Satellite cells play an integral role in normal development of skeletal muscle by providing a source for postmitotic myonuclei and in repair of injured myofibers by serving as the source of myoblasts that participate in the regeneration response. The population of satellite cells in a muscle undergoes an ordered change both in relative and absolute numbers over the course of the postnatal growth period. Quantitative studies have shown that the changes are not the same among muscles or even among the individual myofibers within a muscle. In general, oxidative muscles have a much higher density of satellite cells than do glycolytic muscles. Although the exact reasons for the differences in the population densities are unknown, differences in the growth patterns of muscles or in their activity levels may be related factors. These differences point to the fact that the mechanisms that regulate satellite cell mitotic and fusion behavior are also not the same in all muscles. The activity state of muscle is an important factor in the regulation of satellite cell behavior. Increased functional demand that induces a hypertrophic response results in increased satellite cell mitotic activity, and decreased activity that results in atrophy results in decreased mitotic activity. Finally, elevated satellite cell mitotic activity can be a sensitive indicator of muscle damage, especially when the damage is minimal and difficult to detect by morphological means.