CELLULAR MECHANISMS FOR SARCOPENIA IN THE ELDERLY

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Loss of body protein occurs with advancing age with selective depletion of muscle tissue, is known as sarcopenia. Since the loss of lean body mass is primarily from muscle tissue, it has important implications for the maintenance of muscle strength and function. In addition to the serious consequences for muscle function, sarcopenia also reduces the reserve of amino acids available for mobilization in times of stress. Diminished reserve of amino acids in wasted patients during critical illness is a major determinant of outcome. Muscle protein undergoes continual synthesis and degradation. When the rates of protein synthesis and degradation are balanced, muscle protein mass is maintained, but if protein degradation exceeds synthesis, there will be a loss of muscle protein. At the tissue level, loss of muscle protein in the elderly has been associated with a reduction in the rate at which muscle protein is synthesized with no difference in muscle degradation between younger and older subjects. It is therefore important to consider the factors that control protein synthesis in muscle when seeking the mechanism of muscle wasting in the elderly.