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PURPOSE The present study examined the effect of breath-hold without a Valsalva maneuver during isometric exercise on arterial blood pressure (ABP) and cerebral blood flow (CBF). METHODS Twenty healthy adults (15 men and five women) randomly performed only breath-hold without a Valsalva maneuver (BH), and an isometric handgrip exercise for 30 s at 40% of individual maximal voluntary contraction with continuous breathing (IHG) and with breath-hold without the Valsalva maneuver (IHG-BH). Mean ABP (MAP) and blood velocity in the middle (MCA Vmean) and posterior cerebral arteries (PCA Vmean) were continuously measured throughout each protocol. RESULTS MAP was elevated during the IHG-BH compared with IHG (P

NEW FINDINGS What is the central question of this study? To what extent do hypoxia-induced changes in the peripheral and central respiratory chemoreflex modulate anterior and posterior cerebral oxygen delivery, with corresponding implications for susceptibility to acute mountain sickness? What is the main finding and its importance? We provide evidence for site-specific regulation of cerebral blood flow in hypoxia that preserves oxygen delivery in the posterior but not the anterior cerebral circulation, with minimal contribution from the central respiratory chemoreflex. External carotid artery vasodilatation might prove to be an alternative haemodynamic risk factor that predisposes to acute mountain sickness. ABSTRACT The aim of the present study was to determine the extent to which hypoxia-induced changes in the peripheral and central respiratory chemoreflex modulate anterior and posterior cerebral blood flow (CBF) and oxygen delivery (CDO2 ), with corresponding implications for the pathophysiology of the neurological syndrome, acute mountain sickness (AMS). Eight healthy men were randomly assigned single blind to 7 h of passive exposure to both normoxia (21% O2 ) and hypoxia (12% O2 ). The peripheral and central respiratory chemoreflex, internal carotid artery, external carotid artery (ECA) and vertebral artery blood flow (duplex ultrasound) and AMS scores (questionnaires) were measured throughout. A reduction in internal carotid artery CDO2 was observed during hypoxia despite a compensatory elevation in perfusion. In contrast, vertebral artery and ECA CDO2 were preserved, and the former was attributable to a more marked increase in perfusion. Hypoxia was associated with progressive activation of the peripheral respiratory chemoreflex (P 0.05). Symptom severity in participants who developed clinical AMS was positively related to ECA blood flow (Lake Louise score, r = 0.546-0.709, P = 0.004-0.043; Environmental Symptoms Questionnaires-Cerebral symptoms score, r = 0.587-0.771, P = 0.001-0.027, n = 4). Collectively, these findings highlight the site-specific regulation of CBF in hypoxia that maintains CDO2 selectively in the posterior but not the anterior cerebral circulation, with minimal contribution from the central respiratory chemoreflex. Furthermore, ECA vasodilatation might represent a hitherto unexplored haemodynamic risk factor implicated in the pathophysiology of AMS.

New findings What is the central question of this study? What is the effect of exercise countermeasure on microgravity-induced change in cerebral blood flow? What is the main finding and its importance? Jump exercise training as a countermeasure did not modify this heterogeneous cerebral blood flow response to the HDBR, suggesting that this method is effective in preventing cardiovascular system deconditioning but is not good for cerebral haemodynamics. Abstract This study aimed to examine the effect of exercise countermeasure on cerebral blood flow (CBF) response to long-term -6° head-down bed rest (HDBR) in all cerebral arteries and veins. Twenty male volunteers were exposed to HDBR for 60 days with (training group, n = 10) or without jump (control group, n = 10) exercise training as countermeasure to spaceflight. The blood flow in the neck conduit arteries (internal carotid and vertebral artery; ICA and VA) and veins (internal jugular and vertebral veins; IJV and VV) was measured, using ultrasonography before (baseline) HDBR, on the 30th day of HDBR, and on the 57th day of HDBR. Long-term HDBR causes a heterogeneous CBF response between the anterior and the posterior brain or between arteries and veins. Long-term HDBR decreased anterior cerebral arterial and venous blood flow, while posterior cerebral arterial and venous blood flows were well maintained. However, an exercise jump training did not change HDBR-induced heterogenous CBF (control vs. training; ICA, P = 0.643; VA, P = 0.542; ECA, P = 0.644; IJV, P = 0.980; VV, P = 0.999). These findings suggest that jump exercise training did not modify this heterogeneous CBF response to long-term HDBR. This article is protected by copyright. All rights reserved.

KEY POINTS The cerebral fluid response to exercise, including the arterial and venous cerebral blood flow (CBF) and cerebrospinal fluid (CSF), currently remains unknown. We used time-resolved phase-contrast magnetic resonance imaging to assess changes in CBF and CSF flow dynamics during moderate-intensity rhythmic handgrip (RHG) exercise in young healthy men and women. Our data demonstrated that RHG increases the cerebral arterial inflow and venous outflow while decreasing the pulsatile CSF flow during RHG. Furthermore, changes in blood stroke volume at the measured arteries, veins, and sinuses and CSF stroke volume at the cerebral aqueduct were positively correlated with each other during RHG. Male and female participants exhibited distinct blood pressure responses to RHG, but their cerebral fluid responses were similar. These results collectively suggest that RHG influences both CBF and CSF flow dynamics in a way that is consistent with the Monro-Kellie hypothesis to maintain intracranial volume-pressure homeostasis in young healthy adults. ABSTRACT Cerebral blood flow (CBF) increases during exercise, but its impact on cerebrospinal fluid (CSF) flow remains unknown. This study investigated CBF and CSF flow dynamics during moderate-intensity rhythmic handgrip (RHG) exercise in young healthy men and women. Twenty-six participants (12 women) underwent the RHG and resting control conditions in random order. Participants performed 3 sets of RHG, during which cine phase-contrast magnetic resonance imaging (PC-MRI) was performed to measure blood stroke volume (SV) and flow rate in the internal carotid (ICA) and vertebral (VA) arteries, the internal jugular vein (IJV), the superior sagittal (SSS) and straight sinuses (SRS), and CSF SV and flow rate in the cerebral aqueduct of Sylvius. Blood pressure, end-tidal CO2 (EtCO2 ), heart rate (HR), and respiratory rate were simultaneously measured during cine PC-MRI scans. Compared with control conditions, RHG showed significant elevations of HR, mean arterial pressure, and respiratory rate with a mild reduction of EtCO2 (all P < 0.05). RHG decreased blood SV in the measured arteries, veins, and sinuses and CSF SV in the aqueduct (all P < 0.05). Conversely, RHG increased blood flow in the ICA, VA, and IJV (all P < 0.05). At the aqueduct, RHG decreased the absolute CSF flow rate (P = 0.0307), which was calculated as a sum of the caudal and cranial CSF flow rates. Change in the ICA SV was positively correlated with changes in the IJV, SSS, SRS, and aqueductal SV during RHG (all P < 0.05). These findings demonstrate a close coupling between the CBF and CSF flow dynamics during RHG in young healthy adults.

