Iron Status and the Acute Post-Exercise Hepcidin Response in Athletes

by Benjamin Bunting BA(Hons) PGCert

Ben Bunting BA(Hons) PGCert Sports and Exercise Nutrition Level 2 Strength and Conditioning CoachWritten by Ben Bunting: BA(Hons), PGCert. Sport & Exercise Nutrition. British Army Physical Training Instructor (MFT).  


The acute post-exertion hepcidin response (ATPR) is a vital mechanism for maintaining and optimizing the health of athletes. However, the study of its physiology is still in its infancy. Therefore, it is unclear if the ATPR is a good indicator of an athlete's iron status. It is also unclear whether the ATPR is a sufficient indicator of the effects of exercise on the body. This article seeks to address these questions. Specifically, it will examine the role of iron in the acute post-exertion hepcidin responses of athletes. It will also examine the mechanisms involved in these responses.

The role of Iron

Iron is one of the most important components of the human body and plays a vital role in oxygen transport, energy metabolism and immune defense. However, it can be depleted during intense training. A deficiency can result in impaired sports performance. Therefore, it is important to identify and monitor iron status using inflammatory biomarkers.

Various studies have investigated the influence of exercise on hematological parameters, including iron. These studies focused on iron levels in hemoglobin and transferrin. A new study investigated the effect of acute exercise on iron regulatory proteins.


Hepcidin is a 25-amino acid disulfide-rich peptide that plays a major role in erythropoiesis and iron homeostasis. Its function is to balance the need for iron against the threat of infection. It is produced by hepatocytes. It is also produced by macrophages and neutrophils.

During inflammation, hepcidin is induced by interleukin-6 (IL-6). The IL-6-induced inflammation activates the JAK/STAT3 pathway. This pathway controls hepcidin transcription.

Inhibition of IL-6 reduces hepcidin expression. However, hepcidin still contributes to hemoglobin production in the erythroid lineage. It inhibits iron efflux from the cell surface and blocks intestinal iron absorption. The hepcidin molecule contains four disulfide bonds. This structure is similar to many antimicrobial peptides. Its structure may be a relic of evolutionary origin.

Hepcidin is mainly produced by hepatocytes. Its autocrine effects on liver cells may be important in the regulation of iron metabolism. It can also be produced in a number of other cell types.

Hepcidin is a major contributor to anemia of chronic disease (ACD). It also increases in inflammatory conditions. It is also elevated in multiple myeloma and in rheumatic diseases. It is also associated with iron-refractory anemia.

Hereditary hemochromatosis also involves Hepcidin. It is the main regulator of iron incorporation into erythrocytes. It also regulates iron storage in the transferrin compartment of erythrocytes. It is also an inhibitor of the cellular efflux of iron. It is a hormone produced in the myeloid cell membrane.

Hepcidin is present in human urine and the levels measured by various methods vary considerably. These differences are due to the fact that hepcidin isoforms have different molecular structures.

The effects of exercise

In one study, a group of athletes was evaluated for changes in TIBC and hepcidin. It was shown that increased iron level after acute exercise is transient and insufficient to cause acute systemic effects. Both hepcidin and TIBC values increased within 3 hours of exercise and decreased again during the recovery period. It was not observed that lactoferrin and transferrin levels changed.

The study also demonstrated that exercise can lead to disturbances in iron metabolism. This may occur due to hemolysis. During intense physical activity, oxidative stress results in biochemical changes in the membrane of erythrocytes, which can lead to an increase in intravascular hemolysis.

The increase in iron and hepcidin levels after acute exercise can be related to the presence of an inflammatory response. These changes can be useful in cases of unclear situations.

However, establishing specific reference intervals for some hematological and biochemical parameters is still required. To examine this, a group of highly qualified athletes were tested for TIBC and iron levels. The study was performed until exhaustion. The changes in these parameters were compared with baseline data. The findings suggest that the increase in TIBC and hepcidin after acute exercise is insufficient to cause acute systemic effects in restrained athletes.

Serum was collected before and after each running session. Blood samples were analysed for hepcidin, TIBC, lactoferin, and interleukin-6. TIBC correlated with iron levels and was a good indicator of changes in the iron concentration. TIBC is a reflection of transferrin activity and is usually used to characterize dynamic changes in iron levels during training.

Moreover, the study was not able to establish a relationship between the changes in TIBC and hepcidin and exercise duration. Further investigations should be conducted to establish a direct association between the two. In addition, future studies could include other biomarkers such as TNF-, IL-2, and IL-6.

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Iron and Energy Metabolism

Iron deficiency is common in athletes. It is most commonly encountered in endurance sports. In addition, it is more prevalent in females. The average prevalence of iron deficiency in women is 2.2%. The condition is more common in adolescent and menstruating females.

Different studies have described the effects of endurance exercise on hepcidin regulation. However, there are few studies examining the relationship between physical activity and iron absorption in athletes.

