Ivabradine reduced left ventricular mass in healthy rats undergoing anaerobic exercise compared to controls (p<0.008) and induced significant bradycardia.
RCT (n=36)
randomized into six groups
Does ivabradine modulate cardiac structure and electrophysiology in healthy rats undergoing different exercise modalities?
Ivabradine attenuates exercise-induced cardiac hypertrophy and overrides training-related bradycardia in healthy rats, highlighting the pivotal role of heart rate in physiological remodeling.
p-value: p=<0.008
Abstract Background/Introduction Exercise induces physiological cardiac remodeling ("athlete's heart"), with aerobic training causing eccentric hypertrophy and anaerobic training leading to concentric hypertrophy. Ivabradine, a selective heart rate-lowering agent, mitigates pathological remodeling, but its role in exercise-induced adaptations in healthy hearts is poorly understood. Understanding this interaction could inform strategies to optimize cardiovascular health in active populations. Purpose This study aimed to investigate how ivabradine modulates cardiac structure, electrophysiology, and peripheral neuromuscular function in healthy rats undergoing different exercise modalities. Methods Thirty-six male Sprague-Dawley rats were randomized into six groups (n=6): anaerobic (high-intensity loaded swimming), aerobic (moderate-intensity endurance), endurance (high-intensity intermittent), and each with ivabradine (10 mg/kg/day orally) (An+Iva, Ae+Iva, En+Iva). Over 30 days, rats followed tailored swimming protocols. Transthoracic echocardiography, surface ECG, and gastrocnemius EMG assessed cardiac remodeling, heart rate, and neuromuscular function at baseline and endpoint. Results Aerobic exercise increased left ventricular internal diameter in diastole (LVIDd) versus anaerobic (p0.008), indicating eccentric remodeling. Ivabradine reduced left ventricular mass in An+Iva compared to An and Ae groups (p0.008).(Table-1) Ivabradine induced significant bradycardia, with Ae+Iva showing lower heart rate and longer RR interval than An (p0.008). (Table-2) No EMG changes were observed. Conclusion(s) Ivabradine attenuates exercise-induced cardiac hypertrophy and overrides training-related bradycardia in healthy rats, highlighting heart rate’s pivotal role in physiological remodeling. These findings suggest potential applications for heart rate modulation in optimizing exercise-related cardiovascular adaptations.Table-1For image description, please refer to the figure legend and surrounding text. Table-2For image description, please refer to the figure legend and surrounding text.
Asal et al. (Mon,) conducted a rct in healthy (n=36). Ivabradine vs. Exercise without ivabradine was evaluated on Cardiac remodeling (left ventricular mass) and heart rate (p=<0.008). Ivabradine reduced left ventricular mass in healthy rats undergoing anaerobic exercise compared to controls (p<0.008) and induced significant bradycardia.