title: Oxidative stress and delayed-onset muscle damage after exercise.
abstract: Reactive oxygen species (ROS) produced during exercise may be involved in delayed-onset muscle damage related to inflammation. To investigate this hypothesis, we studied whether oxidative stress increases nuclear translocation of nuclear factor-kappaB and chemokine expression in skeletal muscle using myotube L6 cells. We also assessed whether prolonged acute exercise could increase these parameters in rats. In L6 cells, H(2)O(2) induced nuclear translocation of p65 and increased the expression of cytokine-induced neutrophil chemoattractant-1 (CINC-1) and monocyte chemoattractant protein-1 (MCP-1), whereas preincubation with alpha-tocopherol limited the increase in these proteins. Sprague Dawley rats were divided into the following groups: rested control, exercised, rested with a high alpha-tocopherol diet, and exercised with a high alpha-tocopherol diet. After 3 weeks of acclimation, both exercise groups ran on a treadmill at 25 m/min for 60 min. Exercise increased nuclear p65, CINC-1, and MCP-1 in gastrocnemius muscle cells, but these changes were ameliorated by the high alpha-tocopherol diet. Increases in myeloperoxidase and thiobarbituric acid-reactive substrates were ameliorated by a high alpha-tocopherol diet, as were the histological changes. Neutrophil activity was not altered by either exercise or a high alpha-tocopherol diet. These results indicate that delayed-onset muscle damage induced by prolonged exercise is partly related to inflammation via phagocyte infiltration caused by ROS and that alpha-tocopherol (an antioxidant) can attenuate such inflammatory changes.
authors.affiliation: Department of Inflammation and Immunology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, 602-8566, Japan. waoi@koto.kpu-m.ac.jp
authors.forename: Wataru
authors.initials: W
authors.lastname: Aoi
authors.forename: Yuji
authors.initials: Y
authors.lastname: Naito
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Takanami
authors.forename: Yukari
authors.initials: Y
authors.lastname: Kawai
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Sakuma
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ichikawa
authors.forename: Norimasa
authors.initials: N
authors.lastname: Yoshida
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Yoshikawa
mesh_terms: D021581:Active Transport, Cell Nucleus; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002135:Calcium-Binding Proteins / Q000378:metabolism; D002460:Cell Line; D018932:Chemokine CCL2 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007249:Inflammation; D008562:Membrane Glycoproteins / Q000378:metabolism; D051379:Mice; D018482:Muscle, Skeletal / Q000293:injuries / Q000378:metabolism / Q000473:pathology*; D016328:NF-kappa B / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D009195:Peroxidase / Q000378:metabolism; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050863:Synaptotagmin I; D050857:Synaptotagmins; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors; D014158:Transcription, Genetic; D024502:alpha-Tocopherol / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D002135:Calcium-Binding Proteins; D018932:Chemokine CCL2; D018925:Chemokines; D008562:Membrane Glycoproteins; D016328:NF-kappa B; D009419:Nerve Tissue Proteins; D017382:Reactive Oxygen Species; D050863:Synaptotagmin I; D017392:Thiobarbituric Acid Reactive Substances; D050857:Synaptotagmins; D006861:Hydrogen Peroxide; D009195:Peroxidase; D024502:alpha-Tocopherol