Abstract

Oxidation produces reactive oxygen species (ROS), which cause peroxidation, enzyme inhibition and genetic damage in muscle cells. Genetic damage to cells and tissues caused by ROS facilitates aging. Therefore, the functional capacity of the antioxidant system against ROS is important to protect cells and tissues. The health benefits of regular exercise are well documented in a large number of reports. Moderate exercise can result in greater health benefits than vigorous exercise, because intense activity may be more susceptible to producing oxidative damage. Evidence would appear, as an indirect sign of muscle cell damage, such as an increase in lipid peroxidation, glutathione oxidation, and oxidative protein damage. During exercise, increased aerobic metabolism is a potential source of ROS in mitochondria. In muscle cells, mitochondria are one important source of reactive intermediates that include superoxides, hydrogen peroxide, and possibly hydroxyl radicals. Furthermore, a recent report suggested the occurrence of inter-mitochondrial complementation through exchange of genetic contents. This complementation could be a mitochondria-specific mechanism for avoiding expression of deletion-mutant mitochondria DNA from oxidative stress. Unfortunately, because research focusing on oxidative stress and antioxidants following exercise has up to now been narrow in scope, the mechanism linking oxidative stress and antioxidants in muscle tissue during exercise is not fully understood. Knowledge of the mechanism of ROS formation during exercise will be useful for health promotion for elderly as well as young exercise enthusiasts and may lead to the prevention of oxidative stress and damage associated with physical activity. This review paper provides a brief account of how exercise leads to oxidative stress and the link with antioxidants, and implys appropriate exercise regmen as prevention of oxidative stress for elderly individuals. Verf.-Referat