Journal of Applied Physiology
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J Appl Physiol 92: 2409-2418, 2002. First published February 8, 2002; doi:10.1152/japplphysiol.00376.2001
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Vol. 92, Issue 6, 2409-2418, June 2002

The off rate of Ca2+ from troponin C is regulated by force-generating cross bridges in skeletal muscle

Ying Wang and W. Glenn L. Kerrick

Department of Physiology and Biophysics, University of Miami School of Medicine, Miami, Florida 33101

The effects of dissociation of force-generating cross bridges on intracellular Ca2+, 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 Ca2+ 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 Ca2+ concentrations and caused actomyosin ATPase rate to decrease at submaximal Ca2+ and increase at maximal Ca2+ activation. These results suggest that dissociation of force-generating cross bridges during a twitch causes the off rate of Ca2+ from troponin C to increase (a decrease in the Ca2+ affinity of troponin C), thus decreasing the Ca2+ 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 Ca2+ concentrations.

force; intracellular calcium ion; actomyosin adenosinetriphosphatase; mechanical length perturbation; deactivation


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