What Is Ferritin? What It Measures and What It Means for Athletes
Table of Contents
Key Takeaways: What Is Ferritin
- Ferritin is the body’s primary iron storage mechanism. It makes iron available for critical cellular processes while protecting lipids, DNA and proteins from the potentially toxic effects of iron.[1] A single ferritin molecule can sequester up to 4,500 iron atoms.[2]
- A ferritin blood test is an indirect marker of total body iron stores. Low serum ferritin is highly specific for iron deficiency, and without concurrent inflammation it is both highly specific and sensitive.[2]
- “Normal” lab limits are often set too low. A serum ferritin below 30 µg/L has high specificity and sensitivity for diagnosing iron deficiency in adults, yet reference interval studies report a median lower limit of normal of only 8 µg/L in females and 25 µg/L in males.[3]
- Ferritin rises with inflammation and hard training. It is an acute phase protein, increased during periods of inflammation and after intensive exercise, so it should be read alongside hemoglobin and transferrin saturation.[2][4]
- Iron deficiency is common in athletes. It is found in ~15–35% of female and ~5–11% of male athlete cohorts, and a recent review cites estimates of up to 60% in female athletes.[4][5]
- Athletes need sport-relevant thresholds. Swiss sports medicine recommendations use a cut-off of 30 µg/L for athletes over 15 years, while a 2024 review classes ferritin above 50 µg/L (with adequate hemoglobin and transferrin saturation) as healthy and 35–50 µg/L as sub-optimal.[6][7]
- More iron is not automatically better. Iron supplementation in non-iron-deficient athletes does not improve performance, and in one marathon study 15.0% of male recreational runners had ferritin above 200 µg/L.[7][8]
- In my clinical experience, the athlete target sits above the laboratory’s lower limit. I aim for a ferritin above 30 µg/L in athletes, while the lower reference limit for women in our laboratory is 15 µg/L; the athlete recommendation is a consensus among sports physicians rather than a national treatment guideline.
- Ferritin is rarely read on its own. I usually check hemoglobin or a full blood count and MCV with it, and when ferritin is high, CRP and a broader iron panel.
- IV iron needs a clear indication. In Finland, at least in public health care, the criteria are strict, and in my understanding the indications for athletes are the same as for the sedentary population.
Introduction: What Is Ferritin and Why Should Athletes Care?
Estimates of iron deficiency in female athletes reach up to 60%, and in high-level iron-deficient female athletes endurance performance was negatively affected by 3%–4%.[5] A result marked “normal” says little about what the number means for training, recovery or racing.
So, what is ferritin? In short, it is the protein your cells use to store iron safely. In clinical medicine, ferritin is predominantly used as a serum marker of total body iron stores.[1] For athletes, interpretation is harder than it looks. Ferritin is an acute phase protein, and its levels are increased during periods of inflammation and after intensive exercise, so the same athlete can produce different results depending on when and how blood is drawn.[4]
From a sports medicine perspective, ferritin is best read as one part of a bigger picture rather than a pass-or-fail number. This article explains what ferritin is, what a ferritin blood test measures, what low and high results mean, which thresholds are used in athletes, and how to test and act on the result.
In my clinical work, ferritin is one of the most frequently measured laboratory tests, and many patients already know it as the iron deficiency marker. The usual trigger is fatigue: exhausted patients often ask for ferritin themselves. The typical patient who requests it is a burned-out woman, often in the busy years of life, with a background of anemia, or pregnant. Men ask for it too, but in my experience less often. This may reflect awareness of the effect of menstruation and an assumption that iron deficiency is more common in women than in men. In the occupational health setting where I work, ferritin is also part of the basic laboratory panel for women, mainly because women may become anemic more easily due to menstruation. At the same time, ferritin has become something of a fashionable marker for exhaustion, and many people try to explain their fatigue with ferritin alone.
