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We sought to determine how whole body heating acutely influences radial artery function, characterized using flow-mediated dilation (FMD) and low-flow-mediated constriction (L-FMC), and the mechanistic role of shear rate modification on radial artery functional characteristics during heating. Eleven young healthy men underwent whole body heating (water-perfused suit) sufficient to raise the core temperature by +1°C. Trials were repeated with (heat + WC) and without (heat) the application of a wrist cuff located distal to the radial artery examined, known to prevent increases in mean and anterograde shear rates but increase retrograde shear rate. Radial artery characteristics were assessed throughout each trial, with FMD and L-FMC assessed before and upon reaching the target core temperature. Heat markedly increased radial artery mean and anterograde shear rates, along with radial artery diameter and blood flow ( P < 0.05). Heat + WC abolished the heat-induced increase in mean and anterograde shear rates ( P > 0.05) but markedly increased retrograde shear rate ( P < 0.05). Concomitantly, increases in radial artery diameter and blood flow were decreased (heat + WC vs. heat, P < 0.05). Heat attenuated FMD (8.6 ± 1.2% vs. 2.2 ± 1.4%, P < 0.05), whereas no change in FMD was observed in heat + WC (7.8 ± 1.2% vs. 10.8 ± 1.2%, P > 0.05). In contrast, L-FMC was not different in either trial ( P > 0.05). In summary, acute whole body heating markedly elevates radial artery shear rate, diameter, and blood flow and diminishes FMD. However, marked radial artery vasodilation and diminished FMD are absent when these shear rate changes are prevented. Shear rate modifications underpin the radial artery response to acute whole body heat stress, but further endothelium-dependent vasodilation (FMD) is attenuated likely as the vasodilatory range limit is approached. NEW & NOTEWORTHY We observed that acute whole body heating elevates radial artery shear rate, diameter, and blood flow. This results in a diminished flow-meditated dilatation (FMD) but does not change low-flow-mediated constriction (L-FMC). Preventing shear rate changes during whole body heating reduces radial artery vasodilation and reverses FMD reductions but has no effect on L-FMC. These findings indicate that shear rate changes underpin conduit artery responses to acute whole body heat stress, but further endothelium-dependent flow-mediated vasodilation is attenuated as the vasodilatory range limit is approached.

South Asians living in the United Kingdom have a 1.5-fold greater risk of ischemic stroke than the general population. Impaired cerebrovascular carbon dioxide (CO 2 ) reactivity is an independent predictor of ischemic stroke and cardiovascular mortality. We sought to test the hypothesis that cerebrovascular CO 2 reactivity is reduced in South Asians. Middle cerebral artery blood velocity (MCA V m ) was measured at rest and during stepwise changes in end-tidal partial pressure of CO 2 ( P E T C O 2 ) in South Asian ( n = 16) and Caucasian European ( n = 18) men who were young (~20 yr), healthy, and living in the United Kingdom. Incremental hypercapnia was delivered via the open-circuit steady-state method, with stages of 4 and 7% CO 2 (≈21% oxygen, nitrogen balanced). Cerebrovascular CO 2 reactivity was calculated as the change in MCA V m relative to the change in P E T C O 2 . MCA V m was not different in South Asians [59 (9) cm/s, mean (standard deviation)] and Caucasian Europeans [61 (12) cm/s; P > 0.05]. Similarly, cerebrovascular CO 2 reactivity was not different between the groups [South Asian 2.53 (0.76) vs. Caucasian European 2.61 (0.81) cm·s -1 ·mmHg -1 ; P > 0.05]. Brachial artery flow-mediated dilation was lower in South Asians [5.48 (2.94)%] compared with Caucasian Europeans [7.41 (2.28)%; P < 0.05]; however, when corrected for shear rate no between-group differences in flow-mediated dilation were observed ( P > 0.05). Flow-mediated dilation was not correlated with cerebrovascular CO 2 reactivity measures. In summary, cerebrovascular CO 2 reactivity and flow-mediated dilation corrected for shear rate are preserved in young healthy South Asian men living in the United Kingdom. NEW & NOTEWORTHY Previous reports have identified an increased risk of ischemic stroke and peripheral endothelial dysfunction in South Asians compared with Caucasian Europeans. The main finding of this study is that cerebrovascular carbon dioxide reactivity (an independent predictor of ischemic stroke) is not different in healthy young South Asian and Caucasian European men.

Purpose: Prevalence of cardiovascular disease (CVD) is greater in South Asians (SAs) than White Europeans (WEs). Endothelial dysfunction and blunted forearm vasodilatation to environmental stressors have been implicated in CVD. We investigated whether these features are present in young SA men., Methods: In 15 SA and 16 WE men (19-23 years), we compared changes in forearm blood flow, arterial blood pressure (ABP), forearm vascular conductance (FVC), heart rate, and electrodermal resistance (EDR; sweating) following release of arterial occlusion (reactive hyperaemia endothelium-dependent) and 5 single sounds at 5-10 min intervals (stressors)., Results: All were normotensive. Peak reactive hyperaemia was smaller in SAs than WEs (FVC increase: 0.36 ± 0.038 vs 0.44 ± 0.038 units; P < 0.05). Furthermore, in WEs, mean FVC increased at 5, 15, and 20 s of each sound (vasodilatation), but increased at 5 s only in SAs, decreasing by 20 s (vasoconstriction). This reflected a smaller proportion of SAs showing forearm vasodilatation at 15 s (5/15 SAs vs 11/16 WEs: P < 0.01), the remainder showing vasoconstriction. Concomitantly, WEs showed greater bradycardia and EDR changes. Intra-class correlation analyses showed that all responses were highly reproducible over five sounds in both WEs and SAs. Moreover, sound-evoked changes in ABP and FVC were negatively correlated in each ethnicity (P < 0.01). However, WEs showed preponderance of forearm vasodilatation and depressor responses; SAs showed preponderance of vasoconstriction and pressor responses., Conclusions: Endothelium-dependent vasodilatation is blunted in young SA men. This could explain their impaired forearm vasodilatation and greater pressor responses to repeated environmental stressors, so predisposing SAs to hypertension and CVD.