Abstract 1322: Exercise Stimulates Angiogenesis and Improves β-Adrenergic Receptor Signaling in the Failing Heart
Cardiac angiogenesis is impaired in the failing heart. Exercise is shown to stimulate cardiac angiogenesis in physiologic conditions and in infarcted hearts. The aim of this study was to evaluate whether exercise might ameliorate angiogenesis mechanisms in the failing heart. Another aim was to establish the relationship between the exercise-induced improvement of cardiac β-adrenergic receptor (β-AR) signalling and increased angiogenesis in a rat model of post-ischemic HF. At 1 month from surgical ligation of left anterior descending coronary artery, 40 adult (4 month), male, WKY rats, with an infarct size ≥ 40% (assessed by Echo), were randomized into 2 groups: Group 1 (20 rats stabulated under controlled conditions for 1 month), Group 2 (20 rats undergone to a training program consisted of a 45 min/day treadmill exercise at a speed of 17 m/min, 5 days/wks for 12 wks. 10 sham operated animals were also included. After this period, cardiac performance was evaluated by in vivo (Echocardiography) and in vitro (single myocyte contractility) studies; myocardial blood flow (MBF) and coronary flow reserve (CFR) by dyed beads dilution assay; cardiac capillary density by histology; cardiac β-AR signalling by β-AR density, GRK2 expression, and ISO-stimulated cAMP production; cardiac VEGF expression by western blotting. Data are illustrated in the table⇓. Our results indicate that exercise stimulates angiogenesis, increases myocardial perfusion, restores β-AR signalling, and improves failing myocytes contractility. The reduced cardiac VEGF levels reflect the comprehensive improvement in local ischemia induced by training.