Sarcopenia

Sarcopenia is the degenerative loss of skeletal muscle mass (0.5–1% loss per year after the age of 50), quality, and strength associated with aging. Sarcopenia is a component of the frailty syndrome. It is often a component of cachexia. It can also exist independently of cachexia; whereas cachexia includes malaise and is secondary to an underlying pathosis (such as cancer), sarcopenia may occur in healthy people and does not necessarily include malaise. The term is from Greek σάρξ sarx, 'flesh' and πενία penia, 'poverty'. Sarcopenia is characterized first by a muscle atrophy (a decrease in the size of the muscle), along with a reduction in muscle tissue quality, characterized by such factors as replacement of muscle fibres with fat, an increase in fibrosis, changes in muscle metabolism, oxidative stress, and degeneration of the neuromuscular junction and leading to progressive loss of muscle function and frailty. Sarcopenia is determined by two factors: initial amount of muscle mass and rate at which aging decreases muscle mass. Due to the loss of independence associated with loss of muscle strength, the threshold at which muscle wasting becomes a disease is different pathologically from person to person. Simple circumference measurement does not provide enough data to determine whether or not an individual is suffering from severe sarcopenia. Sarcopenia is also marked by a decrease in the circumference of distinct types of muscle fibers. Skeletal muscle has different fiber-types, which are characterized by expression of distinct myosin variants. During sarcopenia, there is a decrease in 'type 2' fiber circumference (Type II), with little to no decrease in 'type I' fiber circumference (Type I), and deinervated type 2 fibers are often converted to type 1 fibers by reinnervation by slow type 1 fiber motor nerves. Satellite cells are small mononuclear cells that abut the muscle fiber. Satellite cells are normally activated upon injury or exercise. These cells then differentiate and fuse into the muscle fiber, helping to maintain its function. One theory is that sarcopenia is in part caused by a failure in satellite cell activation. Extreme muscle loss is often a result of both diminishing anabolic signals, such as growth hormone and testosterone, and promotion of catabolic signals, such as pro-inflammatory cytokines. Oxidized proteins increase in skeletal muscle with age and leads to a buildup of lipofuscin and cross-linked proteins that are normally removed via the proteolysis system. These proteins compile in the skeletal muscle tissue, but are dysfunctional. This leads to an accumulation of non-contractile material in the skeletal muscle. This helps explain why muscle strength decreases severely, as well as muscle mass, in sarcopenia. One group has suggested that the evolutionary basis for the failure of the body to maintain muscle mass and function with age is that the genes governing these traits were selected in a Late Paleolithic environment in which there was a very high level of obligatory muscular effort, and that these genetic parameters are therefore ill-matched to a modern lifestyle characterized by high levels of lifelong sedentary behavior. Epidemiological research into the developmental origins of health and disease has shown that early environmental influences on growth and development may have long-term consequences for human health. Low birth weight, a marker of a poor early environment, is associated with reduced muscle mass and strength in adult life. One study has shown that lower birth weight is associated with a significant decrease in muscle fibre score, suggesting that developmental influences on muscle morphology may explain the widely reported associations between lower birth weight and sarcopenia.