Exercise training increases anabolic and attenuates catabolic and apoptotic processes in aged skeletal muscle of male rats
Abstract
Aging results in significant loss of mass and function of the skeletal muscle, which negatively impacts the quality of life. In this study we investigated whether aerobic exercise training has the potential to alter anabolic and catabolic pathways in the skeletal muscle. Five and twenty eight month old rats were used in the study. Aging resulted in decreased levels of follistatin/mTOR/Akt/Erk activation and increased myostatin/Murf1/2, proteasome subunits, and protein ubiquitination levels. In addition, TNF-α, reactive oxygen species (ROS), p53, and Bax levels were increased while Bcl-2 levels were decreased in the skeletal muscle of aged rats. Six weeks of exercise training at 60% of VO2max reversed the age-associated activation of catabolic and apoptotic pathways and increased anabolic signaling. The results suggest that the age-associated loss of muscle mass and cachexia could be due to the orchestrated down-regulation of anabolic and up-regulation of catabolic and pro-apoptotic processes. These metabolic changes can be attenuated by exercise training.
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Aging activates mitochondria-dependent apoptotic pathways in aged rats as result of down-regulated Bcl-2 and up-regulated Bax along with increased cleaved caspase-3.
“Similarly, aging activates the mitochondria-dependent apoptotic pathways in the aged rats as a result of down-regulated Bcl-2 and up-regulated Bax along with increased cleaved caspase-3 [38].”
From Lifelong Aerobic Exercise Alleviates Sarcopenia by Activating Autophagy and Inhibiting Protein Degradation via the AMPK/PGC-1α Signaling Pathway (2021) · cites this paper as [38]
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- Authors
- Ziaaldini, M. M., Koltai, E., Csende, Z., Goto, S., Boldogh, I., Taylor, A. W., & Radak, Z.
- Affiliations
- Semmelweis University (HU)
- Juntendo University (JP)
- The University of Texas Medical Branch at Galveston (US)
- Western University (CA)
- Corresponding author
- Radak, Zsolt
- Venue
- Experimental Gerontology
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 67
- Pages
- 9-14
- ISSN
- 0531-5565 (ISSN-L)
- OpenAlex
- W2068554185
- Cited by
- 72
- References
- 49
- Citations by year
- 2025: 5 · 2024: 4 · 2023: 3 · 2022: 7 · 2021: 6 · 2020: 7 · 2019: 6 · 2018: 13 · 2017: 11 · 2016: 8 · 2015: 2
- FWCI
- 4.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental Gerontology (publishedVersion)
- PubMed (publishedVersion)
- Repository of the Academy's Library (Library of the Hungarian Academy of Sciences) (acceptedVersion)
- Funders
- OTKA (K 112810)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Keywords
- exercise training, skeletal muscle aging, sarcopenia, cachexia, anabolic signaling, catabolic pathways, apoptosis, follistatin, myostatin, proteasome, ubiquitination, TNF-α, reactive oxygen species, p53, Bax, Bcl-2, muscle mass loss
- MeSH terms
- Aging, Animals, Male, Physical Conditioning, Animal, Signal Transduction, Rats, Wistar, Apoptosis, Reactive Oxygen Species, Muscle, Skeletal, Follistatin, Myostatin
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