Smoking is an established risk factor for cardiovascular disease. It has also been shown to result in endothelial dysfunction as assessed by flow-mediated dilation (FMD) in response to reactive hyperemia (RH)-induced increases in shear stress. Handgrip exercise (HGEX) is an emerging alternative method to increase shear stress for FMD assessment (HGEX-FMD) and the purpose of this study was to identify the impact of smoking on HGEX-FMD in young healthy subjects. Brachial artery RH-FMD and HGEX-FMD (10-minute bout of HGEX) was assessed in eight smokers (S) and 14 non-smokers (NS) (age 21 ± 2 years). Brachial artery diameter and mean blood velocity were assessed with echo and Doppler ultrasound, respectively. Shear stress was estimated by shear rate (SR = brachial artery blood velocity/diameter). The SR stimulus did not differ between groups for either test (RH-FMD (SR area under the curve until peak diameter measurement), p = 0.897; HGEX-FMD (average SR over 10-minute exercise bout), p = 0.599). The RH-FMD magnitude was not significantly different between groups (S: 7.7 ± 2.2% vs NS: 7.9 ± 2.4%, p = 0.838); however, the HGEX-FMD magnitude was significantly impaired in smokers (S: 6.1 ± 3.4% vs NS: 9.6 ± 3.6%, p = 0.037). In conclusion, HGEX-FMD assessment detected vascular dysfunction in young healthy smokers while RH-FMD did not. This suggests that HGEX-FMD may be useful in the early detection of smoking-induced impairments in endothelial function. Further research is required to explore this phenomenon in other populations and to isolate underlying mechanisms.

Acute mental stress can impair brachial artery (BA) flow-mediated dilation (FMD) in response to reactive hyperemia (RH) induced increases in shear stress. Handgrip exercise (HGEX) is emerging as a useful tool to increase shear stress for FMD assessment; however, the impact of acute mental stress on HGEX-FMD is unknown. The purpose of this study was to determine whether acute mental stress attenuates RH- and HGEX-induced BA-FMD to a similar extent. In 2 counterbalanced visits, 16 healthy males (19-27 years of age) performed RH-FMD or HGEX-FMD tests after a counting control task (prestress FMD) and a speech and arithmetic stress task (poststress FMD). BA diameter and mean blood velocity were assessed with echo and Doppler ultrasound, respectively. Shear stress was estimated using shear rate (SR = BA blood velocity/BA diameter). Mean arterial pressure (MAP), heart rate (HR), and salivary cortisol were used to assess stress reactivity. Results are expressed as mean ± SE. The stress task elevated MAP (Δ24.0 ± 2.6 mm Hg) and HR (Δ15.5 ± 1.9 beats·min(-1)), but not cortisol (prestress vs. poststress: 4.4 ± 0.7 nmol·L(-1) vs. 4.7 ± 0.7 nmol·L(-1); p = 0.625). There was no difference between the pre- and poststress SR stimulus for RH (p = 0.115) or HGEX (p = 0.664). RH-FMD decreased from 5.2% ± 0.6% prestress to 4.1% ± 0.5% poststress (p = 0.071); however, stress did not attenuate HGEX-FMD (prestress vs. poststress: 4.1% ± 0.6% vs. 5.3% ± 0.6%; p = 0.154). The pre- to poststress change in FMD was significantly different in the RH-FMD vs. the HGEX-FMD test (-1.1% ± 0.6% vs. +1.1% ± 0.8%; p = 0.015). In conclusion, acute mental stress appears to have a disparate impact on FMD stimulated by RH vs. HGEX induced increases in shear stress.

Exercise elevates conduit artery shear stress and stimulates flow-mediated dilation (FMD). However, little is known regarding the impact of acute psychological and physical stress on this response. The purpose of this study was to examine the impact of the Trier Social Stress Test (TSST (speech and arithmetic tasks)) and a cold pressor test (CPT) with and without social evaluation (SE) on exercise-induced brachial artery FMD (EX-FMD). A total of 59 healthy male subjects were randomly assigned to 1 of 3 conditions: TSST, CPT, or CPT with SE. During 6 min of handgrip exercise, brachial artery EX-FMD was assessed before and 15 and 35 min poststress with echo and Doppler ultrasound. Shear stress was estimated as shear rate, calculated as brachial artery mean blood velocity/brachial artery diameter. Results are means ± SD. All conditions elicited significant physiological stress responses. Salivary cortisol increased from 4.6 ± 2.4 nmol/L to 10.0 ± 5.0 nmol/L (p < 0.001; condition effect: p = 0.292). Mean arterial pressure increased from 98.6 ± 12.1 mm Hg to 131.9 ± 18.7 mm Hg (p < 0.001; condition effect: p = 0.664). Exercise shear rate did not differ between conditions (p = 0.592), although it was modestly lower poststress (prestress: 72.3 ± 4.5 s(-1); 15 min poststress: 70.8 ± 5.4 s(-1); 35 min poststress: 70.6 ± 6.1 s(-1); trial effect: p = 0.011). EX-FMD increased from prestress to 15 min poststress in all conditions (prestress: 6.2% ± 2.8%; 15 min poststress: 7.9% ± 3.2%; 35 min poststress: 6.6% ± 2.9%; trial effect: p < 0.001; condition effect: p = 0.611). In conclusion, all conditions elicited similar stress responses that transiently enhanced EX-FMD. This response may help to support muscle perfusion during stress.

No abstract

Endothelial function is impaired in smokers as measured via handgrip exercise (HGEX) induced flow mediated dilation (FMD). The goal of this pilot study was to determine whether the dilation and reconstriction dynamics of FMD were impaired in young male smokers. 8 smokers and 14 non smokers (age 21 ± 2) performed 10 minutes of rhythmic HGEX bracketed by 4 minutes of arterial compression to ensure rapid shear stress onset and return to baseline. Brachial artery diameter and blood velocity assessed via echo and Doppler ultrasound. Shear stress estimated as shear rate (SR = brachial artery blood velocity/diameter). Dynamic parameters: time to onset of dilation and reconstriction (TD1); rate of dilation and reconstriction(Tau1). Alpha set at P<0.1, data ± SD. SR stimulus did not differ between groups(p=0.60). TD1 of dilation was longer in smokers (29.7 ± 17.0 s) vs. non smokers (17.5 ± 11.9 s)(p=0.06), and Tau1 was faster among smokers (27.5 ± 9.5 s vs. 48.6 ± 32.4 s, p = 0.09). Constriction dynamics were not different between groups (p>0.1). Among smokers, dilation tau1 was faster than reconstriction tau1(27.5 ± 9.5 s vs. 72.3 ± 56.4 s, p=0.06), whereas there were no differences between onset and constriction dynamics among non‐smokers (p=0.43). These results suggest that smoking impacts the dynamics of the vascular response to shear stress with a preferential impact on dilation vs. reconstriction. Grant Funding Source: Supported by NSERC and CFI