Int J Sports Med 2017; 38(08): 588-596
DOI: 10.1055/s-0043-106740
Physiology & Biochemistry
© Georg Thieme Verlag KG Stuttgart · New York

Endurance Exercise in Hypoxia, Hyperoxia and Normoxia: Mitochondrial and Global Adaptations

Axel Przyklenk
1   Institute of Cardiology and Sports Medicine – Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Cologne, Germany
,
Boris Gutmann
2   Institute of Movement and Neuroscience, German Sport University Cologne, Cologne, Germany
,
Thorsten Schiffer
3   Outpatient Clinic for Sports Traumatology and Public Health Consultation, German Sport University Cologne, Cologne, Germany
,
Wildor Hollmann
4   Institute of Cardiology and Sports Medicine, German Sport University Cologne, Cologne, Germany
,
Heiko K. Strueder
2   Institute of Movement and Neuroscience, German Sport University Cologne, Cologne, Germany
,
Wilhelm Bloch
1   Institute of Cardiology and Sports Medicine – Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Cologne, Germany
,
Andreas Mierau
2   Institute of Movement and Neuroscience, German Sport University Cologne, Cologne, Germany
,
Sebastian Gehlert
1   Institute of Cardiology and Sports Medicine – Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Cologne, Germany
› Author Affiliations
Further Information

Publication History



accepted 07 March 2017

Publication Date:
02 June 2017 (online)

Abstract

We hypothesized short-term endurance exercise (EN) in hypoxia (HY) to exert decreased mitochondrial adaptation, peak oxygen consumption (VO2peak) and peak power output (PPO) compared to EN in normoxia (NOR) and hyperoxia (PER). 11 male subjects performed repeated unipedal cycling EN in HY, PER, and NOR over 4 weeks in a cross-over design. VO2peak, PPO, rate of perceived exertion (RPE) and blood lactate (Bla) were determined pre- and post-intervention to assess physiological demands and adaptation. Skeletal muscle biopsies were collected to determine molecular mitochondrial signaling and adaptation. Despite reduced exercise intensity (P<0.05), increased Bla and RPE levels in HY revealed higher metabolic load compared to PER (P<0.05) and NOR (n.s.). PPO increased in all groups (P<0.05) while VO2peak and mitochondrial signaling were unchanged (P>0.05). Electron transport chain complexes tended to increase in all groups with the highest increase in HY (n.s.). EN-induced mitochondrial adaptability and exercise capacity neither decreased significantly in HY nor increased in PER compared to NOR. Despite decreased exercise intensity, short term EN under HY may not necessarily impair mitochondrial adaptation and exercise capacity while PER does not augment adaptation. HY might strengthen adaptive responses under circumstances when absolute training intensity has to be reduced.

 
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