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Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201
Ischemia of active skeletal muscle stimulates neuronal afferents within the muscle, which elicits a reflex increase in systemic arterial pressure (SAP), heart rate (HR), and cardiac output (CO) termed the muscle metaboreflex. We investigated whether activation of the muscle metaboreflex elicits increases in ventricular performance using conscious, chronically instrumented dogs trained to run on a treadmill (3.2 km/h, 0% grade). The muscle metaboreflex was activated via progressive partial vascular occlusion of the terminal aorta during control experiments and with HR maintained constant via a pacemaker connected to ventricular electrodes (225 beats/min). In control experiments, hindlimb ischemia elicited substantial increases in SAP, HR, and CO (+53.9 ± 4.3 mmHg, +32.4 ± 4.5 beats/min, and +1.57 ± 0.22 l/min, respectively; all changes P < 0.05), whereas stroke volume (SV) remained unchanged with reflex activation (control 45.9 ± 2.3 vs. 46.1 ± 2.4 ml, P > 0.05). During metaboreflex activation at constant HR, SV significantly increased such that the increases in CO and SAP were not significantly different from control experiments (+1.77 ± 0.56 l/min and +57.4 ± 3.8 mmHg, P > 0.05 vs. control experiments). No significant change in central venous pressure occurred in either experiment, indicating no Frank-Starling effect on SV. We conclude that muscle metaboreflex-induced increases in ventricular contractility act to sustain SV despite decreases in ventricular filling time due to the tachycardia such that the sustained SV coupled with the tachycardia elicits substantial increases in CO that contribute importantly to the reflex increase in SAP.
skeletal muscle ischemia; sympathetic nervous system; muscle afferents; arterial blood pressure; skeletal muscle blood flow
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