What Is Ferritin? The Body’s Iron Storage Protein
Ferritin is an iron storage protein. It is the primary iron storage mechanism in the body and is critical to iron homeostasis.[1] Iron is essential for life, but in excess it is toxic. Ferritin solves this problem: it makes iron available for critical cellular processes while protecting lipids, DNA and proteins from the potentially toxic effects of iron.[1] By capturing and buffering iron, ferritin plays a key role in maintaining iron homeostasis.[2]
A protein shell that stores iron
Ferritin is a 24-subunit molecule composed of two structurally distinct subunits: the light chain (molecular weight 19 kilodalton) and the heavy chain (molecular weight 21 kilodalton).[2] The iron-free form of the protein, apoferritin, forms a roughly spherical container within which ferric iron is stored as a ferrihydrite mineral.[1] One ferritin molecule can sequester up to 4,500 Fe3+ atoms.[2]
The two subunits do different jobs. Through its ferroxidase activity, the heavy-chain subunit transforms ferrous iron (Fe2+) into the less toxic ferric state (Fe3+).[2] The ratio of H and L subunits varies widely depending on tissue type and can be modified in inflammatory and infectious conditions.[1]
Ferritin, hemoglobin and iron: a simple way to think about it
A useful analogy: the iron in hemoglobin is the iron currently at work, carrying oxygen in red blood cells. Ferritin is the savings account — the reserve your body draws on when demand rises or intake falls. When people ask “what is ferritin?”, the most practical answer is that it tells you how much is left in that account. As the next section shows, the blood test is an indirect estimate of that reserve, not a direct count of it.
What Does a Ferritin Blood Test Measure?
If you searched “what is ferritin” after getting a blood test back, this is the part that matters most. Ferritin is mostly found as a cytosolic protein inside cells, but small quantities of ferritin emerge into the serum.[2] That serum ferritin is what the blood test measures, and it is assumed to be relatively iron-poor and almost entirely made up of light-chain subunits.[2] In other words, the test does not count the iron in your stores directly. Because it is proportional to total body iron stores, ferritin is an indirect marker of iron status.[2]
Why a low ferritin is so informative
Among the laboratory values within an iron panel, serum ferritin is the most useful in diagnosing iron deficiency.[1] A low serum ferritin (<12 µg/L) is highly specific for iron depletion, and only two conditions other than iron deficiency were known to lower serum ferritin at the time of that review: hypothyroidism and ascorbate (vitamin C) deficiency.[1] When concurrent inflammation is absent, ferritin is a highly specific and sensitive parameter for the diagnosis of iron deficiency.[2]
In practical terms, a low ferritin result is highly specific for low iron stores.[1]
Why a normal ferritin can still mislead
The reverse is not true. A review reports that a cut-off of 40 µg/L improves diagnostic sensitivity in patients whose conditions are not complicated by infection or inflammation, and, citing an earlier study, that 25% of women with absent stainable bone marrow iron had serum ferritin levels greater than 15 µg/L.[1] A ferritin value that looks acceptable can therefore coexist with depleted stores.
That is why ferritin status is rarely interpreted on its own. For athletes, the minimum markers to consider are serum ferritin, hemoglobin concentration and transferrin saturation, with serum soluble transferrin receptor, hemoglobin mass and C-reactive protein listed as additional markers.[4]
In many of my patients, ferritin is the first value to point toward iron deficiency, and hemoglobin may begin to fall as the deficiency progresses. That is why I do not test ferritin in isolation: I usually order hemoglobin or a full blood count alongside it, which gives a much better picture of the situation. In the clinic we also look at MCV, and microcytic anemia further supports iron deficiency. If MCV is not low, the picture can become more complicated, especially when MCV is high, because megaloblastic anemia may be involved. In that case the anemia does not necessarily arise from iron deficiency in the same way, and ferritin alone may not point to its cause. When the complaint is fatigue, I also look at thyroid function tests. If anemia is suspected or I am working through the differential diagnosis of iron deficiency, folate and vitamin B12 are usually checked too, and, depending on the clinical presentation, vitamin D may end up in the same panel.
Normal Ferritin Levels: Why “Normal” Is Not Always Enough
The reference range printed on a lab report describes a population sample. It does not tell you what is optimal, and for ferritin that difference matters.
A systematic review in The Lancet Haematology states that a serum ferritin concentration of less than 30 µg/L has a high specificity and sensitivity for diagnosing iron deficiency in adults, but the laboratory-reported lower limit of normal (LLN) is typically lower.[3] Across 37 studies covering 21,882 females and 23,650 males, the ferritin LLN was a median of 8 µg/L in females and 25 µg/L in males.[3] The five most used commercial ferritin assays reported a median LLN of 11 µg/L for females and 22 µg/L for males.[3]
The authors concluded that the data behind these reference intervals are at high risk of bias, because individuals at risk of iron deficiency were not excluded from the presumed normal population, and that these LLNs might be contributing to underdiagnosis of iron deficiency.[3] They suggest evidence-based laboratory clinical decision limits to diagnose iron deficiency.[3]
The practical consequence is easy to picture. A hypothetical female athlete with a ferritin of 12 µg/L could sit inside many laboratories’ normal range while being below the 30 µg/L level that identifies iron deficiency with high accuracy.