We examined the acute impact of both low- and high-glycemic index (GI) breakfasts on plasma brain-derived neurotrophic factor (BDNF) and dynamic cerebral autoregulation (dCA) compared with breakfast omission. Ten healthy men (age 24 ± 1 yr) performed three trials in a randomized crossover order; omission and Low-GI (GI = 40) and High-GI (GI = 71) breakfast conditions. Middle cerebral artery velocity (transcranial Doppler ultrasonography) and arterial pressure (finger photoplethysmography) were continuously measured for 5 min before and 120 min following breakfast consumption to determine dCA using transfer function analysis. After these measurements of dCA, venous blood samples for the assessment of plasma BDNF were obtained. Moreover, blood glucose was measured before breakfast and every 30 min thereafter. The area under the curve of 2 h postprandial blood glucose in the High-GI trial was higher than the Low-GI trial ( P < 0.01). The GI of the breakfast did not affect BDNF. In addition, both very-low (VLF) and low-frequency (LF) transfer function phase or gains were not changed during the omission trial. In contrast, LF gain (High-GI P < 0.05) and normalized gain (Low-GI P < 0.05) were decreased by both GI trials, while a decrease in VLF phase was observed in only the High-GI trial ( P < 0.05). These findings indicate that breakfast consumption augmented dCA in the LF range but High-GI breakfast attenuated cerebral blood flow regulation against slow change (i.e., the VLF range) in arterial pressure. Thus we propose that breakfast and glycemic control may be an important strategy to optimize cerebrovascular health.

Passive stretching reduces stiffness in the lower limb arteries of the stretched limb. To address this physiological mechanism, we measured the change in shear rate in the posterior tibial artery during a single bout of one-legged passive calf stretching compared with that in the non-stretched leg. The diameter, mean blood velocity, blood flow, and shear rate in the posterior tibial artery were measured using Doppler ultrasound before (baseline), during, and after a one-legged passive intermittent calf stretching procedure (six repetitions of 30-s static stretch with 10-s relaxation) in nine healthy young men. In the posterior tibial artery of the stretched leg, the arterial diameter significantly decreased from baseline during the stretching period (baseline vs. stretching period of the 6th set, 0.19 ± 0.01 vs. 0.18 ± 0.01 cm, P

International audience; The increasing number of older adults has seen a corresponding growth in those affected by neurovascular diseases, including stroke and dementia. Since cures are currently unavailable, major efforts in improving brain health need to focus on prevention, with emphasis on modifiable risk factors such as promoting physical activity. Moderate-intensity continuous training (MICT) paradigms have been shown to confer vascular benefits translating into improved musculoskeletal, cardiopulmonary and cerebrovascular function. However, the time commitment associated with MICT is a potential barrier to participation, and high-intensity interval training (HIIT) has since emerged as a more time-efficient mode of exercise that can promote similar if not indeed superior improvements in cardiorespiratory fitness for a given training volume and further promote vascular adaptation. However, randomised controlled trials (RCTs) investigating the impact of HIIT on the brain are surprisingly limited. The present review outlines how the HIIT paradigm has evolved from a historical perspective and describes the established physiological changes including its mechanistic bases. Given the dearth of RCTs, the vascular benefits of MICT are discussed with a focus on the translational neuroprotective benefits including their mechanistic bases that could be further potentiated through HIIT. Safety implications are highlighted and components of an optimal HIIT intervention are discussed including practical recommendations. Finally, statistical effect sizes have been calculated to allow prospective research to be appropriately powered and optimise the potential for detecting treatment effects. Future RCTs that focus on the potential clinical benefits of HIIT are encouraged given the prevalence of cognitive decline in an ever-ageing population.

The present study examined the effect of muscle metaboreflex on blood flow in different cerebral arteries. Eleven healthy participants performed isometric, one-leg knee extension at 30% maximal voluntary contraction for 2 min. Activated muscle metaboreflex was isolated for 2 min by post-exercise muscle ischemia (PEMI). The contralateral internal carotid (ICA), vertebral (VA), and ipsilateral external carotid arteries (ECA) blood flows were evaluated using Doppler ultrasound. The ICA blood flow increased at the beginning of exercise (P = 0.004) but returned to the baseline level at the end of exercise (P = 0.055). In contrast, the VA blood flow increased and it was maintained until the end of the exercise (P = 0.011), while the ECA blood flow gradually increased throughout the exercise (P = 0.001). These findings indicate that isometric exercise causes a heterogeneous cerebral blood flow response in different cerebral arteries. During PEMI, the conductance of the VA as well as that of the ICA was significantly lower compared with the baseline value (P = 0.020 and P = 0.032, at PEMI90), while the conductance of the ECA was not different from the baseline (P = 0.587), suggesting that the posterior and anterior cerebral vasculature were similarly affected during exercise by activation of muscle metaboreceptors, but not in the non-cerebral artery. Since ECA branches from ICA, the balance in the different influence of muscle metaboreflex on ECA (vasodilation via exercise-induced hypertension) and ICA (vasoconstriction) may contribute to the decrease in ICA blood flow at the end of isometric exercise.

Interval exercise has been determined to be more effective than continuous exercise for achieving improvement in the cardiovascular function of individuals suffering from cardiovascular disease. However, whether interval exercise improves the cerebrovascular function remains unclear. As per our hypothesis, interval exercise induces a higher cerebrovascular shear rate (SR) than continuous exercise. In this study, 11 adult men randomly performed continuous exercise for 12 min or work‐equivalent (57.6 kJ/exercise session) interval exercise of semi‐recumbent cycling. The SR in the internal carotid artery (ICA) represents an index of the cerebrovascular SR, which was measured during both the exercises using Doppler ultrasonography. Both the aerobic exercise modes increased the ICA SR. Moreover, the average ICA SR of the interval exercise for the final 4 min of exercise or 2 min of recovery was significantly higher than that for continuous exercise (exercise, 351 ± 75 vs. 330 ± 61/s, p = .038; recovery, 327 ± 86 vs. 290 ± 56/s, p = .014). To our knowledge, this is the first study to show that aerobic interval exercise increased the ICA SR more than equivalent work volume of aerobic continuous exercise. Thus, aerobic interval exercise may be more effective at stimulating the cerebrovasculature, resulting in greater improvements in cerebrovascular function as compared to continuous aerobic exercise in healthy adult men. These findings provide some important information that would help enhance exercise therapy programs for patients with arteriosclerosis, especially in the cerebral circulation., Internal carotid artery image and cerebrovascular parameters during continuous and interval exercise by Doppler ultrasonography.

