Exercise, aging, and muscle protein metabolism

Abstract

Age-associated alterations in muscle protein quantity and quality that adversely affect muscle structure, composition, and function have been referred to as sarcopenia. Muscle protein is metabolically active, and the age-associated loss of muscle protein mass is related to a loss of physical function and an inability to perform activities of daily living (physical frailty). It is important to maintain adequate reserves of muscle protein and amino acids as we age. As in all cachectic conditions, sarcopenia can be explained by an imbalance between the rates of muscle protein synthesis and muscle proteolysis, in which net muscle protein balance is negative. This review summarizes evidence that supports the notion that: (a). advancing age and physical frailty are associated with a reduction in the fasting rate of mixed and myosin heavy chain protein synthesis, which contributes to muscle protein wasting in advancing age; (b). this impairment can be corrected because resistance exercise acutely and dramatically increases the rate of muscle protein synthesis in men and women aged 76 years and older; and (c). resistance exercise training maintains a modest increment in the rate of muscle protein synthesis and contributes to muscle hypertrophy and improved muscle strength in frail elderly men and women. The cellular mechanisms responsible for these adaptations, as well as the role of nutrition and hormone replacement in reversing sarcopenia, require further investigation.