title: 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.
authors.affiliation: Center for Mitochondrial Biology and Medicine, Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology and Frontier Institute of Life Science, FIST, Xi'an Jiaotong University, Xi'an 710049, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.affiliation: Center for Mitochondrial Biology and Medicine, Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology and Frontier Institute of Life Science, FIST, Xi'an Jiaotong University, Xi'an 710049, China.
authors.forename: Yunhua
authors.initials: Y
authors.lastname: Peng
authors.affiliation: Center for Mitochondrial Biology and Medicine, Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology and Frontier Institute of Life Science, FIST, Xi'an Jiaotong University, Xi'an 710049, China.
authors.forename: Zhihui
authors.initials: Z
authors.lastname: Feng
authors.affiliation: Center for Mitochondrial Biology and Medicine, Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology and Frontier Institute of Life Science, FIST, Xi'an Jiaotong University, Xi'an 710049, China.
authors.forename: Wen
authors.initials: W
authors.lastname: Shi
authors.affiliation: State Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing 100094, China.
authors.forename: Lina
authors.initials: L
authors.lastname: Qu
authors.affiliation: State Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing 100094, China.
authors.forename: Yinghui
authors.initials: Y
authors.lastname: Li
authors.affiliation: Center for Mitochondrial Biology and Medicine, Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology and Frontier Institute of Life Science, FIST, Xi'an Jiaotong University, Xi'an 710049, China; Tianjin Key Laboratory of Exercise Physiology and Sports Medicine, Tianjin University of Sport, Tianjin, 300381, China. Electronic address: j.liu@mail.xjtu.edu.cn.
authors.forename: Jiankang
authors.initials: J
authors.lastname: Liu
authors.affiliation: Center for Mitochondrial Biology and Medicine, Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology and Frontier Institute of Life Science, FIST, Xi'an Jiaotong University, Xi'an 710049, China. Electronic address: jglong@mail.xjtu.edu.cn.
authors.forename: Jiangang
authors.initials: J
authors.lastname: Long
mesh_terms: D000108:Acetylcarnitine / Q000008:administration & dosage; D000818:Animals; D008928:Mitochondria / Q000187:drug effects* / Q000473:pathology; D063269:Mitochondrial Turnover / Q000187:drug effects*; D009133:Muscular Atrophy / Q000178:diet therapy* / Q000378:metabolism / Q000473:pathology; D020966:Muscular Disorders, Atrophic / Q000178:diet therapy* / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects; D010626:Phenylethyl Alcohol / Q000008:administration & dosage / Q000031:analogs & derivatives; D051381:Rats; D015398:Signal Transduction / Q000235:genetics; D008063:Thioctic Acid / Q000008:administration & dosage; D014451:Ubiquinone / Q000008:administration & dosage / Q000031:analogs & derivatives
chemical_list: C005975:3,4-dihydroxyphenylethanol; D014451:Ubiquinone; D000108:Acetylcarnitine; D008063:Thioctic Acid; C024989:coenzyme Q10; D010626:Phenylethyl Alcohol
keywords: Acetyl-l-carnitine; CoQ(10); Free radicals; Hydroxytyrosol; Lipoic acid; Mitochondria; Muscle atrophy; Reloading; Unloading