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Exercise training has been reported to prevent the age-induced decline in muscle mass and fragmentation of mitochondria, as well as to affect autophagy and mitophagy. The interaction between these pathways during aging as well as the similarity between such changes in human and mouse skeletal muscle is however not fully understood. Therefore the aim of the present study was to test the hypothesis that cellular degradation pathways, including apoptosis, autophagy and mitophagy are coordinately regulated in mouse and human skeletal muscle during aging and lifelong exercise training through a PGC-1α-p53 axis. Muscle samples were obtained from young untrained, aged untrained and aged lifelong exercise trained men, and from whole-body PGC-1α knockout mice and their littermate controls that were either lifelong exercise trained or sedentary young and aged. Lifelong exercise training prevented the aging-induced reduction in PGC-1α, p53 and p21 mRNA as well as the increase in LC3II and BNIP3 protein in mouse skeletal muscle, while aging decreased the BAX/Bcl-2 ratio, LC3I and BAX protein in mouse skeletal muscle without effects of lifelong exercise training. In humans, aging was associated with reduced PGC-1α mRNA as well as decreased p62 and p21 protein in skeletal muscle, while lifelong exercise training increased BNIP3 protein and decreased p53 mRNA. In conclusion, there was a divergent regulation of autophagy and apoptosis in mouse muscle with aging and lifelong exercise training, whereas healthy aged human skeletal muscle seemed rather robust to changes in apoptosis, autophagy and mitophagy markers compared with mouse muscle at the investigated age., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Exercise has long been recognized as a powerful physiological stimulus for a wide variety of metabolic adaptations with implications for health and performance. The metabolic effects of exercise occur during and after each exercise bout and manifest as cumulative adaptive responses to successive exercise bouts. Studies on the beneficial effects of exercise have traditionally focused on the biosynthesis of metabolic proteins and organelles. However, the recycling of cellular components by autophagy has recently emerged as an important process involved in the adaptive responses to exercise. This review covers the regulation of autophagy by exercise, with emphasis on the potential autophagy-dependent beneficial effects of exercise., (Copyright © 2017 Cold Spring Harbor Laboratory Press; all rights reserved.)