Cellular Degradation Machineries in Age-Related Loss of Muscle Mass (Sarcopenia)

One of the most characteristic features of the aged is a change in body composition and human cross-sectional and longitudinal studies consistently demonstrate gain in fat mass and decline in lean mass (Attaix et al., 2005). Skeletal muscle mass is gradually reduced through both atrophy and loss of myofibers, and along with this connective tissue and intramyocellular lipids increase (Fig. 1) (St-Onge, 2005). Although sarcopenia is widely recognized it remains poorly understood and has not received appropriate attention until quite recently. Sarcopenia is often assumed to have a multi-factorial background (Adamo and Farrar, 2006; Attaix et al., 2005; Paddon-Jones and Rasmussen, 2009; Roth et al., 2006; Solomon and Bouloux, 2006). A sedentary life-style combined with periods of prolonged bed-rest during illnesses has well-established detrimental effects on muscle mass and function (Janssen et al., 2002). Skeletal muscles do not only generate the power to let us move but collectively they are a highly significant component of the systemic metabolic homeostasis machinery. The progressive loss of muscle mass with advancing age is evident in both the ‘healthy’ aging population and specialist patient populations. The reduced functional muscle mass is associated with increased morbidity, frailty and reduced quality of life (Baumgartner et al., 1998a). The prevalence of sarcopenia increases with about 5% per year and typically begins in the fourth decade of life (Baumgartner et al., 1998b). After the age of 50 years 1-2 % of the muscle mass is lost annually. Individuals with clinically manifest sarcopenia have 4 times greater risk of disability, three times greater risk of balance impairment, and 3 times greater risk of falling (Baumgartner et al., 1998b). Sarcopenia is the single most common etiology to falls and fall-associated fractures in elderly.