Physical exercise stimulates autophagy in normal skeletal muscles but is detrimental for collagen VI-deficient muscles
Open accessAbstract
Autophagy is a catabolic process that provides the degradation of altered/damaged organelles through the fusion between autophagosomes and lysosomes. Proper regulation of the autophagic flux is fundamental for the homeostasis of skeletal muscles in physiological conditions and in response to stress. Defective as well as excessive autophagy is detrimental for muscle health and has a pathogenic role in several forms of muscle diseases. Recently, we found that defective activation of the autophagic machinery plays a key role in the pathogenesis of muscular dystrophies linked to collagen VI. Impairment of the autophagic flux in collagen VI null (Col6a1–/–) mice causes accumulation of dysfunctional mitochondria and altered sarcoplasmic reticulum, leading to apoptosis and degeneration of muscle fibers. Here we show that physical exercise activates autophagy in skeletal muscles. Notably, physical training exacerbated the dystrophic phenotype of Col6a1–/– mice, where autophagy flux is compromised. Autophagy was not induced in Col6a1–/– muscles after either acute or prolonged exercise, and this led to a marked increase of muscle wasting and apoptosis. These findings indicate that proper activation of autophagy is important for muscle homeostasis during physical activity.
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Exercise promotes the synthesis of new proteins but simultaneously activates autophagy-lysosome and ubiquitin-proteasome degradative systems.
“In fact, exercise does promote the synthesis of new proteins but simultaneously activates autophagy–lysosome and ubiquitin–proteasome-degradative systems4.”
From Mechanisms of muscle atrophy and hypertrophy: implications in health and disease (2021) · cites this paper as [4]
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- Authors
- Grumati, P., Coletto, L., Schiavinato, A., Castagnaro, S., Bertaggia, E., Sandri, M., & Bonaldo, P.
- Affiliations
- University of Padua (IT)
- Veneto Institute of Molecular Medicine (IT)
- Corresponding author
- Sandri, Marco
- Bonaldo, Paolo
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2011-12
- Volume
- 7
- Issue
- 12
- Pages
- 1415-1423
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- PMC
- PMC3288016
- OpenAlex
- W2171103810
- Cited by
- 267
- References
- 41
- Citations by year
- 2026: 11 · 2025: 12 · 2024: 8 · 2023: 13 · 2022: 13 · 2021: 23 · 2020: 17 · 2019: 19 · 2018: 24 · 2017: 24 · 2016: 23 · 2015: 31 · 2014: 19 · 2013: 15 · 2012: 15
- FWCI
- 6.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Autophagy (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- Funders
- European Commission
- Fondazione Telethon
- Università degli Studi di Padova
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Keywords
- physical activity, skeletal muscle, collagen VI deficiency, muscular dystrophy, autophagic flux, muscle atrophy, apoptosis, mitochondrial dysfunction, sarcoplasmic reticulum, muscle homeostasis, exercise-induced muscle damage
- MeSH terms
- Animals, Autophagy, Mice, Inbred C57BL, Physical Conditioning, Animal, Time Factors, Muscle, Skeletal, Wasting Syndrome, Collagen Type VI, Mice
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