Iron deficiency in Athletes – Challenges and Future of Sports Nutrition

Ryunosuke Takahashi^1, Katsuhiko Hata^2, Koji Okamura^3, Takako Fujii²

1. The Institute of Health and Sports Science, Chuo University. Tokyo. Japan
2. Department of Sports and Medical Science, Graduate School of Emergency Medical System, Kokushikan University, Tokyo, Japan.
3. Exercise Nutrition Laboratory, Graduate School of Sport Sciences, Osaka University of Health and Sport Sciences.

OPEN ACCESS

PUBLISHED: 27 Febuary 2025

CITATION: TAKAHASHI, Ryunosuke et al. Iron deficiency in Athletes – Challenges and Future of Sports Nutrition. Medical Research Archives. Available at: <https://esmed.org/MRA/mra/article/view/6354>.

COPYRIGHT: © 2025 European Society of Medicine. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 ISSN 2375-1924

DOI: https://doi.org/10.18103/mra.v13i2.6354

ABSTRACT

Iron deficiency is one of the world’s most common nutritional problems: according to the WHO, approximately 30% of the female population aged 15-49 years suffers from iron deficiency anemia. Women are more likely than men to have inadequate dietary iron intake. Women are also more likely to suffer from iron deficiency because iron is also lost through menstrual bleeding. Many athletes, not just women, have also been diagnosed with iron deficiency. Iron plays an important role in oxygen transport and energy metabolism in the body and is therefore very important for athletes with high oxygen requirements, especially endurance athletes. However, despite its importance, many studies, particularly in endurance athletes, have shown a tendency towards low serum ferritin levels. This paper focuses on iron deficiency in athletes and describes the relationship between iron deficiency and exercise. Particular attention will be paid to the effects of different types of exercise on iron nutritional status and the issues that arise.

Keywords: Athlete, Aerobic exercise, Resistance exercise, iron deficiency, Sports nutrition

Introduction

Iron is a micronutrient found in very small amounts in the body, but it plays an important role in processes such as oxygen transport and energy metabolism. Iron is also an essential component of hemoglobin, which is required for oxygen transport in red blood cells. Therefore, iron deficiency in an athlete’s body reduces the oxygen transport capacity of active muscles, leading to a decline in athletic performance. In other words, iron is a very important nutrient for athletes with high oxygen requirements, especially endurance athletes. Despite its importance, many athletes have been diagnosed with iron deficiency. Research has been ongoing for a long time, irrespective of athletes.

There have been many studies of the effects of exercise and diet on iron status, and it is known that exercise itself alters iron status. In particular, many studies of athletes have shown a tendency for serum ferritin levels to be low. Many results support this in endurance athletes. Iron deficiency anemia is the most common nutritional disorder in female athletes, and many of these are thought to be due to dietary iron deficiency. However, people who participate in intense exercise are thought to need more iron than non-athletes due to loss of cellular iron caused by excessive sweating and shedding of epithelial cells from the skin and digestive tract, reduced absorption of iron from the digestive tract, and destruction of blood cells due to the intense physical impact on the legs and other parts of the body during some types of exercise. The incidence of iron deficiency is high not only in athletes but also in people who exercise regularly, and most of these cases involve aerobic exercise, so most research on the effects of exercise and the body’s iron nutritional status has been conducted on aerobic exercise. However, few studies have focused on resistance exercise. In recent years, the effect of resistance exercise in improving iron nutritional status has been suggested. Therefore, we will focus on the different effects of aerobic and resistance exercise on the iron nutritional status of iron-deficient athletes, as well as the issues necessary for the prevention and improvement of iron-deficient athletes, which will be discussed below.

Iron distribution in the body

Approximately 60–70% of the iron in the whole body is present as part of the hemo in the hemoglobin.