Background Maximal aerobic capacity, e.g. maximal oxygen uptake (V̇O2max), is not constant, and it has a time-dependent variation based on the condition of individual. On the other hand, arterial properties play an important role in determining aerobic performance, and lower arterial stiffness is associated with higher cardiorespiratory fitness levels. This study examined whether individual variations in maximal aerobic performance are associated with arterial stiffness. Methods Twenty-four (mean age, 19.8 ± 0.2 y) and 10 (mean age, 21.2 ± 0.2 y) recreationally active young men and women participated in Experiment 1 (Ex1) and in Experiment 2 (Ex2), respectively. Aerobic performance was assessed using a graded power test (Ex1) or a 1500-m time trial (Ex2). Simultaneously, brachial-ankle pulse wave velocity (baPWV) was measured as an index of arterial stiffness in both Ex1 and Ex2 before the exercise trials. In both experiments, subjects returned for measurement of baPWV and V̇O2max or 1500-m time trial at 1 month after first measurements. Results No significant differences in mean baPWV, V̇O2max or 1500-m run time were seen between first and second visits. Mean baPWV was significantly lower on days when participants showed higher V̇O2max or better 1500-m run time (P = 0.001 each) than on days when participants showed lower V̇O2max or worse 1500-m run time. In addition, a significant relationship was seen between individual changes in baPWV from first to second visits and changes in V̇O2max (P=0.0001) or 1500-m run time (P=0.04). Conclusion These findings suggest that individual day-to-day variations in maximal aerobic performance are associated with variations in arterial stiffness.

Previous studies have reported that even a single bout of dynamic exercise improves cognitive performance. However, the acute effect of the interval handgrip (HG) exercise protocol, which is effective in reducing resting blood pressure, on cognitive performance is poorly understood. Cognitive performance was assessed in 17 young healthy subjects before and after a resting control (e.g., time control) and the interval HG exercise (Exercise), which consisted of four trials of 2-min HG exercise at 25% of maximum voluntary contraction with 3-min recovery in between each trial. Mean arterial blood pressure (MAP) and middle cerebral artery blood velocity (MCA V) were measured continuously throughout the experiment. Memory recognition and executive function were assessed using memory recognition and Go/No-Go tasks, respectively. During interval HG exercise, MAP and mean MCA V increased from the resting baseline condition (both P < 0.049) and returned to the resting baseline levels during recovery after the interval HG exercise (both P = 1.000). The reaction time and performance accuracy of the memory recognition task did not change in either the time control condition or Exercise condition (P = 0.514 and P = 0.414 respectively). However, the changes in reaction time of Go/No-Go task from the baseline in Exercise condition was significantly shorter than that in time-control condition (P = 0.004) without affecting performance accuracy (P = 0.482). The results of the present study show that an acute interval HG exercise could improve the processing speed in executive function despite no post-exercise improvement in hemodynamic parameters in young healthy subjects. These findings suggest that the interval HG exercise is a useful exercise mode that can be expected to have a positive effect on the processing speed in executive function regardless of cardiovascular adaptation to exercise.

We sought to determine whether gravity-induced changes in intracranial pressure influence cerebral blood flow regulation. Accordingly, nine young healthy men were studied while supine (0°) and during mild changes in hydrostatic pressure induced by head-up tilt at +20° and +10° (HUT+20 and HUT+10) and head-down tilt at -20° and -10° (HDT-20, HDT-10). Blood flows were measured in the internal and external carotid and vertebral arteries (ICA, ECA, and VA). Intraocular pressure (IOP) was measured as an indicator of hydrostatic changes in intracranial pressure. A posture change from HUT+20 to HDT-20 increased IOP by +5.1 ± 1.9 mmHg (

We investigated that the effects of hypercapnia-induced elevations in cerebral perfusion during a heat stress on global cerebrovascular responses to an orthostatic challenge. Seven volunteers completed a progressive lower-body negative pressure (LBNP) challenge to presyncope during heat stress, with or without breathing a hypercapnic gas mixture. Administration of the hypercapnic gas mixture increased the partial pressure of end-tidal CO2 greater than pre-heat stress alone, and increased both internal carotid artery (ICA) and vertebral artery (VA) blood flows (P P

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.

International audience; The present study examined if repeated bouts of micro- and hypergravity during parabolic flight (PF) alter structural integrity of the neurovascular unit (NVU) subsequent to free radical-mediated changes in regional cerebral perfusion. Six participants (5♂, 1♀) aged 29 ± 11 years were examined before, during and after a 3h PF and compared to six sex and age-matched (27 ± 6 years) normogravity controls. Blood flow was measured in the anterior (middle cerebral artery, MCA; internal carotid artery, ICA) and posterior (vertebral artery, VA) circulation (duplex ultrasound) in-flight over the course of 15 parabolas. Venous blood was assayed for free radicals (electron paramagnetic resonance spectroscopy), nitric oxide (NO, ozone-based chemiluminescence) and NVU integrity (chemiluminescence/ELISA) in normogravity before and after exposure to 31 parabolas. While MCA velocity did not change (P > 0.05), a selective increase in VA flow was observed during the most marked gravitational transition from micro- to hypergravity (P < 0.05). Increased oxidative-nitrosative stress defined by a free radical-mediated reduction in NO and elevations in glio-vascular GFAP and S100ß were observed after PF (P < 0.05), the latter proportional to the increase in VA flow (r = 0.908, P < 0.05). In contrast, biomarkers of neuronal-axonal damage (neuron-specific enolase, neurofilament light-chain, ubiquitin carboxy-terminal hydrolase L1 and tau) did not change (P > 0.05). Collectively, these findings suggest that the cumulative effects of repeated gravitational transitions may promote minor blood-brain barrier disruption, potentially related to the combined effects of haemodynamic (posterior cerebral hyperperfusion) and molecular (systemic oxidative-nitrosative) stress.

In the present study, we hypothesized that habitual cigarette smoking attenuates endothelial function in the cerebral circulation as well as that of the peripheral circulation in young adults. To test this hypothesis, we measured cerebrovascular and peripheral flow‐mediated dilation (FMD) in young smokers and nonsmokers in the present study. Ten healthy nonsmokers and 10 smokers participated in the study. We measured blood velocity and diameter in the brachial artery and internal carotid artery (ICA) using Doppler ultrasound. We identified shear‐mediated dilation in the brachial artery and ICA by the percentage change in peak diameter during hyperemia stimulation (reactive hyperemia and hypercapnia). We measured the baseline diameter and the shear rate area under the curve from the onset of hyperemia to peak dilation in the brachial artery and ICA, finding the measurements of the smokers and those of the nonsmokers did not differ (p > .05). In contrast to brachial FMD (5.07 ± 1.79% vs. 7.92 ± 3.01%; smokers vs. nonsmokers, p = .019), FMD in the ICA was not attenuated in the smokers compared with that of the nonsmokers (5.46 ± 2.32% vs. 4.57 ± 2.70%; p = .442). These findings indicate that in young healthy smokers, cerebral endothelial function was preserved, and the response of cerebral endothelial function to smoking was different from that of peripheral vasculature., Peripheral FMD was lower in young healthy smokers than that in nonsmokers, indicating that habitual smoking attenuates peripheral endothelial function. In contrast, cerebral endothelial function was preserved in young healthy smokers. These findings suggest that the response of cerebral endothelial function to smoking is different from that of peripheral vasculature.

