Cerebral vascular response during a hypercapnic challenge with and without simultaneous activation of the sympathetic nervous system

Introduction: Cerebral vascular function/health is crucial for the maintenance of neurocognitive function and prevention of various neurocognitive and cerebral vascular conditions/diseases. Cerebral vascular function is commonly assessed by evaluating the vasodilatory response to a hypercapnic stimuli. A larger vasodilatory response is associated with more positive outcomes, while a blunted response is associated with an increased risk of cerebral vascular and neurocognitive diseases in the future. However, it remains unclear whether simultaneous activation of the sympathetic nervous system (SNS) can attenuate cerebral vasodilation during a hypercapnic challenge. Hypothesis: Therefore, this study tested the hypothesis that cerebral vascular vasodilatory responsiveness to a hypercapnic stimulus would be blunted when SNS activation is superimposed upon this stimulus. Methods: Nineteen individuals (10 males, age: 21±3 years, BMI: 24±4 kg/m 2 ) participated. Throughout data collection cerebral blood flow was continuously indexed as mean blood velocity in the middle cerebral artery via trans-cranial Doppler (MCAVmean) and beat-to-beat arterial blood pressure was continuously assessed via photoplethysmography (MAP). Arterial carbon dioxide (CO 2 ) tension was indexed as end-tidal CO 2 assessed on a breath-by-breath basis. Following 10-min of quiet supine rest, individuals were exposed to a 4-min hypercapnic challenge induced by breathing 6% CO 2 gas. The first 2-min were conducted under normal conditions (i.e. CO 2 gas alone), and the last 2-min were conducted while the individual submerged one hand into an ice water slurry to induce activation of the sympathetic nervous system (i.e. cold pressor test, CPT). Cerebral vasodilatory responsiveness during each phase was assessed as cerebral vascular conductance (CVCi, MCAVmean/MAP). Responses during the 1 st two-min of hypercapnia were analyzed as the % change in CVCi relative to baseline (i.e. normocapnia) and the effect of simultaneous activation of the sympathetic nervous system was assessed as the % change in CVCi during combined hypercapnia + CPT (i.e. last 2-min) relative to hypercapnia alone (i.e. 1 st 2-min). Results: Hypercapnia alone increased CVCi by 38±14 % ( p< 0.001). When the CPT was superimposed during the final 2-mins of hypercapnia, CVCi was slightly, yet significantly, decreased relative to the hypercapnia alone condition (34±18 % vs. 38±14 %, p= 0.04). Conclusion: These preliminary data suggest that SNS activation modestly restrains the cerebral vasodilatory responsiveness to a hypercapnic stimuli. This may have implications for understanding how sympathetic activation influences cerebral vascular health, particularly under conditions of stress. The University of Texas at Arlington College of Nursing and Health Innovation 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.