Exercise as therapeutic angiogenesis: Post-myocardial infarction

Post-myocardial infarction the left ventricle goes through a deleterious remodeling process that places a significant strain on the remaining viable myocardium. Like skeletal muscle the myocardium has demonstrated a remarkable plasticity response to both physiological and pathological stimuli. The purpose of this study was to demonstrate the temporal and spatial response of exercise induced therapeutic angiogeneis in a post-myocardial infarction rat model. Male Sprague-Dawley rats were randomly assigned to sham, sedentary myocardial infarction, and exercise myocardial infarction groups. Two weeks post-ligation the exercise myocardial infarction groups were trained on a rodent treadmill for 2 weeks, 4 weeks, and 8 weeks. Upon completing the respective training program the rats were sacrificed. To test the affect of the groups and time on therapeutic angiogenesis, transverse cross-sections of the myocardium were stained using indirect immunohistochemistry with an antibody against the endothelial cell marker CD-31. Using a point to count technique capillary density was measured in the left ventricle, the septum, and in the right ventricle. A significant main effect for the groups was found in all three regions of the myocardium (p < .05). However, no main effect for time or group and time interaction was found when measuring capillary density. These results suggest that exercise training post-myocardial infarction induces therapeutic angiogenesis in the viable myocardium.