Mammalian muscle fiber types: comparison of excitation-contraction coupling mechanisms.
The mechanism of fatigue of single skeletal muscle fibers appears to involve failure or inactivation of excitation-contraction (EC) coupling. The communication between transverse tubule (TT) and sarcoplasmic reticulum (SR) membranes, whereby plasmalemma voltage controls SR Ca2+ release, may involve inositol trisphosphate (IP3) as a chemical signal. IP3 has already been shown to cause SR Ca2+ release in skeletal fast-twitch fibers; the purpose of this paper is to show that IP3 has similar effects on rabbit slow twitch fibers from soleus muscle. IP3 appears to trigger SR Ca2+ release via a mechanism which is independent of the Ca2+ induced one, since it elicits regenerative SR Ca2+ release in the presence of 20 mM procaine. IP3 also acts at a step in EC coupling beyond TT depolarization, making it a likely candidate for a TT-SR chemical signal. The possible relationship of an IP3 chemical signaling mechanism to skeletal muscle fiber fatigue and mammalian fiber type differences are discussed.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D066298:In Vitro Techniques; D015544:Inositol 1,4,5-Trisphosphate; D007295:Inositol Phosphates / Q000502:physiology; D009119:Muscle Contraction; D009132:Muscles / Q000378:metabolism*; D010716:Phosphatidylinositols / Q000378:metabolism; D010807:Physical Endurance
D007295:Inositol Phosphates; D010716:Phosphatidylinositols; D015544:Inositol 1,4,5-Trisphosphate; D002118:Calcium