Maximum Rate Of Shortening Research Articles

Temperature dependence of the crossbridge cycle during unloaded shortening and maximum isometric tetanus in frog skeletal muscle.

The primary objective of this study was to determine if the rate limiting step in the crossbridge cycle was the same during maximum rate of shortening and during maintenance of maximum tension in an isometric contraction. To this end the temperature dependence, Q10, of the crossbridge cycle was estimated during unloaded shortening and maximum isometric tetanus. Isolated semitendinosus muscles from the frog were studied at 0 and 10 degrees C. Crossbridge cycling during unloaded shortening was determined from the velocity of unloaded shortening estimated by the slack step technique. Crossbridge cycling during maintained isometric tetanus was determined from the steady rate of energy liberation during the tetanus after allowance for energy liberation due to Ca2+ cycling. The Q10 of the velocity of unloaded shortening was 2.5 and that of the steady rate of energy liberation was 4.6. After correction for the temperature dependence of energy liberation associated with Ca2+ cycling (5.7), the estimated Q10 of the steady rate of energy liberation became 3.9. These estimates of the Q10 of the crossbridge cycle are significantly different. These results support the conclusion that the rate limiting steps during unloaded shortening and maximum isometric force maintenance occur at different steps in the crossbridge cycle. Further the high Q10 of the energy liberation due to Ca2+ cycling may relate to the high concentration of parvalbumin in frog muscle. A second objective of this study was to document in the same muscle the variation of Q10s of mechanical and energetic properties of contraction. Over this temperature range the Q10s ranged from 1.1 to 5.7.

Contractility of isolated bovine ventricular myocytes is enhanced by intracellular injection of cardioactive glycosides. Evidence for an intracellular mode of action.

The contractions of isolated bovine left ventricular myocytes were evaluated by optically measuring the extent of unloaded shortening (ES), the maximal rate of shortening (MRS) and the maximal rate of re-lengthening (MRL). Ouabain, digoxin or digitoxin were intracellularly injected by 2 sec long pressure pulses via the microelectrodes. Their i.c. concentration was estimated to be 2-5 nM. Within 1-4 min after the injection, ES, MRS and MRL increased by more than 2-fold. The contractility renormalized within the following 20 min. Injection of solutions without glycosides did not increase the contractility. An interaction of the injected glycoside with the e.c. ouabain receptor could be largely excluded because a) the amount of the released glycoside was too small for e.c. effects, b) 500 nM e.c. antidigoxin, c) 20 mM [K]o or d) covalent binding of digoxin to HSA did not prevent the increase in contractility due to the i.c. injections. Since contractility also increased when the injections were performed at Na-free conditions, [Na]i-load is not necessary for the effect of i.e. glycosides. The increased contractility due to the injected glycosides was not observed when the contractility prior to the injection was already potentiated, e.g. by greater than 3.6 mM [Ca]o or by stimulation at frequencies greater than 1.25 Hz. The results are interpreted by the hypothesis that the i.c. glycosides facilitate the release of activator calcium from the SR. The possible i.c. modes of action are discussed as well as the idea that e.c. applied glycosides internalize and mediate inotropy via the i.e. mechanism.