Maintaining mobility is a critical element for the quality of life. Skeletal muscle, the primary organ for locomotion, undergoes age-associated deterioration in size, structure, and function. Recent research suggests that oxidative stress is an important etiology for sarcopenia. The level of oxidative stress imposed on aging muscle is influenced by two fundamental biological processes: the increased generation of reactive oxygen species (ROS) and age-associated changes in antioxidant defense. It appears that despite increased ROS production, aging muscle has a decreased gene expression of antioxidant enzymes possibly due to a diminished ability for cell signaling. A major benefit of nonexhaustive exercise is to induce a mild oxidative stress that stimulates the expression of certain antioxidant enzymes. This is mediated by the activation of redox-sensitive signaling pathways. For example, gene expression of muscle mitochondrial (Mn) superoxide dismutase is enhanced after an acute bout of exercise preceded by an elevated level of NF-kappaB and AP-1 binding. An increase in de novo protein synthesis of an antioxidant enzyme usually requires repeated bouts of exercise. Aging does not abolish but seems to attenuate training adaptations of antioxidant enzymes. Thus, for senescent muscle, training should be assisted with supplementation of exogenous antioxidants to research the optimal level of defense.