Reloading Functionally Ameliorates Disuse-Induced Muscle Atrophy by Reversing Mitochondrial Dysfunction, and Similar Benefits Are Gained by Administering a Combination of Mitochondrial Nutrients
Abstract
We previously found that mitochondrial dysfunction occurs in disuse-induced muscle atrophy. However, the mitochondrial remodeling that occurs during reloading, an effective approach for rescuing unloading-induced atrophy, remains to be investigated. In this study, using a rat model of 3-week hindlimb unloading plus 7-day reloading, we found that reloading protected mitochondria against dysfunction, including mitochondrial loss, abnormal mitochondrial morphology, inhibited biogenesis, and activation of mitochondria-associated apoptotic signaling. Interestingly, a combination of nutrients, including α-lipoic acid, acetyl-L-carnitine, hydroxytyrosol, and CoQ10, which we designed to target mitochondria, was able to efficiently rescue muscle atrophy via a reloading-like action. It is suggested that reloading ameliorates skeletal muscle atrophy through the activation of mitochondrial biogenesis and the amelioration of oxidative stress. Nutrient administration acted similarly in unloaded rats. Here, the study of mitochondrial remodeling in rats during unloading and reloading provides a more detailed picture of the pathology of muscle atrophy.
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CoQ10 administration ameliorates disuse-induced skeletal muscle atrophy via activation of mitochondrial biogenesis and amelioration of oxidative stress in SD rats, and reduces MuRF-1, MAFbx, and FoxO3 expression.
“Similarly, Liu et al. reported that CoQ10 administration ameliorates disuse-induced skeletal muscle atrophy via the activation of mitochondrial biogenesis and the amelioration of oxidative stress in SD rats. In addition, the expression of MuRF-1, MAFbx, and Forkhead box O3 (FoxO3) were reduced by the CoQ10 [68].”
From Nutraceuticals in the Prevention and Treatment of the Muscle Atrophy (2021) · cites this paper as [68]
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- Authors
- Liu, J., Peng, Y., Feng, Z., Shi, W., Qu, L., Li, Y., Liu, J., & Long, J.
- Affiliations
- Tianjin University of Sport (CN)
- Xi'an Jiaotong University (CN)
- China Astronaut Research and Training Center (CN)
- Corresponding author
- Liu, Jing
- Liu, Jiankang
- Long, Jiangang
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2014-04
- Volume
- 69
- Pages
- 116-128
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W1970403178
- Cited by
- 55
- References
- 43
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 3 · 2023: 5 · 2022: 2 · 2021: 6 · 2020: 11 · 2019: 4 · 2018: 4 · 2017: 3 · 2016: 5 · 2015: 4 · 2014: 1
- FWCI
- 1.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Opening Foundation of the State Key Laboratory of Space Medicine Fundamentals and Application, the China Astronaut Research and Training Center (SMFA10K07)
- Shaanxi Province Science and Technology Research and Development Program (2013K12-01-10)
- New Century Excellent Talents in University, Tianjin Applied Basic and Frontier Tech Major Project (12JCZDJC34400), Tianjin higher Education Sci-tech Development Project (20112D05), and the National Natural Science Foundation of China (31070740)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Spaceflight effects on biology
- Keywords
- muscle atrophy, disuse, reloading, mitochondrial dysfunction, mitochondrial biogenesis, hindlimb unloading, mitochondrial remodeling, mitochondrial morphology, apoptosis, oxidative stress, alpha-lipoic acid, acetyl-L-carnitine, hydroxytyrosol, coenzyme Q10, skeletal muscle
- MeSH terms
- Acetylcarnitine, Animals, Thioctic Acid, Mitochondria, Muscular Atrophy, Phenylethyl Alcohol, Ubiquinone, Signal Transduction, Oxidative Stress, Muscular Disorders, Atrophic, Rats, Mitochondrial Turnover
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