DIHYDROPYRIDINE AND RYANODINE RECEPTOR BINDING AFTER ECCENTRIC CONTRACTIONS IN MOUSE SKELETAL MUSCLE

Abstract

193 The purpose of this study was to determine if alterations in the dihydropyridine (DHP) and/or ryanodine (RY) receptors explain the excitation-contraction uncoupling associated with eccentric contraction-induced skeletal muscle injury. The left anterior crural muscles of mice were injured in vivo by 150 eccentric contractions. Scatchard analysis of ligand binding of [3H]PN200-110 to the DHP receptor and [3H]ryanodine to the RY receptor were performed on tibialis anterior (TA) muscle homogenates immediately after and 3 d after the injury protocol. Peak isometric tetanic torque of the anterior crural muscles was reduced 45% immediately after the eccentric contractions. TA muscle protein content was reduced 10% 3 d after the injury protocol. Compared with contralateral control muscles, the absolute (pmol/muscle) number (Bmax) of DHP receptors increased ∼20% immediately after and 3 d following the injury protocol, whereas the Kd was unchanged. The Bmax (pmol/muscle) of the RY receptor decreased 17% 3 d after initiation of the injury, whereas Kd was unchanged, when compared with control muscles. These data suggest that a loss or altered sensitivity of the DHP receptor does not contribute to the EC uncoupling associated with eccentric contraction-induced muscle injury. However, reductions in RY receptors may contribute to EC uncoupling 3 d after initiation of the injury. Supported by the Omar Smith Chair