Activation heat in rabbit cardiac muscle.

1. Activation heat was estimated myothermically in right ventricular papillary muscles of rabbits using several different methods. 2. Gradual pre‐shortening of muscles to a length (lmin) where no active force development took place upon stimulation led to relatively low estimates of activation heat (1.59 +/‐ 0.26‐2.06 +/‐ 0.57 mJ g‐1 blotted wet weight, mean +/‐ S.E.M., n = 10). 3. Quick releases applied during the latency period, before force development, from lmax to various muscle lengths allowed a heat‐stress relation to be established. The zero‐stress intercept of this relation estimated the activation heat to be 3.27 +/‐ 0.40 mJ g‐1; this was close to the experimentally measured value of 3.46 +/‐ 0.39 mJ g‐1 (mean +/‐ S.E.M., n = 23) found by quick release from lmax to lmin. 4. The magnitude of the activation heat measured by the quick‐release technique is dependent upon the extracellular Ca2+ concentration and there is good correlation between activation heat magnitude and peak developed stress. 5. In agreement with expectations based on the aequorin data of Allen & Kurihara (1982) a prolonged period of time spent at a short length is shown to depress the subsequently determined activation heat. 6. Hyperosmotic solutions (2.5 x normal) only abolished active stress development at low stimulus rates (0.2 Hz) and the activation heat measured at lmax under these conditions was 2.03 +/‐ 0.12 mJ g‐1 (mean +/‐ S.E.M., n = 6). This value was significantly lower than the latency release estimate of activation heat in the same preparations (2.93 +/‐ 0.39 mJ g‐1). 7. The latency release method of estimating activation heat results in activation heat values that account for approximately 30% of total active energy flux per contraction; a fraction comparable to that found in skeletal muscle. Calculations based on the data suggest that, under our experimental conditions, total Ca2+ release per beat lies between 50 and 100 nmol g‐1 wet weight which would produce less than half‐maximal myofibrillar ATPase activity when allowance is made for the passive Ca2+‐buffering capacity of the myocardial cell.