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Abstract

Apelin is an exercise-induced peptide that declines with age and is positively associated with exercise-induced benefits in older individuals. This molecule may therein have a potential role in combatting sarcopenia—age-related progressive loss of muscle mass and strength—when combined with exercise; however, the molecular mechanisms behind its autocrine function remain unclear. PURPOSE: To investigate how aerobic exercise impacts skeletal muscle apelin signaling, focusing on its potential in counteracting the age-related loss of skeletal muscle. METHODS: 22 Fisher 344 male rats (3- and 21-month-old) were obtained from NIA rodent colonies. Experimental groups were randomly divided: young sedentary (Y, n=5); young exercise (YEx, n=5); old sedentary (O, n=6); old exercise (OEx, n=6). YEx and OEx groups were subjected to an aerobic training protocol (10–12 m/min, 15° incline, 60 min/day, 5 days/10 weeks). At the end of the experiment, the tibialis anterior muscle (TA) was collected, weighed, and snap frozen for subsequent biochemical analysis. Specifically, gene expression of apelin (APLN) and Murf-1 (TRIM63) were detected by reverse transcription polymerase chain reaction (RT-PCR). Separate two-way ANOVAs were used to evaluate significance at a level of pRESULTS: Both O (pCONCLUSION: These results demonstrated that the old rats showed maladaptive responses to the aerobic training in this study, such as reduced body mass, reduced apelin levels, and increased expression of an atrophy-related gene. Our data further emphasizes the importance of exercise dosing, wherein more research is needed to evaluate muscle fiber size, the mechanisms underlying age-related and training-induced changes, and to determine the best exercise regimen for improving muscle quality during aging.

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