title: Changes in indices of antioxidant status, lipid peroxidation and inflammation in human skeletal muscle after eccentric muscle actions.
abstract: This study investigated the effects of chronic muscle inflammation on indices of antioxidant status and muscle injury after eccentric exercise. Eight subjects each performed 70 maximal voluntary eccentric muscle actions on an isokinetic dynamometer, using the knee extensors of a single leg. Venous blood samples were collected into serum and EDTA tubes 5 and 3 days before exercise, immediately before exercise, and then again on days 3, 4, 5, 6, 7, 10 and 12 after the bout. Needle biopsies were taken from the vastus lateralis of six subjects, a week before exercise (baseline), and again on days 4 and 7 post-exercise. The concentrations of malondialdehyde in plasma and muscle were used as markers of lipid peroxidation. Creatine kinase activity, beta-glucuronidase activity and total antioxidant capacity were determined in serum. In muscle, aqueous and bound total antioxidant capacity, the aqueous sulphydryl concentration, and beta-glucuronidase and glucose-6-phosphate dehydrogenase activity were determined. No changes were detected in serum total antioxidant capacity, serum creatine kinase and beta-glucuronidase after the baseline biopsy. After exercise serum creatine kinase and beta-glucuronidase were elevated although other serum measures were unchanged. In muscle, aqueous and bound total antioxidant capacity, sulphydryls, glucose-6-phosphate dehydrogenase and beta-glucuronidase were all elevated. Despite evidence of inflammation in this study, muscle antioxidant status was not compromised, and malondialdehyde was unaltered in muscle and plasma. Therefore, this study provides no evidence that chronic muscle inflammation compromises antioxidant status or increases lipid peroxidation.
authors.affiliation: Muscle Research Centre, Department of Medicine, University Clinical Departments, Liverpool University, c/o The Duncan Building, Daulby Street, Liverpool L69 3GA, U.K.
authors.forename: R
authors.initials: R
authors.lastname: Child
authors.forename: S
authors.initials: S
authors.lastname: Brown
authors.forename: S
authors.initials: S
authors.lastname: Day
authors.forename: A
authors.initials: A
authors.lastname: Donnelly
authors.forename: H
authors.initials: H
authors.lastname: Roper
authors.forename: J
authors.initials: J
authors.lastname: Saxton
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D000975:Antioxidants / Q000032:analysis*; D015415:Biomarkers / Q000032:analysis; D003402:Creatine Kinase / Q000378:metabolism; D004558:Electric Stimulation; D015444:Exercise / Q000502:physiology*; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005966:Glucuronidase / Q000378:metabolism; D006801:Humans; D007537:Isometric Contraction; D007717:Knee; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D018482:Muscle, Skeletal / Q000737:chemistry / Q000201:enzymology / Q000293:injuries*; D009220:Myositis / Q000503:physiopathology*; D018709:Statistics, Nonparametric; D013439:Sulfhydryl Reagents / Q000032:analysis; D014527:Uric Acid / Q000032:analysis
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D013439:Sulfhydryl Reagents; D014527:Uric Acid; D008315:Malondialdehyde; D005954:Glucosephosphate Dehydrogenase; D003402:Creatine Kinase; D005966:Glucuronidase