Age-Associated declines in mitochondrial biogenesis and protein quality control factors are minimized by exercise training
Open accessAbstract
A decline in mitochondrial biogenesis and mitochondrial protein quality control in skeletal muscle is a common finding in aging, but exercise training has been suggested as a possible cure. In this report, we tested the hypothesis that moderate-intensity exercise training could prevent the age-associated deterioration in mitochondrial biogenesis in the gastrocnemius muscle of Wistar rats. Exercise training, consisting of treadmill running at 60% of the initial Vo(2max), reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass (succinate dehydrogenase, citrate synthase, cytochrome-c oxidase-4, mtDNA), SIRT1 activity, AMPK, pAMPK, and peroxisome proliferator-activated receptor gamma coactivator 1-α, UCP3, and the Lon protease. Exercise training also decreased the gap between young and old animals in other measured parameters, including nuclear respiratory factor 1, mitochondrial transcription factor A, fission-1, mitofusin-1, and polynucleotide phosphorylase levels. We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.
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Studies in rodents have reported increased or unchanged Drp1 content in aged skeletal muscles.
“Indeed, studies in rodents have reported increased [49,50,51] or unchanged [34,47,52,54] Drp1 content in aged skeletal muscles.”
From Mitochondrial Dynamics and Mitophagy in Skeletal Muscle Health and Aging (2021) · cites this paper as [51]
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- Authors
- Koltai, E., Hart, N., Taylor, A. W., Goto, S., Ngo, J. K., Davies, K. J. A., & Radak, Z.
- Affiliations
- Semmelweis University (HU)
- University of Southern California (US)
- Corresponding author
- Radak, Zsolt
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2012-07-15
- Volume
- 303
- Issue
- 2
- Pages
- R127-R134
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- PMC
- PMC3404634
- OpenAlex
- W2136544814
- Cited by
- 152
- References
- 60
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 2 · 2023: 12 · 2022: 4 · 2021: 16 · 2020: 10 · 2019: 14 · 2018: 19 · 2017: 11 · 2016: 9 · 2015: 13 · 2014: 13 · 2013: 13 · 2012: 4
- FWCI
- 5.53
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Environmental Health Sciences (3R01-ES 003598-22S2, R01ES003598)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- exercise training, mitochondrial biogenesis, mitochondrial protein quality control, skeletal muscle aging, gastrocnemius, SIRT1, AMPK, PGC-1α, UCP3, Lon protease, mitofusin 1, mitochondrial fission, mitochondrial mass, mitochondrial DNA, succinate dehydrogenase, citrate synthase, cytochrome c oxidase, NRF1, TFAM, treadmill running, Wistar rats
- MeSH terms
- Adaptation, Physiological, Aging, Animals, Male, Membrane Proteins, Mitochondria, Muscle, Physical Conditioning, Animal, Transcription Factors, Rats, Wistar, Muscle, Skeletal, Models, Animal, Mitochondrial Proteins, Nuclear Respiratory Factor 1, Rats
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