Anticipatory mental stress blunted sympathetic baroreflex sensitivity (p=0.048), which correlated with increased diastolic blood pressure variability (r=0.533, p<0.001) in healthy adults.
Does anticipatory mental stress increase beat-to-beat blood pressure variability through blunted sympathetic baroreflex sensitivity in healthy adults?
Anticipatory mental stress blunts sympathetic baroreflex sensitivity, which correlates with increased diastolic blood pressure variability, suggesting a physiological mechanism for stress-induced cardiovascular risk.
Absolute Event Rate: 0% vs 0%
Introduction: Elevated blood pressure variability (BPV) is associated with greater cardiovascular risk. At rest, beat-to-beat BPV is closely linked to sympathetic baroreflex sensitivity (sBRS). Therefore, factors which dampen sBRS, such as mental stress exposure, may increase BPV and cardiovascular risk. However, whether stress-induced blunting of baroreflex sensitivity results in larger beat-to-beat blood pressure oscillations remains unknown. The purpose of this study is to investigate whether mental stress-induced reductions in sBRS are associated with elevated BPV. We hypothesized that sBRS would be reduced during stress, and that the magnitude of sBRS reductions would be proportional to increases in BPV. Methods: 40 healthy adults (21 males, 19 females; age 22 ± 5 years; BMI 24 ± 3 kg/m 2 ) completed a 10-minute resting baseline and a 5-minute anticipatory stress task. The anticipatory stress task was a 5-minute speech preparation phase of a standardized Trier Social Stress Test (TSST). Continuous heart rate (ECG), beat-to-beat blood pressure (finger plethysmography), and muscle sympathetic nerve activity (MSNA; microneurography) were recorded throughout. Changes in average systolic (SBP) and diastolic (DBP), as well as their variability quantified using the standard deviation (SBP-BPV & DBP-BPV) were calculated from baseline to the anticipatory stress task. Similarly, average changes in muscle sympathetic nerve activity (MSNA), as well as sBRS were quantified. Pearson correlations were used to examine the relationships between changes in blood pressure, BPV, MSNA, and sBRS. Results: Anticipatory stress increased SBP (base: 112±10 vs. stress: 121±13 mmHg, p< 0.001), DBP (base: 67±6 vs. stress: 72±7 mmHg, p< 0.001), and heart rate (base: 66 ± 8 vs. stress: 73 ± 11 beats/min, p < 0.001), while MSNA was reduced (base: 18 ± 9 vs. stress: 15 ± 8 bursts/min, p < 0.001). sBRS was blunted during anticipatory stress compared to baseline (base: –3.3 ± 1.6 vs. stress: –2.8 ± 1.6 bursts/100 hb/mmHg, p = 0.048). DBP-BPV increased (4.3 ± 1.1 vs. 4.6 ± 1.0 mmHg, p = 0.025), while SBP-BPV remained unchanged (base: 5.5±1.6 vs. stress: 5.4±1.3 mmHg, p=0.339). Changes in MSNA were negatively associated with changes in DBP (r=-0.389, p=0.013) but unrelated to changes in DBP-BPV (r=0.054, p=0.740). Conversely, changes in sBRS were not associated with changes in average DBP (r=-0.276, p=0.085), but were positively associated with changes in DBP-BPV (r=0.533, p< 0.001). Conclusion: These findings indicate that anticipatory mental stress elicits reductions in sBRS which are associated with elevated BPV. Together, these findings suggest that psychological stress may increase cardiovascular risk through impaired baroreflex function and increased BPV. 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.
Murvich et al. (Fri,) reported a other. Anticipatory mental stress blunted sympathetic baroreflex sensitivity (p=0.048), which correlated with increased diastolic blood pressure variability (r=0.533, p<0.001) in healthy adults.