Effects of an Acute Exercise Bout on Serum Hepcidin Levels

Abstract

Iron deficiency is a frequent and multifactorial disorder in the career of athletes, particularly in females. Exercise-induced disturbances in iron homeostasis produce deleterious effects on performance and adaptation to training; thus, the identification of strategies that restore or maintain iron homeostasis in athletes is required. Hepcidin is a liver-derived hormone that degrades the ferroportin transport channel, thus reducing the ability of macrophages to recycle damaged iron, and decreasing iron availability. Although it has been suggested that the circulating fraction of hepcidin increases during early post-exercise recovery (~3 h), it remains unknown how an acute exercise bout may modify the circulating expression of hepcidin. Therefore, the current review aims to determine the post-exercise expression of serum hepcidin in response to a single session of exercise. The review was carried out in the Dialnet, Elsevier, Medline, Pubmed, Scielo and SPORTDiscus databases, using hepcidin (and “exercise” or “sport” or “physical activity”) as a strategy of search. A total of 19 articles were included in the review after the application of the inclusion/exclusion criteria. This search found that a single session of endurance exercise (intervallic or continuous) at moderate or vigorous intensity (60–90% VO2peak) stimulates an increase in the circulating levels of hepcidin between 0 h and 6 h after the end of the exercise bout, peaking at ~3 h post-exercise. The magnitude of the response of hepcidin to exercise seems to be dependent on the pre-exercise status of iron (ferritin) and inflammation (IL-6). Moreover, oxygen disturbances and the activation of a hypoxia-induced factor during or after exercise may stimulate a reduction of hepcidin expression. Meanwhile, cranberry flavonoids supplementation promotes an anti-oxidant effect that may facilitate the post-exercise expression of hepcidin. Further studies are required to explore the effect of resistance exercise on hepcidin expression.

The Effect of Vitamin D3 Supplementation on Hepcidin, Iron, and IL-6 Responses after a 100 km Ultra-Marathon

“…Generally, physical exercises induce an increase in serum hepcidin concentrations during the early recovery phase [17]. In our study, the post-exercise hepcidin results (post) are consistent with earlier studies reporting significant changes in marathon runners [47].…”

“…During and after a 100 km run the regulation of hepcidin and iron metabolism can be controlled with two opposite metabolic pathways: first, the occurrence of inflammation and an increased IL-6 serum concentration which can induce hepcidin synthesis; and second, elevated erythropoiesis activity, which can suppress the elevation of this hormone in serum [15,16]. Thus, although IL-6 is an undoubted co-operator to the post-exercise hepcidin response, it seems that there are additional factors that cooperate during prolonged exercise to achieve the adequate level of this hormone [17].…”

Beneficial Effect of Ubiquinol on Hematological and Inflammatory Signaling during Exercise

“…Regular physical exercise is associated with numerous health benefits including a lower risk of all-cause mortality [37,38], nevertheless, strenuous exercise specially in amateur athletes, promotes the generation of oxidative stress and a pro-inflammatory state, which are one of the main reasons for the muscular aggression observed in high intensity exercise, together with other physiological alterations such as sports anemia [12], characterized by hematological changes including decrease in RBC, hemoglobin, and hematocrit [12,13,15]. These changes reduce oxygen supply and energy production which could regulate the aerobic performance capacity [17], which could lead to a reduction in the physical performance, incorrect adaptation to training protocols, and other possible physiological alterations [12].…”

Partial sleep deprivation after an acute exercise session does not augment hepcidin levels the following day

“…However, attention to hepcidin (an iron regulating hormone) has been growing as a key factor contributing to iron deficiency in endurance athletes (Badenhorst et al., 2016; Peeling et al., 2017). Sufficient evidence has revealed that various types of exercise increase the serum hepcidin level during the postexercise period (Badenhorst et al., 2015a; Domínguez et al., 2018; Goto, Kasai, Kojima, & Ishibashi, 2018; Goto, Sumi, Kojima, & Ishibashi, 2017; Peeling et al., 2017). Moreover, the increase in postexercise hepcidin level has been attributed to exercise‐induced increases in interleukin (IL)‐6 in iron sufficient individuals (Badenhorst et al., 2015a, 2015b; Peeling, 2010).…”