Rainbow trout (Oncorhynchus mykiss) are likely to experience acute changes in both temperature and oxygen availability and, like many other organisms, exhibit behavioural selection of low temperatures during hypoxia that acts to reduce metabolism and alleviate the demands on the heart. To investigate whether low temperature protects cardiac performance during anoxia, we studied the effects of an acute temperature change, from 10 degrees C to either 5 degrees C, 15 degrees C or 18 degrees C, upon the performance of in situ perfused trout hearts before, during and after exposure to 20 min of anoxia. Routine cardiac workload mimicked in vivo conditions at the given temperatures, and the effects of anoxia were evaluated as maximal cardiac performance before and after 20 min of anoxic perfusion. Functional data were related to maximal activities of glycolytic enzymes and energetic status of the heart at the termination of the experiment. At high oxygenation, maximum cardiac output and power output increased with temperature (Q10 values of 1.8 and 2.1, respectively) as a result of increased heart rate. Hypoxia tolerance was inversely related to temperature. At 5 degrees C, the hearts maintained routine cardiac output throughout the 20 min period of anoxia, and maximal cardiac performance was fully restored following reoxygenation. By contrast, cardiac function failed sooner during anoxia as temperature was increased and maximal performance after reoxygenation was reduced by 25%, 35% and 55% at 10 degrees C, 15 degrees C and 18 degrees C, respectively. Increased functional impairment following anoxic exposure at elevated temperature occurred even though both cardiac glycolytic enzyme activity and the rate of lactate production were increased proportionally with cardiac work. Nonetheless, there was no indication of myocardial necrosis, as biochemical and energetic parameters were generally unaffected by anoxia.