Influence of spontaneous bursts of muscle sympathetic nerve activity on the femoral artery and vein flow in young healthy adults

Spontaneously occurring bursts of sympathetic nerve activity contribute to the moment-to-moment control of blood pressure by evoking an alpha-adrenergic mediated arterial vasoconstriction. However, the venous system also receives a rich sympathetic innervation, contains alpha-adrenergic receptors, and venoconstriction has been elicited by sympatho-excitatory stimuli (e.g., hypoxia, exercise) in some studies. Herein we tested the hypothesis that spontaneously occurring bursts of sympathetic activity evoke dynamic changes in venous tone and consequently, flow. In nine healthy volunteers (4 women, 26±7 years, 24±4 kg·m 2 ; mean±SD) simultaneous 10-minute recordings of femoral artery and vein blood flow (duplex ultrasound), muscle sympathetic nerve activity (MSNA, microneurography), and blood pressure (finger photoplethysmography) were made. Sympathetic transduction was quantified as the change in mean arterial pressure (MAP), femoral artery flow, and femoral vein flow, following spontaneous bursts of MSNA using signal-averaging techniques. As expected, sympathetic bursts were accompanied by a transient increase in MAP (peak +3.2±1.2 mmHg), while MAP fell following cardiac cycles not associated with a sympathetic burst (nadir -1.1±0.6 mmHg). Similarly, sympathetic bursts were followed by a transient decrease in femoral artery blood flow (nadir -9.2±4.6 ml/min), whereas increases were exhibited following cardiac cycles not associated with a sympathetic burst (peak +2.5±2.6 ml/min). In contrast, sympathetic bursts evoked comparatively smaller, less consistent and directionally opposite changes in femoral vein flow (average over 15 cardiac cycles +2.1±6.0 ml/min), while small decreases were observed following cardiac cycles not associated with a sympathetic burst (-0.8±1.7 ml/min). Collectively, these findings indicate that spontaneously occurring bursts of sympathetic nerve activity exert a minimal contribution to the moment-to-moment control of femoral venous flow in young healthy humans. Further studies examining sympathetic venous transduction during physiological stressors (e.g., exercise), and in other venous beds (e.g., mesenteric) and populations (e.g., hypertension) are warranted. JPF is supported by a Health Research Council Programme grant (19/687). This abstract was presented at the American Physiology Summit 2025 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.