3 research outputs found

    Cardioprotective Effect of High Intensity Interval Training and Nitric Oxide Metabolites (NO2-, NO3-)

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    Background: The aim of this study was to investigate the effects of High-Intensity Interval Training (HIIT) on nitric oxide metabolites (NO2-, NO3-) and myocardial infarct size after Ischemia/Reperfusion (I/R) injury in healthy male rats. Methods: A total of 44 Wistar rats were randomly divided into 4 groups including HIIT (n=8), HIIT + IR protocol (n=14), control (n=8), and control + IR (n=14). Each training session of HIIT consisted of 1 hour of exercise in three stages: 6-minute running at 50-60% VO2max for warm-up; 7 intervals of 7-minute running on treadmill with a slope of 50 to 20° (4 minutes with an intensity of 80-100% VO2max and 3 minutes at 50-60% VO2max); and 5-minute running at 50-60% VO2max for cool-down. The control group did not participate in any exercise program. Nitric Oxide (NO) and its metabolites were measured by using Griess reaction test.   Results: The results showed that eight weeks of exercise training exerted a significantly increasing effect on nitrite (8.55 µmol per liter, equivalent to 34.79%), nitrate (62.02 µmol per liter, equivalent to 149.48%), and NOx (66 µmol per liter, equivalent to 98.11%) in the HIIT group compared with the control group. The results showed myocardial infract size (IS) was significantly smaller (23.2%, P<0.001) in the exercise training group compared with the control group. Conclusion: Incremental changes in NO-NO3-, NO2- axis are one of mechanisms through which HIIT program can protect the heart from I/R injury and decrease myocardial infarction

    Protective effects of atorvastatin on myocardium in hypertensive rats

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    Background and Aim: Previous studies have shown that arterial hypertension induces cardiac hypertrophy and myocardial oxidative stress. The aim of the present study was to assess the effects of treatment by atorvastatin, as an antioxidant, to prevent myocardial oxidative stress and cardiac hypertrophy in hypertensive rats. Materials and Methods: In this experimental study, 20 male Wistar rats were randomly divided into four equal groups, including sham, sham treated, hypertensive, and hypertensive treated. The rats were made acutely hypertensive by aortic constriction above the renal arteries. After 21 days, the carotid artery pressure of the subjects was recorded and, under anaesthesia their hearts were removed and weighed. Then, the left atrium of each was excised. After tissue homogenation, superoxide dismutase (SOD) and catalase (CAT) activities, as well as glutathione (GSH) and malondialdehyde (MDA) levels of myocardium were determined through biochemical methods. Results: In the hypertensive groups, mean arterial hypertension and cardiac hypertrophy (heart weight/body weight, g/kg) increased70% and 76%, respectively. Aortic constriction significantly increased arterial pressure and cardiac hypertrophy index respectively SOD and CAT activities were significantly lower than in the sham animals ,P<0.05.Besides, arterial hypertension decreased GSH content of myocardium by 59% ,but it increased MDA level by 62%. Finally, it was found that atorvastatin treatment only prevented from the reduction of CAT activity. Conclusion: Arterial hypertension induces cardiac hypertrophy concomitant with oxidative stress in rat myocardium. Treatment with atorvastatin can prevent hypertension-induced oxidative stress

    Alteration in cardiac uncoupling proteins and eNOS gene expression following high-intensity interval training in favor of increasing mechanical efficiency

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    Objective(s):High-intensity interval training (HIIT) increases energy expenditure and mechanical energy efficiency. Although both uncoupling proteins (UCPs) and endothelial nitric oxide synthase (eNOS) affect the mechanical efficiency and antioxidant capacity, their effects are inverse. The aim of this study was to determine whether the alterations of cardiac UCP2, UCP3, and eNOS mRNA expression following HIIT are in favor of increased mechanical efficiency or decreased oxidative stress. Materials and Methods: Wistar rats were divided into five groups: control group (n=12), HIIT for an acute bout (AT1), short term HIIT for 3 and 5 sessions (ST3 and ST5), long-term training for 8 weeks (LT) (6 in each group). The rats of the training groups were made to run on a treadmill for 60 min in three stages: 6 min running for warm-up, 7 intervals of 7 min running on treadmill with a slope of 5° to 20° (4 min with an intensity of 80-110% VO2max and 3 min at 50-60% VO2max), and 5-min running for cool-down. The control group did not participate in any exercise program. Rats were sacrificed and the hearts were extracted to analyze the levels of UCP2, UCP3 and eNOS mRNA by RT-PCR. Results:UCP3 expression was increased significantly following an acute training bout. Repeated HIIT for 8 weeks resulted in a significant decrease in UCPs mRNA and a significant increase in eNOS expression in cardiac muscle. Conclusion:This study indicates that Long term HIIT through decreasing UCPs mRNA and increasing eNOS mRNA expression may enhance energy efficiency and physical performance
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