In my medical training at the University of Helsinki, anemia was emphasized as the measure that matters: we were taught on the hematology course that a low ferritin is not a problem as long as the patient does not become anemic. In practice, however, a number of patients feel they benefit from iron supplementation when their ferritin is low, and athletes may experience improved performance as well.
Restless legs syndrome and periodic limb movement disorder are contexts in which ferritin is handled differently. In my patients with these conditions, ferritin is generally aimed toward the upper third, even when there is no actual anemia and the ferritin is not particularly low to begin with. Pregnancy is similar: restless legs can appear, and I see fairly low ferritin levels in quite a few pregnant patients.
At the upper end, ferritin reference ranges vary with the assay used, although the upper cut-off is typically set to 200 µg/L in women and 300 µg/L in men.[2]
High Ferritin: Inflammation, Exercise and Iron Overload
A high ferritin is often read as “plenty of iron”. Usually it is not that simple. In routine medical practice, only 10% of hyperferritinemia cases are related to iron overload; the rest are a result of acute phase reactions and reactive increases in ferritin due to underlying conditions.[2] The usual underlying causes are inflammation, metabolic syndrome, chronic alcohol consumption, cellular damage and malignancy.[2]
Inflammation
All forms of inflammation, regardless of their cause, may elevate ferritin levels, which is why ferritin is recognized as an acute phase reactant.[2] Pro-inflammatory cytokines stimulate the synthesis of both ferritin and hepcidin, leading to hyperferritinemia, iron retention in macrophages and less iron being available for red blood cell production.[2] Very high values are not diagnostic on their own: ferritin above 1000 µg/L is regarded as a non-specific marker of pathology.[2]
In practice, many laboratory panels already offer ferritin and CRP as a combination. Because ferritin is an acute phase protein, a high ferritin value can be read alongside CRP to judge whether inflammation may be affecting it. In my view, the limitation is that a patient may have mild inflammation that does not raise CRP, and then the interpretation remains unclear.
Exercise and training load
Training can push ferritin up too. In eight male junior world elite rowers followed through a 4-week training camp, serum ferritin was significantly higher at day 7, during the initial increase in training load, than at the start of camp (90.37 vs 68.50 ng/mL; 1 ng/mL equals 1 µg/L).[9] In the same study, ferritin followed hepcidin’s rise at the initial increase in training load.[9] This rise appeared even though samples were drawn after an overnight fast and at least 14 hours after the last training session.[9]
True iron overload
Iron overload is real, and athletes are not immune to it. A slow and progressive increase in ferritin over time can suggest ongoing iron overload, and an elevated transferrin saturation can support that suspicion; transferrin saturation above 45% in women and above 50% in men is generally regarded as elevated.[2] One review suggests that an elevated ferritin combined with a transferrin saturation above 45% should prompt genetic confirmation of hemochromatosis.[1] C282Y homozygosity (HFE) is the most common monogenic disorder in northern European populations, with a prevalence of 0.5%, although penetrance is incomplete.[2]
In one study of recreational marathon runners, this was found mainly in men. Among 170 recreational runners in the Zürich marathon, after excluding those with elevated C-reactive protein, iron overload, as defined in the study (plasma ferritin >200 µg/L), was found in 19 of 127 men (15.0%) but only 2 of 43 women (4.7%).[8] Iron depletion showed the opposite pattern: 1.6% of men versus 28.0% of women.[8] The authors suggested that supplements should only be used if tests of iron status indicate deficiency.[8]
When a patient’s ferritin is high, I usually order more tests: iron values and a broader anemia panel including transferrin, soluble transferrin receptor, transferrin saturation and serum iron concentration, together with a full blood count. These often take the assessment quite far. Very high ferritin values may be caused by hemochromatosis or another hematological disease, and after the basic investigations these patients are usually referred on to specialist hematology care.
