CHANGES IN FORCE AND CYTOSOLIC CA2+ CONCENTRATION AFTER LENGTH CHANGES IN ISOLATED RAT VENTRICULAR TRABECULAE

1. Changes in cytosolic [Ca2+] ([Ca2+](i)) were measured in isolated r at trabeculae that had been micro-injected with fura-2 salt, in order to investigate the mechanism by which twitch force changes following a n alteration of muscle length. 2. A step increase in length of the mus cle produced a rapid potentiation of twitch force but not of the Ca2transient. The rapid rise of force was unaffected by inhibiting the sa rcoplasmic reticulum (SR) with ryanodine and cyclopiazonic acid. 3. Th e force-[Ca2+](i) relationship of the myofibrils in situ, determined f rom twitches and tetanic contractions in SR-inhibited muscles, showed that the rapid rise of force was due primarily to an increase in myofi brillar Ca2+ sensitivity, with a contribution from an increase in the maximum force production of the myofibrils. 4. After stretch of the mu scle there was a further, slow increase of twitch force which was due entirely to a slow increase of the Ca2+ transient, since there was no change in the myofibrillar force-[Ca2+](i) relationship. SR inhibition slowed down, but did not alter the magnitude of, the slow force respo nse. 5. During the slow rise of force there was no slow increase of di astolic [Ca2+](i), whether or not the SR was inhibited. The same was t rue in unstimulated muscles. 6. We conclude that the rapid increase in twitch force after muscle stretch is due to the length-dependent prop erties of the myofibrils. The slow force increase is not explained by length dependence of the myofibrils or the SR, or by a rise in diastol ic [Ca2+](i). Evidence from tetani suggests the slow force responses r esult from increased Ca2+ loading of the cell during the action potent ial.