Cerebrovascular Responses to Acute Increases in Glycemia in Healthy Young Adults

Introduction: Individuals with metabolic syndrome or type 2 diabetes face elevated risks of stroke and vascular dementia, yet the early mechanisms underlying cerebrovascular dysfunction remain unclear. Emerging evidence shows that even brief episodes of increased glycemia can disturb cardiovascular control and impair arterial blood pressure (ABP) regulation in healthy adults. We therefore propose that an acute increase in glycemia may also disrupt the regulation of cerebral blood flow (CBF) by impairing dynamic cerebral autoregulation (dCA). Objectives: The aim of this study was to assess the acute effects of increased glycemia on the regulation of CBF and ABP in healthy young adults. Methods: Ten healthy young adults (28±7 years; BMI=22±4 kg/m 2 ; fasting glucose 4.54±0.41 mmol/L) attended the laboratory in a fasted state for assessments of blood glucose (capillary sampling), CBF, and ABP regulation at baseline and at 30-minute intervals for 2 hours following ingestion of a 75g glucose solution. CBF was assessed via middle cerebral artery velocity (MCAv) using transcranial Doppler (WAKIe, Atys Medical), while ABP was continuously recorded using finger photoplethysmography (NIBP, ADInstruments). CBF and ABP regulation were characterized by their mean levels and spectral variability (power spectral density; PSD) at rest and during forced ABP oscillations induced by 0.10 Hz paced breathing. Frequency-domain properties were quantified using Fast Fourier analysis, and dCA was assessed using transfer function analysis between mean ABP and MCAv. Cerebrovascular responses across the 2-hour post–glucose ingestion period were compared using two-way ANOVA. Associations between glycemic, ABP, and CBF responses were assessed using Pearson’s correlations of their respective incremental areas under the curve during the 2-hour post–glucose ingestion period. Results: Blood glucose levels increased within the normal physiological range during the 2-hour post-ingestion period (iAUC: 227 ± 75 mmol/L·min). Increases in glycemia were accompanied by significant elevations in mean ABP (baseline= 98±4 vs. 120 min=108±6 mmHg, P=0.002) and ABP variability (baseline=3.59±0.78 vs. 120 min=7.20±2.19 mmHg 2 , P=0.039), confirming that an acute rise in glycemia challenged systemic ABP regulation. Despite these changes, there were no detrimental alterations in CBF mean levels, CBF variability, or dCA, suggesting that in healthy young adults, cerebral autoregulatory mechanisms effectively maintain stable CBF during acute glycemic elevations. However, exploratory post-hoc analyses revealed a strong positive association between the magnitude of the glycemic response and impaired CBF regulation (r=0.814, P=0.004), indicating that individuals exhibiting larger glycemic excursions may display early signs of cerebrovascular vulnerability. Conclusion: An acute increase in glycemia may compromise ABP regulation, yet cerebral autoregulatory mechanisms appear sufficient to preserve stable CBF in healthy young adults. The association between greater glycemic responses and altered CBF regulation suggests that individuals with less effective glucose control may be more susceptible to early cerebrovascular dysfunction, an observation that warrants further investigation. 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.