Iron plays a very important role in the human body, especially in terms of oxygen transport and energy metabolism during exercise. Therefore, the supply, utilization and storage of iron are crucial for athletes [1]. However, iron deficiency is frequently found in some athletes, especially women and adolescents, with an increasing risk of depleting iron stores to a stage of functional or absolute iron deficiency [2], [3]. Published evidence suggests that a key determinant of athlete performance is iron metabolism [1], [4] and there is growing interest in the mechanisms that affect iron metabolism in athletes. The change of hepcidin caused by exercise has been emphasized as an important factor in the change of iron metabolism of athletes.

Hepcidin is a cysteine-rich antimicrobial peptide, encoded by the HAMP gene, and is a key molecule in the regulation of iron absorption and metabolism in the body [5]. It not only controls iron release to the circulation but also regulates iron absorption in the intestines [6], which maintains the absorption of dietary iron and the distribution of iron among the body tissues [7]. Hepcidin is produced primarily by hepatocytes [8]. Other tissues and cells, such as macrophages, have been shown to express hepcidin as well, though at a much lower level. So far, it has been demonstrated that hepcidin expression can be influenced by inflammation [9], body iron status [10], erythropoiesis, as well as hypoxia [11]. The increase of hepcidin level will degrade iron transporters [12] and divalent metal ion transporters, leading to blocked duodenal iron absorption, decreased cell iron efflux and ability to recover iron from macrophages [6], and decreased serum iron, leading to anemia.

The iron content in the human body is not only affected by whether sufficient iron is taken in the diet, but also affected by inflammation caused by exercise [13]. The discovery of hepcidin provided a link between iron deficiency and concomitant inflammation [12]. Domínguez et al. experiments showed that the increase of interleukin 6 (IL-6) levels after exercise is closely related to the enhanced synthesis of Hepcidin [14]. Some studies have shown that hepcidin is a reactant in the acute phase and a key regulator of iron homeostasis in the whole body. Many reports on the elevation of hepcidin level 24 hours after exercise show that serum iron and inflammatory parameters will increase sharply immediately after exercise, and then serum iron will decrease due to the elevation of hepcidin level [15], [16], [17]. At the same time, the increase of hepcidin level after exercise is also thought to be caused by the increase of so-called unstable iron pool [11] caused by enhanced hemolysis [18].

In conclusion, the exact relationship between hepcidin expression, IL-6 and iron metabolism and the molecules involved is still unclear [6]. Therefore, this review aims to explore the effect of exercise on serum hepcidin level as a mediator of iron absorption in human body, and the relationship between hepcidin level, inflammatory status, and iron metabolism markers.