HEAT PRODUCED BY RABBIT PAPILLARY-MUSCLE DURING ANOXIA AND REOXYGENATION

Resting heat rate was measured in superfused rabbit papillary muscles at 20-degrees-C during 40 minutes of anoxia and subsequent reoxygenati on. To reveal the nature of the reactions underlying energy output und er such conditions, the data obtained were compared with values predic ted from data on chemical change. Before and after the anoxic period, muscles were stimulated at 0.2 Hz, during which time the contraction-r elated heat rate was measured. During anoxia, muscles were kept at res t or stimulated at 1 Hz. Stimulation was switched off intermittently t o determine resting heat rate. Before anoxia, resting heat rate was 8. 7 +/- 1.1 (mean +/- SEM) mW . g dry wt-1. During anoxia, it decreased to 38% and 50% of the preanoxic level in resting and stimulated muscle s, respectively (P<.05). In resting muscles, heat rate increased with reoxygenation in approximately 10 to 15 minutes to 1.3 times the prean oxic level, whereas this was 3.7 times in stimulated muscles. Resting heat rate returned within 65 (resting muscles) or 150 (stimulated musc les) minutes to the baseline. The ratio of force- and contraction-rela ted heat rate, ie, the economy of contraction, was not different befor e and after anoxia. We estimated that the heat produced by muscles dur ing anoxia was not different from the heat to be expected from the hyd rolysis of creatine phosphate, the breakdown of nucleotides, and the f ormation of lactate. The overshoot in resting heat during reoxygenatio n of resting muscles could be accounted for by the resynthesis of the energy store. The much larger overshoot in resting heat of stimulated muscles was due to the contracture. The finding that the economy of co ntraction was not altered by anoxia and reoxygenation suggests that bo th sarcoplasmic reticulum Ca2+-ATPase and myofibrillar ATPase are depr essed by anoxia and that the enhancement of cytosolic calcium transien ts with reoxygenation, reported in other studies on papillary muscle, results from reduced binding of calcium rather than from enhanced rele ase.