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Autophagy is not required to sustain exercise and PRKAA1/AMPK activity but is important to prevent mitochondrial damage during physical activity.
- Source :
-
Autophagy [Autophagy] 2014; Vol. 10 (11), pp. 1883-94. Date of Electronic Publication: 2014 Oct 30. - Publication Year :
- 2014
-
Abstract
- 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.
- Subjects :
- AMP-Activated Protein Kinases genetics
Animals
Antioxidants chemistry
Autophagy-Related Protein 7
Female
Glucose metabolism
Homeostasis
Male
Mice
Mice, Knockout
Muscle Contraction
Oxidative Stress
Physical Conditioning, Animal
AMP-Activated Protein Kinases metabolism
Autophagy physiology
Microtubule-Associated Proteins genetics
Mitochondria physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1554-8635
- Volume :
- 10
- Issue :
- 11
- Database :
- MEDLINE
- Journal :
- Autophagy
- Publication Type :
- Academic Journal
- Accession number :
- 25483961
- Full Text :
- https://doi.org/10.4161/auto.32154