Sarcopenia and Its Intervention

Abstract

The world’s elderly population is expanding rapidly, and we are now faced with the significant challenge of maintaining or improving physical activity, independence, and quality of life in the elderly. Sarcopenia, the age-related loss of skeletal muscle mass, is characterized by a deterioration of muscle quantity and quality leading to a gradual slowing of movement, a decline in strength and power, increased risk of fall-related injury, and often, frailty. Muscle loss has been linked with several proteolytic systems, including the ubuiquitin-proteasome and lysosome-autophagy systems. Although many factors are considered to regulate age-dependent muscle loss, this gentle atrophy is not affected by factors known to enhance rapid atrophy (denervation, hindlimb suspension, etc.). In addition, defects in Akt-mammalian target of rapamycin (mTOR) and serum response factor (SRF)-dependent signaling have been found in sarcopenic muscle. Intriguingly, more recent studies indicate an apparent functional defect in autophagy-dependent signaling in sarcopenic muscle. Resistance training combined with amino acid-containing supplements is often utilized to prevent age-related muscle wasting and weakness. Treatment with ursolic acid seems to be effective as therapeutic agents for sarcopenia, because they attenuate the degenerative symptoms of cachexic muscle. Pharmacological, hormonal, and supplemental approaches have been tried to attenuate sarcopenia, but did not obtain outstanding results. In this review, we summarize the current understanding of the adaptation of many regulators in sarcopenia and more recent therapeutic strategies (myostatin inhibition, supplementation with ghrelin or ursolic acid, etc.) for counteracting sarcopenia.