Govus, A. D, Peeling, P., Abbiss, C. R, Lawler, N. G, Swinkels, D. W, Laarakkers, C. M, Thompson, K. G, Peiffer, J. J, Gore, C. J & Garvican-Lewis, LA. (2017). Live high, train low – influence on resting and post-exercise hepcidin levels. Scandinavian Journal of Medicine and Science in Sports,27(7), S. Harridge. 704-713. Denmark: Wiley-Blackwell Publishing Ltd.. Retrieved from https://doi.org/10.1111/sms.12685
The post‐exercise hepcidin response during prolonged ( > 2 weeks) hypoxic exposure is not well understood. We compared plasma hepcidin levels 3 h after exercise [6 × 1000 m at 90% of maximal aerobic running velocity (vVO2max)] performed in normoxia and normobaric hypoxia (3000 m simulate altitude) 1 week before, and during 14 days of normobaric hypoxia [196.2 ± 25.6 h (median: 200.8 h; range: 154.3–234.8 h) at 3000 m simulated altitude] in 10 well‐trained distance runners (six males, four females). Venous blood was also analyzed for hepcidin after 2 days of normobaric hypoxia. Hemoglobin mass (Hbmass) was measured via CO rebreathing 1 week before and after 14 days of hypoxia. Hepcidin was suppressed after 2 (Cohen's d = −2.3, 95% confidence interval: [−2.9, −1.6]) and 14 days of normobaric hypoxia (d = −1.6 [−2.6, −0.6]). Hepcidin increased from baseline, 3 h post‐exercise in normoxia (d = 0.8 [0.2, 1.3]) and hypoxia (d = 0.6 [0.3, 1.0]), both before and after exposure (normoxia: d = 0.7 [0.3, 1.2]; hypoxia: d = 1.3 [0.4, 2.3]). In conclusion, 2 weeks of normobaric hypoxia suppressed resting hepcidin levels, but did not alter the post‐exercise response in either normoxia or hypoxia, compared with the pre‐exposure response.
Mary MacKillop Institute for Health Research