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Epidemiological and objective studies report an association between sedentary time and lower risk of the metabolic syndrome (MetS) and its risk factors in young and middle-age adults. To date, there is a lack of objective data on the association between sedentary time and MetS among older adults.The association between objectively measured sedentary time (accelerometry) with MetS and MetS components was examined in a large sample of older adults with mobility limitations (N=1198; mean age=78.7 ± 5.3 years) enrolled in the Lifestyle Interventions and Independence for Elders (LIFE) study. Participants were divided into tertiles according to percentage of daily sedentary time, and the relation between sedentary time with MetS and MetS components was examined after adjusting for age, sex, ethnicity, and BMI.Participants in the highest sedentary time tertile had significantly higher odds of MetS (OR=1.54) (95% CI 1.13 to 2.11) in comparison with participants in the lowest tertile (p=0.03). Participants in the highest sedentary time tertile had larger waist circumference (p=0.0001) and lower HDL-C (p=0.0003) than participants in the lowest sedentary time tertile.Sedentary time was strongly related to higher odds of MetS. These results, based on objectively measured sedentary time, suggest that sedentary time may represent an important risk factor for the development of MetS in older adults with high likelihood for disability.

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.