KEY POINTS: Chronic mountain sickness (CMS) is a maladaptation syndrome encountered at high altitude (HA) characterised by severe hypoxaemia that carries a higher risk of stroke and migraine and is associated with increased morbidity and mortality. We examined if exaggerated oxidative‐inflammatory‐nitrosative stress (OXINOS) and corresponding decrease in vascular nitric oxide bioavailability in patients with CMS (CMS+) is associated with impaired cerebrovascular function and adverse neurological outcome. Systemic OXINOS was markedly elevated in CMS+ compared to healthy HA (CMS−) and low‐altitude controls. OXINOS was associated with blunted cerebral perfusion and vasoreactivity to hypercapnia, impaired cognition and, in CMS+, symptoms of depression. These findings are the first to suggest that a physiological continuum exists for hypoxaemia‐induced systemic OXINOS in HA dwellers that when excessive is associated with accelerated cognitive decline and depression, helping identify those in need of more specialist neurological assessment and targeted support. ABSTRACT: Chronic mountain sickness (CMS) is a maladaptation syndrome encountered at high altitude (HA) characterised by severe hypoxaemia that carries a higher risk of stroke and migraine and is associated with increased morbidity and mortality. The present cross‐sectional study examined to what extent exaggerated systemic oxidative‐inflammatory‐nitrosative stress (OXINOS), defined by an increase in free radical formation and corresponding decrease in vascular nitric oxide (NO) bioavailability, is associated with impaired cerebrovascular function, accelerated cognitive decline and depression in CMS. Venous blood was obtained from healthy male lowlanders (80 m, n = 17), and age‐ and gender‐matched HA dwellers born and bred in La Paz, Bolivia (3600 m) with (CMS+, n = 23) and without (CMS−, n = 14) CMS. We sampled blood for oxidative (electron paramagnetic resonance spectroscopy, HPLC), nitrosative (ozone‐based chemiluminescence) and inflammatory (fluorescence) biomarkers. We employed transcranial Doppler ultrasound to measure cerebral blood flow (CBF) and reactivity. We utilised psychometric tests and validated questionnaires to assess cognition and depression. Highlanders exhibited elevated systemic OXINOS (P < 0.05 vs. lowlanders) that was especially exaggerated in the more hypoxaemic CMS+ patients (P < 0.05 vs. CMS−). OXINOS was associated with blunted cerebral perfusion and vasoreactivity to hypercapnia, impaired cognition and, in CMS+, symptoms of depression. Collectively, these findings are the first to suggest that a physiological continuum exists for hypoxaemia‐induced OXINOS in HA dwellers that when excessive is associated with accelerated cognitive decline and depression, helping identify those in need of specialist neurological assessment and support.

New findings What is the central question of this study? A heterogeneous cerebral blood flow (CBF) response in the cerebral arteries has been demonstrated in several physiological conditions, and it might be attributable to different physiological properties. However, the whole cerebral haemodynamic response to weightlessness remains unknown. What is the main finding and its importance? Long-term head-down bed rest caused a heterogeneous CBF response between the anterior and posterior cerebral arteries and between the cerebral arteries and veins. Especially, in contrast to the anterior cerebral circulation, the posterior arterial and venous CBFs were well maintained throughout weightlessness. Abstract In this study, we investigated the whole cerebral haemodynamic response to long-term head-down bed rest (HDBR). We hypothesized that long-term exposure to weightlessness influences cerebral blood flow (CBF) or CBF distribution among cerebral arteries and veins because of the different physiological roles of each cerebral vessel. To test this hypothesis, 10 male volunteers were exposed to -6 deg HDBR for 60 days. Blood flows in the internal carotid artery, external carotid artery and vertebral artery or internal jugular vein and vertebral vein were measured using ultrasonography before and on days 30 and 57 of the HDBR. The internal carotid artery blood flow was reduced on day 30 (P = 0.019) and had returned to the baseline level by day 57. In contrast, the vertebral artery blood flow remained unaltered throughout the HDBR (P = 0.626). The internal jugular vein blood flow was reduced on day 30 (P = 0.009), whereas the vertebral vein blood flow remained unaltered (P = 0.397). These findings suggest that long-term HDBR causes a heterogeneous CBF response between the anterior and posterior cerebral circulation in the both arteries and veins. The posterior arterial and venous CBFs were well maintained throughout HDBR, and these CBF responses to HDBR were different from the anterior cerebral circulation.

The aim of the present study was to assess carotid baroreflex (CBR) function during acute changes in otolithic activity in humans. To address this question, we designed a set of experiments to identify the modulatory effects of microgravity on CBR function at a tilt angle of −2°, which was identified to minimize changes in central blood volume during parabolic flight. During parabolic flight at 0 and 1 g, CBR function curves were modeled from the heart rate (HR) and mean arterial pressure (MAP) responses to rapid pulse trains of neck pressure and neck suction ranging from +40 to −80 Torr; CBR control of HR (carotid-HR) and MAP (carotid-MAP) function curves, respectively. The maximal gain of both carotid-HR and carotid-MAP baroreflex function curves were augmented during microgravity compared with 1 g (carotid-HR, −0.53 to −0.80 beats·min−1·mmHg−1, P < 0.05; carotid-MAP, −0.24 to −0.30 mmHg/mmHg, P < 0.05). These findings suggest that parabolic flight-induced acute change of otolithic activity may modify CBR function and identifies that the vestibular system contributes to blood pressure regulation under fluctuations in gravitational forces. NEW & NOTEWORTHY The effect of acute changes in vestibular activity on arterial baroreflex function remains unclear. In the present study, we assessed carotid baroreflex function without changes in central blood volume during parabolic flight, which causes acute changes in otolithic activity. The sensitivity of both carotid heart rate and carotid mean arterial pressure baroreflex function was augmented in microgravity compared with 1 g, suggesting that the vestibular system contributes to blood pressure regulation in humans on Earth.

