The trace element iron plays a number of crucial physiological roles within the body. Despite its importance, iron deficiency remains a common problem among athletes. As an individual's iron stores become depleted, it can affect their well-being and athletic capacity. Recently, altered iron metabolism in athletes has been attributed to postexercise increases in the iron regulatory hormone hepcidin, which has been reported to be upregulated by exercise-induced increases in the inflammatory cytokine interleukin-6. As such, when hepcidin levels are elevated, iron absorption and recycling may be compromised. To date, however, most studies have explored the acute postexercise hepcidin response, with limited research seeking to minimize/attenuate these increases. This review summarizes the current knowledge regarding the postexercise hepcidin response under a variety of exercise scenarios and highlights potential areas for future research-such as: a) the use of hormones though the female oral contraceptive pill to manipulate the postexercise hepcidin response, b) comparing the use of different exercise modes (e.g., cycling vs. running) on hepcidin regulation.
OBJECTIVES: The post-exercise interleukin-6 (IL-6) and hepcidin response was investigated during the hormone-deplete and hormone-replete phases of an estradiol and progestogen regulated oral contraceptive cycle (OCC). DESIGN: Counterbalanced, repeated measures cross-over study. METHODS: Ten active female monophasic oral contraceptive pill (OCP) users completed two 40 min treadmill running trials at 75% of their pre-determined peak oxygen uptake velocity (vVO2peak). These trials were randomly performed in two specific phases of the OCC: (a) Day 2-4, representing a hormone-free withdrawal period (D-0); (b) Day 12-14, representing the end of the first week of active hormone therapy (D+7). Venous blood samples were drawn pre-, post- and 3h post-exercise. RESULTS: In both trials, serum IL-6 was significantly elevated (p<0.05) immediately post-exercise, while serum hepcidin was significantly elevated (p<0.05) 3h post-exercise, with no significant differences recorded between trials. CONCLUSIONS: These findings suggest that exercise performed during the different phases (D-0 vs. D+7) of a monophasic OCP regulated cycle does not alter exercise induced IL-6 or hepcidin production. As such, future studies looking to investigate similar variables post-exercise, may not need to 'control' for different phases of the OCC, provided participants are current monophasic OCP users.