AJP - Heart and Circulatory Physiology, Vol 271, Issue 5 1739-H1745, Copyright © 1996 by American Physiological Society
Skeletal muscle beta-adrenoreceptors and phosphate metabolism abnormalities in heart failure in rats
Z. Chati, C. Michel, J. M. Escanye, P. M. Mertes, C. Ribuot, D. Canet and F. Zannad
Department of Cardiology and Pharmacology, University of Henri Poincare, Nancy, France.
To investigate the mechanisms leading to skeletal muscle metabolic
abnormalities in chronic heart failure (CHF), we studied phosphate
metabolism and skeletal muscle beta-adrenoreceptors (beta-AR) in rats 12-14
wk after coronary ligation (CL). We performed 31P magnetic resonance
spectroscopy in the gastrocnemius muscle during motor activity produced by
electrical stimulation (5 Hz). The initial slope of phosphocreatine (PCr)
depletion was higher in the CL rats compared with sham-operated rats
(Pi/PCr/time: 0.211 +/- 0.045 vs. 0.113 +/- 0.029; P < 0.05). During
recovery, both PCr resynthesis rate and maximal rate of oxidative ATP
synthesis were reduced threefold in the CL rats compared with controls (11
+/- 2 vs. 37 +/- 7 mmol.l-1.min-1, P < 0.04; and 20 +/- 3 vs. 79 +/- 18
mmol.l-1.min-1, P < 0.03, respectively). There were no significant
differences either for the skeletal muscle density (13 +/- 6 vs. 15 +/- 3
fM/mg) or for the affinity (0.244 +/- 0.149 vs. 0.246 +/- 0.146 nM) of
beta-AR between the two groups. This study showed that, although in
moderate CHF skeletal muscle metabolic abnormalities can be demonstrated,
these changes could not be explained by skeletal muscle beta-adrenergic
receptor alterations in this experimental model.
