The Arterial Baroreflex Buffers Muscle Metaboreflex-Induced Coronary Vasoconstriction

• Published in: Physiology (Bethesda, Md.) Md.), 2024-05, Vol.39 (S1)
• Main Authors: Mannozzi, Joseph, Kohrman, Andrew, Kim, Jong-Kyung, O'Leary, Donal S.
• Format: Article
• Language: English
• ISSN: 1548-9213; 1548-9221
• DOI: 10.1152/physiol.2024.39.S1.713

Abstract only The ability to increase cardiac output and thereby skeletal muscle blood flow during dynamic exercise is paramount to maintaining exercise workload. Increases in cardiac output are driven via increases in heart rate, ventricular function, and central blood volume mobilization which raises arterial blood pressure, in part, due to activation of the muscle metaboreflex. The increase in cardiac sympathetic tone also activates coronary vascular alpha-adrenergic receptors which restrains increases in coronary blood flow which limits increases in ventricular function. During submaximal dynamic exercise, the muscle metaboreflex acts primarily to raise cardiac output with little net peripheral vasoconstriction. However, after sinoaortic baroreceptor denervation (SAD), the muscle metaboreflex causes increases in both cardiac output and total peripheral resistance indicating that the baroreflex buffers the muscle metaboreflex mainly via restraint of peripheral vasoconstriction. To what degree the arterial baroreflex restrains muscle metaboreflex-induced coronary vasoconstriction is unknown. Therefore, we utilized our chronically instrumented canine model to evaluate if SAD would significantly impact muscle metaboreflex-induced coronary vasoconstriction. Canines were chronically instrumented to measure cardiac output, left circumflex coronary artery blood flow, hindlimb blood flow and arterial blood pressure. During steady-state mild treadmill exercise (3.2 kph, 0% grade) the muscle metaboreflex was activated via partial inflation of vascular occluders placed distal to the hindlimb blood flow probe. Metaboreflex activation caused substantial increases in cardiac output, heart rate, cardiac power, coronary blood flow, and arterial blood pressure. Assessment of coronary vasodilation was performed via linear regression of the relationship between coronary vascular conductance (CVC; coronary blood flow/mean arterial pressure) vs. cardiac power (CP, an index of O 2 demand). Experiments were performed at least 2 weeks after chronic bilateral SAD. Muscle metaboreflex activation after SAD caused a significantly greater pressor response driven by increases in both cardiac output and total peripheral resistance. Furthermore, after SAD the slope of the CVC-CP relationship was significantly lower during muscle metaboreflex activation (0.072 ml/min/mmHg/Watt, control vs 0.033 ml/min/mmHg/Watt, SAD; p