In standard sports nutrition practices, nutritional deficiencies are not readily acknowledged, apart from iron that is. Simone do Carmo digs deeply into the iron and athletic performance literature.

Iron is an essential micronutrient in the diet of elite and recreational athletes alike. It is key to the formation of haemoglobin in red blood cells, the protein that is responsible for carrying oxygen from the lungs to the bodily tissues. Adults have around three to five grams of iron in the body, most of which is bound to haemoglobin (Hb) (1). Without sufficient iron availability, oxygen uptake into the tissues is reduced - this compromises performance, especially aerobic capacity, which depends strongly on the oxygen-carrying capacity of the blood. More specifically, as the brain has a high demand for oxygen, low iron levels in the body can make an athlete feel lethargic and unmotivated to train or perform. Iron availability is also vital in maintaining energy release from the mitochondrial electron-transport chain, that is needed to support physical exercise. If low iron levels are not treated, an athlete is likely to develop iron deficiency anaemia (IDA), one of the most common micronutrient deficiencies encountered in athletes, especially females and adolescents.

Why are athletes at a greater risk of iron depletion?

Athletes are thought to be at a greater risk of developing iron depletion through many exercise-related physiological mechanisms, including micro-ischaemia of the gut lining during intensive training or events such as marathons or Ironman triathlons. However, iron losses through blood present in urine and sweating do not seem to be relevant and although haemolysis through ‘foot strike’ damage (the mechanical damage of red blood cells associated with running) has also been suggested, the recovery of blood constituents has been shown to be complete, with no loss of iron (2). On the other hand, increased intramuscular pressure as a result of intense exercise may cause damage to the muscular tissues and induce haemolyses. Marathon runners may be particularly susceptible because their red blood cells have been shown to have increased osmotic fragility due to the loss of the protein spectrin within the cell membrane (3).

Recent evidence suggests that there is another, more pertinent, mechanism that relates to a marked increase in hepcidin, a hormone produced in the liver that is responsible for regulating iron metabolism in the gut and macrophages (4). Iron storage does occur in the muscle, where iron is bound to myoglobin, but most of it is stored in the liver; more specifically in the hepatocytes, where iron is bound to ferritin. To have an optimal iron balance, metabolism is tightly regulated by both hepcidin (known as the store regulator) and erythroid regulators (known as the systemic regulators) (1). The marked increase in hepcidin levels after exercise leads to a blockage of iron absorption and disruption of iron transference from macrophages to immature red blood cells. Conversely, hepcidin production is suppressed by the production of red blood cells, as well as anaemia, which encourages iron absorption from macrophages and red blood cells in the gut (2).

The post-exercise acute inflammatory response may also play a role in stimulating hepcidin production (5). A study in women showed a significant increase in hepcidin levels three hours after running. This marked increase was preceded by increases in the inflammatory cytokine interleukin-6 (IL-6) and followed by decreases in iron levels nine hours after running (6). Although other studies have also found elevated levels of hepcidin after different exercise modalities, and these were generally associated with increased IL-6 levels, this association is not always present. This could be due to differences in exercise intensity, with low intensity exercise not being adequate to up-regulate hepcidin (5). One study found that a 100km ultra-marathon increased both inflammatory markers IL-6 and C-reactive protein, yet this was not accompanied by increases in hepcidin levels (7).

Interestingly, exercise also seems to increase the erythroid regulator known as myonectin in skeletal muscle, which in turn seems to have an inhibitive effect on hepcidin production (1). This increases iron delivery to tissues from absorption in the gut and the liver stores. After the stress of blood loss, red cell production is known to be triggered by erythropoietin (EPO), which results in the release of erythroferrone (an erythroid regulator) from immature red blood cells, leading to supressed hepcidin production. As a result, iron absorption, haemoglobin synthesis and red blood cell production are increased. There is some evidence to suggest that in response to feeding and exercise, myonectin produced in skeletal muscle triggers fatty acid uptake by adipocytes and hepatocytes (5). Considering the function of erythroferrone in red blood production, it is suggested that the regulation of myoglobin (the iron and oxygen binding protein in muscle) is a consequence of myonectin release. Further research is needed to gain a better understanding of the inhibitory effect of myonectin on hepcidin as this could undermine the production of exercise/inflammatory-mediated hepcidin and have implications for the development of IDA.

How much iron do athletes need?

