Aim: The present study was to investigate the protective effects and mechanisms of heat preconditioning (HP) on myocardial injury induced by the overload training. Methods: A total of 25 male Sprague-Dauley (SD) rats were randomly divided into three groups: control group, training group and HP group. The activities of creatine kinase (CK), catalase (CAT) and superoxide dismutase (SOD) of myocardium, apoptosis index (AI), expressions of Bcl-2, Bax, caspase-3, caspase-9, ICAM-1, VCAM-1, and PECAM-1 were determined after 8-week overload training. Results: Results showed the CK activity, myocardial apoptosis rate and AI in training group were significantly higher than control group and HP group (P0.05). The Bcl-2 expression in HP group was significantly higher than control group and training group, while the ratio of Bcl-2/Bax of training group was significantly lower than control group and HP group. The expressions of caspase-3, caspase-9, ICAM-1, VCAM-1 and PECAM-1 in training group and HP group were significantly higher than control group. Significant differences in the expressions of caspase-3, and caspase-9 was also noted between training group and HP group, but there was no marked difference in the expressions of ICAM-1, VCAM-1 and PECAM-1 between these two groups. Conclusion: HP could adjust the activities of CK, CAT and SOD, regulate the expressions of apoptosis-related genes and adhesion molecules resulting in enhanced capacity against overload training induced injury and reduced damage to the myocardium.
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