Abstract

This chapter discusses oxidative stress and the pathogenesis of sarcopenia. Sarcopenia, an important contributor to senile physical frailty, is characterized by age-dependent changes in muscle mass, fiber-type composition, and innervation. The chapter also discusses changes in skeletal muscle functions, metabolic capacity, and morphological changes in skeletal muscle with aging. Changes in muscle function—such as decreased strength and endurance and metabolic capacity—also occur in skeletal muscle with aging. Hypothesized causes of sarcopenia include denervation-reinnervation, contraction-induced injury, satellite cell changes, and oxidative stress/damage. Oxidative stress of mitochondrial origin may contribute to the age-dependent development of sarcopenia in a focal way. Understanding the mechanism by which caloric restriction (CR) attenuates the development of sarcopenia may result in effective clinical therapy. Sarcopenia universally afflicts older people and causes physical frailty. Studies designed to elucidate the etiology and pathogenesis of sarcopenia will provide insights into preventive strategies and therapies. Recent advances in stem-cell biology are worthy of vigorous pursuit. These lines of research will eventually produce sarcopenia-specific interventions that will contribute to an increased span of robust health for humans.

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