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The Journal of Sports Medicine and Physical Fitness 2013 February;53(1):93-100

Copyright © 2013 EDIZIONI MINERVA MEDICA

lingua: Inglese

Effects of heat preconditioning on overload training induced myocardial injury

Yang Y. ¹, Li Z. ², Liu H. ¹, Shi W. ³, Zhang J. ³ ✉

¹ College of Health Science, Wuhan Institute of Physical Education, Wuhan, China; ² Renmin Hospital, Wuhan University, Wuhan, China; ³ Graduate Department, Wuhan Institute of Physical Education, Wuhan, China

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 (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.
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.