High-intensity interval exercise (HIIE) improves cerebral executive function (EF), but the improvement in EF is attenuated after repeated HIIE, perhaps because of lower lactate availability for the brain. This investigation examined whether improved EF after exercise relates to brain lactate uptake. Fourteen healthy, male subjects performed 2 HIIE protocols separated by 60 min of rest. Blood samples were obtained from the right internal jugular venous bulb and from the brachial artery to determine arterial-venous differences across the brain for lactate (a-v difflactate), glucose (a-v diffglucose), oxygen (a-v diffoxygen), and brain-derived neurotrophic factor (BDNF; a-v diffBDNF). EF was evaluated by the color-word Stroop task. The first HIIE improved EF for 40 min, whereas the second HIIE improved EF only immediately after exercise. The a-v diffglucose was unchanged, whereas the a-v diffBDNF increased similarly after both HIIEs, and the a-v difflactate increased, but the increase was attenuated after the second HIIE, compared with the first HIIE ( P < 0.05). The EF after HIIE correlated with the a-v difflactate ( r2 = 0.62; P < 0.01). We propose that attenuated improvement in EF after repeated HIIE relates to reduced cerebral lactate metabolism and is, thereby, linked to systemic metabolism as an example of the lactate shuttle mechanism.-Hashimoto, T., Tsukamoto, H., Takenaka, S., Olesen, N. D., Petersen, L. G., Sorensen, H., Nielsen, H. B., Secher, N. H., Ogoh, S. Maintained exercise-enhanced brain executive function related to cerebral lactate metabolism in men.

Although hypoxia has the potential to impair the cognitive function, the effects of acute hypoxia on the high-order brain function (executive and/or inhibitory processing) and somatosensory ascending processing remain unknown. We tested the hypothesis that acute hypoxia impairs both motor executive and inhibitory processing and somatosensory ascending processing. Fifteen healthy subjects performed two sessions ( sessions 1 and 2), consisting of electroencephalographic event-related potentials with somatosensory Go/No-go paradigms and somatosensory-evoked potentials (SEPs) under two conditions (hypoxia and normoxia) on different days. On 1 day, participants breathed room air in the first and second sessions of the experiment; on the other day, participants breathed room air in the first session, and 12% O2 in the second session. Acute hypoxia reduced the peak amplitudes of Go-P300 and No-go-P300, and delayed the peak latency of Go-P300. However, no significant differences were observed in the peak amplitude or latency of N140, behavioral data, or the amplitudes and latencies of individual SEP components between the two conditions. These results suggest that acute hypoxia impaired neural activity in motor executive and inhibitory processing, and delayed higher cognitive processing for motor execution, whereas neural activity in somatosensory processing was not affected by acute hypoxia. NEW & NOTEWORTHY Hypoxia has the potential to impair the cognitive function, but the effects of acute hypoxia on the cognitive function remain debatable. We investigated the effects of acute hypoxia on human cognitive processing using electroencephalographic event-related potentials and somatosensory-evoked potentials. Acute normobaric hypoxia impaired neural activity in motor executive and inhibitory processing, but no significant differences were observed in neural activity in somatosensory processing.

We have recently demonstrated that heterogeneous cerebral blood flow (CBF) response in each cerebral artery may contribute to the maintenance of circulatory homeostasis in the brain. However, to what extent weightlessness associated with fluid shift from peripheral to central circulations influences distribution of CBF in each cerebral artery remains unknown. We hypothesised that dry immersion-induced fluid shift (weightlessness condition) would cause heterogeneous CBF response in each cerebral artery. During and after a 3-day dry immersion, internal carotid (ICA), external carotid (ECA) and vertebral arteries (VA) blood flows were measured by Doppler ultrasonography using an 8-MHz linear transducer. Although the 3-day dry immersion and the 2-day recovery period did not change blood flow in each cerebral artery, both ICA and VA conductance decreased during dry immersion on day 2 and day 3 (ICA, 2.95 and 3.23 ml min−1 mmHg−1; VA, 1.10 and 1.05 ml min−1 mmHg−1) from the baseline (ICA, 3.47 ml min−1 mmHg−1, P = 0.027; VA, 1.23 ml min−1 mmHg−1, P = 0.004). In addition, Pearson correlation analysis demonstrated that the 3-day dry immersion-induced a decrease in cardiac output (P = 0.004) was associated with changes in ICA (P = 0.046) and VA blood flow (P = 0.021), but not ECA blood flow (P = 0.466). These findings suggest that short exposures to weightlessness via a cephalad redistribution of fluid volume and blood flow in the human body influenced cerebral vasculature in each cerebral artery but did not cause heterogeneous CBF response in each cerebral artery. This article is protected by copyright. All rights reserved

High cerebral pressure and flow fluctuations could be a risk for future cerebrovascular disease. This study aims to determine whether acute systemic vasoconstriction affects the dynamic pulsatile hemodynamic transmission from the aorta to the brain. We applied a stepwise lower body negative pressure (LBNP) (−10, −20, and −30 mmHg) in 15 young men to induce systemic vasoconstriction. To elucidate the dynamic relationship between the changes in aortic pressure (AoP; estimated from the radial arterial pressure waveforms) and the cerebral blood flow velocity (CBFV) at the middle cerebral artery (via a transcranial Doppler), frequency-domain analysis characterized the beat-to-beat slow oscillation (0.02–0.30 Hz) and the intra-beat rapid change (0.78–9.69 Hz). The systemic vascular resistance gradually and significantly increased throughout the LBNP protocol. In the low-frequency range (LF: 0.07–0.20 Hz) of a slow oscillation, the normalized transfer function gain of the steady-state component (between mean AoP and mean CBFV) remained unchanged, whereas that of the pulsatile component (between pulsatile AoP and pulsatile CBFV) was significantly augmented during −20 and −30 mmHg of LBNP (+28.8% and +32.4% vs. baseline). Furthermore, the relative change in the normalized transfer function gain of the pulsatile component at the LF range correlated with the corresponding change in systemic vascular resistance ( r = 0.41, P = 0.005). Regarding the intra-beat analysis, the normalized transfer function gain from AoP to CBFV was not significantly affected by the LBNP stimulation ( P = 0.77). Our findings suggest that systemic vasoconstriction deteriorates the dampening effect on the pulsatile hemodynamics toward the brain, particularly in slow oscillations (e.g., 0.07–0.20 Hz). NEW & NOTEWORTHY We characterized the pulsatile hemodynamic transmission from the heart to the brain by frequency-domain analysis. The low-frequency transmission was augmented with a mild LBNP stimulation partly due to the elevated systemic vascular resistance. A systemic vasoconstriction deteriorates the dampening effect on slow oscillations of pulsatile hemodynamics toward the brain.

