Acute mental stress and its impact on systemic vascular endothelial function in obese adults

Background and aims: Everyday life stressors such as acute mental stress can result in transient impairments in vascular endothelial function (2). Similarly, obesity is known to impair arterial smooth muscle function (1). However, their combined effect remains unknown. To investigate this, we determined to what extent a battery of neuropsychometric tests further compounded vascular endothelial dysfunction in obese adults related to non-obese controls. Methods: Eight obese [26 (mean) ± 8 (SD) years old; BMI = 33 ± 4] and 8 non-obese (21 ± 4 years old; BMI = 25 ± 3) male participants were recruited. Brachial artery flow-mediated dilatation (FMD, Acuson P50, Siemens) was measured 1 hour before and immediately following a standardised battery of neuropsychometric tests. Following a 1-min baseline, the occluding cuff (distal) was inflated (>250mmHg) for 5 min and a subsequently released for 5-min into recovery. Brachial artery diameter and flow were recorded continuously throughout the test. Baseline data correspond to the 1-min average pre cuff inflation and peak diameter was measured as the average of the highest 3 values recorded. Data were analysed using automated edge-detection and wall-tracking software (Brachial Tools, Medical Imaging Application). Following confirmation of distribution normality (Shapiro-Wilk W tests), data were analysed using a 2-way (Time x Group) repeated measures ANOVA. Data are expressed as mean ± SD with significance set at P < 0.05. Results: Psychometric stress was shown to impair FMD (Pre: 5.3 ± 1.4% vs. Post: 4.4 ± 1.4%, P < 0.05). The obese group also displayed a lower FMD than their non-obese peers during both FMD tests (P<0.05). The obese further exhibited a decrease in baseline flow from 0.11 ± 0.02 m/sec before to 0.08 ± 0.02 m/sec after acute mental stress (P<0.05). Conclusion: The present results confirmed that acute mental stress impairs systemic vascular endothelial function. Contrary to our original hypothesis, this impairment was not further compounded by obesity.