Hemo iron, other than hemoglobin, accounts for approximately 5% of iron in vivo and acts as an oxygen transporter in tissues. Non-hemo iron enzymes include those involved in oxidation reactions. In mitochondria, these non-hemo iron enzyme groups are more abundant than in cytochromes. Approximately 25% of the body’s iron is stored as ferritin and hemosiderin. When iron loss is less than iron intake, apoferritin synthesis increases with increasing iron intake, and iron adsorption onto ferritin within free polyribosomes proceeds, increasing ferritin stores in the liver. At the same time, hepatic hemosiderin stores are increased, apoferritin synthesis in the reticuloendothelial system and in the endoplasmic reticulum of hepatocytes is enhanced, and serum ferritin is also increased. Conversely, when iron loss is greater than iron uptake, iron is released from ferritin in the liver and serum iron concentration increases. In addition, iron stored in the reticular system and hepatocytes is released into the peripheral blood at a rate of approximately 20–25 mg/day, while serum iron is taken up by erythroblasts (in the bone marrow). Iron incorporated into erythroblasts is used for hemoglobin synthesis, and erythroblasts differentiate into erythrocytes and are released into the peripheral blood. Erythrocytes released into the peripheral blood eventually age and are phagocytosed by reticuloendothelial macrophages. Approximately 85% of the iron in erythrocytes phagocytosed by reticuloendothelial macrophages is released back into the body in the form of transferrin and ferritin, and the remainder is stored in the form of ferritin. Thus, iron uptake into erythroblasts is complemented and maintained by iron supply from macrophages.

The aim of this study was to understand iron metabolism in vivo and to provide a clear assessment of the challenges in sports nutrition.

Regulation of iron in the body

Many studies have been conducted on the effects of training and nutrition (nutrients) on athletes. In particular, hepcidin, an iron-regulating hormone synthesized in the liver, has attracted considerable attention. Hepcidin plays an important role in iron homeostasis. Hepcidin, a peptide hormone, is secreted by hepatocytes. The main iron flux of hepcidin is shown in

Dietary iron is primarily absorbed in the duodenum. Hepcidin also negatively regulates the release of recycled iron from macrophages and stored iron from hepatocytes. Iron and hepcidin regulate each other via endocrine feedback. When iron is high, hepcidin production by hepatocytes increases, limiting iron uptake and the release of stored iron. When iron is deficient, hepcidin production by hepatocytes is reduced and more iron is released into the plasma. Specific forms of iron that increase hepcidin synthesis include diiron plasma transferrin and hepatocyte-stored iron.

In iron deficiency, low hepcidin levels increase ferroportin activity in duodenal epithelial cells and reduce iron stores in intestinal epithelial cells. Iron deficiency in intestinal epithelial cells reduces the activity of oxygen- and iron-dependent prolyl hydroxylases, which target hypoxia-inducible factor (HIF) for degradation in the proteasome and stabilization of HIF. HIF2α is an apical iron importer. Normalization of HIF2α regulates dietary iron import into the apex and the activity of hepcidin-regulated ferroportins, and increases intestinal iron absorption in iron-deficient states. Both extracellular iron (in the form of iron transferrin) and intracellular iron regulate hepcidin synthesis. However, the mechanism underlying intracellular iron sensing remains unclear.

Dietary iron contains two main types of iron: heme iron and non-heme iron. However, it is known that the majority of dietary iron intake is non-heme iron. Dcytb at the intestinal epithelial cell membrane reduces non-heme iron to divalent iron, which is then taken up into the cell by DMT1. The heme iron and the iron taken up by the intestinal epithelial cells are transported to the cytoplasm by heme carrier protein 1 (HCP1). It is then degraded by heme oxygenase and released as an iron ion. Iron in the cytoplasm is exported into the circulation by ferroportins located in the basement membrane of the intestinal epithelium. The iron released from ferroportin is oxidized to trivalent iron by membrane-bound hefaestin or soluble ceruloplasmin. It is then bound to transferrin in the blood and transported in a safe form for distribution throughout the body.

