Interventions based on the possibility that oxidative stress contributes to sarcopenia

Skeletal muscle is a tissue which accounts for a large part of the body's total oxygen consumption at rest, due to its large mass and the majority of oxygen consumption during vigorous physical activity. Also, skeletal muscle and nervous tissues do not possess the very high repair capacities that occur in more mitotically active tissues. Accordingly, oxidative stress may accumulate with age in these tissues and contribute to the development of sarcopenia; however, this possibility has not been thoroughly investigated. Although long-term intervention studies which test the hypothesis that oxidative stress contributes to sarcopenia have not been conducted, recent findings using the caloric restriction (CR) paradigm for studying retarded aging processes indirectly support this concept. Several research directions appear important to pursue, including the measurement of free radical production in skeletal muscle at diverse ages, antioxidant supplementation as an intervention for retarding the development of sarcopenia, the use of genetically manipulated animal models, and determining the influence ofCR on oxidative stress in specific skeletal muscles and individual fibers and neurons therein. THE free radical theory of aging was first proposed byHarman (1956), and has generated much investigation. He hypothesized that aging results from macromolecular damage caused by free radicals generated as a result of normal metabolism. The initial emphasis was on membrane molecules. More recently, Harman (1983) and several oth-ers (e.g., Fleming et al., 1982; Bandy and Davison, 1990