PurposeA “low-flow mediated constriction” (L-FMC) is evoked in the radial artery by the inflation of an ipsilateral wrist cuff to a supra-systolic pressure. We sought to test the hypothesis that the radial artery L-FMC response is augmented immediately following acute dynamic leg exercise in young healthy individuals.MethodsTen healthy and recreationally active men (23 ± 4 years) undertook a 30-min trial of incremental dynamic leg cycling exercise (10 min at 50, 100 and 150 W) and a 30-min time control trial (seated rest). Trials were randomly assigned and performed on separate days. Radial artery characteristics (diameter, blood flow and shear rate) were assessed throughout each trial, with L-FMC and flow-mediated vasodilatation (FMD) assessments conducted prior to and immediately following (10 min) trials.ResultsDynamic leg cycling exercise increased radial artery blood flow, along with mean, retrograde and anterograde shear rate (P < 0.05). Blood flow profiles were unchanged during the time control trial (P > 0.05). Following exercise L-FMC was increased (mean [SD]; − 5.6 [3.3] vs. − 10.1 [3.8] %, P < 0.05), while it was not different in the time control condition (− 8.1 [3.2] vs. − 6.7 [3.4] %, P > 0.05). FMD was not different following either the exercise or time control trials (P > 0.05), but the composite end-point of L-FMC + FMD was enhanced post-exercise (P < 0.05).ConclusionsDynamic exercise with a large muscle mass acutely augments the vasoconstrictor response of the radial artery in response to a reduction in blood flow (L-FMC) in young healthy individuals. The time course of this post-exercise response and the underlying vasoregulatory mechanisms require elucidation.

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 (CO2) reactivity is an independent predictor of ischemic stroke and cardiovascular mortality. We sought to test the hypothesis that cerebrovascular CO2 reactivity is reduced in South Asians. Middle cerebral artery blood velocity (MCA Vm) was measured at rest and during stepwise changes in end-tidal partial pressure of CO2 ([Formula: see text]) 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% CO2 (≈21% oxygen, nitrogen balanced). Cerebrovascular CO2 reactivity was calculated as the change in MCA Vm relative to the change in [Formula: see text]. MCA Vm 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 CO2 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 CO2 reactivity measures. In summary, cerebrovascular CO2 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.

Diving evokes a pattern of physiological responses purported to preserve oxygenated blood delivery to vital organs such as the brain. We sought to uncouple the effects of trigeminal nerve stimulation on cerebral blood flow (CBF) from other modifiers associated with the diving response, such as apnoea and changes in arterial carbon dioxide tension. Thirty-seven young healthy individuals participated in separate trials of facial cooling (FC, 3 min) and cold pressor test (CPT, 3 min) under poikilocapnic (Protocol 1) and isocapnic conditions (Protocol 2), facial cooling while either performing a breath-hold (FC +BH) or breathing spontaneously for a matched duration (FC −BH) (Protocol 3), and BH during facial cooling (BH +FC) or without facial cooling (BH −FC) (Protocol 4). Under poikilocapnic conditions neither facial cooling nor CPT evoked a change in middle cerebral artery blood flow velocity (MCA v mean ; transcranial Doppler) (P > 0.05 vs. baseline). Under isocapnic conditions, facial cooling did not change MCA v mean (P > 0.05), whereas CPT increased MCA v mean by 13% (P < 0.05). Facial cooling with a concurrent BH markedly increased MCA v mean (Δ23%) and internal carotid artery blood flow (ICA Q ; duplex Doppler ultrasound) (Δ26%) (P < 0.001), but no change in MCA v mean and ICA Q was observed when facial cooling was accompanied by spontaneous breathing (P > 0.05). Finally, MCA v mean and ICA Q were similarly increased by BH either with or without facial cooling. These findings suggest that physiological factors associated with BH, and not facial cooling (i.e. trigeminal nerve stimulation) per se, make the predominant contribution to increases in CBF during diving in humans. K E Y W O R D S blood flow, brain, diving response 1 wileyonlinelibrary.com/journal/eph Experimental Physiology. 2020;105:940-949.

