Advancing age is associated with a reduction in skeletal muscle protein and muscle force production capabilities; a syndrome referred to as sarcopenia. This process occurs in healthy, normal aging, but is accelerated by physical inactivity, degenerative or other disease conditions. Incorporation of 13C-leucine into skeletal muscle protein, as measured by isotope dilution mass spectrometry, provides a measure of muscle protein synthesis. Decreased muscle mass and strength are associated with an increased risk of falling, and therefore, increased risk for hip fracture. Reduced muscle strength with aging can also result in physical disability and frailty, a loss of independent function, and contributes to escalating health care costs. The biological consequences of advancing age and the progressive decline in physical activity with age contribute to sarcopenia. Exercise training programs have the potential to improve overall fitness, muscle force generation, and improve quali ty of life. The physiological and functional benefits of increased muscular activity have been reported, even into the 9th decade of life (1). Thus, human skeletal muscle protein maintains the ability to respond to an exercise-induced increase in contractile activity throughout. The ability to adapt may be limited by other biological processes. Circulating concentrations and the pulsatile release patterns of several hormones that regulate metabolism are reduced with age. By virtue of their anabolic actions on body proteins, low serum growth hormone (GH), testosterone, dehydroepiandrosterone (DHEA), and perhaps estrogen, along with reduced insulin action, have all been implicated as mediators of the muscle protein wasting aging. We review the efficacy of recombinant human growth hormone (rhGH) replacement therapy and resistance exercise training to enhance muscle protein mass and contractile force output in elderly men and women.
NIH ExPorter
NIH ExPorter