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

Ying Wang, W. Glenn L. Kerrick

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)2409-2418
Number of pages10
JournalJournal of applied physiology
Issue number6
StatePublished - 2002


  • Actomyosin adenosinetriphosphatase
  • Deactivation
  • Force
  • Intracellular calcium ion
  • Mechanical length perturbation

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation


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