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Cardiovascular Research 2002 56(2):260-268; doi:10.1016/S0008-6363(02)00540-0
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Cardiac and skeletal muscle energy metabolism in heart failure: beneficial effects of voluntary activity

Elvira De Sousaa, Patrick Lechênea, Dominique Fortina, Benoît N’Guessanb, Souad Belmadania, Xavier Bigardb, Vladimir Vekslera and Renée Ventura-Clapiera,*

aU-446 INS.E.RM, Université Paris-Sud, 5 rue Jean-Baptiste Clément 92296 Châtenay-Malabry, France
bCRSSA, 38702 La-Tronche, Cedex, France

renee.ventura{at}cep.u-psud.fr

* Corresponding author. Tel.: +33-1-4683-5762; fax: +33-1-4683-5475.

Objective: Mitochondrial function and metabolic profile of slow and fast skeletal muscles and cardiac muscle are altered in chronic heart failure (CHF), suggesting a generalized metabolic myopathy in this disease. The aim of this study was to investigate the potential beneficial effects of voluntary activity on cardiac and skeletal muscle energetics in heart failure. Methods: Heart failure was induced in rats by aortic stenosis. Four months after surgery, part of sham and CHF animals were randomly assigned to activity cages equipped with running wheels for 8 weeks or kept sedentary. Mitochondrial capacity and regulation were measured using saponin skinned fibers in left ventricle, slow and fast skeletal muscles, and metabolic and myosin profiles were established. Results: Despite four times lower performances of CHF rats, alterations in metabolic and myosin parameters (oxidative capacity, mitochondrial enzymes, cytosolic and mitochondrial creatine kinase, myosin heavy chains) observed in all muscles of CHF animals were almost fully restored in soleus muscle though unchanged in heart and fast skeletal muscles. Conclusions: These results show the powerful beneficial effect of physical activity specifically on active slow oxidative skeletal muscle in CHF, without the worsening of cardiac muscle metabolism.

KEYWORDS Energy metabolism; Glycolysis; Heart failure; Mitochondria; Oxidative phosphorylation


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