Our previous study demonstrated that a single bout of stretching exercises acutely reduced arterial stiffness. We hypothesized that this acute vascular response is due to regional mechanical stimulation of the peripheral arteries. To test this hypothesis, we examined the effect of a single bout of passive one leg stretching on arterial stiffness, comparing the stretched and the non-stretched leg in the same subject. Twenty-five healthy young men (20.9 ± 0.3 years, 172.5 ± 1.4 cm, 64.1 ± 1.2 kg) volunteered for the study. Subjects underwent a passive calf stretching on one leg (six repetitions of 30-s static stretch with a 10-s recovery). Pulse wave velocity (PWV, an index of arterial stiffness), blood pressure (BP), and heart rate (HR) were measured before and immediately, 15, and 30 min after the stretching. Femoral–ankle PWV (faPWV) in the stretched leg was significantly decreased from baseline (835.0 ± 15.9 cm/s) to immediately (802.9 ± 16.8 cm/s, P

We hypothesized that cerebral blood flow (CBF) regulation in the posterior circulation differs from that of the anterior circulation during a cold pressor test (CPT) and is accompanied by elevations in arterial blood pressure (ABP) and sympathetic nervous activity (SNA). To test this, dynamic cerebral autoregulation (dCA) in the middle and posterior cerebral arteries (MCA and PCA) were measured at three different conditions: control, early phase of the CPT, and the late phase of the CPT. The dCA was examined using a thigh cuff occlusion and release technique. The MCA and PCA blood velocities were unchanged at CPT compared with the control conditions despite an elevation in the ABP. The dCA in both the MCA and PCA remained unaltered at CPT. These findings suggest that CPT-induced elevations in the ABP and SNA did not cause changes in the CBF regulation in the posterior circulation compared with the anterior circulation.

This study aimed to test our hypothesis that acute hypotension attenuates brachial flow-mediated dilation (FMD) as an index of endothelial function in healthy humans. Twelve healthy men (21.8 ± 1.6 years, body mass index; 22.2 ± 1.6 kg/m2) participated in this study. Brachial FMD was measured in three trials: standardized FMD protocol (control trial), abrupt decrease in blood pressure (BP) via thigh cuff inflation–deflation (hypotension trial) and decrease in shear rate (SR) via a shortened forearm occlusion time (SR reduction trial). Brachial diameter and blood velocity were measured using Duplex ultrasound. Mean arterial pressure during reactive hyperaemia showed a marked decrease in the hypotension trial (− 23.7 ± 6.0 mmHg), but not in the control and SR reduction trials. SR area under the curve was attenuated in the SR reduction trial (P

This brief review summarizes the current knowledge on sex differences in baroreflex function, with a major focus on studies in humans. It has been demonstrated that healthy women have blunted cardiovagal baroreflx sensitivity during a rapid (i.e., within seconds) hypertensive stimulus, but baroreflex sensitivity is similar between the sexes during a hypotensive stimulus. Normal aging decreases cardiovagal baroreflex sensitivity and the rate of decline is similar in men and women. Cardiovagal baroreflex sensitivity is reduced in pathological conditions such as hypertension and type II diabetes, and the reduction is greater in female patients than male patients. There is no clear sex difference in sympathetic baroreflex sensitivity among young individuals, however, with women of more advanced age, sympathetic baroreflex sensitivity decreases, which appears to be associated with greater arterial stiffness compared with similarly aged men. The blunted sympathetic baroreflex sensitivity in older women may predispose them to an increased prevalence of hypertension and cardiovascular disease.

Females are more prone to cognitive decline, stroke and neurodegenerative disease, possibly due to more marked reductions in cerebral blood flow and cerebrovascular reactivity to CO2 (CVRCO2HYPER) in later life. To what extent regular exercise confers selective neuroprotection in females remains unestablished. To examine this, 73 adults were prospectively assigned to 1 of 4 groups based on sex (male, ♂ vs. female, ♀) and physical activity status (trained, ≥ 150 minutes of moderate-vigorous intensity aerobic exercise/week; n = 18♂ vs. 18♀ vs. untrained, no formal exercise; n = 18♂ vs. 19♀). Middle cerebral artery velocity (MCAv, transcranial Doppler ultrasound), mean arterial pressure (MAP, finger photoplethysmography) and end-tidal CO2 (capnography) were assessed at rest during normocapnea and hypercapnea (5% CO2) enabling CVRCO2HYPER to be assessed. Cerebrovascular resistance/conductance indices (CVRi/CVCi) were calculated as MAP/MCAv and MCAv/MAP. Maximal oxygen uptake (VO2MAX) was determined during incremental semi-recumbent cycling ergometry to volitional exhaustion. Despite having a lower VO2MAX, females were characterized by selective elevations in MCAv, CVRCO2HYPER and lower CVRi (P

A strict adequate perfusion pressure via arterial baroreflex for the delivery of oxygen to the tissues of the body is well established; however, the importance of baroreflex for cerebral blood flow (CBF) is unclear. On the other hand, there is convincing evidence for arterial baroreflex function playing an important role in maintaining brain homeostasis, e.g., cerebral metabolism, cerebral hemodynamics, and cognitive function. For example, mild cognitive impairment attenuates the sensitivity of baroreflex, and Alzheimer’s disease further decreases it. These clinical findings suggest that CBF and cerebral function are affected by systemic blood pressure regulation via the arterial baroreflex. However, dysfunction of arterial baroreflex is likely to affect CBF regulation as well as the underlying neuronal function, but identifying how this is achieved is arduous since neurological diseases affect systemic as well as cerebral circulation independently. Recent insights into the influence of blood pressure regulation via the arterial baroreflex on cerebral function and blood flow regulation may help elucidate this important question. This review summarizes some update findings regarding direct (autonomic regulation) and indirect (systemic blood pressure regulation) contributions of the arterial baroreflex to the maintenance of cerebral vasculature regulation.

This review summarizes the interaction between the regulatory system of respiration and cerebral vasculature. Some clinical reports provide evidence for the association between these two physiological regulatory systems. Physiologically, arterial carbon dioxide concentration is mainly regulated by two feedback control systems: respiration and cerebral blood flow. In other words, both of these systems are sensitive to the same mediator, i.e., carbon dioxide, at a set point. In addition, respiratory dysfunction alters various physiological factors that affect the cerebral vasculature. Therefore, it is physiologically plausible that these systems are closely linked. The regulation of arterial carbon dioxide concentration affected by respiration and cerebral blood flow may be a key factor for a rise in the risk of brain disease in the patients with respiratory dysfunction. For example, the management of respiratory disease (e.g., patients with chronic obstructive pulmonary disease) and the use of prophylactic therapy are essential to reduce the risk of stroke.

