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Updated: May 31, 2025

Supramaximal Intensity Hypoxic Exercise and Vascular Function Assessment in Mice
Published on: March 15, 2019
Effect of repeated sprint training in hypoxia on acute and chronic redox balance modulation
M Chambion-Diaz1,2, R Faiss3, V Pialoux1,4
1LIBM, Team Atherosclerosis, Thrombosis and Physical Activity, University Claude Bernard Lyon 1, Univ Lyon, Lyon, France.
Abstract:
Little is known regarding the effects high-intensity training performed in hypoxia on the oxidative stress and antioxidant systems. The aim of this study was to assess the potential effect of 4 weeks of repeated sprint training in hypoxia (RSH) on the redox balance. Forty male well-trained cyclists were matched into two different interventions (RSH, n = 20) or in normoxia, RSN, n = 20) and tested twice (before (Pre-) and after (Post-) a 4-week of training) for performance (repeated sprint ability (RSA) test), oxidative stress, and antioxidant status. Antioxidant enzyme activity (Superoxide Dismutase, Glutathione Peroxidase, and catalase), NO metabolites (NOx: nitrites and nitrates), ferric reducing antioxidant power, Malondialdehyde (MDA), nitrotyrosine, and carbonyls were measured in plasma. At Post-, MDA, and carbonyls increased (p < 0.05) in the RSN group both at rest (+90.6%) and also acutely in response to RSA (+22.9%); but not in RSH. At Post-, in the RSH group, catalase increased (p < 0.05) both at rest (+44.7%) and in response to the RSA test (+66.3%). At Post-, SOD, and nitrotyrosine decreased after RSA and at rest, regardless of the group (p = 0.0012 and p = 0.0413, respectively). At Post-, NOx decreased after the RSA test, regardless of the group (p < 0.05). In conclusion, several weeks of RSH training limits the increase in oxidative stress markers both at rest and in response to RSA test. Moreover, such training downregulated SOD activity, possibly due to an overproduction of reactive oxygen species. These findings could constitute a paradigm shift with a better enzymatic adaptation after RSH concomitant with a distinct reactive oxygen species (ROS) production between RSH and RSN.
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