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RESEARCH PRODUCT

Exercise as a Model to Study Oxidative Stress

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Physical exercise generates free radicals. The major source of radicals in exercise appears to be extracellular. Our experiments show that xanthine oxidase is a key player in the generation of superoxide during exercise. Mitochondrial contribution appears to be less important: during high oxygen utilization by mitochondria in state 3, the proportion of oxygen that is converted to superoxide is on an order of magnitude lower than in resting, state 4 conditions. Exercise-induced radicals constitute a double-edged sword: high intensity ­exercise causes the generation of relatively high concentrations of radicals that cause oxidative stress and eventually damage. On the other hand, low intensity training activates the expression of antioxidant genes and other cell adaptations to exercise. This has practical implications: antioxidant supplements are useful after exhaustive exercise (which causes damage) but should not be used in training (because oxidant-dependent adaptations are prevented). Thus, exercise is an excellent physiological model to understand oxidative stress and subsequent cellular adaptations to such stress.