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

Abstract

Muscle metaboreflex activation (MMA) during dynamic exercise induces a substantial increase in cardiac work and oxygen demand via a significant increase in heart rate, ventricular contractility and afterload. This increase in cardiac work should lead to coronary metabolic vasodilation. However, in this situation, little if any coronary vasodilation is observed. It is unclear if this lack of coronary vasodilation, which occurs as a result of increased coronary sympathetic stimulation due to MMA, suppresses any further increases in left ventricular contractility (LVC). The purpose of this study was to determine if this lack of coronary vasodilation leads to a buffered increase in LVC. Using chronically instrumented, conscious dogs we measured arterial pressure, cardiac output (CO), circumflex blood flow (CxBF), and calculated coronary vascular conductance (CVC), maximal derivative of ventricular pressure (dp/dt), and preload recruitable stroke work (PRSW) at rest and during mild exercise (2mph) before and after MMA. Experiments were repeated after alpha-1 adrenergic blockade (prazosin ∼50 ìg/kg). During prazosin we observed significantly greater increases in CVC, CxBF, CO, dP/dt, and PRSW, with MMA, over that of the control condition. We conclude that the lack of coronary vasodilation limits further improvement in LVC. NIH HL 55473