Effects of heat preconditioning on overload training induced myocardial injury

The present study was to investigate the protective effects and mechanisms of heat preconditioning (HP) on myocardial injury induced by the overload training.

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 showed the CK activity, myocardial apoptosis rate and AI in training group were significantly higher than control group and HP group (P<0.05), while the activities of CAT and SOD of training group and HP group were slightly lower than control group (P>0.05). 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.

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.