All of our previous work, and that of other investigators, shows that the trout heart only partially recovers following brief exposure to severe hypoxia or anoxia (i.e. it is hypoxia-sensitive). However, in preliminary studies, we found evidence to suggest that rainbow trout reared at a farm in Oregon (USA) have a significant degree of inherent myocardial hypoxia tolerance. To evaluate whether hearts from these trout are indeed hypoxia-tolerant, and thus to determine whether intra-specific variation in rainbow trout myocardial hypoxia tolerance exists, we measured in situ cardiac function and monitored myoglobin and lactate dehydrogenase (LDH) release (both indices of myocardial damage) in hearts that were exposed to varying durations (10-30 min) of severe hypoxia (P(O2) =5-10 mmHg). There was a strong positive relationship between the duration of severe hypoxia and the degree of post-hypoxic myocardial dysfunction. However, the resulting dysfunction was modest, with hearts exposed to 30 min of severe hypoxia recovering 77% of their initial maximum cardiac output. Furthermore, myoglobin was not detected in the perfusate, and ventricular LDH activity did not vary in response to the duration of severe hypoxia. These data (1) indicate that trout from this farm have extremely hypoxia-tolerant hearts; (2) suggest that considerable intra-specific variation exists in trout myocardial hypoxia tolerance; and (3) provide preliminary evidence that trout hearts are not irreversibly damaged, but are merely 'stunned', following brief periods (10-30 min) of severe hypoxia.