The augmented cerebral hemodynamic pulsatility could lead to the elevated risk of cerebrovascular disease. To determine the impact of an acute orthostatic challenge on a pulsatile component of cerebral hemodynamics, mild lower body negative pressure (LBNP, -30 mmHg) was applied to 29 men. Middle cerebral artery blood flow velocity (MCAv) was measured by transcranial Doppler technique. Stroke volume (SV) was estimated by the Modelflow method with adjustment by the Doppler ultrasound-measured SV at rest. SV, peak and pulsatile MCAv, and pulsatility index were significantly lower during the LBNP stimulation than those at the baseline (e.g., supine resting) (P < 0.05 for all), whereas mean arterial pressure and mean MCAv remained unchanged. The change in SV with the LBNP stimulation significantly correlated with corresponding changes in peak and pulsatile MCAv (r = 0.617, P < 0.001; r = 0.413, P = 0.026, respectively). These results suggest that pulsatile components of cerebrovascular hemodynamics are dampened during the transient period of orthostatic challenge (as simulated using LBNP) when compared to supine rest, and which is partly due to the modified SV.

Habitual stretching exercise increases carotid arterial compliance, and acute stretching exercise increases arterial compliance in patients with myocardial infarction. However, it is not known whether this arterial adaptation is sustained after exercise. The aim of this study was to examine the effect of a single bout of stretching exercise on the time course of systemic, central, and peripheral arterial stiffness in healthy young subjects.Twenty-six healthy young men performed static stretching exercise involving the entire body (trunk, upper limb, and lower limb) for 40 mins. Pulse-wave velocity (PWV; an index of arterial stiffness), blood pressure, and heart rate were measured before and 0, 15, 30, and 60 mins after stretching exercise.Femoral-ankle PWV and brachial-ankle PWV were reduced relative to baseline 15 and 30 mins after acute stretching (P0.05); however, these arterial responses were not sustained for longer periods, and both PWV values returned to the baseline levels within 60 mins. By contrast, carotid-femoral PWV was unchanged.These results suggest that chronic and sufficient repetition of muscle stretch stimulation may result in chronic high arterial compliance, although a single bout of stretch exercise acutely affects arterial compliance.

The present study was designed to explore to what extent low-intensity resistance exercise-induced acute hypertension influences intracranial cerebral perfusion.Twelve healthy participants performed one-legged static knee extension exercise at 30% maximal voluntary contraction for 2 min. Blood flow to the internal and external carotid arteries (ICA/ECA) were evaluated by duplex ultrasonography.ICA blood flow increased and reached a plateau before stabilizing 60 s into exercise despite continued increases in cardiac output and arterial blood pressure. ICA conductance significantly decreased by -14.4% ±13.8% at the end of exercise (P0.01), whereas in contrast, ECA blood flow (P0.01) and conductance were shown to increase (P0.05).The present findings demonstrate that low-intensity resistance exercise was associated with vasodilation of the ECA that was accompanied by vasoconstriction of the ICA. We propose that the heterogeneity and reciprocal regulation of intracranial cerebral blood flow reflect an adaptive neuroprotective mechanism that serves to protect the brain and associated vasculature against the structural damage associated with resistance exercise-induced hypertension.

New Findings What is the central question of this study? Dynamic cerebral autoregulation (CA) is impaired by sympathetic blockade, and the external carotid artery (ECA) vascular bed may prevent adequate internal carotid artery blood flow. We examined whether α1-receptor blockade-induced attenuation of dynamic CA is related to reduced ECA vasoconstriction. What is the main finding and its importance? α1-Receptor blockade attenuated dynamic CA, but in contrast to our hypothesis did not affect the ECA blood flow response to acute hypotension. These findings suggest that the recovery of cerebral blood flow during acute hypotension is unrelated to vasoconstriction within the ECA territory. External carotid artery (ECA) vasoconstriction may defend internal carotid artery (ICA) blood flow during acute hypotension. We hypothesized that the α1-receptor blockade-induced delay in ICA recovery to the baseline level from acute hypoperfusion is related to attenuated ECA vasoconstriction. The ICA and ECA blood flow were determined by duplex ultrasound during thigh-cuff release-induced acute hypotension while the α1-receptor blocker prazosin [1 mg (20 kg)−1] was administered to nine seated young healthy men. Both ICA (mean ± SD; by 17 ± 8%, P = 0.005) and ECA (by 37 ± 15%, P

Drinking coffee causes caffeine-induced physiological alterations such as increases in arterial blood pressure, sympathetic nerve activity, cerebral vasoconstriction, etc., and these physiological alterations may be associated with a reduced risk of cerebral vascular disease. However, the effect of coffee drinking on dynamic cerebral blood flow (CBF) regulation remains unclear. The aim of this study was to test our hypothesis that coffee drinking enhances dynamic cerebral autoregulation. Twelve healthy young subjects participated in the present study. After a 5 min baseline measurement in a semi-recumbent position on the hospital bed, each subject drank water (CON) as a placebo condition or coffee beverage (Coffee INT). Arterial blood pressure and middle cerebral artery blood velocity (MCAv) were measured continuously throughout the experiment. At 30 min after the intake of either water or coffee, dynamic cerebral autoregulation was examined using a thigh cuffs occlusion and release technique. Each condition was randomly performed on a different day. Under Coffee INT condition, mean arterial blood pressure was increased (P = 0.01) and mean MCAv was decreased (P = 0.01) from the baseline. The rate of regulation (RoR), as an index of dynamic cerebral autoregulation, during coffee condition was significantly higher than that during CON (P = 0.0009). The findings of the present study suggest that coffee drinking augments dynamic CBF regulation with cerebral vasoconstriction. This phenomenon may be associated with a reduction in the risk of cerebral vascular disease.

What is the central question of this study? The cardiopulmonary baroreflex inhibits adjustment of sympathetic vasomotor outflow during mild-intensity dynamic exercise. However, it is unclear how suppression of sympathetic vasomotor outflow by the cardiopulmonary baroreflex is modulated by a powerful sympatho-excitatory drive from the exercise pressor reflex, central command and/or the arterial chemoreflex. What is the main finding and its importance? Hypoxia-induced heightened sympathetic nerve activity during dynamic exercise attenuated cardiopulmonary baroreflex control of sympathetic vasomotor outflow. This could facilitate the redistribution of blood flow to the active muscles by sympathetically mediated vasoconstriction of inactive muscles. Muscle sympathetic nerve activity (MSNA) does not increase during mild-intensity dynamic leg exercise in normoxic conditions, despite activation of central command and the exercise pressor reflex. Suppression of MSNA could be caused by muscle pump-induced loading of cardiopulmonary baroreceptors. In contrast, MSNA increases during mild dynamic leg exercise in hypoxic conditions. We hypothesized that hypoxic exercise, which induces a powerful sympatho-excitatory drive from the exercise pressor reflex, central command and/or arterial chemoreflex, attenuates cardiopulmonary reflex control of sympathetic vasomotor outflow. To test this hypothesis, MSNA was recorded during leg cycling in hypoxic conditions and with increased central blood volume by increasing the pedalling frequency to change the cardiopulmonary baroreflex. Subjects performed two leg cycle exercises at different pedal cadences of 60 and 80 r.p.m. (60EX and 80EX trials, respectively) in two (haemodynamic and MSNA) measurement conditions while breathing a hypoxic gas mixture (inspired oxygen fraction = 0.12). Thoracic impedance, stroke volume and cardiac output were measured non-invasively using impedance cardiography. During the MSNA test, MSNA was recorded via microneurography at the right median nerve at the elbow. Changes in thoracic impedance, stroke volume and cardiac output during the 80EX trial were greater than those during the 60EX trial. The MSNA burst frequency during hypoxic exercise in the 80EX trial (39 ± 4 bursts min(-1)) did not differ from that during the 60EX trial (39 ± 3 bursts min(-1)). These results suggest that the cardiopulmonary baroreflex of sympathetic vasomotor outflow during dynamic exercise is modulated by heightened hypoxia-induced sympathetic nerve activity.

