Journal
AUTOPHAGY
Volume 10, Issue 11, Pages 1883-1894Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.32154
Keywords
skeletal muscle; exercise; mitochondria; AMPK; metabolism; autophagy
Categories
Funding
- Telethon-Italy [TCP04009]
- ERC [282310-MyoPHAGY]
- European Union (MYOAGE) [223576]
- Leducq Foundation
- Italian Ministry of Education (MiUR) [PRIN 2010/2011]
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Physical activity has been recently documented to play a fundamental physiological role in the regulation of autophagy in several tissues. It has also been reported that autophagy is required for exercise itself and for training-induced adaptations in glucose homeostasis. These autophagy-mediated metabolic improvements are thought to be largely dependent on the activation of the metabolic sensor PRKAA1/AMPK. However, it is unknown whether these important benefits stem from systemic adaptations or are due solely to alterations in skeletal muscle metabolism. To address this we utilized inducible, muscle-specific, atg7 knockout mice that we have recently generated. Our findings indicate that acute inhibition of autophagy in skeletal muscle just prior to exercise does not have an impact on physical performance, PRKAA1 activation, or glucose homeostasis. However, we reveal that autophagy is critical for the preservation of mitochondrial function during damaging muscle contraction. This effect appears to be gender specific affecting primarily females. We also establish that basal oxidative stress plays a crucial role in mitochondrial maintenance during normal physical activity. Therefore, autophagy is an adaptive response to exercise that ensures effective mitochondrial quality control during damaging physical activity.
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