تأثیر هشت هفته تمرین تناوبی شدید بر بیان ژن نیتریک اکساید سنتاز اندوتلیالی و فاکتور رشد اندوتلیالی عروق و بیان پروتئین مولکول چسبنده سلول اندوتلیالی رتها بعد از انفارکتوس میوکارد

Abstract

Introduction: Myocardial Infarction is one of greatest cause of death worldwide which cause enlargement of left ventricle and loss of capillaries. Angiogenesis and adequate growth of capillaries after MI is essential. The mechanism of exercise-induced benefit and angiogenesis in ischemic heart disease remains poorly defined. This study was designed to investigate the effects of eight weeks of high intensity interval training on endothelial constitutive nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and Platelet-endothelial cell adhesion molecule-1 (PECAM-1/CD31) in rats with myocardial infarction. Methods: 13 male Wistar rats weighing 250 to 300 grams were assigned into two groups: the experimental group or HIIT (42 minutes running on a treadmill on an interval basis, each interval four minutes with intensity of 85-90 and three minutes of active recovery with 40- 50 % VO 2 max, Five days a week for eight weeks) and the control group (without training intervention). Genes expression of eNOS, VEGF were investigated by the PCR technique and protein expression of CD31 was investigated by western blotting test. Data were analyzed using SPSS (version 16) with Independent sample t-test (P≤0.05).\xa0 Results: Endothelial constitutive nitric oxide synthase in high intensity interval training group (8.43) was significantly higher than the control group (2.85) (P=0.001) vascular endothelial growth factor in high intensity interval training group (0.097) was significantly higher than control group (0.019) (P=0.05) and Platelet-endothelial cell adhesion molecule-1 in high intensity interval training group (1.345) was significantly higher than control group (0.626) (P=0.01). Conclusion: Eight weeks of high intensity interval training with intensity 85-90 % VO 2 max increased endothelial constitutive nitric oxide synthase and vascular endothelial growth factor and Platelet-endothelial cell adhesion molecule-1.