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Am J Physiol Regul Integr Comp Physiol 258: R352-R357, 1990;
0363-6119/90 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 258, Issue 2 352-R357, Copyright © 1990 by American Physiological Society


ARTICLES

Evidence of a slow-to-fast fiber type transition in skeletal muscle from spontaneously hypertensive rats

L. Ben Bachir-Lamrini, B. Sempore, M. H. Mayet and R. J. Favier
Laboratoire de Physiologie, Faculte de Medecine Grange Blanche, Universite Claude Bernard, Lyon, France.

The histochemical, biochemical, and electrophysiological properties of selected muscles were evaluated in spontaneously hypertensive rats (SHR) and compared with their normotensive Wistar-Kyoto (WKY) counterparts. As early as 4 wk of age, slow muscles (soleus) of SHR displayed a significant alteration in fiber type distribution with a decrease of slow-twitch fibers (from 64 to 53%) and a simultaneous increase of type IIA-fibers (from 19 to 39%). In addition, soleus from young SHR had a significant enhancement of both oxidative (citrate synthase, 3-hydroxyacyl-CoA dehydrogenase) and glycolytic [lactate dehydrogenase (LDH)] capacities, which could be partly related to a capillary rarefaction. During development (from the 4th to the 12-14th wk), in the soleus muscle the histochemical differences between SHR and WKY were amplified, whereas most of the enzymatic differences between strains were abolished, except for a significantly higher LDH activity. These histochemical changes had only marginal repercussions on soleus electrophysiological properties. SHR animals had a significantly higher basal metabolic rate, which could not be accounted for by elevation of thyroid hormones. The origin of the slow-to-fast fiber type transition in slow muscle remains unclear but could be related to the increased level of plasma catecholamines in SHR. Indeed, chronic treatment of rats with a beta 2-receptor agonist has been reported to cause slow-to-fast muscle fiber transition [R. J. Zeman, R. Ludemann, T. G. Easton, and J. D. Etlinger. Am. J. Physiol. 254 (Endocrinol. Metab. 17): E726-E732, 1988].


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