Both acute hypoxia and physical exercise are known to increase oxidative stress. This randomized prospective trial investigated whether the addition of moderate exercise can alter oxidative stress induced by continuous hypoxic exposure.
Fourteen male participants were confined to 10-d continuous normobaric hypoxia (FIO2 = 0.139 ± 0.003, PIO2 = 88.2 ± 0.6 mm Hg, ∼4000-m simulated altitude) either with (HCE, n = 8, two training sessions per day at 50% of hypoxic maximal aerobic power) or without exercise (HCS, n = 6). Plasma levels of oxidative stress markers (advanced oxidation protein products [AOPP], nitrotyrosine, and malondialdehyde), antioxidant markers (ferric-reducing antioxidant power, superoxide dismutase, glutathione peroxidase, and catalase), nitric oxide end-products, and erythropoietin were measured before the exposure (Pre), after the first 24 h of exposure (D1), after the exposure (Post) and after the 24-h reoxygenation (Post + 1). In addition, graded exercise test in hypoxia was performed before and after the protocol.
Maximal aerobic power increased after the protocol in HCE only (+6.8%, P < 0.05). Compared with baseline, AOPP was higher at Post + 1 (+28%, P < 0.05) and nitrotyrosine at Post (+81%, P < 0.05) in HCS only. Superoxide dismutase (+30%, P < 0.05) and catalase (+53%, P < 0.05) increased at Post in HCE only. Higher levels of ferric-reducing antioxidant power (+41%, P < 0.05) at Post and lower levels of AOPP (−47%, P < 0.01) at Post + 1 were measured in HCE versus HCS. Glutathione peroxidase (+31%, P < 0.01) increased in both groups at Post + 1. Similar erythropoietin kinetics was noted in both groups with an increase at D1 (+143%, P < 0.01), a return to baseline at Post, and a decrease at Post + 1 (−56%, P < 0.05).
These data provide evidence that 2 h of moderate daily exercise training can attenuate the oxidative stress induced by continuous hypoxic exposure.
1Department of Automation, Biocybernetics and Robotics, “Jozef Stefan” Institute, Ljubljana, SLOVENIA; 2Center of Research and Innovation on Sports, University Claude Bernard Lyon 1, Villeurbanne, FRANCE; 3Department of Environmental Physiology, School of Technology and Health, Royal Institute of Technology, Stockholm, SWEDEN; and 4Faculty of Biology and Medicine, ISSUL, Institute of Sport Sciences, University of Lausanne, Lausanne, SWITZERLAND
Address for correspondence: Tadej Debevec, Ph.D., Department of Automation, Biocybernetics and Robotics, Jozef Stefan Institute, Jamova 39, 1000, Ljubljana, Slovenia; E-mail: email@example.com.
Submitted for publication April 2013.
Accepted for publication June 2013.