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 @entity413 homeostasis. These autophagy-mediated metabolic improvements are thought to be largely dependent on the activation of the metabolic sensor @entity52892 /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, @entity30527 knockout @entity19 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, @entity52892 activation, or @entity413 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.

Autophagy is not required to sustain exercise and XXXX /AMPK activity but is important to prevent mitochondrial damage during physical activity.

@entity19 :: ('10090', 'Species') :: ['mice'] @entity52892 :: ('105787(Tax:10090)', 'Gene') :: ['PRKAA1'] @entity30527 :: ('74244(Tax:10090)', 'Gene') :: ['muscle-specific, atg7'] @entity413 :: ('MESH:D005947', 'Chemical') :: ['glucose']
@entity52892 :: (105787(Tax:10090),Gene) :: ['PRKAA1']