Athletes have greater physiological demands and requirements for iron as a result of the exercise-related physiological mechanisms described above. Endurance athletes are at a greater risk of iron depletion due to the greater physiological demands of their exercise. This applies especially to the female endurance athlete because of the heightened loss of iron through menstruation (8) and the adolescent athlete due to the demands of growth and development (9). The human body is able to absorb only 1-2mg of iron from a typical diet that contains 15-20mg of iron (3). In addition, iron has two different forms, known as haem found in animal sources (10 per cent), and non-haem found in plant-based sources (90 per cent), the latter of which is poorly absorbed because the iron is primarily in a non-bioavailable form. Therefore, athletes should pay particular attention to their diet in order to maintain an adequate iron status. Specific dietary recommendations for athletes of different sports are currently lacking; however dietary iron recommendations are 1.3 to 1.7 times higher for athletes than non-athletes. Furthermore, the iron requirements for vegetarians are 1.8 higher than for meat eaters (10). To ensure that athletes are meeting these requirements, they should increase their consumption of a variety of iron-rich foods such as red meat, seafood, eggs, lentils, beans and spinach.

Some components of food can interfere with or enhance iron absorption when combined in the same meal. Non-haem sources are particularly susceptible to interference, but their absorption can be enhanced by adding a haem source, such as red meat, or a food rich in ascorbic acid (e.g. broccoli, cauliflower or citrus fruit) in the same meal. Despite the lack of interventional studies, there is some preliminary evidence to suggest that fructose can increase iron bioavailability in human intestinal epithelial and liver cells (11). Additionally, athletes are also often advised to avoid consuming tea or coffee during their meal due to the tannic acid that binds to iron and inhibits its absorption in the gut (12). The methylating nutrients folate, vitamin B6 and B12 are also essential for haemoglobin synthesis and any deficiencies in these micronutrients may cause vitamin deficiency anaemia (13, 14). An athlete can also meet these vitamin needs by consuming the iron-rich foods described above.

How to diagnose iron depletion and IDA

Correct diagnosis of IDA requires the assessment of an athlete’s dietary intake, their clinical symptoms and continuous monitoring of their iron blood levels, rather than a one-off blood test. Athletes may have to consider additional supplementation if they present a basal serum ferritin level (marker of the body’s iron stores) of <30 µg/L. The aim of supplementation should be to restore serum ferritin levels to approximately 60 µg/L and evidence suggests that 100mg of haem iron per day (equivalent to approximately 1kg of cooked liver or 3kg of cooked beef) is an appropriate amount to restore an athlete’s iron status within a couple of months (3). The first line, and most widely used form of therapy, is oral iron due to its safety and effectiveness; however this might not be sufficient for some athletes who may have to take iron intravenously. The most common oral iron supplements contain the ferrous form of iron, such as ferrous fumarate, sulphate and gluconate. Because of their higher solubility, these are better absorbed than supplements containing the ferric form of iron. The reported differences between the above ferrous forms is the amount of iron they contain that is available for absorption: 33, 20 and 12 per cent respectively. However, other recent studies have shown that these ferrous iron supplements are essentially the same in terms of bioavailability (15).

When it comes to Hb levels, the lower laboratory cut-off levels for male and female athletes are <140g/litre and <120g/litre, respectively (2). In IDA, both ferritin and Hb levels are lowered. However, one must not forget that intense exercise increases plasma volume in the blood and can dilute haemoglobin levels. This is known as ‘sports anaemia’, a transitory, pseudo condition that does not have an effect on performance. It is likely to occur when training load is increased or at the start of a new training programme, which is why continuous monitoring of iron blood levels is so important.

Many iron supplementation studies have shown beneficial effects in restoring iron balance, and in some cases have improved performance. A study in 42 iron-depleted (serum ferritin <16 µg/L), non-anaemic (Hb levels >120g/d) women investigated the effects of iron depletion during a 15km cycle after they were randomised to receive either 100mg of ferrous sulphate or a placebo every day for six weeks. Their aerobic training was standardised during the six-week period. The iron-supplemented group revealed an increase in serum ferritin levels and a greater decrease in 15km time compared to the placebo group, suggesting that iron deficiency without anaemia still impairs favourable adaptions to aerobic training. In slightly anaemic active women (Hb levels <120g/d), eight weeks of 100mg/day of iron supplementation improved their aerobic capacity and reduced blood lactate concentrations after a submaximal cycle. A recent study in female volleyball players also showed that significant iron supplementation (11 weeks of 325mg/day) prevented declines in iron stores and benefitted strength and power performance parameters, such as the bench-press, half-squat, power clean and others (16). There are many studies that show similar findings, which seems to suggest that both iron-deficient athletes with and without anaemia can benefit from iron supplementation to restore iron balance and enhance their performance. And while female endurance athletes seem to respond better to iron supplementation than their male counterparts, further research is required to expose the mechanisms behind this (3).