Iron is a vital component of hemoglobin. It plays an important role in energy metabolism and oxygen transport. It is also a critical component of muscle enzymes and is essential for the immune system. In athletes, iron deficiency can cause various health problems. However, the optimal intake of iron is related to dietary intake and energy requirements. In addition, training load and competition period can affect iron levels. Therefore, it is recommended to monitor basic blood tests and therapeutic measures to ensure optimal iron status.

Acute exercise is associated with a significant increase of nutrient turnover, which includes iron. However, this increase is transient. It is not enough to trigger a post-exercise hepcidin response. The hepcidin response is attenuated in athletes with low iron and ferritin stores. This may be due to the effects of erythropoietin stimulation on the bone marrow.

Hepcidin is a key protein in the regulation of iron levels. Acute exercise has been shown to stimulate hepcidin production. In addition, hepcidin levels are reduced by hypoxia and decreased by iron requirements. This may result in an inverse homeostatic function.

Iron Regulation

Iron is an essential component of hemoglobin and plays a significant role in energy metabolism and oxygen transport. Athletes are often susceptible to iron deficiency and should regularly monitor their blood parameters.

Acute exercise is a stimulus that triggers a sequence of reactions to regulate iron levels. A small rise in iron concentrations following exercise has been reported in a few studies. It appears to be transient, though, and may not cause acute systemic effects in restrained athletes.

A recent study aimed to explore the effect of acute exercise on iron-related proteins. In particular, it investigated the acute post-exercise hepcidin response in athletes. This response occurs in response to a hypoxia-induced inverse homeostatic function in the body. It has been characterized by a reduction in circulating hepcidin.

After the first three hours of exercise, TIBC values were significantly elevated. During the post-exercise rest period, these values reverted to baseline. This indicates that the released iron was absorbed by circulating transferrin. In addition, a relatively rapid mechanism of regulation was involved, as apotransferrin was utilised. 

Compared with the control group, the iron deficient athletes had lower serum ferritin, iron, and hepcidin levels. Furthermore, they showed a decreased TIBC level. This difference suggests that the increased iron levels may have occurred due to a haemolytic or inflammatory stimulus. This may be due to the high training level of the participants. However, future investigation could confirm this association in a larger sample.

During the acute-phase response, the body is prone to inflammation. This inflammatory response is one of the mechanisms that disturb iron management during intense training. Athletes should be monitored using inflammatory biomarkers such as high-sensitivity C-reactive protein and soluble transferrin receptors. Inflammatory markers may also be useful when iron status is unclear.

Athletes should have their blood parameters evaluated before and after each running session. These measurements should be repeated every six to eight weeks. In addition, basic blood tests should be repeated at least 8 weeks after start of oral therapy, nutritional measures, or iv-iron administration.

An acute exercise response is often associated with increased iron levels. The mechanism behind this increase is unclear. However, it is believed that an acute exercise stimulus induces a sequence of reactions to regulate iron levels. Physiological stress and inflammation caused by intense training can also alter iron management in athletes. In this regard, this study investigated the effects of acute exercise on iron regulatory proteins.

In this study, blood samples were collected before, after and during incremental exercise performed on a treadmill. The hematological parameters studied included serum ferritin, hepcidin, iron concentration, and TIBC. The results show that serum ferritin increased significantly after the exercise. The hepcidin and IL-6 values did not change significantly during the study. 

Iron deficiency in athletes is a common problem. It affects the immune system, energy metabolism, and oxygen transport. Therefore, the proper utilization of iron is necessary for optimal functioning. It is essential to maintain adequate iron stores and to monitor the effect of intense training on them.

Hepcidin is a liver-produced peptide that helps to regulate the iron absorption process. Athletes with low iron and ferritin stores are susceptible to hepcidin bursts. As a result, hepcidin may contribute to the development of iron deficiency.


There is considerable debate over the role of iron status in sports performance. In some athletes, the presence of iron deficiency may negatively affect performance. Moreover, different nutritional factors influence the uptake of iron.

As a result, maintaining optimal iron status is essential for athletes. There is a growing body of research examining the role of exercise and hepcidin in regulating the body's iron homeostasis.

The hepcidin response to physical activity is a complex process that is influenced by a number of factors. The intensity of an athlete's physical activity plays an important role in determining the magnitude of the post-exercise hepcidin response. In addition, the duration and type of exercise may affect the hepcidin response. 

Athletes with sub-optimal iron status had a significant increase in post-exercise hepcidin. They also had lower serum ferritin levels. Despite these results, there was no clear evidence to support a time-dependent effect of iron supplementation on the hepcidin response. Rather, the increase in post-exercise hepcidin may have been due to the reduced ability of the body to absorb iron. This may explain why the response was not affected by an oral iron isotope.

The hepcidin response was induced by a high energy deficit during exercise. The release of muscle-derived Interleukin-6 (IL-6) is a critical component of this inflammatory response. The half-life of IL-6 is relatively short, meaning that its release peaks shortly after exercise.

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