Iron deficiency

Iron storage deficiency can occur rapidly or very slowly, depending on the balance between iron intake, storage, and iron requirements. Furthermore, the rate at which true iron deficiency occurs in individual tissues and intracellular organelles depends on the intracellular mechanisms of iron recycling and the metabolic turnover rate of iron-containing proteins. Iron is also responsible for transporting oxygen to the muscles during exercise and plays an important role in energy production during exercise. Therefore, iron deficiency leads to reduced athletic performance in endurance sports. Several physiological mechanisms have been proposed to explain iron depletion, including gastrointestinal hemorrhage, hemolysis due to impact, such as on plantar surfaces, iron deficiency in the daily diet, and loss due to heavy sweating. In addition, iron metabolism disorders, such as iron recycling from the spleen and macrophages, and iron absorption in the duodenum via hepcidin, are associated with iron deficiency. Hepcidin regulates iron homeostasis by binding to ferroportin, the only known intracellular iron exporter, and inhibiting its function through occlusion or degradation. Hepcidin plays an important role in iron metabolism in the body. The basolateral membrane contains an iron transporter called ferroportin, which removes iron from the cells. Hepcidin regulates iron levels by binding to ferroportin. In other words, hepcidin produced in the liver binds to ferroportin, and moves from the cell membrane to inside the cell, where it is degraded in lysosomes. When iron is not needed, hepcidin levels increase, leading to a decrease in ferroportin and suppression of iron transport. Conversely, when iron is needed, hepcidin expression decreases, allowing ferroportin to promote iron transport. Under normal conditions, blood iron levels are regulated. However, when excess iron is administered or during inflammation, hepcidin is overproduced, leading to a state of functional iron deficiency where stored iron cannot be utilized. Measuring blood hepcidin concentration is important for determining whether iron metabolism is normal.

Currently, anemia is mainly measured by hemoglobin concentration, which the WHO defines as less than 13 g/dl in men and 12.0 mg/dl in women. Furthermore, in recent years, blood ferritin levels, which reflect iron stores, have garnered attention for determining iron deficiency. The World Health Organization (WHO) recommends a serum ferritin concentration of 15 ng/mL as the cutoff value for iron deficiency in healthy individuals (10-59 years). Many studies have used a serum ferritin cutoff of >30 ng/mL, while broader ranges such as 12-40 ng/mL have also been employed in research on iron deficiency and metabolism. However, Galetti et al., in a study investigating the association of serum ferritin, hepcidin, and iron absorption in young women, recommended a ferritin cutoff of 50 ng/mL for the early detection of iron deficiency. Nachtigall et al. investigated the blood status of 45 long-distance runners and reported that serum ferritin levels were <35 μg/L in 51% of athletes and <20 μg/L in 16%. Reinke et al. studied professional soccer players and elite rowers, finding that some athletes had normal hemoglobin levels but serum ferritin levels below the 12 μg/L cutoff. In animal studies, iron deficiency, in the absence of anemia, has been shown to reduce endurance and exercise capacity. Hinton et al. reported that prescribing iron supplements to women with normal hemoglobin and low serum ferritin levels improved exercise capacity. These results indicate that iron levels in the body may be reduced even when hemoglobin concentrations are within the normal range.

Mielgo Ayuso et al. reported that to screen for iron deficiency, 30–99 ng/mL is considered functional iron deficiency, and a serum ferritin level of at least 100 ng/mL is required. These reports suggest that a higher cutoff value of ferritin may be beneficial when screening for iron deficiency in athletes.

Exercise and iron

1. AEROBIC EXERCISE

Many human studies have reported that aerobic exercise reduces hematocrit, blood hemoglobin concentration, and serum iron levels, and weakens red blood cell membranes. Endurance athletes, particularly elite long-distance athletes, train for long periods of time on multiple occasions throughout the day. Daily training in iron deficiency conditions reduces performance. Davies et al. reported that endurance performance decreased by up to 30% in athletes with iron deficiency anemia. It is well known that factors contributing to iron deficiency anemia in athletes include hemolysis from mechanical stimulation during running, as well as sweating during training and hypertonic sweating. The possibility of increased red blood cell turnover in athletes was also supported by ferrokinetic measurements performed by Ehn et al., who showed that female athletes lost iron 20% faster than non-athletes in experiments using radioactive iron, and that iron loss was faster than in adult males. They also reported that female athletes had normal hemoglobin and plasma iron levels but a latent iron deficiency in their bone marrow.

