Unilateral Transient Partial Reductions In Renal Blood Flow Amplify Muscle Metaboreflex Reponses During Mild Exercise

During exercise cardiovascular performance is maintained and dynamically adjusted via modulation of autonomic activity by several reflexes. The most powerful of these reflexes, termed the muscle metaboreflex, is elicited by activation of skeletal muscle afferents. The resultant increase in sympathetic activity to the heart markedly enhances ventricular function which is restrained by coronary vasoconstriction due to stimulation of coronary vascular a adrenergic receptors. Stifling of maximal ventricular performance has been observed at multiple workloads in previous studies and is thought to be a primary mechanism by which the metaboreflex is capable of eliciting activation of the cardiac sympathetic afferent reflex (CSAR). CSAR is a response to myocardial ischemia that increases sympathetic outflow and contributes to exaggerated metaboreflex responses in both normal and heart failure subjects during exercise. Previous studies from our laboratory have shown that during mild, moderate, and severe exercise, that muscle metaboreflex activation elicits large reductions in renal vascular conductance even in normal subjects, and in heart failure subjects massive reductions in renal blood flow often occur. Large reductions in renal perfusion elicited by metaboreflex activation could cause activation of renal afferents which could elicit further increases in sympathetic tone. However, whether or not metaboreflex mediated renal vasoconstriction in healthy subjects is capable of eliciting renal afferent activation is unknown. Furthermore, even if renal afferents were activated during metaboreflex activation the potential contribution of renal afferent activation to metaboreflex responses is unknown. Thus, in this study we set out to determine, if muscle metaboreflex responses in normal animals could be amplified due to concurrent activation of unilateral renal afferents. We utilized our conscious chronically instrumented canine model to evaluate the hypothesis that renal afferent activation via single partial renal artery occlusion (60% reduction in RBF for 1 min, n=3) during muscle metaboreflex activation would exaggerate metaboreflex responses similar to what has been observed as a result metaboreflex activation with other cardiovascular reflexes like CSAR. We observed that single renal artery occlusion during muscle metaboreflex activation elicited significant increases in mean arterial pressure (+5.6±1 mmHg), cardiac output (+0.6±0.1 L/min), heart rate (+11.5±2 bpm), non-ischemic vascular conductance (+2.8±0.3 mL/mmHg), and left ventricular dP/dtmax (+645.6±197 mmHg/s), in normal animals during exercise at 3.2 kph. Furthermore, we evaluated the effects of renal occlusion alone in the absence of metaboreflex activation at rest and during exercise and observed that unilateral renal arterial occlusion of 60% is not sufficient to induce significant hemodynamic changes. This suggests that if the conditions for renal afferent activation are met, they likely serve as a sympathetic amplifier of muscle metaboreflex activation. This work was supported by NHLBI 055473. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.