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Free Radic Res. 2014 Jan;48(1):30-42. doi: 10.3109/10715762.2013.825043. Epub 2013 Oct 7.

Free radicals and sprint exercise in humans.

Author information

1
Department of Physical Education, University of Las Palmas de Gran Canaria, Campus Universitario de Tafira s/n , Las Palmas de Gran Canaria, Canary Island , Spain.

Abstract

Sprint exercise ability has been critical for survival. The remarkably high-power output levels attained during sprint exercise are achieved through strong activation of anaerobic, and to a lesser extent, aerobic energy supplying metabolic reactions, which generate reactive oxygen and nitrogen species (RONS). Sprint exercise may cause oxidative stress leading to muscle damage, particularly when performed in severe acute hypoxia. However, with training oxidative stress is reduced. Paradoxically, total plasma antioxidant capacity increases during the subsequent 2 h after a short sprint due to the increase in plasma urate concentration. The RONS produced during and immediately after sprint exercise play a capital role in signaling the adaptive response to sprint. Antioxidant supplementation blunts the normal AMPKα and CaMKII phosphorylation in response to sprint exercise. However, under conditions of increased glycolytic energy turnover and muscle acidification, as during sprint exercise in severe acute hypoxia, AMPKα phosphorylation is also blunted. This indicates that an optimal level of RONS-mediated stimulation is required for the normal signaling response to sprint exercise. Although RONS are implicated in fatigue, most studies convey that antioxidants do not enhance sprint performance in humans. Although currently controversial, it has been reported that antioxidant ingestion during training may jeopardize some of the beneficial adaptations to sprint training.

PMID:
23879691
DOI:
10.3109/10715762.2013.825043
[Indexed for MEDLINE]

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