| Purpose: A major problem facing sports medicine is to objectively estimate thecirculatory system in athletes. It's well know that Athlete's heart is a physiological adaptation of the heart to intensive physical training. Over the last several decades the insight into cardiovascular adaptation of endurance sporting people has largely increased. Physical activity is associated with hemodynamic changes and alters the loading conditions of the heart. There echocardiographic studies have confirmed that the ventricular wall of an athlete has been physiologically thickness and dilatation by prolonged training, including an increase in chamber size, wall thickness and a decrease in the resting heart rate.Athlete's heart and hypertrophic cardiomyopathy have characteristics that overlap and sometimes make differential diagnosis difficult. Sudden cardiac death of suspected healthy young athletes is a rare, but deeply moving event.Usually, the affected athlete has been completely free of symptoms,as unrecognized inflammatory, hypertrophic or dilated cardiomyopathies are the most frequent causes. Sudden death occurs not infrequently in athletes during intense physical exertion. The fact that the changes in the cardiovascular system in athletes occur during performance of the intense physical exercises is exist; therefore, improper training may cause pathologicalchanges in this system. There are many researches suggest that apoptosis is a basic physiological process which has been associated with the tissue remodeling in cardiovascular system. Increasing evidence has suggested that exercise to cardiovascular system can induce apoptosis. Exercise may increase free radicals production.The area of antioxidant supplementation and its ameliorating effects on exercise-induced free radical damage (including lipid peroxidation) has attracted much interest in recent years. The theoretical benefits of using antioxidant vitamin E supplements helps to safeguard cell membranes from quenching oxygen free radicals.Athletic myocardium hypertrophy with electrocardiographic and echocardiographic manifestations makes it possible to define the athlete's heart as a special physiological notion. However, the question whether anatomic and functional changes in the athlete's heart remain within physiological ranges is still poorly understood. To test the changes in the during the circulatory system during endurance training and antioxidant intervention and the relationship between these indices and the circulatory system response to the physical exercise in rats, the objective of this paper was to study the structural and functional indices of the Cardiovascular System of rats by conventional and molecular methods.Methods: Forty-eight male Sprague Dawley rats were divided randomly into sixgroups. Swimming exercise with loads for 60 minutes per day for 4 weeks was used as an exercise protocol. Group A (n=8) was the control group, in which rats did not perform any exercise and were treated with oral placebo. In Group B (n=8) , rats were treated as Group A ,but they performed acute exercise before killed in the lastday of the fourth week. Group C (n=8) was the control group with VE supplementation, in which rats were treated with oral 50mg/kg of VE. In Group D (n=8) , rats did not perform any exercise and were treated with oral 50mg/kg of VE, they performed acute exercise before killed in the last day of the fourth week. In Group E (n=8) , rats performed endurance training for 4 weeks and were treated with oral placebo. In Group F (n=8) ,rats performed endurance training for 4 weeks and were treated with oral 50mg/kg of VE. Group B,D,E,F were killed 24 hours later after performed one bout exhaust exercise in the last day of fourth week. And transmission electron microscope was used to study the structure of myocardium. In addition, the inflammatory mediator TNF-a , free radical nitric oxide (NO) and nitric oxide synthase (NOS) in the blood of the rats was measured.Results: The present study suggest that exercise and VE supplementation triggeredthe initial stage of apoptosis in the myocardium,but exhibited typical signs of apoptosis in the vascular endothelial cells of rat. Nitric oxide in the blood samples taken after exhaust exercise decrease significantly between the Group A and B ( 29.31 ±22.15nmol/L vs 6.47±2.46 nmol/L,P<0.05 ) ,but high in the Group E significantly (18.72±20.23nmol/Lvs 6.47±2.46 nmol/L,P<0.05 ) . And overshooting response of NOS was observed In the Group F (P<0.05 ) .The concentration of tumor necrosis factor alpha(TNF-a) increased in the Group E when compared with all the other five groups(P<0.05).there was no significant difference between the other groups.Conclusion: The results of this study indicate that chronic endurance training andVE supplementation help boost the immune function. Our studies have shown that combining VE and exercise training can provide powerful antioxidant protection, which is related to the adjustment of the concentration of TNF-a, NO and the total NOS activity in the blood. They suggest that these changes are a normal physiologic adaptation to prolonged training and VE supplementation does provide cardiovascular system efficiency benefit in physical stress. These data suggest that prior vitamin E supplementation may exert a protective effect against exhaust exercise-induced damage. Therefore, chronic endurance training and exogenous antioxidants may have a prophylactic effect in keeping the balance mechanism between proliferation , apoptosis and anti-oxidation. All of our findings should be considered as preliminary. Numerous additional questions regarding the antioxidant needs for physical activity remain to be answered. Therefore, further studies will be done to study the mechanism of endurance training and antioxidant intervention in the health protection of cardiovascular system.
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