Animal studies have shown that aerobic exercise can reduce or ameliorate the reduction in biological markers of iron caused by iron deficiency. Perkkio et al. observed that aerobic exercise (treadmill running) in iron-deficient rats significantly increased hemoglobin concentration, endurance, and VO2max relative to iron-deficient resting rats. In contrast, no decrease in hemoglobin concentration was observed in iron-sufficient rats that exercised relative to the non-exercising groups. Willis et al. also reported that aerobic exercise (treadmill running) results in significantly higher hemoglobin concentrations in iron-deficient rats than in resting rats.

2. RESISTANCE EXERCISE

There are very few studies on the effects of resistance exercise on iron metabolism in vivo in comparison to aerobic exercise. Unlike aerobic exercise, resistance exercise promotes the synthesis of somatic proteins, and the faster the nutritional intake following exercise, the higher the muscle protein synthesis.

Mild resistance exercise has been reported to improve latent iron deficiency in young women without iron supplementation. Matsuo et al. reported that when women with latent iron deficiency performed resistance exercise (dumbbell exercise) for 12 weeks, there was a significant increase in serum ferritin levels, hemoglobin concentration, red blood cell count, and total iron binding capacity, and that daily mild resistance exercise improved non-anemic iron deficiency and prevented iron deficiency anemia. Additionally, Matsuo et al. found that resistance exercise alleviated iron deficiency anemia in rats that climbed a 2-meter wire tower to obtain water. This effect suggests that resistance exercise is related to an increase in ALAD activity, an enzyme involved in heme biosynthesis. Rats that habitually engaged in climbing exercises showed increased bone marrow ALAD activity after exercise. Matsuo et al. compared iron-deficient rats that had habitually engaged in climbing or swimming exercises for 8 weeks, and reported that while swimming exercise did not change bone marrow ALAD activity, climbing exercise increased ALAD activity. This result suggests that resistance exercise may increase hemoglobin concentration, unlike aerobic exercise.

Fujii et al. have also reported that voluntary resistance exercise, such as climbing, is effective in reducing iron deficiency anemia. However, it has been speculated that even if resistance exercise increases the ability to biosynthesize heme, blood hemoglobin levels may not recover if the supply of iron, the material for hemoglobin, from diet or stored iron is inadequate. Although some observations have been made on the effects of resistance exercise on iron nutrition in the body, the number of publications is significantly lower than that on aerobic exercise. Further research is needed to update the in vivo iron recycling capacity and the possibility of different iron uptakes depending on the type of exercise.

Diet

The first step in optimizing iron supplementation in athletes is to correct any existing iron deficiencies. For iron deficiency, the initial step is usually to improve dietary intake. Iron intake of 14 mg per day should be targeted. This is approximately twice the recommended amount for an average Japanese individual. Additionally, the recommended iron intake for female endurance runners is 18 mg/day, posing a significant burden for athletes.

Clenin et al suggest that iron deficiency in athletes can be treated by dietary modification, oral supplementation, or intravenous/intramuscular supplementation. Under normal conditions, macrophages efficiently recycle old red blood cells. Iron absorption from the daily diet is estimated to be approximately 15–20% for hemo iron and 5–10% for non-hemo iron, and the absorption of iron from the daily diet is thought to be approximately 10% of the ingested iron.

It is important for athletes to include meat, fish, whole grains, and green vegetables in their diets. In addition, although meat-derived proteins promote iron absorption, not all proteins have this effect (meat factor). In addition, meat intake increases non-hemo iron absorption by a factor of 2, although not all animal proteins have this effect. Lyle et al. found in a long-term study of aerobic dancers that the consumption of one meat-containing meal per day was associated with the maintenance of serum ferritin levels and reported that it was effective. Furthermore, Tetens et al. reported that serum ferritin levels are maintained in women of childbearing age who consume a meat-based diet, but that these levels are reduced in women who consume a plant-based diet. Fujii et al. reported that a protein intake of >1.0 g/kg BW/day, of which animal-derived protein was approximately 50%, resulted in no anemic individuals among athletes.