What Ferritin Means for Athletes
Iron deficiency is common in sport
For athletes, the question “what is ferritin?” has a practical edge. Although iron deficiency is most common in female athletes (~15–35% of athlete cohorts deficient), approximately 5–11% of male athlete cohorts also present with it.[4] A recent systematic review cites estimates of iron deficiency in up to 60% of female athletes.[5]
In my clinical experience, I often see low ferritin in athletes, particularly in female athletes who also menstruate. I frequently meet female athletes who are vegetarian, and they may have poorer iron absorption on top of that. Athletes may also notice a decline in performance more readily than other patients, because they see it directly in their sport. Many want to maximize their athletic performance, which may lead them to seek an appointment and ask for ferritin to be measured.
Why athletes struggle to keep iron: hepcidin
Hepcidin is the master iron regulatory hormone.[10] When elevated, it reduces intestinal iron absorption and macrophage iron release.[1] Exercise transiently increases hepcidin for 3–6 h post-exercise, likely as a result of the exercise-induced inflammatory response and the associated increase in the cytokine interleukin-6 (IL-6).[4]
An individual participant data meta-analysis found that exercise is associated with a 1.5–2.5-fold increase in hepcidin concentrations, and that the size of the change from before exercise to 3 h after exercise was largely attributable to exercise duration.[10] The authors note that hepcidin is likely a major contributor to the prevalence of iron deficiency in athletes.[10] Put simply, a long session may briefly reduce how much dietary iron is absorbed.
What low iron does to performance
A systematic review of 23 studies comprising 669 athletes (age range 13–47 years) across 16 sports examined high-level, iron-deficient female athletes, defined as serum ferritin <40 µg/L.[5] Iron deficiency negatively affected endurance performance by 3%–4%, while endurance performance improved by 2%–20% when iron-deficient athletes were treated with 100 mg/day of elemental iron for up to 56 days via oral supplementation, or bi-daily via parenteral administration over 8–10 days.[5] Maximal aerobic capacity improved by 6%–15% following 16–100 mg/day of elemental iron for 36–126 days.[5] Study quality was moderate (77%), and most studies (n = 18) had group sizes of 20 athletes or fewer.[5]
A 3–4% deficit can be a meaningful disadvantage in competition.
Low hemoglobin is not always iron deficiency
Hemoglobin is affected by shifts in plasma volume, which can produce a pseudo-anemia commonly referred to as sports anemia; this does not appear to have any negative effects on performance.[4] That is one more reason to read ferritin, hemoglobin and transferrin saturation together.
What Is Ferritin Telling You? Athlete Thresholds and How to Test
General-population reference ranges were not designed with athletes in mind, so sports medicine uses its own thresholds for ferritin status.
From a clinical perspective, this is a consensus among sports physicians rather than a national treatment guideline, so it does not show up in the laboratory reference range, and mainstream medicine does not usually take a position on athlete-specific questions. In my experience, many athletes are unaware of the athlete-specific recommendation. It often comes as a surprise to female athletes that ferritin should preferably be above 30 µg/L when the lower reference limit is 15 µg/L, at least in the laboratory we use in Finland.
Athlete-specific ferritin thresholds
Swiss sports medicine recommendations state that in healthy male and female athletes over 15 years, ferritin values <15 µg/L are equivalent to empty stores and values from 15 to 30 µg/L to low iron stores, so a cut-off of 30 µg/L is appropriate.[6] For children aged 6–12 years and adolescents aged 12–15 years, cut-offs of 15 and 20 µg/L are recommended.[6] As an exception in adult elite sport, a ferritin value of 50 µg/L should be attained before altitude training, as iron demands are increased in that setting.[6]
A 2024 review in the International Journal of Sports Medicine combined several published sources into a guide for categorizing an athlete’s iron status (the treatment column shows approaches adapted from the review, not automatic indications; the choice between oral and parenteral iron requires individual assessment):[7]
| Classification | Serum ferritin | Other markers | Common treatment approach |
|---|---|---|---|
| Healthy iron status | >50 µg/L | Transferrin saturation >16%; Hb F >120 g/L, M >130 g/L | Not applicable |
| Sub-optimal iron stores | 35–50 µg/L | — | Nutritional assessment |
| Iron depletion | 25–35 µg/L | — | Nutritional assessment and potential oral iron supplement |
| Iron deficiency non-anemia (IDNA) | 15–25 µg/L | Transferrin saturation <16% | Nutritional assessment and oral iron supplement |
| Iron deficiency anemia (IDA) | <15 µg/L | Hb F <120 g/L, M <130 g/L | Parenteral iron |
