title: Increased muscle oxidative potential following resistance training induced fibre hypertrophy in young men.
abstract: Some evidence suggests that resistance training may lower relative muscle mitochondrial content via "dilution" of the organelle in a larger muscle fibre. Such an adaptation would reduce fatigue resistance, as well as compromise oxidative ATP synthesis and the capacity for fatty-acid oxidation. We investigated the effect of resistance training on mitochondrial enzymes of the citric acid cycle (citrate synthase; CS) and beta-oxidation (beta-hydroxyacyl CoA dehydrogenase; beta-HAD), as well as markers of the potential for glucose phosphorylation (hexokinase; HK) and glycolysis (phosphofructokinase; PFK). Twelve untrained men (21.9 +/- 0.5 y; 1.79 +/- 0.03 m; 83.2 +/- 3.2 kg) participated in a 12 week progressive resistance-training program. Muscle biopsies were taken from the vastus lateralis before (PRE) and after (POST) training. Training increased mean muscle fibre cross-sectional area (p < 0.05) and the activities of CS (PRE = 4.53 +/- 0.44 mol.kg protein(-1).h(-1); POST = 5.63 +/- 0.40 mol.kg protein(-1).h(-1); p < 0.001) and beta-HAD (PRE = 2.55 +/- 0.28 mol.kg protein(-1).h(-1); POST = 3.11 +/- 0.21 mol.kg protein(-1).h(-1); p < 0.05). The activity of HK increased 42% (p < 0.05), whereas the activity of PFK remained unchanged. We conclude that resistance training provides a stimulus for improving muscle oxidative potential, as reflected by the increased activities of CS and beta-HAD following resistance training induced hypertrophy.
authors.affiliation: Department of Kinesiology, Exercise Metabolism Research Group, McMaster University, 1280 Main St. W, Hamilton, ON L8S 4K1, Canada.
authors.forename: Jason E
authors.initials: JE
authors.lastname: Tang
authors.forename: Joseph W
authors.initials: JW
authors.lastname: Hartman
authors.forename: Stuart M
authors.initials: SM
authors.lastname: Phillips
mesh_terms: D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000328:Adult; D001707:Biopsy, Needle; D001823:Body Composition; D002950:Citrate (si)-Synthase / Q000378:metabolism; D015444:Exercise / Q000502:physiology*; D006593:Hexokinase / Q000378:metabolism; D006801:Humans; D006984:Hypertrophy; D008297:Male; D008931:Mitochondria, Muscle / Q000201:enzymology; D018485:Muscle Fibers, Skeletal / Q000201:enzymology / Q000648:ultrastructure; D053580:Muscle Strength; D018482:Muscle, Skeletal / Q000201:enzymology* / Q000648:ultrastructure; D010084:Oxidation-Reduction; D025221:Phosphofructokinases / Q000378:metabolism; D014891:Weight Lifting / Q000502:physiology*; D016474:Weight-Bearing / Q000502:physiology
chemical_list: D000255:Adenosine Triphosphate; D015094:3-Hydroxyacyl CoA Dehydrogenases; D002950:Citrate (si)-Synthase; D025221:Phosphofructokinases; D006593:Hexokinase