To clarify the roles of Ca2+ and crossbridge kinetics in determining the cardiac contraction profile, we analyzed the rate of tension development following nitrophenyl-EGTA photolysis and the rate of relaxation following diazo-2 photolysis in the absence and presence of phosphate (Pi, 5 mM) in rat skinned ventricular trabeculae. The rate of tension development was fitted with a single exponential function. The rate constant (kc) increased not only with an increase in prephotolysis tension (initial activation level) under the same postphotolysis tension (final Ca2+ level), but also with an increase in postphotolysis tension under the same prephotolysis tension. Pi increased kc, though decreased both the prephotolysis and postphotolysis tension greatly. The rate of relaxation was fitted with a double-exponential function. The rate constants of both initial rapid phase (kr1), which was higher than kc, and subsequent slow (kr2) relaxation were almost independent of either the prephotolysis tension or the postphotolysis tension (i.e. the extent of relaxation). Pi increased both kr1 and kr2 by about twofold. These results apparently contradicting both the "steric blocking model" and the "kinetic model", and can be explained in terms of the changes in number of tension-generating crossbridges through the Ca2+-dependent cooperative thin filament activation/inactivation associated with the Pi-modulated changes in number of tension-generating crossbridges. The thin filament activation kinetics seems to be slower than its inactivation.