Authors: Hartman, Joseph W.; Phillips, Stuart M.; Tang, Jason E.

Source: Applied Physiology, Nutrition, and Metabolism, Volume 31, Number 5, October 2006 , pp. 495-501(7)

Publisher: NRC Research Press

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 β-oxidation (β-hydroxyacyl CoA dehydrogenase; β-HAD), as well as markers of the potential for glucose phosphorylation (hexokinase; HK) and glycolysis (phosphofructokinase; PFK). Twelve untrained men (21.9 ± 0.5y; 1.79 ± 0.03m; 83.2 ± 3.2kg) 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 ± 0.40mol·kg protein^-1·h^-1; p < 0.001) and β-HAD (PRE = 2.55 ± 0.28 mol·kg protein^-1·h^-1; POST = 3.11 ± 0.21mol·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 β-HAD following resistance training induced hypertrophy.

D'après certaines études, l'entraînement à la force réduit la concentration relative de mitochondries dans les muscles du fait de la « dilution » de l'organelle dans une fibre musculaire de plus grande dimension. Il appert qu'une telle adaptation amoindrit la résistance à la fatigue et compromet la capacité oxydative de synthèse de l'ATP et la capacité d'oxydation des acides gras. Nous avons analysé l'effet d'un programme d'entraînement à la force sur les enzymes mitochondriaux du cycle de l'acide citrique (citrate synthase; CS) et de la β-oxydation (β-hydroxyacyl CoA déshydrogénase; β-HAD), sur les marqueurs des enzymes de la phosphorylation du glucose (hexokinase; HK) et de la glycolyse (phosphofructokinase; PFK). Douze hommes non entraînés (21,9 ± 0,5 ans; 1,79 ± 0,03m; 83,2 ± 3,2kg) participent à un programme progressif d'entraînement à la force d'une durée de 12 semaines. On prélève des échantillons de tissu musculaire du vaste externe avant (PRE) et après (POST) ledit programme. L'entraînement augmente la surface de section moyenne des fibres musculaires (p < 0,05) et les activités de la CS (PRE = 4,53 ± 0,44 mol·kg protéine^-1·h^-1; POST = 5,63 ± 0,40mol·kg protéine^-1·h^-1; p < 0001) et de la β-HAD (PRE = 2,55 ± 0,28 mol·kg protéine^-1·h^-1; POST = 3,11 ± 0,21mol·kg protéine^-1·h^-1; p < 0,05). L'activité de la HK augmente de 42 % (p < 0,05) et celle de la PFK ne change pas. En conclusion, l'entraînement à la force améliore le potentiel oxydatif du muscle comme le révèle l'augmentation de l'activité de la CS et de la β-HAD à la suite d'un programme d'entraînement à la force causant l'hypertrophie.

Document Type: Research article

Publication date: 2006-10-01

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• This bimonthly journal has a 30-year history of publishing, first as the Canadian Journal of Sport Sciences, and later as the Canadian Journal of Applied Physiology. It publishes original research articles, reviews, and commentaries, focussing on the application of physiology, nutrition, and metabolism to the study of human health, physical activity, and fitness. The published research, reviews, and symposia will be of interest to exercise physiologists, physical fitness and exercise rehabilitation specialists, public health and health care professionals, as well as basic and applied physiologists, nutritionists, and biochemists.
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