Heat stress limits the injury associated with myocardial ischaemia and reperfusion, an effect previously attributed to enhanced endogenous anti-oxidant activity. We examined the influence of heat stress on the calcium paradox, an injury in which oxidant stress is not thought to play a major role. Twenty-four hours following sham or true heat stress, rabbits were re-anaesthetized and hearts either removed for stress protein analysis (n = 8), or Langendorff-perfused (n = 20) and subjected to a calcium paradox. Ten minutes following calcium repletion (Ca2+ = 1.3 mM), left ventricular developed pressure was better preserved in heat stress vs control hearts (38.3 +/- 5.0 vs 18.8 +/- 4.1 mmHg, respectively, P = 0.003) whilst contracture, measured by left ventricular end-diastolic pressure, was diminished (21.6 +/- 4.7 vs 39.9 +/- 5.2 mmHg, respectively, P = 0.02). Creatine phosphokinase release at 1 min was less in heat stress vs control hearts (10.6 +/- 8.6 vs 86.4 +/- 33.7 U/min/g, respectively, P = 0.01). The myocardial content of the 72 kDa stress protein was elevated eight-fold in heat stress vs control hearts (2.8 +/- 0.2 vs 0.4 +/- 0.1 U, respectively, P = 0.01). This study suggests that some portion of the stress protein response represents a form of cardiac adaptation capable of limiting myocyte injury independent of antioxidant mechanisms.