Acute mental stress did not impair endothelial function, and vitamin C disrupted the relationship between cortisol reactivity and changes in FMD post-stress. This suggests that acute mental stress does not universally impair endothelial function and that reactive oxygen species signaling may influence the interaction between FMD and stress responses.

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A temporary depression in reactive hyperemia stimulated flow‐mediated dilation (RH‐FMD) has been observed in young healthy individuals after an acute bout of mental stress. While it has been shown that a post‐stress reduction in RH‐FMD persists for 90 minutes in middle‐aged participants, it is unclear whether the impairment is similarly prolonged in a young healthy population. The objective of this pilot study was therefore to examine brachial artery RH‐FMD at 90 minutes post‐acute mental stress in young healthy volunteers. Doppler and echo ultrasound were used to obtain brachial artery diameter and velocity respectively. The shear stress stimulus was characterized as the shear rate (SR = velocity/diameter) area under the curve (SR‐AUC) during the first 30 seconds following forearm cuff deflation. Data are mean ± SD. Four men and two women aged 22.2 ± 3.7 years participated. RH‐FMD was assessed at baseline and 90 minutes following a stress task based on the Trier Social Stress Test (TSST). The average subjective stress rating for the TSST was 6.7 ± 1.8 (on a subjective scale of 1‐10). SR‐AUC was not significantly different at baseline (2304.9 ± 1055.2) compared to 90 minutes post‐mental stress (3022.9 ± 1224.7; P = 0.171). RH‐FMD was significantly lower in participants at 90 minutes post‐stress (6.7 ± 5.5%) compared to baseline (9.3 ± 3.7%; P = 0.025). These preliminary findings suggest that acute mental stress can have a prolonged (90 minute) detrimental effect on endothelial function in young healthy adults. Funded by NSERC and CFI.