The loss of fast motor units and the concomitant loss of type II fibers result in loss in muscle power necessary for actions such as rising from a chair, climbing steps, or regaining posture after a perturbation Givinostat of balance. The extent of skeletal muscle power loss with age has been

confirmed by studies of cycle ergometry in which the cycle velocity at maximal power was measured. In a study of human volunteers ranging in age from 20 to 90 years, Kostka et al. found that velocity at maximal power decreased by roughly 18% between ages 20–29 and 50–59 and by a further 20% between 60–69 and 80–89 [15]. In addition to studies examining muscle power and contraction velocities, other studies have cross-sectionally examined age-related changes in strength, showing strength declines as great as 30–35% [16]. These alterations in strength have been linked primarily to declines in muscle mass as well as reductions in power per unit area and force per unit area, as nonmuscle tissue components replace lost muscle fiber [17]. Another morphologic aspect of aging skeletal muscle is the infiltration of muscle tissue components

by lipid, which can be contained within adipocytes as well as deposited within muscle fiber. The aging process is thought to result in increased frequency of adipocytes within muscle tissue. As with precursor cells in bone marrow, liver, and kidney, muscle satellite cells can express both adipocytic and a myocytic phenotypes, and recent studies have reported that expression of the adipocytic phenotype is increased with age [18–21]. This process PFT�� mouse is still relatively poorly understood in terms of its extent and spatial distribution. Another well-known source of adiposity in muscle tissue is through increased deposition of lipid within muscle fibers

[22–28]. This type of lipid distribution, often referred to as intramyocellular lipid, may result from net buildup of lipid due to reduced oxidative capacity of muscle fibers with aging [22, 29]. Neurologic underpinnings Suplatast tosilate of muscle atrophy The correct functioning of motor neurons is essential to the survival of muscle fibers. Age-related neurodegeneration may contribute importantly to the effects of age on muscle structure, including loss of muscle fibers, atrophy of muscle fibers, and increased clustering of muscle fibers as denervated fibers are Tariquidar recruited into viable motor units. Multiple levels of the nervous system are affected by age, including the motor cortex (beyond the scope of this review), the spinal cord, peripheral neurons, and the neuromuscular junction. Within the spinal cord, there is a substantial decline in the number of alpha motor neurons, and there may be a preferential loss in those motor neurons supplying fast motor units. Other reports have noted age-related losses in peripheral nerve fibers and alterations of their myelin sheaths.