to the editor: Sarcopenia has been defined initially as the decrease of muscle mass and function during aging. As pointed out by Hepple et al. (2), this definition has been extended to muscle atrophy situations such as undernourishment or acute catabolic states (ACS) like sepsis and cancer. Sarcopenia is not the result of pathology and has been reported among healthy, well nourished, physically active elderly subjects (3). It is a slow process, taking place over decades, whereas muscle loss during ACS occurs in days or weeks. Sarcopenia in an individual can even result from the random succession of ACS because the capacity to recover muscle mass lost during ACS decreases with aging (1, 4). How can you explain that "sarcopenia" results from "sarcopenia" if you do not make the difference with the lifetime processes and the acute catabolic condition? One of the clearest experimental evidence that the loss of muscle mass with aging is explained by different mechanisms relatively to ACS is that in the fasting state, a clear decreased muscle protein synthesis rate has been rarely demonstrated in old individuals (5), whereas it is classically shown during ACS. The slow erosion of muscle mass during aging is partly explained by a lower sensitivity of muscle anabolism to meal intake (5). Thus the strategies to limit muscle loss during aging are probably not the same as during ACS due to the slow kinetics involved and differences in underlying mechanisms. In conclusion, we really think that the term "sarcopenia" should be limited to the age-related alteration of muscle mass and function.
