Regulatory Roles of Exercise⁃regulated Circadian Rhythm in Muscular Atrophy / 中国生物化学与分子生物学报

As people age, the population of the elderly increases rapidly. With the change of work and lifestyle, the problems such as reduced physical activity and irregular routine become more serious, which results in the significantly increased incidence of skeletal muscle atrophy, and reduced health status and life quality of elderly. At the same time, the imbalance of diets, the decrease of physical activity, and the fluctuation of hormone levels further aggravate the occurrence of skeletal muscle atrophy, and its pathological mechanisms mainly correlated with chronic inflammation, mitochondrial dysfunction, deficient autophagy, increased apoptosis, impaired muscle satellite cell function, and disrupted circadian rhythm. Skeletal muscles, as the largest peripheral biological clock of the body, can affect the fiber structure, mitochondrial function, and muscle mass of skeletal muscles by regulating the circadian core genes BMAL1 and CLOCK. As an important intervention strategy to improve skeletal muscle masses, exercise can also activate the circadian signal pathway and regulate its phase, thus improving muscle regeneration and muscle strengths and delaying muscle atrophy. Therefore, from the perspective of circadian rhythm, this article summarizes the occurrence of muscular atrophy and the molecular mechanism of potential exercise intervention to provide new ideas for the targeted regulation of the prevention, treatment, and rehabilitation of muscular atrophy.

Advance in Role of Mitochondrial Quality Control in Exercise for Sarcopenia (review) / 中国康复理论与实践

Sarcopenia is a process in which skeletal muscle mass and strength are gradually declining, resulting a main health challenge for the old adults. Mitochondria can maintain the integrity of structure and function of skeletal muscle by improving biosynthesis, antioxidant defense, fusion/fission dynamics and mitophagy. Mitochondrial dysfunction is a important factor leading to the complex etiology of sarcopenia. Exercise can regulate mitochondrial quality control pathways by activating mitochondrial biogenesis and mitophagy to maintain optimal mitochondrial function, thereby delaying and preventing the onset and progression of sarcopenia.

Regulatory roles of microRNAs in sarcopenia and exercise intervention / 生理学报

Sarcopenia is an age-related degenerative disease, in which skeletal muscle mass and function are reduced during aging process. Physical intervention is one of the most effective strategies available for the treatment of sarcopenia. Studies have shown that microRNAs (miRNAs), as important regulators of gene expression, play an important role in maintaining the homeostasis of senescent skeletal muscle cells by regulating skeletal muscle cell development (proliferation and differentiation), mitochondrial biogenesis, protein synthesis and degradation, inflammatory response and metabolic pathways. Furthermore, exercise can combat age-related changes in muscle mass, composition and function, which is associated with the changes in the expression and biological functions of miRNAs in skeletal muscle cells. In this article, we systematically review the regulatory mechanisms of miRNAs in skeletal muscle aging, and discuss the regulatory roles and molecular targets of exercise-mediated miRNAs in muscular atrophy during aging process, which may provide novel insights into the prevention and treatment of sarcopenia.

Regulatory Role of Exercise-induced Autophagy in Rehabilitation of Sarcopenia (review) / 中国康复理论与实践

Sarcopenia is an aging-related disease with a significant reduction in mass and strength of skeletal muscle due to the imbalance between protein synthesis and degradation. Autophagy acts as a conserved mechanism regulating the balance of protein metabolism in body and can be regulated by multiple signaling pathways such as AMP-activated protein kinase (AMPK), insulin like growth factor (IGF)/ protein kinase B (Akt)/ mammalian target of rapamycin (mTOR) and phosphatidylinositol 3 kinase (PI3K)/Akt/mTOR induced by exercise. Exercise-activated autophagy regulates skeletal muscle remodeling and homeostasis under different physiological and pathological conditions, which is the key to skeletal muscle health maintenance. This article reviewed the regulator roles and potential molecular mechanisms of varying exercise-induced autophagy in the prevention, treatment and rehabilitation of sarcopenia.