title: 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.
authors.affiliation: Research Institute of Sport Science, Semmelweis University, Budapest, Hungary.
authors.forename: Mohammad Mosaferi
authors.initials: MM
authors.lastname: Ziaaldini
authors.affiliation: Research Institute of Sport Science, Semmelweis University, Budapest, Hungary.
authors.forename: Erika
authors.initials: E
authors.lastname: Koltai
authors.affiliation: Department of Biomechanics, Semmelweis University, Budapest, Hungary.
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Csende
authors.affiliation: Department of Exercise Physiology, School of Health and Sport Science, Juntendo University, Chiba, Japan.
authors.forename: Sataro
authors.initials: S
authors.lastname: Goto
authors.affiliation: Department of Microbiology and Immunology, Sealy Center for Molecular Medicine, University of Texas Medical Branch at Galveston, Galveston, TX 77555, USA.
authors.forename: Istvan
authors.initials: I
authors.lastname: Boldogh
authors.affiliation: Faculty of Health Sciences, The University of Western Ontario, London, Ontario, Canada.
authors.forename: Albert W
authors.initials: AW
authors.lastname: Taylor
authors.affiliation: Research Institute of Sport Science, Semmelweis University, Budapest, Hungary. Electronic address: radak@tf.hu.
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Radak
mesh_terms: D000375:Aging / Q000378:metabolism* / Q000473:pathology / Q000502:physiology; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D038681:Follistatin / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology; D055435:Myostatin / Q000378:metabolism; D010805:Physical Conditioning, Animal; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology
chemical_list: D038681:Follistatin; C525913:Mstn protein, rat; D055435:Myostatin; D017382:Reactive Oxygen Species
keywords: Aging; Exercise; Follistatin; Myostatin; Reactive oxygen species; Skeletal muscle