Research Progress of Exercise Regulating Endoplasmic Reticulum Unfolding Protein Response to Improve Sarcopenia

The prevention and treatment of sarcopenia is an urgent public health problem. Endoplasmic reticulum unfolded protein response(UPRER) is a key target to maintain protein homeostasis in aging skeletal muscle, so it is important to explore the role of UPRERin sarcopenia. Exercise is known to weaken endoplasmic reticulum stress(ERS), increase protein synthesis of aging skeletal muscle, maintain protein homeostasis and improve skeletal muscle function by regulating UPRER. Acute exercise may have the role to activate protein kinase RNA-like ER kinase/activating transcription factor 4(PERK/ATF4), inositol-requiring protein 1/X-box binding protein 1(IRE1/Xbp1) and ATF6 signal axes via UPRER, and thus to promote protein synthesis of aging skeletal muscle, and finally to improve protein homeostasis. In addition, the “phasic” is the most important characteristic in the abovementioned effects, i.e.,the effect is not obvious at 0~3 h after exercise, gradually significant at 12~48 h, and fall back after 48 h, especially in resistance exercise. Long-term endurance/resistance exercise may also mediate UPRERto activate PERK/ATF4 and IRE1/Xbp1 signal axis, and then promote protein synthesis of aging skeletal muscle, and finally improved protein homeostasis. It is suggested that exercise can optimize UPRER, improve the expression of related proteins on PERK/ATF4 and IRE1/Xbp1 signal axis of aging skeletal muscle to weaken ERS, so as to maintain the skeletal muscle homeostasis and the functional integrity of aging skeletal muscle. In the future,the research on the regulation of sarcopenia by exercise-mediated UPRERis expected to provide useful references for the prevention and treatment of sarcopenia.