| Summary: | 碩士 === 臺北市立大學 === 運動科學研究所 === 105 === Background and purpose: Hypertension is reported to cause endothelial dysfunction and reduced nitric oxide (NO) bioavailability, thereby resulting in various cardiovascular diseases. Exercise is well known to ameliorate high blood pressure and cardiovascular function. In addition to exercise, previous studies have indicated that vegetarian diet or low calorie diet effectively ameliorates hypertension and reduces risk factors of cardiovascular disease. However, its physiological mechanism was still unclear. Therefore, the aim of this study was to investigate effects of long-term exercise and low-methionine diet on the cardiovascular function and their physiological mechanisms in the animal model of hypertension. Methods: In this study, spontaneously hypertensive rats were used and randomly divided into control (CON), low methionine diet (MET), exercise training(EX), and combined low methionine diet and exercise training (MET+EX) groups. The exercise training group was given 60 minutes per day, 5 days per week for a total of 24 weeks. Moreover, the low methionine diet group was given a low concentration of methionine (0.172%) per day for 24 weeks. At the end of the intervention, the parameters of vasorelaxation and liver oxidative and antioxidant activities were measured and compared among four groups. Results: We found that the single-dose and dose-dependent acetylcholine-induced vasorelaxation was significantly higher in MET, EX, and MET+EX groups than that in the CON group. However, after the pre-treatment with the inhibitor, L-NAME or wortmannin, there was no significant difference among four groups.. The activities of liver superoxide
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dismutase and catalase were significantly greater in MET, EX, and MET+EX groups than those in the CON group. However, no significant difference was found in liver MDA concentration among four groups. Conclusion: This study suggested that twenty-four weeks of combined exercise training and low methionine diet effectively improved hypertension-induced vascular endothelial dysfunction and enhanced liver antioxidant activity.
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