Autophagy is required for exercise training-induced skeletal muscle adaptation and improvement of physical performance
Vitor A. Lira,Mitsuharu Okutsu,Mei Zhang,Nicholas P. Greene,Rhianna C. Laker,David S. Breen,Kyle L. Hoehn,Zhen Yan +7 more
TLDR
It is demonstrated that increased basal autophagy is required for endurance exercise training‐induced skeletal muscle adaptation and improvement of physical performance and revealed that endurance exerciseTraining‐induced increases in basal autophile, including mitophagy, only take place if an enhanced oxidative phenotype is achieved.Abstract:
Pathological and physiological stimuli, including acute exercise, activate autophagy; however, it is unknown whether exercise training alters basal levels of autophagy and whether autophagy is required for skeletal muscle adaptation to training. We observed greater autophagy flux (i.e., a combination of increased LC3-II/LC3-I ratio and LC3-II levels and reduced p62 protein content indicating a higher rate of initiation and resolution of autophagic events), autophagy protein expression (i.e., Atg6/Beclin1, Atg7, and Atg8/LC3) and mitophagy protein Bnip3 expression in tonic, oxidative muscle compared to muscles of either mixed fiber types or of predominant glycolytic fibers in mice. Long-term voluntary running (4 wk) resulted in increased basal autophagy flux and expression of autophagy proteins and Bnip3 in parallel to mitochondrial biogenesis in plantaris muscle with mixed fiber types. Conversely, exercise training promoted autophagy protein expression with no significant increases of autophagy flux and m...read more
Citations
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Autophagy--a key player in cellular and body metabolism.
Kook Hwan Kim,Myung-Shik Lee +1 more
TL;DR: The role of autophagy in various tissues in the regulation of energy metabolism and the development of diseases related to altered metabolism is described and the potential of pharmacological modulation of Autophagy as a treatment for human metabolic disorders is discussed.
Journal ArticleDOI
Mitochondrial Quality Control and Muscle Mass Maintenance.
Vanina Romanello,Marco Sandri +1 more
TL;DR: The current knowledge linking mitochondria-dependent signaling pathways to muscle homeostasis in aging and disease is outlined and the resulting implications for the development of novel therapeutic approaches to prevent muscle loss are outlined.
Journal ArticleDOI
Ampk phosphorylation of Ulk1 is required for targeting of mitochondria to lysosomes in exercise-induced mitophagy
Rhianna C. Laker,Joshua C. Drake,Rebecca J. Wilson,Vitor A. Lira,Vitor A. Lira,Bevan M. Lewellen,Karen A. Ryall,Carleigh C. Fisher,Mei Zhang,Jeffrey J. Saucerman,Laurie J. Goodyear,Mondira Kundu,Zhen Yan +12 more
TL;DR: It is shown that acute treadmill running in mice causes mitochondrial oxidative stress at 3–12 h and mitophagy at 6’h post-exercise in skeletal muscle and that Ulk1 activation is dependent on Ampk, and that exercise-induced metabolic adaptation requiresUlk1.
Journal ArticleDOI
Autophagy and the cell biology of age-related disease
TL;DR: How the autophagy pathway restricts cellular damage and degeneration, and the impact of these functions towards tissue health and organismal lifespan is examined.
Journal ArticleDOI
Role of PGC-1α during acute exercise-induced autophagy and mitophagy in skeletal muscle.
TL;DR: Results suggest that mitochondrial turnover is increased following exercise and that this effect is at least in part coordinated by PGC-1α.
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