Age effect on myocellular remodeling: Response to exercise and nutrition in humans

Aging is associated with decline in muscle mass and muscle functions. Muscle strength declines disproportionate to the decline in muscle mass indicating that muscle quality or protein quality also declines with age. Human studies have shown a progressive decline in muscle protein synthesis including proteins in the contractile apparatus and mitochondria with age. However, the decline in muscle protein synthesis is disproportionate to the decline in muscle mass that occurs with age prompting to hypothesize that muscle protein degradation also declines with age. A decline in mitochondrial capacity to synthesize ATP is likely a limiting factor of both synthesis and degradation, which are ATP dependent processes. In support of the above hypothesis, several studies have shown a decline in whole body protein turnover (synthesis and degradation). The timely and efficient degradation of irreversibly damaged or modified proteins is critical to maintain the quality of protein. It is proposed that a failure to degrade the damaged proteins and replacing them with newly synthesized proteins contribute to age related decline in muscle mass and quality of muscle proteins. The underlying molecular mechanism of these age related changes in human muscle needs further investigation.

► Decreased protein turnover with age may diminish protein quality.
► Exercise training increases protein turnover and protein quality.
► Decreased muscle mitochondrial capacity with age may decrease protein turnover.
► Feeding enhances the anabolic effects of exercise independent of age.
► Methods are needed to examine the turnover of individual proteins.