Oxygen, although is highly required for living, can be toxic because it can be easily changed into oxygen free radicals (reactive oxygen species, ROS) and generates oxidative stress. [1][2][3][4][5] This oxidative stress will cause endothelial lesion and will be responded by endothelial cells through nitric oxide (NO) response and immunological response pathway. 6-8 The immunological response begins by increasing cytokines production, activated coagulation factors, and reactivation of platelet in acute thrombotic process. However, acute thrombotic process, which is an initial part of protective mechanism to fix the lesion, often change to become continuous process because of abundance oxidative stress, and then generates various levels of acute coronary syndromes. 3,5 Several studies showed that acute exercise on treadmill test with high intensity Bruce protocol increased oxidative stress because of ROS. 9,10 On the contrary, acute exercise also increased production of NO because of the increment effect of shear stress on endothelial cells. 6,9-15 But, regular exercise Keywords ► acute coronary syndrome ► atherosclerosis ► cardiovascular risk factors ► myocardial infarction ► oxidative stress ► nitric oxide ► cardiac markers ► exercise
AbstractModerate-to-high intensity of exercise training within 2 to 3 months decreases oxygen free radicals (reactive oxygen species, ROS) and increases nitric oxide (NO) in outpatients with myocardial infarction. There is no data about the association of ROS and NO after short-term low-intensity exercise training within 5 days in patients hospitalized with acute myocardial infarction (AMI). A total of 32 male patients with AMI were randomized into two groups: 15 patients with short-term low-intensity exercise training within 5 days formed the training group and 17 patients without such exercise training formed the control group. All patients performed exercise treadmill test with modified Bruce protocol before and after the study. F2-isoprostane and NO concentration of the training group increased slightly after modified Bruce exercise treadmill test. Compared with the control group, NO of the training group was also slightly higher. Baseline NO and uric acid were negative predictor variables for F2-isoprostane in all patients hospitalized with AMI, and triglyceride was a positive predictor variable. After the study, physical capacity of the training group was higher; but heart rate and systolic blood pressure were lower significantly. This study showed that short-term low-intensity exercise training for patients hospitalized with AMI did not change ROS and NO productions, but it improved physical capacity and lowered heart rate and systolic blood pressure. NO was negative predictor variable for F2-isoprostane in controlling ROS changes in dynamic compensation mechanism.