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.

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