The same review notes that a ferritin threshold of 50 µg/L is associated with a hepcidin threshold for increased iron absorption, signaling the onset of early iron deficiency, and that interpreting iron status from a single marker (only serum ferritin) is not recommended.[7]
A three-stage model proposed for athletic populations uses slightly different cut-offs: Stage 1 iron deficiency at ferritin <35 µg/L (Hb >115 g/L, transferrin saturation >16%), Stage 2 iron-deficient non-anemia at ferritin <20 µg/L (Hb >115 g/L, transferrin saturation <16%), and Stage 3 iron deficiency anemia at ferritin <12 µg/L (Hb <115 g/L, transferrin saturation <16%).[4]
The exact numbers differ between frameworks, but the direction is consistent: athlete thresholds sit well above many laboratory lower limits, and 50 µg/L is the level referenced both for healthy iron status and before altitude training.[6][7]
How to test ferritin properly
Because ferritin responds to inflammation and recent exercise, how you test matters almost as much as what you test. A narrative review on iron in athletes recommends that blood samples be collected:[4]
- in the morning, after an overnight fast
- in a rested state, 24+ hours after training
- in a hydrated state, preferably confirmed by a waking urine specific gravity <1.025
- with no muscle-damaging (e.g. eccentric) exercise in the 2–3 days before
- with no recent illness, since inflammation can raise ferritin
The same review recommends screening annually for athletes with no symptoms or history of iron deficiency, and quarterly (or at least biannually) for at-risk individuals.[4] At-risk groups include athletes with low dietary iron intake (e.g. vegetarians and weight-category athletes) and those with increased iron requirements (e.g. growth, altitude, females or endurance athletes); low iron stores may also be an early indication of low energy availability.[4] Swiss recommendations similarly advise following athletes individually and repeating baseline tests (hemoglobin, hematocrit, mean cellular volume, mean cellular hemoglobin and serum ferritin) twice a year.[6]
What to Do About Low Ferritin: Evidence-Based Approaches
Treatment of iron deficiency consists of nutritional counselling, oral iron supplementation or, in specific cases, intravenous injection.[6] It is also important to identify and treat any potential underlying cause of iron deficiency, as this can improve the efficacy of supplementation and prevent recurrence.[4]
Food first
Heme iron sources (from meat) show greater absorptive capacity (~5–35%) than non-heme sources (~2–20%) from a single meal.[4] Vitamin C, meat, poultry and fish can enhance non-heme iron absorption, whereas polyphenols, phytates and calcium, found in tea, coffee, whole grains, legumes and dairy products, can decrease it.[4]
I also often advise patients to pay attention to their diet. I do not necessarily recommend a fully vegetarian diet; if the patient tolerates it, it can be worthwhile to eat meat as well, particularly red meat, when iron levels have been low.
Oral iron supplements
In athlete cohorts, oral iron supplementation at doses of ~100 mg per day over 8–12 weeks has produced 40–80% increases in ferritin.[4] Gastrointestinal discomfort is a common side effect of oral iron supplements.[4]
Alternate-day dosing may improve results. In two randomized controlled trials in iron-depleted women (serum ferritin ≤25 µg/L) aged 18–40 years, 60 mg of iron given on alternate days for 28 days produced a cumulative fractional absorption of 21.8% compared with 16.3% when the same doses were given on consecutive days for 14 days; total iron absorbed was 175.3 mg versus 131.0 mg.[11] Splitting a 120 mg dose into two 60 mg doses did not significantly change fractional or total absorption.[11] These participants were not athletes, but the finding underpins the suggestion that alternate-day supplementation may increase efficacy in athletes through better fractional absorption.[4]
Timing matters too. Hepcidin shows a strong diurnal variation, with the lowest levels in the morning and a steady increase throughout the day, so the review suggests that optimal iron intake may be as far away from exercise as possible, with a preference for the morning over the evening.[4]
In my practice, iron supplementation is often started when a patient has low ferritin and a clear decline in performance, whether at work or in sport. In an individual patient it is not always clear whether iron actually helps or whether the exhaustion simply comes in waves, but many patients want to rule out that possibility, or at least know that something has been done about it. For athletes, the ferritin threshold is often held a little higher than for the sedentary population, because ferritin may affect performance in many athletes even before it falls below the laboratory reference limit. In athletes I aim for a ferritin above 30 µg/L, and preferably somewhat higher, especially when the patient clearly has performance-related symptoms. The lower reference limit for women in our laboratory is 15 µg/L, which may be a little low for an athlete. For this reason, especially in female athletes, I may start iron supplementation more readily and at a lower threshold.
