Abstract: BACKGROUND: Studies have shown that long-term regular aerobic exercises can lower blood pressure and improve ventricular remodeling caused by hypertensive myocardial hypertrophy and myocardial fibrosis.
OBJECTIVE: To investigate the effects of swimming exercise preconditioning on myocardial apoptosis and remodeling in mice during pressure overload compensatory period.
METHODS: Male C57B/L6 mice aged 6-7 weeks were randomly divided into control group, exercise group, operation group and operation+exercise group. Mice in the exercise and operation+exercise groups were subjected to 4-week swimming exercises (90 minutes per session, twice per day, and 7 days per week). Transverse aorta constriction was then used to construct a model of myocardial remodeling in the operation and operation+exercise groups. The aorta was ligated with a 27G needle to make the aorta constricted by more than 70%. Two weeks later, cardiac ultrasonography was performed and myocardial samples were collected to observe the apoptosis of myocardial cells. The expression levels of heat shock protein 70 and P53 proteins in mouse myocardial tissue were detected by western blot. The expression levels of P53, Bcl-2 and Bax in mice were detected by RT-PCR.
RESULTS AND CONCLUSION: The heart was in the compensatory stage at 2 weeks after TAC surgery. Compared with the control group, the heart weight index and left ventricular shorting rate were significantly increased in the operation group (P < 0.01), the ventricular wall thickness and myocardial fibrosis were significantly increased (P < 0.01), but the heart function was not significantly decreased. Compared with the operation group, the ventricular wall thickness was significantly lower in the operation+exercise group (P < 0.05), and the level of myocardial fibrosis and apoptosis cell count were significantly decreased (P < 0.01). Western blot results showed that compared with the control group, the protein expression of P53 in the operation group was significantly increased (P < 0.01), and the protein expression of heat shock protein 70 was significantly decreased (P < 0.01). Compared with the operation group, the protein expression of P53 in the operation+exercise group was decreased (P < 0.05), and the protein expression of heat shock protein 70 was increased (P < 0.05). RT-PCR results showed that compared with the control group, the expression of Bax mRNA and P53 mRNA in the operation group was increased (P < 0.01), while the expression of Bcl-2 mRNA and Bcl-2/Bax value decreased (P < 0.01). Compared with the operation group, the expression level of Bax mRNA was decreased (P < 0.05), the expression level of P53 mRNA was decreased (P < 0.01), the expression level of Bcl-2 mRNA was increased (P < 0.01), and the ratio of Bcl-2/Bax was significantly increased (P < 0.01). To conclude, the mouse heart is in the compensatory phase of pathological myocardial hypertrophy after 2 weeks of aortic constriction surgery. A 4-week exercise preconditioning can enhance the mouse heart function in the early stage of pressure overload, and maintain and delay the pathological development of compensatory myocardial remodeling in the early stage. The myocardial protection induced by exercise preconditioning may be related to the up-regulation of heat shock protein 70 and Bcl-2 expression and the inhibition of P53 and Bax expression, thereby inhibiting myocardial cell apoptosis.

Key words: exercise preconditioning, hypertension, myocardial remodeling, heat shock protein, apoptosis