Journal
FREE RADICAL RESEARCH
Volume 48, Issue 1, Pages 30-42Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/10715762.2013.825043
Keywords
exercise; antioxidant; redox signaling; reactive oxygen species; xanthine dehydrogenase/xanthine oxidase
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Funding
- Ministerio de Educacion y Ciencia [DEP2009-11638, DEP2010-21866]
- Ministerio de Educacion y Ciencia (FEDER)
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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 AMPK alpha 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, AMPK alpha 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.
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