Myofilaments: The End Effector of E-C Coupling

Abstract

When cytoplasmic [Ca] rises, the myofilaments are activated in a [Ca]-dependent manner, thereby transducing the chemical signal and chemical energy (ATP) into mechanical force or shortening. Under physiological conditions, skeletal muscle contractile force can be varied by summation of contractions, tetanus and recruitment of additional fibers. Cardiac muscle, on the other hand, functions as a syncytium such that each cell contracts at every beat. The heart must also relax between contractions. Thus, there is neither the practical possibility of recruitment of additional cells, nor summation, nor tetanization to alter the force of contraction to meet altered demands. Therefore, in cardiac muscle, the force of contraction is varied in large part by changes in the peak [Ca]_i reached during systole (as well as sarcomere length).