Some athletes without iron deficiency take iron injections in order to rapidly increase their stores; however these do not seem to have a beneficial effect on their performance. Indeed, iron overloading may be counterproductive, as shown in cyclists, due to increased oxidative stress (17). Another study in runners without iron deficiency showed that iron supplementation did not improve their aerobic capacity or time-trial performance (5). Some people may also develop a condition called haemochromatosis with excessive use, which causes tissue damage and can result in serious health complications, including cancer and heart disease (5). Therefore, iron supplementation should not be encouraged in athletes without iron deficiency.


Having an optimal iron balance is vital to maintaining oxygen uptake into the tissues and the energy release needed to support physical exercise. Athletes are at a greater risk of developing iron depletion due to exercise-induced mechanisms. A better understanding of these mechanisms could provide valuable information for implementing prevention and treatment strategies. If low iron levels are not treated, athletes are likely to develop IDA. Therefore, athletes should pay particular attention to their dietary intake by consuming a variety of iron-rich foods to ensure they meet their higher requirements. Some athletes may need to consider supplementation if a correct diagnosis is made after assessing their habitual dietary intake, clinical symptoms and with continuous monitoring of their blood markers. There is evidence to show that the correct use of iron supplementation can restore iron balance and may have a beneficial effect on an athlete’s performance. Conversely, the incorrect use of iron supplementation is likely to be counterproductive and may cause detrimental effects to an athlete’s health.


  1. Lawen A (2015). Is erythroferrone finally the long sought-after systemic erythroid regulator of iron? World J Biol Chem. 6(3):78-82.
  2. Clenin G et al (2015). Iron deficiency in sports - definition, influence on performance and therapy. Swiss Med Wkly. 145:w14196.
  3. Zourdos M et al (2015). A brief review: the implications of iron supplementation for marathon runners on health and performance. J Strength Cond Res. 29(2):559-565.
  4. Peeling P (2010). Exercise as a mediator of hepcidin activity in athletes. Eur J Appl Physiol. 110(5):877-883.
  5. Buratti P et al (2015). Recent advances in iron metabolism: relevance for health, exercise, and performance. Med Sci Sports Exerc. 47(8):1596-604.
  6. Newlin MK et al (2012). The effects of acute exercise bouts on hepcidin in women. Int J Sport Nutr Exerc Metab. 22(2):79-88.
  7. Kasprowicz K et al (2013). Running a 100-km ultra-marathon induces an inflammatory response but does not raise the level of the plasma iron-regulatory protein hepcidin. J Sports Med Phys Fitness. 53(5):533-7.
  8. Alaunyte I et al (2015). Iron and the female athlete: a review of dietary treatment methods for improving iron status and exercise performance. J Int Soc Sports Nutr. 12:38.
  9. Desbrow B et al (2014). Sports Dietitians Australia position statement: sports nutrition for the adolescent athlete. Int J Sport Nutr Exerc Metab. 24(5):570-584.
  10. AIS Sports Nutrition (2009). Iron - are you getting enough? (Accessed November 2016)
  11. Christides T & Sharp P (2013). Sugars increase non-heme iron bioavailability in human epithelial intestinal and liver cells. PLoS One. 8(12):e83031.
  12. Zijp I et al (2000). Effect of tea and other dietary factors on iron absorption. Crit Rev Food Sci Nutr. 40(5):371-398.
  13. Koury M & Ponka P (2004). New insights into erythropoiesis: the roles of folate, vitamin B12, and iron. Annu Rev Nutr. 24:105-131.
  14. Stover P & Field M (2015). Vitamin B-6. Adv Nutr. 6(1):132-133.     
  15. Johnson-Wimbley T & Graham D (2011). Diagnosis and management of iron deficiency anemia in the 21st century. Therap Adv Gastroenterol. 4(3):177-184.
  16. Mielgo-Ayuso J et al (2015). Iron supplementation prevents a decline in iron stores and enhances strength performance in elite female volleyball players during the competitive season. Applied Physiology, Nutrition, and Metabolism. 40(6):615-622.
  17. De Matos L et al (2013). The use of exogenous iron by professional cyclists pervades abdominal organs but not the heart. International Journal of Cardiology. 167(5):2341-2343.