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Role of free Radicals

Excesive Exercise

Oxidative stress and subsequent damage to cellular proteins, lipids, and nucleic acids, as well as changes to the glutathione system, are well documented in response to aerobic exercise. However, far less information is available on anaerobic exercise-induced oxidative modifications. Recent evidence indicates that high intensity anaerobic work does result in oxidative modification to the above-mentioned macromolecules in both skeletal muscle and blood. Also, it appears that chronic anaerobic exercise training can induce adaptations that act to attenuate the exercise-induced oxidative stress. These may be specific to increased antioxidant defenses and/or may act to reduce the generation of pro-oxidants during and after exercise. However, a wide variety of exercise protocols and assay procedures have been used to study oxidative stress pertaining to anaerobic work. Therefore, precise conclusions about the exact extent and location of oxidative macromolecule damage, in addition to the adaptations resulting from chronic anaerobic exercise training, are difficult to indicate. Fortunately, regular endurance exercise results in adaptations in the skeletal muscle antioxidant capacity, which protects myocytes against the deleterious effects of oxidants and prevents extensive cellular damage. The effects of chronic exercise on the up-regulation of both antioxidant enzymes and the glutathione antioxidant defense system have also been discussed. Primary antioxidant enzymes superoxide dismutase, glutathione peroxidase, and catalase will be discussed as well as glutathione, which is an important nonenzymatic antioxidant. Growing evidence indicates that exercise training results in an elevation in the activities of both superoxide dismutase and glutathione peroxidase along with increased cellular concentrations of glutathione in skeletal muscles. It seems plausible that increased cellular concentrations of these antioxidants will reduce the risk of cellular injury, improve performance, and delay muscle fatigue. A major vascular adaptation to exercise training is increased expression of the endothelial cell nitric oxide synthase. This has been demonstrated in dogs, mice, rats, and pigs. Furthermore, chronic exercise training in humans enhances endothelium-dependent vasodilatation and increases plasma levels of nitrate and nitrite, the oxidation products of NO. This phenomenon seems to have therapeutic implications, in that exercise training increases endothelium-dependent vasodilatation in humans with heart failure. Because endothelial production of NO has numerous antiatherosclerotic properties, including inhibition of adhesion molecule expression, prevention of platelet aggregation, and inhibition of vascular smooth muscle proliferation, increased eNOS expression in response to exercise may explain in part the beneficial effects of exercise in preventing cardiovascular disease.

References

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