Aging is associated with a progressive decline in skeletal muscle mass and function (sarocopenia). Despite several years of research, controversy exists regarding the manifestations and causes of sarcopenia. In the former respect, whereas a preferential loss of so-called "fast-twitch" muscle fibers occurs in rat models of aging, this appears unlikely in human skeletal muscle. In the latter respect, whereas a decline in physical activity with aging contributes to whole-muscle atrophy, it cannot explain the marked heterogeneity in muscle fiber size seen in aged muscles. Similarly, systemic alterations, such as reduced blood levels of anabolic hormones and nutritional deficits, although involved in modulating the degree of whole-muscle atrophy, cannot explain the observation that only some fibers atrophy and die while most appear unaffected. A further significant question remaining is that if death of some muscle fibers is normal and perhaps advantageous (that is, by removing malfunctioning cells), what is the capacity for muscle fiber regeneration in adult skeletal muscle and can this process be augmented in aging muscles?