Abstract
Exercise training is one of the most effective interventional strategies for sarcopenia in aged people. Nevertheless, the underlying mechanisms are not well recognized. Increasing studies have reported abnormal regulation of autophagy in aged skeletal muscle. Our current study aims to explore the efficiency of exercise interventions, including treadmill exercise, resistance exercise, alternating exercise with treadmill running and resistance exercise, and voluntary wheel running, on 21-month-old rats with sarcopenia and to detect the underlying mechanisms. Results showed the declined mass of gastrocnemius muscle with deficient autophagy and excessive apoptosis as a result of up-regulated Atrogin-1 and MuRF1, declined Beclin1 level and LC3-II/LC3-I ratio, accumulated p62, increased Bax, and reduced Bcl-2 levels, and also exhibited a defective mitochondrial quality control due to declined PGC-1α, Mfn2, Drp1, and PINK1 levels. However, 12-week exercise interventions suppressed the decline in mass loss of skeletal muscle, accompanied by down-regulated Atrogin-1 and MuRF1, increased Beclin1 level, improved LC3-II/LC3-I ratio, declined p62 level, and reduced Bax and increased Bcl-2 level, as well as enhanced mitochondrial function due to the increased PGC-1α, Mfn2, Drp1, and PINK1 levels. Moreover, exercise interventions also down-regulated the phosphorylation of Akt, mTOR, and FoxO3a, and up-regulated phosphorylated AMPK to regulate the functional status of autophagy and mitochondrial quality control. Therefore, exercise-induced autophagy is beneficial for remedying sarcopenia by modulating Akt/mTOR and Akt/FoxO3a signal pathways and AMPK-mediated mitochondrial quality control, and resistance exercise exhibits the best interventional efficiency.
Highlights
As the population undergoes rapid aging, the number of elderly patients with aging-related diseases is increasing
Myofilaments showed a regular arrangement, following the nucleus situated at the side of skeletal muscle fibers; irregular shapes and nucleus aggregation were observed in the skeletal muscle of the rats from the OC group
A significant reversal was detected in the OT, OR, and OV groups (Figure 1B), suggesting that the aging-induced atrophy of skeletal muscle could be alleviated by regular exercise interventions
Summary
As the population undergoes rapid aging, the number of elderly patients with aging-related diseases is increasing. Maintaining or optimizing the functional status of autophagy can delay skeletal muscle atrophy and improve skeletal muscle function Multiple interventions, such as dietary supplements, calorie limitation, and physical exercise, on alleviating sarcopenia have been widely discussed, exercise intervention may be the appropriate approach (Phu et al, 2015). Previous studies have shown that exercise-induced AMPK can regulate energy metabolism and promote mitochondrial biosynthesis in skeletal muscle, participate in the quality control of skeletal muscle, regulate inflammatory responses, and inhibit muscular atrophy (Brault et al, 2010; Drake et al, 2016; Liu and Chang, 2018). We hypothesize that exercise can regulate Akt/mTOR and Akt/FoxO3a signal pathways to induce autophagy and cooperate with AMPK-mediated mitochondrial quality control to alleviate sarcopenia. The atrophy of type II myofibers in skeletal muscle is a prominent feature of sarcopenia (Sayed et al, 2016), so the gastrocnemius muscle was selected as the subject of this study
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