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Abstract
Iron is an important mineral element used by the body in a variety of metabolic and physiologic processes. These processes are highly active when the body is undergoing physical exercises. Prevalence of exercise-induced iron deficiency anemia (also known as sports anemia) is notably high in athletic populations, particularly those with heavy training loads. The pathogenesis of sports anemia is closely related to disorders of iron metabolism, and a more comprehensive understanding of the mechanism of iron metabolism in the course of physical exercises could expand ways of treatment and prevention of sports anemia. In recent years, there have been remarkable research advances regarding the molecular mechanisms underlying changes of iron metabolism in response to physical exercises. This review has covered these advances, including effects of exercise on duodenum iron absorption, serum iron status, iron distribution in organs, erythropoiesis, and hepcidin’s function and its regulation. New methods for the treatment of exercise-induced iron deficiency are also discussed.
Highlights
Iron is an essential trace element in the human body
We found that hepatic hepcidin mRNA significantly increased in rats trained with strenuous exercise, which was associated with an obvious decrease in duodenal divalent metal transporter 1 (DMT1) and FPN1 expression [20]
Iron deficiency is commonly found in strenuous exercised athletes. In addition to those well-known processes of iron loss, such as hemolysis, hematuria, sweating and gastrointestinal bleeding, exercise-induced up-regulation of hepcidin expression might be the main reason that results in iron deficiency in athletes
Summary
Iron is an essential trace element in the human body. It is important for the synthesis of hemoglobin and oxygen delivery, and plays a key role in the electron transport chain as well as the production of energy in mitochondria [1,2]. Sports anemia and hepcidin exercise can increase erythropoietic activity in marrow [25], it was found that erythrocyte numbers, haemoglobin levels and haematocrit values were significantly decreased after intensive training [20,26] This observation may be resulted from the reduced iron absorption in small intestine and the decreased iron export to the circulation from parenchymal cells and macrophages. Studies by Theurl et al [127] demonstrated that inhibition of hepcidin expression by using the soluble hemojuvelin-Fc (sHJV.Fc) in a rat model of AI resulted in the mobilization of iron stores, increase of serum iron levels, stimulation of erythropoiesis, and correction of anemia. BMP modulators as potential drugs to reduce hepcidin expression should have a great specificity
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