Vertebrate muscles contain satellite cells that are quiescent myoblasts that have the ability to proliferate, differentiate, and fuse together to form new muscle fibers. The satellite cells are found between muscle fibers and its surrounding basal lamina (Carlson 1995). One theory of sarcopenia is that either the depletion or impairment of satellite cells with age produces the loss of muscle fibers once the remaining satellite cells are unable to repair normal muscle damage (Edstrom and Ulfhake, 2005). Animal studies support this theory as both declines in satellite cell number and replicative potential decline with aging. Interestingly, the slow-twitch type I muscle fibers, which are better preserved in aging muscle, have a greater number of satellite cells than the fast-twitch type II fibers (Carlson, 1995).
Although sarcopenia appears to be a universal phenomenon during aging, ultimately the importance is its impact on older people. Consequently, human studies have and will continue to play important roles in elucidating the consequences of sarcopenia on strength, functioning, and mortality. Additionally, these clinical studies have provided insights into the role nutrition, endocrine changes, lifestyle factors, and comorbid disease could play in the development of sarcopenia. These insights often have provided starting points for subsequent cell culture and animal experiments. Also, the characterization of the clinical effects of sarcopenia provides a framework to ultimately test the effects of treatments developed through human studies or model systems. As a result of the importance of human studies, we will begin with a review of methods used in patient-oriented sarcopenia research.
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