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.