Cited by 146Autophagy in Disease and TherapyExercise and Physiological ResponsesMetabolism, Diabetes, and Cancer

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

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Lo Verso, Francesca, Carnio, Silvia, Vainshtein, Anna, Sandri, Marco·2014·Autophagy

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.

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Authors
Lo Verso, F., Carnio, S., Vainshtein, A., & Sandri, M.
Affiliations
  • Veneto Institute of Molecular Medicine (IT)
  • York University (CA)
  • University of Padua (IT)
Corresponding author
Sandri, Marco
Venue
Autophagy
Published
2014-10-30
Volume
10
Issue
11
Pages
1883-1894
ISSN
  • 1554-8627 (ISSN-L)
  • 1554-8635
OpenAlex
W1994408958
Cited by
146
References
38
Citations by year
2026: 5 · 2025: 5 · 2024: 12 · 2023: 13 · 2022: 6 · 2021: 21 · 2020: 11 · 2019: 12 · 2018: 20 · 2017: 13 · 2016: 16 · 2015: 12
FWCI
10.32
Type
journal article
Language
en
Open access
Locations
  • Autophagy (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Figshare (submittedVersion, cc-by)
  • Padua Research Archive (University of Padova) (submittedVersion)
  • Figshare (cc-by)
Funders
  • Fondation Leducq
  • Fondazione Telethon
  • Consiglio Nazionale delle Ricerche
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
physical activity, skeletal muscle, mitochondrial damage, mitochondrial quality control, oxidative stress, muscle contraction, glucose homeostasis, sex differences, physical performance
MeSH terms
Autophagy-Related Protein 7, Animals, Antioxidants, Autophagy, Female, Glucose, Homeostasis, Male, Microtubule-Associated Proteins, Mitochondria, Muscle Contraction, Physical Conditioning, Animal, Mice, Knockout, Oxidative Stress, Mice, AMP-Activated Protein Kinases

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