Journal of Applied Physiology AJP: Endocrinology and Metabolism
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J Appl Physiol (February 8, 2002). doi:10.1152/japplphysiol.00376.2001
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Articles in PresS, published online ahead of print February 8, 2002
J Appl Physiol, 10.1152/jap.00376.2001
Submitted on April 20, 2001
Accepted on February 1, 2002

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

Ying Wang1 and Wallace G L Kerrick1*

1 Department of Physiology and Biophysics, University of Miami School of Medicine, Miami, Florida, USA

* To whom correspondence should be addressed. E-mail: wkerrick{at}miami.edu.

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 non-overlap stretch, or an unloaded shortening during a twitch caused a transient increase in intracellular Ca2+ compared to 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 (TnC) to increase (a decrease in the Ca2+ affinity of TnC), 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.




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