INTRODUCTION High-intensity interval exercise (HIIE) is more effective at increasing metabolic and cardiovascular health compared with moderate-intensity continuous exercise for patients with cardiovascular disease, but exhaustive high-intensity continuous exercise attenuates dynamic cerebral autoregulation (CA). This study assessed the effect of HIIE on dynamic CA. METHODS Nine healthy men (age, 24 ± 3 yr; mean ± SD) warmed up at 50%-60% maximal workload (Wmax) for 5 min before HIIE including four 4-min bouts of exercise at 80%-90% Wmax interspaced by four 3-min bouts at 50% to 60% Wmax. Transcranial Doppler determined middle cerebral artery mean blood velocity (MCA Vmean), and brachial artery catheterization determined mean arterial pressure (MAP). Dynamic CA was evaluated by transfer function analysis of changes in MAP and MCA Vmean. RESULTS The HIIE increased MAP (from 92 ± 9 to 104 ± 10 mm Hg; P < 0.0125), whereas MCA Vmean did not change. Transfer function phase increased and coherence decreased during HIIE (P < 0.0125 vs rest, respectively), whereas gain was unchanged. CONCLUSIONS The results suggest that dynamic CA is unaffected during HIIE, indicating that the brain is protected from fluctuations in MAP. Thus, we propose that HIIE may be beneficial for brain-related health as maintenance of cerebral perfusion in contrast to high-intensity continuous exercise.

The role of the sympathetic nervous system in cerebral blood flow (CBF) regulation remains unclear. Previous studies have primarily measured middle cerebral artery blood velocity to assess CBF. Recently, there has been a transition toward measuring internal carotid artery (ICA) and vertebral artery (VA) blood flow using duplex Doppler ultrasound. Given that the VA supplies autonomic control centers in the brainstem, we hypothesized that graded sympathetic activation via lower body negative pressure (LBNP) would reduce ICA but not VA blood flow. ICA and VA blood flow were measured during two protocols: protocol 1, low-to-moderate LBNP (−10, −20, −30, and −40 Torr) and protocol 2, moderate-to-high LBNP (−30, −50, and −70 Torr). ICA and VA blood flow, diameter, and blood velocity were unaffected up to −40 LBNP. However, −50 and −70 LBNP evoked reductions in ICA and VA blood flow [e.g., −70 LBNP: percent change (%∆)VA-baseline = −27.6 ± 3.0] that were mediated by decreases in both diameter and velocity (e.g., −70 LBNP: %∆VA-baseline diameter = −7.5 ± 1.9 and %∆VA-baseline velocity = −13.6 ± 1.7), which were comparable between vessels. Since hyperventilation during −70 LBNP reduced end-tidal pressure of carbon dioxide ([Formula: see text]), this decrease in [Formula: see text] was matched via voluntary hyperventilation. Reductions in ICA and VA blood flow during hyperventilation alone were significantly smaller than during −70 LBNP and were primarily mediated by decreases in velocity (%∆VA-baseline velocity = −8.6 ± 2.4 and %∆VA-baseline diameter = −0.05 ± 0.56). These data demonstrate that both ICA and VA were unaffected by low-to-moderate sympathetic activation, whereas robust reflex-mediated sympathoexcitation caused similar magnitudes of vasoconstriction in both arteries. Thus, contrary to our hypothesis, the ICA was not preferentially vasoconstricted by sympathetic activation. NEW & NOTEWORTHY Our study demonstrates that moderate-to-high reflex-mediated sympathetic activation with lower body negative pressure (LBNP) decreases internal carotid artery and vertebral artery blood flow via reductions in both vessel diameter and blood velocity. This vasoconstriction was primarily sympathetically mediated as voluntary hyperventilation alone, to isolate the effect of decreases in end-tidal pressure of carbon dioxide that occurred during LBNP, resulted in a significantly smaller vasoconstriction. In contrast to our hypothesis, these data indicate a lack of heterogeneity between the anterior and posterior cerebral circulations in response to sympathoexcitation.

Posttraumatic stress disorder (PTSD) is associated with structural and functional alterations in a number of interacting brain regions, but the physiological mechanism for the high risk of cerebrovascular disease or impairment in brain function remains unknown. Women are more likely to develop PTSD after a trauma than men. We hypothesized that cerebral blood flow (CBF) regulation is impaired in women with PTSD, and it is associated with impairment in cognitive function. To test our hypothesis, we examined dynamic cerebral autoregulation (CA) and cognitive function by using a transfer function analysis between arterial pressure and middle cerebral artery blood velocity and the Stroop Color and Word test (SCWT), respectively. We did not observe any different responses in these hemodynamic variables between women with PTSD ( n = 15) and healthy counterparts (all women; n = 8). Cognitive function was impaired in women with PTSD; specifically, reaction time for the neutral task of SCWT was longer in women with PTSD compared with healthy counterparts ( P = 0.011), but this cognitive dysfunction was not affected by orthostatic stress. On the other hand, transfer function phase, gain, and coherence were not different between groups in either the supine or head-up tilt (60°) position, or even during the cognitive challenge, indicating that dynamic CA was well maintained in women with PTSD. In addition, there was no relationship between cognitive function and dynamic CA. These findings suggest that PTSD-related cognitive dysfunction may not be due to compromised CBF regulation. NEW & NOTEWORTHY Cognitive function was impaired; however, dynamic cerebral autoregulation (CA) as an index of cerebral blood flow regulation was not impaired during supine and 60° head-up tilt in women with PTSD compared with healthy females. In addition, there was no relationship between cognitive function and dynamic CA. These findings suggest that the mechanism of PTSD-related cognitive dysfunction may not be due to CBF regulation.