Abstract

Reactive oxygen species (ROS) play an important role as mediators of skeletal muscle damage and inflammation after strenuous exercise. These ROS arise largely from increases in mitochondrial oxygen consumption and electron transport flux. Bouts of intense exercise are associated with increases in lipid peroxidation, generating malondialdehyde and F(2alpha)-isoprostanes, and the release of muscle enzymes like lactate dehydrogenase and creatine kinase. Dietary and enzymatic antioxidant defenses appear to play a protective role in muscle cells by reducing associated oxidative damage to lipids, nucleic acids, and protein. However, studies of the use of dietary antioxidants like vitamin E to reduce exercise-induced muscle injury have met with mixed success. The equivocal nature of these results appear to reflect a diversity of factors including the antioxidant(s) tested, the nature and timing of the exercise, the age and fitness of the subjects, and the methodology for assessing oxidative stress.