Abstract
Sarcopenia is an aging-induced syndrome characterized by a progressive reduction of skeletal muscle mass and strength. Increasing evidence has attested that appropriate and scientific exercise could induce autophagy or optimize the functional status of autophagy, which plays a critical role in senescent muscular dystrophy. As a publicly recognized strategy for extending lifespan and improving the health of the elderly, the underlying mechanisms of lifelong regular aerobic exercise for the prevention of sarcopenia have not been fully elucidated. To explore the role of lifelong aerobic exercise in the beneficial regulation of autophagic signaling pathways in senescent skeletal muscle, the natural aging mice were used as the sarcopenia model and subjected to lifelong treadmill running to evaluate corresponding parameters related to skeletal muscle atrophy and autophagic signaling pathways. Compared with the young control mice, the aged mice showed a significant reduction in skeletal muscle mass, gastrocnemius muscle weight/body weight (GMW/BW) ratio, and cross-sectional areas (CSA) of skeletal muscle fibers (p < 0.01). In contrast, lifelong aerobic exercise effectively rescued these reduced biomarkers associated with muscle atrophy. Moreover, as shown in the activated AMPK/PGC-1α signaling pathway, lifelong aerobic exercise successfully prevented the aging-induced impairment of the ubiquitin-proteasome system (UPS), excessive apoptosis, defective autophagy, and mitochondrial dysfunction. The exercise-induced autophagy suppressed the key regulatory components of the UPS, inhibited excessive apoptosis, and optimized mitochondrial quality control, thereby preventing and delaying aging-induced skeletal muscle atrophy.
Highlights
During the aging process, skeletal muscle shows a gradual decline in mass, strength, and movement capability, which is called sarcopenia [1]
Previous analysis for the internal structure of skeletal muscle has demonstrated that aging-induced skeletal muscle atrophy is mainly manifested as the atrophy of type II fibers [19]
The gastrocnemius muscle weight/body weight (GMW/BW) ratio of the mice from the lifelong aerobic exercise (OE) group showed considerable rescuing upon lifelong aerobic exercise intervention when compared with that from the OC group (p < 0.01). This result suggested that lifelong aerobic exercise effectively improved the sarcopenia index (SI) value of the aged mice and prevented the mass decline of skeletal muscle caused by aging (Table 1)
Summary
Skeletal muscle shows a gradual decline in mass, strength, and movement capability, which is called sarcopenia [1]. There is irrefutable evidence that the main role of resistance exercise is to improve the quality and strength of skeletal muscle, while aerobic exercise plays a crucial role in maintaining the maximum aerobic capacity and cellular homeostasis of the aging skeletal muscle [14]. Both exercise methods can activate autophagic signaling in the aged skeletal muscle [15]. We speculated that lifelong aerobic exercise could induce autophagy and suppress excessive apoptosis, reduce protein degradation, and improve mitochondrial quality control through the AMPK/PGC-1α signaling pathways, thereby preventing and delaying sarcopenia
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