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Pflugers Archiv : European journal of physiology1994; 427(3-4); 257-263; doi: 10.1007/BF00374532

Effect of exercise on hexokinase distribution and mitochondrial respiration in skeletal muscle.

Abstract: Horses were subjected to treadmill running at 65% (submaximal) or 100% (maximal) VO2,max to examine the effects of exercise on subcellular distribution of hexokinase (HK) and on mitochondrial respiration. It is hypothesized that the fraction of HK bound to mitochondria will be reduced due to an elevation of glucose-6-phosphate (G-6-P) concentration in the exercising muscle and that such release of HK from mitochondria will depress oxidative phosphorylation. Changes in muscle G-6-P concentration, pH, subcellular HK distribution, mitochondrial respiration and other metabolites were determined in biopsy samples pre-exercise, immediately post-exercise and during the recovery phase. The fraction of HK associated with mitochondria decreased from 38% to 7% at the end of maximal exercise; exercise at VO2,max also reduced respiratory capacity of muscle homogenates by 20% and was associated with a fivefold increase in muscle [G-6-P], a potent agent known to dissociate HK from mitochondria. The HK distribution returned to normal within 60 min after exercise and the reassociation of the HK with mitochondria parallelled the removal of muscle G-6-P. No changes in muscle HK distribution and respiration were found following the submaximal exercise despite the fact that G-6-P was slightly elevated. Muscle concentrations of adenosine triphosphate, creatine phosphate and glycogen and pH dropped after exercise while lactate concentration increased. The amount of mitochondria-bound HK was also altered in vitro in a preparation of mitochondria isolated from rat skeletal muscle to examine the effect of the bound HK on mitochondrial respiration.(ABSTRACT TRUNCATED AT 250 WORDS)
Publication Date: 1994-06-01 PubMed ID: 8072844DOI: 10.1007/BF00374532Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research demonstrates that intense exercise in horses causes a significant decrease in the amount of the enzyme hexokinase associated with muscle mitochondria, and a corresponding decrease in respiratory capacity of the muscle tissue. The result is influenced by the concurrent massive increase in the concentration of glucose-6-phosphate in the working muscles.

Objective and Methodology

  • The research focuses on understanding the effects of exercise at various intensities on the enzyme hexokinase’s subcellular distribution and the mitochondrial respiration in the skeletal muscle of horses.
  • The horses were made to run on a treadmill at 65% (submaximal) and 100% (maximal) of their maximum oxygen uptake (VO2,max) capacities.
  • The researchers hypothesized that the undergoing exercise would cause a reduced fraction of hexokinase bound to the mitochondria due to high glucose-6-phosphate (G-6-P) concentration in the exercising muscles, thereby depressing oxidative phosphorylation.

Findings

  • Exercise resulted in changes in muscle G-6-P concentration, pH, hexokinase distribution, mitochondrial respiration, and other metabolites. These changes were measured using biopsy samples pre, post, and during recovery from exercise.
  • Maximal exercise led to a decrease in the proportion of hexokinase associated with mitochondria from 38% to 7% and a 20% reduction in the muscle tissues’ respiratory capacity. They also noticed a fivefold increase in muscle glucose-6-phosphate levels, which is known to dissociate hexokinase from the mitochondria.
  • The distribution of hexokinase returned to normal within 60 minutes after exercise in correlation with the reduction of muscle glucose-6-phosphate.
  • Mild exercise didn’t exhibit any changes in hexokinase distribution and mitochondrial respiration, although glucose-6-phosphate was slightly elevated.
  • Muscle concentrations of adenosine triphosphate, creatine phosphate, and glycogen dropped post-exercise, and the pH and lactate concentration increased.
  • In vitro studies on isolated rat skeletal muscle mitochondria showed changes in the amount of mitochondria-bound hexokinase, examining its effect on mitochondrial respiration.

Conclusion

  • Essentially, the research study concluded that increased exercise intensity results in a decrease in the amount of the enzyme hexokinase bound to muscle mitochondria and decreases the respiratory capacity of the muscle tissue. The primary influential factor for this change was the increase in the concentration of glucose-6-phosphate in the working muscles.

Cite This Article

APA
Chen J, Gollnick PD. (1994). Effect of exercise on hexokinase distribution and mitochondrial respiration in skeletal muscle. Pflugers Arch, 427(3-4), 257-263. https://doi.org/10.1007/BF00374532

Publication

ISSN: 0031-6768
NlmUniqueID: 0154720
Country: Germany
Language: English
Volume: 427
Issue: 3-4
Pages: 257-263

Researcher Affiliations

Chen, J
  • Department of Veterinary and Comparative Anatomy, Pharmacology, College of Veterinary Medicine, Pullman, WA 99164-6520.
Gollnick, P D

    MeSH Terms

    • Adenosine Triphosphate / metabolism
    • Animals
    • Glucose-6-Phosphate
    • Glucosephosphates / metabolism
    • Glycogen / metabolism
    • Hexokinase / metabolism
    • Horses
    • Hydrogen-Ion Concentration
    • Lactates / metabolism
    • Lactic Acid
    • Magnesium / physiology
    • Male
    • Mitochondria, Muscle / drug effects
    • Mitochondria, Muscle / enzymology
    • Mitochondria, Muscle / metabolism
    • Oxygen Consumption
    • Phosphocreatine / metabolism
    • Physical Exertion / physiology
    • Rats
    • Rats, Sprague-Dawley

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    Citations

    This article has been cited 2 times.
    1. Layec G, Blain GM, Rossman MJ, Park SY, Hart CR, Trinity JD, Gifford JR, Sidhu SK, Weavil JC, Hureau TJ, Amann M, Richardson RS. Acute High-Intensity Exercise Impairs Skeletal Muscle Respiratory Capacity. Med Sci Sports Exerc 2018 Dec;50(12):2409-2417.
      doi: 10.1249/MSS.0000000000001735pubmed: 30102675google scholar: lookup
    2. Tonkonogi M, Harris B, Sahlin K. Mitochondrial oxidative function in human saponin-skinned muscle fibres: effects of prolonged exercise. J Physiol 1998 Jul 1;510 ( Pt 1)(Pt 1):279-86.