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Pretreatment of K+-deprived rat diaphragm with insulin caused a 38% increase in input resistance and a decline in K+ current in the skeletal muscle, resulting in membrane depolarization and deactivation. Depolarization in K+-depleted muscle is induced by insulin-associated blockage of K+ channels and is maintained by triggering noninactivating Na+ channels. Conductance in K+-depleted fibers is opposed by a large leakage current in the absence of insulin. The diminished outward current is distinct from the inward current carried by Ca2+, as demonstrated by the decline in insulin-induced current in nitrendipine.

The effects of calcium and phosphate on glycerinated psoas fibers were determined by adding increasing levels of calcium and orthophosphate (Pi) to bathing solutions. Results show that stiffness (K) was more sensitive to calcium than force (F) and increasing Pi causes a decrease in calcium sensitivity for both K and F. These results suggest that crossbridges can occur in both force-producing and non-force-producing states and that the relative population of these states may be dependent on calcium.