Further, foods rich in vitamin C increase iron absorption, whereas polyphenols found in coffee, tea, and certain plants inhibit iron absorption. This should be considered in the daily diets to avoid anemia.

Treatment

Most oral iron preparations are used in clinical practice. Oral iron tablets, such as ferrous iron (100-200 mg/day), ferrous fumarate (100 mg/day), and dry ferrous sulphate (105-210 mg/day), often cause gastrointestinal symptoms such as nausea, vomiting, and abdominal pain, making it difficult to continue taking them for long periods. To manage these gastrointestinal symptoms, patients can change the time of administration from during the day to before bedtime, or use soluble ferric pyrophosphate (120-240 mg/day), which is essentially a pediatric formulation, in small doses. However, managing these symptoms in practice can be challenging.

Oral iron preparations are often avoided due to their adverse effects on intestinal lesions. Since the daily dose of intravenous iron is limited to 40–120 mg, frequent administration is necessary to ensure reliable iron supplementation. Recently, iron supplements have become common as a preventive measure against anemia, not only for athletes but also for people who do not exercise. Various supplements and products to improve iron balance are available on the market. Brigham et al. reported that a supplement containing ferrous sulfate (39 mg/day of iron) prevented a decrease in serum ferritin levels in female swimmers. Hinton et al. also reported that the administration of ferrous sulfate (36.8 mg/day iron) to late-iron-deficient women significantly increased serum ferritin levels and improved endurance exercise capacity. In addition, Kang et al. reported that supplementation of young female soccer players with iron (40 mg, per day) significantly increased serum ferritin levels and prevented hemoglobin decline. The low doses of iron used in these studies suggest that iron supplements and preparations can improve iron stores, even at low doses.

As mentioned above, the side effects of oral iron supplementation may include gastrointestinal disturbances such as nausea, abdominal pain, and constipation, which may interfere with daily performance and require careful consideration. It is also recommended that athletes monitor their iron status regularly and treat deficiencies as soon as they occur. Clarke et al. recommend hematological testing every 6 months for women and annually for men unless there are other clinical indications. However, no specific ferritin level is recommended for athletes to determine improvements in iron deficiency. Clearer guidelines for iron supplementation and the associated hepcidin response to improve exercise performance are needed. It has been reported that intravenous iron supplementation has no particular advantage over oral supplementation with respect to iron status in athletes. Few studies have used dietary approaches to iron management rather than pharmaceutical iron supplementation in athletes. Dietary iron treatment methods used in the literature include prescription of iron-rich diets and/or hemo-iron-based diets, dietary counselling, and introduction of new iron-rich products into the daily diet. The majority of studies suggest that dietary iron interventions have a beneficial effect on iron status in iron-deficient athletes. However, the direct effects on athletic performance in female athletes are unknown. Nevertheless, it has been suggested that dietary iron interventions may help maintain iron status in female athletes, particularly during periods of intense training and competition.

Conclusions

This review examined the effects of exercise on iron deficiency and provided evidence to support these findings. Exercise induces an inflammatory response. Athletes who exercise daily may develop anemia during chronic inflammation. Inflammation-induced anemia increases iron excretion and inhibits iron absorption. The iron status of athletes should be carefully monitored during training, with particular attention to conditions associated with increased iron loss or demand. Early identification of reduced iron stores and subsequent supplementation may prevent further decline in iron status.

Dietary prevention of iron deficiency anemia is a fundamental aspect of sports nutrition. However, iron is one of the most difficult minerals to consume. The recommended intake is 14 mg, which is a significant burden for athletes. It is therefore important to consider not only iron supplementation, but also an anti-inflammatory diet and the timing of intake. Just as estimated energy intake needs to be considered individually, iron intake needs to be tailored to individual sports.

1. There is therefore an urgent need to determine the appropriate ferritin concentration for athletes.

2. As with estimated energy intake, iron intake needs to be considered on an individual basis.

Acknowledgements

The authors contributed equally to this work.

Disclosure statement

No potential conflicts of interest were disclosed.

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