Live high,train low – influence on resting and post‐exercise hepcidin levels |
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| Authors: | A. D. Govus P. Peeling C. R. Abbiss N. G. Lawler D. W. Swinkels C. M. Laarakkers K. G. Thompson J. J. Peiffer C. J. Gore L. A. Garvican‐Lewis |
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| Affiliation: | 1. Institute for Sport & Physical Activity Research, University of Bedfordshire, Bedford, UK;2. School of Sport Science, Exercise & Health, University of Western Australia, Crawley, Western Australia, Australia;3. Centre for Exercise & Sports Science Research, School of Exercise and Health Science, Edith Cowan University, Joondalup, Western Australia, Australia;4. School of Psychology and Exercise Science, Murdoch University, Murdoch, Western Australia, Australia;5. Department of Laboratory Medicine (TML 830), Radboud University Medical Centre, Nijmegen, The Netherlands;6. Hepcidinanalysis.com, Radboudumc, Geert Grooteplein 10 (TML 830), Nijmegen, The Netherlands;7. Research Institute for Sport & Exercise, University of Canberra, Belconnen, Australian Capital Territory, Australia;8. Department of Physiology, Australian Institute of Sport, Bruce, Australian Capital Territory, Australia;9. Exercise Physiology Laboratory, Flinders University, Bedford Park, South Australia, Australia |
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| Abstract: | 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. |
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| Keywords: | Iron metabolism iron deficiency altitude training hypoxia |
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