Abstract 3644: Endurance Training Induces Physiological Cardiac Hypertrophy Post Myocardial Infarction without Affecting Calcineurin Signaling
Physiological cardiac hypertrophy is characterized by positive effects on myocardial functions associated with increased left ventricular (LV) wall thickness. To date there is no clear evidence whether endurance training is capable of inducing physiological LV hypertrophy post myocardial infarction (MI) and whether calcineurin signaling is involved in the in vivo regulation of the exercise-induced physiological LV hypertrophy. Therefore we tested the null hypothesis that 10-weeks of endurance training would have no effect on LV wall thickness and calcineurin signaling post MI. Permanent ligation of the left anterior descending coronary artery was used to induce MI in twenty two purpose-bred mongrel dogs. The animals were randomly assigned into endurance exercise training group (n= 10) and time control group (n=12). Echocardiography was used to assess the LV wall thickness and western blotting was used to assay total calcineurin A (CnA) protein expression. Calmodulin was immunoprecipitated and CnA protein was assayed in the precipitate to infer the CnA activity. Our results indicated that Citrate Synthase activity of the diaphragm was increased significantly (P<0.05) by 37.4% in the exercise group when compared to time control verifying the effectiveness of the training program. Heart rates at submaximal exercise levels were reduced significantly (P<0.05) by 25 bpm in the exercise group while no significant changes were recorded in the time control. Endurance training induced about 11% significant increase (P<0.025) in LV wall thickness (pre 9.4±0.4, post 10.1±0.4 mm). Whereas there was no significant change in the LV wall thickness of the time control animals (9.6±0.5, post 9.1±0.4 mm). Neither CnA protein expression nor active CnA (CnA bound to calmodulin) was significantly changed with endurance training compared to time control. Furthermore, RT-PCR analysis indicated no changes in calcineurin mRNA with training. These results suggest the clinical importance of cardiac rehabilitation programs based on endurance training modes to improve cardiac function by inducing physiological LV hypertrophy post MI. In addition, our results do not support a role for calcineurin in the in vivo regulation of exercise-induced physiological LV hypertrophy.