bout of Running Increases Hepcidin and Decreases Dietary Iron Absorption in Trained Female and Male Runners
Moderate evidenceBarney DE Jr, Ippolito JR, Berryman CE, et al. · The Journal of Nutrition · 2022
In a study of trained male and female distance runners, hepcidin concentration rose by about 51% after a prolonged run compared with resting conditions, accompanied by a roughly 36% drop in fractional dietary iron absorption. The authors point to an IL-6-driven inflammatory response as the main mechanism linking a single training session to temporarily impaired iron absorption in the following hours.
View studyThe cumulative effect of these three mechanisms means iron deficiency is noticeably more common in runners than in the general population — estimates suggest 15–35% of female runners and 5–11% of male runners are affected, often without obvious symptoms beyond reduced performance and faster fatigue in training. It's worth stressing that this concerns real iron stores, not just a one-off fluctuation in a blood test result.
Practical takeaways for runners
No. Risk rises with training volume and intensity — endurance runners training nearly every day are far more exposed than people running recreationally a few times a week at moderate distances.
Current research points to the hepcidin response as having the largest, most measurable impact on iron absorption after a single training session, though foot-strike hemolysis and gut microbleeding act in parallel and accumulate over the longer term.
Not automatically — the decision to supplement should be made by a doctor based on the full picture (ferritin, complete blood count, symptoms, training load), since unnecessary iron supplementation in people without a genuine deficiency carries its own health risks.
For some people, yes — especially with moderate training load and a diet rich in well-absorbed iron sources. In runners with very high training volume, diet alone sometimes isn't enough, because of hepcidin's temporary block on absorption — in those cases, it's worth discussing with a doctor or a sports dietitian.
dr Anna Kowalczyk
PhD in Molecular Biology (University of Warsaw), 8 years researching cellular aging
Anna studied molecular biology at the University of Warsaw, then spent eight years after her PhD in a lab researching the mechanisms of cellular aging and autophagy. She stumbled into science journalism almost by accident — frustrated by how easily her field's findings get oversimplified in the media, she started a blog explaining the biology of aging in plain language. That blog became the seed of VitMode. Today Anna oversees the entire editorial process, holding every piece to the same rigor her old lab demanded: primary sources, methodology checks, and honesty about the limits of the evidence. Outside work, she's a dedicated boulderer.
If you drink coffee or tea alongside a meal, you're probably losing more iron from your food than you think — and this isn't an approximation from a pop-science article, it's a concrete figure from classic controlled human studies using radiolabeled iron. Coffee served with a standard meal reduced non-heme iron absorption by 35%, and tea by as much as 62% — nearly two-thirds of the iron the body could have absorbed simply passed through unused. Newer research adds a second dimension: this is a dose-dependent polyphenol effect, so strong black tea blocks far more than herbal tea, and adding milk doesn't actually rescue the situation, contrary to popular belief. For people with low ferritin levels or in a risk group for iron deficiency, this is a detail that can genuinely carry clinical weight.
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Iron-deficiency anemia is the most common cause of anemia worldwide, affecting, according to the latest global burden of disease estimates, hundreds of millions of women. The problem is that the symptoms — fatigue, breathlessness, poor concentration — are vague enough to easily blame on stress, lack of sleep, or "just the season." We explain how iron deficiency is actually diagnosed, why a blood count alone may not be enough, and what research shows about the reversibility of symptoms.
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A classic 1980 study found something counterintuitive: on a standard dose, ferritin doesn't rise at all until hemoglobin is already back to normal. If yours is doing the opposite, it's worth understanding what that might mean.
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Ferritin isn't just an iron-storage marker — it's also an acute-phase protein that rises in response to the inflammation triggered by intense exercise. We explain why a test done right after a hard workout or a long-distance race can be misleading.
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4.6Because ferritin reflects iron stores, which are depleted first — changes in the blood count show up later, only once the bone marrow can no longer compensate for the shortage of raw material for red-cell production.
4.5An iron-storage protein whose blood level is the best available indicator of the body's iron stores — though it can be falsely elevated by inflammation, which complicates straightforward interpretation.
4.6Yes — iron deficiency develops in stages, and depleted stores (low ferritin) can precede a drop in hemoglobin by months, which is why fatigue and hair loss can appear with a completely normal blood count.
4.6Not always — ferritin is also an acute-phase protein, so inflammation, infection, liver disease, or obesity can artificially raise its result and mask a genuine iron deficiency.
4.6Low transferrin saturation means the protein that transports iron in the blood is mostly 'empty' — too little iron is circulating in a usable form, making it one of the earliest signals of functional iron deficiency.
Kasia W. 2 weeks ago
Very clearly explained, especially the interactions section — I hadn't seen it laid out this well anywhere else.
Marek T. a month ago
Are you planning to update this with the newest study from this year? I saw an interesting meta-analysis.
