Int J Sports Med 1987; 08: S66-S69
DOI: 10.1055/s-2008-1025706
© Georg Thieme Verlag Stuttgart · New York

Enzymatic Adaptations Consequent to Long-Term Strength Training*

P. A. Tesch1 , P. V. Komi2 , K. Häkkinen2
  • 1Department of Environmental Medicine, Karolinska institutet, Stockholm, Sweden
  • 2Department of Biology of Physical Activity, University of Jyväskylä, Finland
* This study was supported by grants from the Karolinska Institute's Research Funds, the Research Council of the Swedish Sports Federation and the Ministry of Education, Finland and the Finnish Central Sport Federation. The authors also acknowledge the skillful technical assistance of Dr. M. Alén.
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Publication History

Publication Date:
14 March 2008 (online)

Abstract

The muscle enzymatic changes subsequent to 6 months of strength training followed by 3 months of detraining were examined in 21 physically active men. They were assigned either to a heavy-resistance (HR) or an explosive strength (EX) training program. Muscle biopsies were obtained from m. vastus lateralis for the assessment of activities of the enzymes hexokinase (HK), myofibrillar ATPase (ATPase), citrate synthase (CS), phosphofructokinase (PFK), lactate dehydrogenase (LDH), myokinase (MK) and creatine kinase (CK). The activities were measured on freeze-dried tissue samples using fluorometrical assays. Both groups displayed increased (P < 0.01-0.001) fast-twitch (FT) fiber area consequent to training with no concomitant hypertrophy of slow-twitch (ST) fiber area. Mean fiber area increased by 16% (P < 0.001) in HR and 9% (NS) in EX. Following detraining, mean fiber area returned to pre-training value only in EX. HK decreased in both groups (P < 0.01-0.001) and CK decreased in HR (P < 0.05). When the two groups were treated together, all enzymes, except for LDH, decreased their activity (P < 0.05-0.001). It is concluded that 6 months of strength training performed either as heavy-resistance or explosive training is not associated with any increased activities of enzymes reflecting Phosphagen, glycolytic, or oxidative metabolism. Instead, the present results suggest that exercise-induced hypertrophy is accompanied by attentuation of certain enzyme activities of importance for ATP regeneration.

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