Skeletal muscle is a highly plastic tissue that remarkably adapts to diverse stimuli including exercise, injury, disuse, and, as discussed here, aging. Humans achieve peak skeletal muscle mass and strength in mid-life and then experience a progressive decline of up to 50% by the ninth decade. The loss of muscle mass and function with aging is a phenomenon termed sarcopenia. It is evidenced by the loss and atrophy of muscle fibers and the concomitant accretion of fat and fibrous tissue. Sarcopenia has been recognized as a key driver of limitations in physical function and mobility, but is perhaps less appreciated for its role in age-related metabolic dysfunction and loss of organismal resilience. Similar to other tissues, muscle is prone to multiple forms of age-related molecular and cellular damage, including disrupted protein turnover, impaired regenerative capacity, cellular senescence, and mitochondrial dysfunction. The objective of this review is to highlight the clinical consequences of skeletal muscle aging, and provide insights into potential biological mechanisms. In light of population aging, strategies to improve muscle health in older adults promise to have a profound public health impact.
Keywords: Autophagy; Exercise; Mitochondria; Physical function; Sarcopenia; Senescence; Strength.
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