In my practice, the typical scenario is that iron is taken daily, or on alternate days if the patient gets stomach symptoms, and the situation is reassessed after about two to four months. If iron values and possibly hemoglobin normalize, the supplement is often continued as a course rather than indefinitely. In patients with chronically low hemoglobin or ferritin, continuous long-term medication may of course be needed.
Intravenous (parenteral) iron
Parenteral iron has been very effective at improving iron status, with 200–400% increases in ferritin reported from 300–550 mg of iron delivered over a 1- to 42-day period.[4] Newer intravenous formulations can be given as a single total dose over 15–60 min and have a similar safety profile to oral treatment.[7] Adverse reactions can still occur, ranging from a mild rash to anaphylaxis in very rare cases.[4]
IV iron shows greater efficacy in athletes with lower ferritin, and it should only be given in consultation with a sports medicine physician.[7] Athletes in international competition must also consider anti-doping rules: the World Anti-Doping Agency prohibits IV infusions of more than 100 mL within a 12-hour period, both in and out of competition, and a therapeutic use exemption may be required; the current WADA Prohibited List should be checked for exceptions.[7]
Some of my patients ask for intravenous iron, and in my view they fall into two groups. The first are patients who are mainly exhausted and have repeatedly low ferritin without actual anemia; they usually use private health care, often through insurance. The second group have a real underlying condition, such as Crohn’s disease or exceptionally anemizing bleeding, or very troublesome restless legs that have not responded to oral iron. In these situations IV iron may be indicated. In Finland, at least in public health care, the criteria are fairly strict, and IV iron is often not considered unless there is clearly documented anemia and low ferritin (restless legs syndrome being a possible exception), and the patient either does not tolerate oral iron or gets no benefit from it. Simply not wanting to take iron tablets is not an indication. In my understanding, the indications for athletes are the same as for the sedentary population in Finland. IV iron infusions are given in primary care as well as in specialist care.
When not to take iron
Iron supplementation in non-iron-deficient athletes does not appear to improve performance, so indiscriminate use of IV iron is not recommended.[7] Long-term daily oral iron intake or IV supplementation in the presence of normal or even high ferritin values does not make sense and may be harmful.[6]
Conclusion: What Is Ferritin and Why It Matters for Athletes
So, what is ferritin? It is the body’s primary iron storage protein, and serum ferritin is an indirect marker of how much iron the body holds in reserve.[1][2] A low result is highly specific for iron deficiency, yet published lower limits of normal sit at a median of just 8 µg/L in females, far below the 30 µg/L level that identifies iron deficiency with high accuracy.[3] Ferritin also rises with inflammation, and it rose with an increase in training load in one small study of elite rowers, so a normal or high value needs context.[2][9]
In my clinical work, I usually do not read ferritin on its own. I check it together with hemoglobin or a full blood count, MCV and, when ferritin is high, CRP and a broader iron panel. In athletes I aim for a ferritin above 30 µg/L, which is higher than the 15 µg/L lower limit in our laboratory, and I often advise attention to diet, including red meat when the patient tolerates it, alongside any supplementation. In public health care in Finland, IV iron is usually reserved for clear indications.
For athletes, the stakes are concrete: estimates of iron deficiency in female athletes reach up to 60%, and in high-level female athletes iron deficiency was linked to 3%–4% lower endurance performance.[5] Test under standardized conditions, interpret the result against athlete-specific thresholds, correct a true deficiency with food and targeted supplementation, and skip iron you do not need. Do that, and ferritin stops being a confusing number on a lab report and becomes a tool you can act on.
References
- https://doi.org/10.1016/j.blre.2008.08.001
- https://doi.org/10.3390/jcm10092008
- https://doi.org/10.1016/S2352-3026(24)00103-0
- https://doi.org/10.1007/s00421-019-04157-y
- https://doi.org/10.1016/j.jshs.2024.101009
- https://doi.org/10.4414/smw.2015.14196
- https://doi.org/10.1055/a-2211-0813
- https://doi.org/10.1038/ejcn.2010.16
- https://doi.org/10.3389/fphys.2019.01577
- https://doi.org/10.1007/s40279-023-01874-5
- https://doi.org/10.1016/S2352-3026(17)30182-5

