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Research Article Free access | 10.1172/JCI118490

Increased acetyl group availability enhances contractile function of canine skeletal muscle during ischemia.

J A Timmons, S M Poucher, D Constantin-Teodosiu, V Worrall, I A Macdonald, and P L Greenhaff

Department of Physiology and Pharmacology, University Medical School, Queens Medical Center, Nottingham, United Kingdom.

Find articles by Timmons, J. in: PubMed | Google Scholar

Department of Physiology and Pharmacology, University Medical School, Queens Medical Center, Nottingham, United Kingdom.

Find articles by Poucher, S. in: PubMed | Google Scholar

Department of Physiology and Pharmacology, University Medical School, Queens Medical Center, Nottingham, United Kingdom.

Find articles by Constantin-Teodosiu, D. in: PubMed | Google Scholar

Department of Physiology and Pharmacology, University Medical School, Queens Medical Center, Nottingham, United Kingdom.

Find articles by Worrall, V. in: PubMed | Google Scholar

Department of Physiology and Pharmacology, University Medical School, Queens Medical Center, Nottingham, United Kingdom.

Find articles by Macdonald, I. in: PubMed | Google Scholar

Department of Physiology and Pharmacology, University Medical School, Queens Medical Center, Nottingham, United Kingdom.

Find articles by Greenhaff, P. in: PubMed | Google Scholar

Published February 1, 1996 - More info

Published in Volume 97, Issue 3 on February 1, 1996
J Clin Invest. 1996;97(3):879–883. https://doi.org/10.1172/JCI118490.
© 1996 The American Society for Clinical Investigation
Published February 1, 1996 - Version history
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Abstract

Skeletal muscle contractile function is impaired during acute ischemia such as that experienced by peripheral vascular disease patients. We therefore, examined the effects of dichloroacetate, which can alter resting metabolism, on canine gracilis muscle contractile function during constant flow ischemia. Pretreatment with dichloroacetate increased resting pyruvate dehydrogenase complex activity and resting acetylcarnitine concentration by approximately 4- and approximately 10-fold, respectively. After 20-min contraction the control group had demonstrated an approximately 40% reduction in isomeric tension whereas the dichloroacetate group had fatigued by approximately 25% (P < 0.05). Dichloroacetate resulted in less lactate accumulation (10.3 +/- 3.0 vs 58.9 +/- 10.5 mmol.kg-1 dry muscle [dm], P < 0.05) and phosphocreatine hydrolysis (15.6 +/- 6.3 vs 33.8 +/- 9.0 mmol.kg-1 dm, P < 0.05) during contraction. Acetylcarnitine concentration fell during contraction by 5.4 +/- 1.8 mmol.kg-1 dm in the dichloroacetate group but increased by 10.0 +/- 1.9 mmol.kg-1 dm in the control group. In conclusion, dichloroacetate enhanced contractile function during ischemia, independently of blood flow, such that it appears oxidative ATP regeneration is limited by pyruvate dehydrogenase complex activity and acetyl group availability.

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