Abstract
This study explored the relationship between serum ferritin and hepcidin in athletes. Baseline serum ferritin levels of 54 athletes from the control trial of five investigations conducted in our laboratory were considered; athletes were grouped according to values <30 μg/L (SF<30), 30–50 μg/L (SF30–50), 50–100 μg/L (SF50–100), or >100 μg/L (SF>100). Data pooling resulted in each athlete completing one of five running sessions: (1) 8×3 min at 85% vVO2peak; (2) 5×4 min at 90% vVO2peak; (3) 90 min continuous at 75% vVO2peak; (4) 40 min continuous at 75% vVO2peak; (5) 40 min continuous at 65% vVO2peak. Athletes from each running session were represented amongst all four groups; hence, the mean exercise duration and intensity were not different (p>0.05). Venous blood samples were collected pre-, post- and 3 h post-exercise, and were analysed for serum ferritin, iron, interleukin-6 (IL-6) and hepcidin-25. Baseline and post-exercise serum ferritin levels were different between groups (p<0.05). There were no group differences for pre- or post-exercise serum iron or IL-6 (p>0.05). Post-exercise IL-6 was significantly elevated compared to baseline within each group (p<0.05). Pre- and 3 h post-exercise hepcidin-25 was sequentially greater as the groups baseline serum ferritin levels increased (p<0.05). However, post-exercise hepcidin levels were only significantly elevated in three groups (SF30–50, SF50–100, and SF>100; p<0.05). An athlete's iron stores may dictate the baseline hepcidin levels and the magnitude of post-exercise hepcidin response. Low iron stores suppressed post-exercise hepcidin, seemingly overriding any inflammatory-driven increases.
Highlights
The mechanisms relating to iron deficiency in athletes has been increasingly investigated, with a shift in focus from the more traditionally accepted avenues of exercise-induced iron loss such as hemolysis, sweating and gastrointestinal bleeding, to the influence of the iron regulatory hormone known as hepcidin [2,3,4]
No doubt, such timing is synonymous with that at which an athlete may be consuming meals that contain the majority of their dietary iron intake, and as such, it has been suggested that elevated post-exercise hepcidin levels may contribute to the high number of athletes commonly diagnosed with iron deficiency [11]
Significant between group differences were evident for baseline (p = 0.01) and post-exercise (p = 0.01) serum ferritin levels; there were no between group differences for serum iron levels at either time point (p = 0.82 and p = 0.71, respectively)
Summary
The mechanisms relating to iron deficiency in athletes has been increasingly investigated, with a shift in focus from the more traditionally accepted avenues of exercise-induced iron loss such as hemolysis, sweating and gastrointestinal bleeding (for review see [1]), to the influence of the iron regulatory hormone known as hepcidin [2,3,4]. Research investigating the time-course of exerciseinduced hepcidin response shows that the levels of this hormone seem to peak some 3–6 h subsequent to the peak in IL-6 elevation after an exercise bout [3]. No doubt, such timing is synonymous with that at which an athlete may be consuming meals that contain the majority of their dietary iron intake, and as such, it has been suggested that elevated post-exercise hepcidin levels may contribute to the high number of athletes commonly diagnosed with iron deficiency [11]
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