Abstract

The purpose of the present study was to determine the influence of hypoxic exposure during prolonged endurance exercise sessions (79 min in total) on post-exercise hepcidin levels in trained male endurance athletes. Ten endurance athletes (mean ± standard deviation; height: 169.8 ± 7.1 cm, weight: 57.1 ± 5.0 kg) conducted two endurance exercise sessions under either a normobaric hypoxic condition [inspired O2 fraction (FiO2) = 14.5%] or a normoxic condition (FiO2 = 20.9%). Exercise consisted of 10 × 3 min running on a treadmill at 95% of maximal oxygen uptake () with 60s of active rest at 60% of . After 10 min of rest, they subsequently performed 30 min of continuous running at 85% of . Running velocities were significantly lower in the HYPO than in the NOR (P < 0.0001). Exercise-induced blood lactate elevation was significantly greater in the HYPO (P < 0.01). There were significant increases in plasma interleukin-6, serum iron, and blood glucose levels after exercise, with no significant difference between the trials [interaction (trial × time) or main effect for trial, P > 0.05]. Serum hepcidin levels increased significantly 120 min after exercise (HYPO: from 10.7 ± 9.4 ng/mL to 15.8 ± 11.2 ng/mL; NOR: from 7.9 ± 4.7 ng/mL to 13.2 ± 7.9 ng/mL, P < 0.05), and no difference was observed between the trials. In conclusion, endurance exercise at lower running velocity in hypoxic conditions resulted in similar post-exercise hepcidin elevations as higher running velocity in normoxic conditions.

Highlights

  • Iron deficiency is a frequent diagnosis among athletes, endurance athletes[1,2,3,4]

  • Exercise-induced hepcidin responses were similar for the HYPO and the NOR trials [interaction or main effect for trials (P > 0.05, effect sizes (ES) = 0.05), with no significant difference between the trials

  • Considering that exercise-induced hepcidin elevation was successfully impaired by hypoxic exposure for 3h post-exercise[34], recovering under hypoxic conditions could contribute to maintaining appropriate iron levels by reducing hepcidin production

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Summary

Introduction

Iron deficiency is a frequent diagnosis among athletes, endurance athletes[1,2,3,4]. The prevalence of iron deficiency in females competing in various sports was reported to range from 25% to 36%[5,6]. Hepcidin regulates iron metabolism [18] by degrading ferroportin (iron export protein) transport channels in the intestine and on the surfaces of macrophages[19,20].

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