Contractile apparatus and sarcoplasmic reticulum function: effects of fatigue, recovery, and elevated Ca2+

This investigation tested the notion that fatiguing stimulation induces intrinsic changes in the contractile apparatus and sarcoplasmic reticulum (SR) and that these changes are initiated by elevated intracellular Ca2+ concentration ([Ca2+]i). Immediately after stimulation of frog semitendinosus muscle, contractile apparatus and SR function were measured. Despite a large decline in tetanic force (Po), maximal Ca2+-activated force (Fmax) of the contractile apparatus was not significantly altered. However, Ca2+ sensitivity was increased. In conjunction, the rate constant of Ca2+ uptake by the SR was diminished, and the caffeine sensitivity of Ca2+ release was decreased. During recovery, Po, contractile apparatus, and SR function each returned to near-initial levels. Exposure of skinned fibers to 0.5 microM free Ca2+ for 5 min depressed both Fmax and Ca2+ sensitivity of the contractile apparatus. In addition, caffeine sensitivity of Ca2+ release was diminished. Results suggest that fatigue induces intrinsic alterations in contractile apparatus and SR function. Changes in contractile apparatus function do not appear to be mediated by increased [Ca2+]i. However, a portion of the change in SR Ca2+ release seems to be due to elevated [Ca2+]i.