Hypoxia induces ventilatory, cardiovascular and cerebrovascular adjustments to defend against reductions in systemic oxygen delivery. We aimed to determine whether the ventilatory response to moderate acute hypoxia increases cerebral perfusion independently of changes in arterial oxygenation. Eleven young healthy individuals were exposed to four 15 min experimental conditions: (1) normoxia (partial pressure of end-tidal oxygen, P ETO 2 = 100 mmHg), (2) hypoxia (P ETO 2 = 50 mmHg), (3) normoxia with breathing volitionally matched to levels observed during hypoxia (hyperpnoea; P ETO 2 = 100 mmHg) and (4) hypoxia (P ETO 2 = 50 mmHg) with respiratory frequency and tidal volume volitionally matched to levels observed during normoxia (i.e., restricted breathing (RB)). Isocapnia was maintained in all conditions. Middle cerebral artery mean blood velocity (MCA V mean), assessed by transcranial Doppler ultrasound, was increased during hypoxia (58 ± 12 cm/s, P = 0.04) and hypoxia + RB (61 ± 14 cm/s, P < 0.001) compared to normoxia (55 ± 11 cm/s), while it was unchanged during hyperpnoea (52 ± 13 cm/s, P = 0.08). MCA V mean was not different between hypoxia and hypoxia + RB (P > 0.05). These findings suggest that the hypoxic ventilatory response does not increase cerebral perfusion, indexed using MCA V mean , during moderate isocapnic acute hypoxia beyond that elicited by reduced oxygen saturation.

The immersion of the face in cold water evokes a powerful autonomic reflex known as the diving response. It is activated primarily by stimulation of the trigeminal nerve (TGS) that innervates the areas around the forehead and cheeks, but its physiological effects are also modulated by secondary mechanisms such as apnoea. The diving response is believed to act to preserve oxygen delivery to the heart and brain. We sought to determine the relative importance of the TGS and apnoea components of the diving response to the regulation of cerebral blood flow.In 8 young, healthy volunteers (aged 24 ± 3 yr; 2 women), middle cerebral artery velocity (MCAV; transcranial Doppler), arterial blood pressure (Finometer), heart rate (ECG) and the partial pressure of end‐tidal carbon dioxide (PETCO2) were recorded. In addition, internal carotid artery diameter and velocity were measured (ICAV) using duplex Doppler ultrasound, and internal carotid artery flow (ICAQ) calculated. Cerebral vascular conductance (CVC) was calculated as; MCAV or ICAQ/MAP. TGS was evoked by the placement of ice packs on the forehead and cheeks under two conditions; 1) while performing an end‐expiratory breath‐hold (+BH), and 2) while breathing spontaneously (‐BH). The second condition was always undertaken last and its duration was matched to that of the first condition. Data were averaged at baseline (3 min) and at the end of each manoeuvre (last 10 cardiac cycles) and are presented as mean ± SEM.The apnoea was held for 26 ± 3 s. During combined TGS+BH, mean blood pressure (88 ± 5 vs. 101 ± 4 mmHg), MCAV (67 ± 9 vs. 82 ± 8 cm s−1) and ICAQ (309 ± 42 vs. 386 ± 56 ml min−1) were increased (p<0.05), while MCACVC (0.77 ± 0.11 vs 0.81± 0.08 cm s−1/mmHg) and ICACVC (3.49 ± 0.47 vs. 3.84 ± 0.60 ml min−1/mmHg) remained unchanged (P<0.05), and heart rate tended to decline (71 ± 2 vs. 65 ± 3 bpm; P=0.072). In contrast, during TGS–BH, mean blood pressure increased (87 ± 2 vs. 91 ± 2 mmHg: P<0.01), while MCAV (65 ± 7 vs. 66 ± 7 cm s−1), MCACVC (0.75 ± 0.08 vs. 0.73 ± 0.08 cm s−1/mmHg), ICAQ (304 ± 40 vs. 296 ± 41 ml min−1), ICACVC (3.38 ± 0.48 vs. 3.17 ± 0.47 ml min−1/mmHg) and heart rate (67 ± 4 vs. 66 ± 4 bpm) remained unchanged (P>0.05).In summary, cerebral blood flow increased when TGS was coupled with an apnoea, but the independent activation of TGS did not elicit an increase in cerebral blood flow. These findings suggest that physiological factors associated with breath holding (e.g., pressor response, CO2 accumulation) make the predominate contribution to diving response mediated‐increases in cerebral blood flow in humans.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.