Exercise restores muscle stem cell mobilization, regenerative capacity and muscle metabolic alterations via adiponectin/AdipoR1 activation in SAMP10 mice
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Abstract Background Exercise train (ET) stimulates muscle response in pathological conditions, including aging. The molecular mechanisms by which exercise improves impaired adiponectin/adiponectin receptor 1 (AdipoR1)‐related muscle actions associated with aging are poorly understood. Here we observed that in a senescence‐accelerated mouse prone 10 (SAMP10) model, long‐term ET modulated muscle‐regenerative actions. Methods 25‐week‐old male SAMP10 mice were randomly assigned to the control and the ET (45 min/time, 3/week) groups for 4 months. Mice that were maintained in a sedentary condition served controls. Results ET ameliorated aging‐related muscle changes in microstructure, mitochondria, and performance. The amounts of proteins or mRNAs for p‐AMPKα, p‐Akt, p‐ERK1/2, p‐mTOR, Bcl‐XL, p‐FoxO3, peroxisome proliferators‐activated receptor‐γ coactivator, adiponectin receptor1 (adpoR1), and cytochrome c oxidase‐IV, and the numbers of CD34+/integrin‐α7+ muscle stem cells (MuSCs) and proliferating cells in the muscles and bone‐marrow were enhanced by ET, whereas the levels of p‐GSK‐3α and gp91phox proteins and apoptotic cells were reduced by ET. The ET also resulted in increased levels of plasma adiponectin and the numbers of bone‐marrow (BM)‐derived circulating CD34+/integrin‐α7+ MuSCs and their functions. Integrin‐α7+ MuSCs of exercised mice had improved changes of those beneficial molecules. These ET‐mediated aged muscle benefits were diminished by adiponectin and AdipoR1 blocking as well as AMPK inhibition. Finally, recombinant mouse adiponectin enhanced AMPK and mTOR phosphorylations in BM‐derived integrin‐α7+ cells. Conclusions These findings suggest that ET can improve aging‐related impairments of BM‐derived MuSC regenerative capacity and muscle metabolic alterations via an AMPK‐dependent mechanism that is mediated by an adiponectin/AdipoR1 axis in SAMP10 mice.
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A 4-month endurance training program in mice enhanced AdipoR1 gene expression, circulating adiponectin levels, AMPK/PGC-1α-related mitochondrial biogenesis, and Akt/mTOR-mediated protein synthesis and proliferation, showing positive effects on sarcopenia development and muscle health.
“A 4-month endurance training (45 min/time, 3 times/week) program in mice enhanced AdipoR1 gene expression, circulating adiponectin levels, AMPK/PGC-1α-related mitochondrial biogenesis, and Akt/mTOR-mediated protein synthesis and proliferation, showcasing positive effects on sarcopenia development and muscle health [74] (Table 1).”
From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [74]
Chronic exercise training imposed to rodents for 4 to 16 weeks increased circulating ApN levels in some, but not all, studies.
“Chronic exercise training imposed to rodents for 4 to 16 weeks increased circulating ApN levels in some [79,80], but not all [81], studies.”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [80]
Chronic exercise training also induced an increase in muscle AdipoR1 expression in rodents and in humans.
“Chronic exercise training also induced an increase in muscle AdipoR1 expression in rodents [80,87,88] and in humans [82,83].”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [80]
Exercise training may exert beneficial effects on muscle through ApN-AdipoR1 axis.
“These data indicate a contrario that exercise training may exert beneficial effects on muscle through ApN-AdipoR1 axis [80].”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [80]
Exercise training for 4 months attenuated the decline in muscle regeneration and performance in SAMP10 mice, a senescence-accelerated mouse model.
“Exercise training for 4 months attenuated the decline in muscle regeneration and performance in SAMP10 mice, a senescence-accelerated mouse model.”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [80]
Muscle benefits induced by chronic exercise were diminished by ApN or AdipoR1 blockade using specific antibodies directed against either ApN or AdipoR1 for 2 months.
“Muscle benefits induced by chronic exercise were diminished by ApN or AdipoR1 blockade. This blockade was achieved by using specific antibodies directed against either ApN or AdipoR1 for 2 months.”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [80]
These changes were associated with improved exercise force and endurance in aged mice and resulted from activation of AdipoR1-AMPK axis.
“These changes were associated with improved exercise force and endurance in these aged mice and resulted from activation of AdipoR1-AMPK axis [80].”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [80]
In a mouse model of accelerated senescence, ApN mediates the stimulatory effects of exercise on muscle stem cell proliferation while mitigating apoptosis.
“A study conducted in a mouse model of accelerated senescence reported that ApN mediates the stimulatory effects of exercise on muscle stem cell proliferation, while mitigating apoptosis.”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [80]
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- Authors
- Inoue, A., Cheng, X. W., Huang, Z., Hu, L., Kikuchi, R., Jiang, H., Piao, L., Sasaki, T., Itakura, K., Wu, H., Zhao, G., Lei, Y., Yang, G., Zhu, E., Li, X., Sato, K., Koike, T., & Kuzuya, M.
- Affiliations
- Nagoya University (JP)
- Kyung Hee University (KR)
- University of Occupational and Environmental Health Japan (JP)
- Nagoya University Hospital (JP)
- Yanbian University (CN)
- Yanbian University Hospital (CN)
- Hamamatsu University (JP)
- Institutes of Innovation for Future Society, Nagoya University (JP)
- Corresponding author
- Cheng, Xian Wu
- ORCID
- Venue
- Journal of Cachexia Sarcopenia and Muscle
- Publisher
- Wiley
- Published
- 2016-11-29
- Volume
- 8
- Issue
- 3
- Pages
- 370-385
- ISSN
- 2190-5991 (ISSN-L)
- 2190-6009
- PMC
- PMC5476856
- OpenAlex
- W2559359565
- Cited by
- 89
- References
- 55
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 7 · 2023: 13 · 2022: 14 · 2021: 6 · 2020: 11 · 2019: 8 · 2018: 9 · 2017: 3
- FWCI
- 3.46
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Cachexia Sarcopenia and Muscle (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science, and Technology of Japan (23390208, 22390143, 15H04801, 15H04802)
- Japan Takeda Science Foundation (26-007596)
- Novartis Aging and Geriatrics Research Foundation (25-7778)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Keywords
- exercise training, muscle stem cells, adiponectin, AdipoR1, AMPK, mTOR signaling, muscle aging, bone marrow-derived stem cells, integrin alpha7, muscle regeneration, muscle metabolism, mitochondrial function, apoptosis, FOXO3, skeletal muscle
- MeSH terms
- Animals, Body Weight, Cell Movement, Lipids, Male, Mitochondria, Muscle, Muscles, Physical Conditioning, Animal, Regeneration, Signal Transduction, Biomarkers, Cytokines, Muscle, Skeletal, MAP Kinase Signaling System, Myoblasts, Mice, Adiponectin, Muscle Strength, Receptors, Adiponectin
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