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Am J Physiol Cell Physiol 274: C1718-C1726, 1998;
0363-6143/98 $5.00
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Vol. 274, Issue 6, C1718-C1726, June 1998

Effect of clenbuterol on sarcoplasmic reticulum function in single skinned mammalian skeletal muscle fibers

Anthony J. Bakker1, Stewart I. Head2, Anthony C. Wareham3, and D. George Stephenson4

1 Department of Physiology, University of Western Australia, Nedlands 6907; 2 School of Physiology and Pharmacology, University of New South Wales, Sydney 2052; 4 School of Zoology, La Trobe University, Bundoora 3083, Australia; and 3 Division of Neuroscience, School of Biological Sciences, University of Manchester, Manchester M13 9PT, United Kingdom

We examined the effect of the beta 2-agonist clenbuterol (50 µM) on depolarization-induced force responses and sarcoplasmic reticulum (SR) function in muscle fibers of the rat (Rattus norvegicus; killed by halothane overdose) that had been mechanically skinned, rendering the beta 2-agonist pathway inoperable. Clenbuterol decreased the peak of depolarization-induced force responses in the extensor digitorum longus (EDL) and soleus fibers to 77.2 ± 9.0 and 55.6 ± 5.4%, respectively, of controls. The soleus fibers did not recover. Clenbuterol significantly and reversibly reduced SR Ca2+ loading in EDL and soleus fibers to 81.5 ± 2.8 and 78.7 ± 4.0%, respectively, of controls. Clenbuterol also produced an ~25% increase in passive leak of Ca2+ from the SR of the EDL and soleus fibers. These results indicate that clenbuterol has direct effects on fast- and slow-twitch skeletal muscle, in the absence of the beta 2-agonist pathway. The increased Ca2+ leak in the triad region may lead to excitation-contraction coupling damage in the soleus fibers and could also contribute to the anabolic effect of clenbuterol in vivo.

calcium uptake; calcium leak; calcium release; beta -agonist; excitation-contraction coupling; anabolism


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