Autophagy is not required to sustain exercise and PRKAA1/AMPK activity but is important to prevent mitochondrial damage during physical activity

摘要: Physical activity has been recently documented to play a fundamental physiological role in the regulation of autophagy several tissues. It also reported that is required for exercise itself and training-induced adaptations glucose homeostasis. These autophagy-mediated metabolic improvements are thought be largely dependent on activation sensor PRKAA1/AMPK. However, it unknown whether these important benefits stem from systemic or due solely alterations skeletal muscle metabolism. To address this we utilized inducible, muscle-specific, atg7 knockout mice have generated. Our findings indicate acute inhibition just prior does not an impact physical performance, PRKAA1 activation, reveal critical preservation mitochondrial function during damaging contraction. This effect appears gender specific affecting primarily females. We establish basal oxidative stress plays crucial maintenance normal activity. Therefore, adaptive response ensures effective quality control