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Dihydropyridine and ryanodine receptor binding after eccentric contractions in mouse skeletal muscle

¹Muscle Biology Laboratory, Department of Kinesiology and Health, Georgia State University, Atlanta, Georgia 30303; ²Muscle Biology Laboratory, Department of Health and Kinesiology, Texas A&M University, College Station 77843-4243; and ³Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030

Submitted 29 January 2003 ; accepted in final form 11 December 2003

The purpose of this study was to determine whether there are alterations in the dihydropyridine and/or ryanodine receptors that might explain the excitation-contraction uncoupling associated with eccentric contraction-induced skeletal muscle injury. The left anterior crural muscles (i.e., tibialis anterior, extensor digitorum longus, and extensor hallucis longus) of mice were injured in vivo by 150 eccentric contractions. Peak isometric tetanic torque of the anterior crural muscles was reduced 45% immediately and 3 days after the eccentric contractions. Partial restoration of peak isometric tetanic and subtetanic forces of injured extensor digitorum longus muscles by 10 mM caffeine indicated the presence of excitation-contraction uncoupling. Scatchard analysis of [³H]ryanodine binding indicated that the number of ryanodine receptor binding sites was not altered immediately postinjury but decreased 16% 3 days later. Dihydropyridine receptor binding sites increased 20% immediately after and were elevated to the same extent 3 days after the injury protocol. Muscle injury did not alter the sensitivity of either receptor. These data suggest that a loss or altered sensitivity of the dihydropyridine and ryanodine receptors does not contribute to the excitation-contraction uncoupling immediately after contraction-induced muscle injury. We also concluded that the loss in ryanodine receptors 3 days after injury is not the primary cause of excitation-contraction uncoupling at that time.

voltage sensor; sarcoplasmic reticulum calcium release channel; injury

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