The normal skeletal muscle consists of multinucleated cells called fibers. Each muscle fiber is an elongated cell surrounded by a plasma membrane called the sarco-lemma. Fibers contain myofilaments, contractile proteins that are responsible for muscle contractions. These fibers are grouped in fascicles and surrounded by connective tissue, the perimysium (Bossen, 2000). Skeletal muscles are connected to bone by tendons at each end.
One of the most obvious effects of aging is a decline in muscle strength that is largely related to a loss of muscle mass (sarcopenia). After skeletal maturation the total muscle mass declines at an average of 4% per decade until the age of 50 years. In older individuals the rate of loss increases up to 10% per decade (Buckwalter et al., 1993). Local injury and damage to the innervation of muscle fibers occurs throughout life, but in old age the process of collateral sprouting of the neurons appears to become less effective in repairing innervation, and muscle fibers are lost (Campbell et al., 1973; Lexell et al., 1988).
Normal skeletal muscle has the ability of repair and regeneration following local injury of muscle fibers. This process is thought to be critically dependent on the activation of so-called satellite cells, usually quiescent cells detected outside the sarcolemma but within the basal lamina. Satellite cells, first described in 1961 (Mauro, 1961), are now seen as ''spare parts'' for postnatal muscle growth and repair.
The recruitment of the satellite cells is governed by a splice variant of the insulin-like growth factor (IGF)-I, termed mechano growth factor (MGF), which is expressed in response to mechanical stimulation (McKoy et al., 1999; Yang et al., 1996). In an animal model, electrical stimuli led to an increase in muscle mass as well as a concomitant upregulation of MGF mRNA compared to resting control muscles (Goldspink et al., 1992).
The aging organism is much less able to increase MGF levels after high resistance exercise, as compared to muscles of younger individuals (Hameed et al., 2003). Additionally, satellite cell functionality can be decreased by an abnormal accumulation of reactive oxygen species due to a drastic reduction of antioxidant activity in aged satellite cells (Fulle et al., 2005; Short et al., 2005a). This decrease in the antioxidative capacity may cause destabilizing oxidative damage to aging satellite cells, limiting their ability to repair muscle.
Another important factor in the aging process of the skeletal muscle is a decline in mitochondrial function, since the required energy for proper muscle function is generated in mitochondria, which contain their own DNA, called mitochondrial mtDNA (Clayton, 1992). mtDNA abundance and mitochondrial ATP production have been demonstrated to decline with advancing age. The content of several mitochondrial proteins was reduced in older muscles, whereas the level of the oxidative DNA lesion was increased, supporting the oxidative damage theory of aging (Short et al., 2005a).
In contrast, it has been reported that mitochondrial capacities were related to physical activity, but not to age. The mitochondrial theory of aging, which attributes the age-related decline of muscle performance to decreased mitochondrial function, was questioned by these authors (Rasmussen et al., 2003).
Other age-related changes of the skeletal muscle include changes in myosin heavy chain mRNA and protein expression (Short et al., 2005b), myosin heavy chain composition of muscle spindles (Liu et al., 2005), or alterations in the maximal O2 uptake rate (Conley et al., 2000).
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