Do mechanical length perturbations alter intracellular Ca2+ handling and force generation in mouse skeletal muscle?
Dissociation of force-generating cross bridges during a twitch increases the off rate of Ca2+ from troponin C, decreasing Ca2+ sensitivity and resulting in muscle deactivation.
The effects of dissociation of force-generating cross bridges on intracellular Ca 2+ , pCa-force, and pCa-ATPase relationships were investigated in mouse skeletal muscle. Mechanical length perturbations were used to dissociate force-generating cross bridges in either intact or skinned fibers. In intact muscle, an impulse stretch or release, a continuous length vibration, a nonoverlap stretch, or an unloaded shortening during a twitch caused a transient increase in intracellular Ca 2+ compared with that in isometric controls and resulted in deactivation of the muscle. In skinned fibers, sinusoidal length vibrations shifted pCa-force and pCa-actomyosin ATPase rate relationships to higher Ca 2+ concentrations and caused actomyosin ATPase rate to decrease at submaximal Ca 2+ and increase at maximal Ca 2+ activation. These results suggest that dissociation of force-generating cross bridges during a twitch causes the off rate of Ca 2+ from troponin C to increase (a decrease in the Ca 2+ affinity of troponin C), thus decreasing the Ca 2+ sensitivity and resulting in the deactivation of the muscle. The results also suggest that the Fenn effect only exists at maximal but not submaximal force-activating Ca 2+ concentrations.
Wang et al. (Sat,) studied this question.
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