Muscle Metaboreflex Control of Coronary Blood Flow and Ventricular Contractility During Dynamic Exercise in Heart Failure

Abstract

Muscle metaboreflex activation (MMA) during dynamic exercise increases cardiac work and O2 demand via increases in heart rate, ventricular contractility and afterload. This increase in cardiac work should lead to metabolic coronary vasodilation. However, no change in coronary vascular conductance is seen, indicating that the increased sympathetic activity which increased contractility also caused vasoconstriction. In heart failure, cardiac output does not increase with MMA presumably due to impaired left ventricular contractility, and large decreases in coronary vascular conductance are observed. We tested whether this coronary vasoconstriction could explain in part, the reduced ability to increase cardiac performance during MMA. In conscious, chronically instrumented dogs after pacing induced heart failure, MMA responses during mild exercise were observed before and after α1 ‐ adrenergic blockade (prazosin 50‐100 μg/kg). During MMA, the increases in coronary blood flow, coronary vascular conductance, cardiac output, and +dP/dtmax were significantly greater after α1 ‐ adrenergic blockade. We conclude that during heart failure the coronary vasoconstriction limits the ability of muscle metaboreflex to increase left ventricular contractility. NIH HL 55473