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This study evaluated the time-to-time aerobic and anaerobic exercise intensities, calculated using the Global Positioning System (GPS), using laboratory measurements of individual physical fitness throughout the game in each female youth football player. In addition, we examine if the anaerobic exercise index calculated by only GPS data presents this evaluation to examine its validity. In the laboratory, the oxygen uptake (V̇O2) matched with moving speed was identified during an incremental exercise test on the treadmill, and the ventilatory (anaerobic) threshold was also analysed to identify individual aerobic and anaerobic exercise intensities. Using these laboratory data, time-to-time changes in individual relative running intensity (aerobic and anaerobic) were visualised from individual GPS data during a football game, and an individual’s sprint output (ability) during the game was evaluated. An index of running intensity and the percentage of anaerobic exercise over the game provided by the GPS software (equivalent distance index [%EDI] and anaerobic index [AI]) did not present the actual individual exercise intensity (ICC(2,1), absolute agreement=−0.031; P=0.596) and percentage of anaerobic exercise (ICC(2,1), absolute agreement=−0.003; P=0.698) values during the game, respectively. These findings suggest that only GPS measurement cannot present the individual actual exercise intensity during a football game because of different individual fitness levels to the same running speed.

Compared with younger adults, passive heating induced increases in cardiac output are attenuated by ∼50% in older adults. This attenuated response may be associated with older individuals’ inability to maintain stroke volume through ionotropic mechanisms and/or through altered chronotropic mechanisms. The purpose of this study was to identify the interactive effect of age and hyperthermia on cardiac responsiveness to dobutamine-induced cardiac stimulation. Eleven young (26 ± 4 yr) and 8 older (68 ± 5 yr) participants underwent a normothermic and a hyperthermic (baseline core temperature +1.2°C) trial on the same day. In both thermal conditions, after baseline measurements, intravenous dobutamine was administered for 12 min at 5 µg/kg/min, followed by 12 min at 15 µg/kg/min. Primary measurements included echocardiography-based assessments of cardiac function, gastrointestinal and skin temperatures, heart rate, and mean arterial pressure. Heart rate responses to dobutamine were similar between groups in both thermal conditions ( P > 0.05). The peak systolic mitral annular velocity (S′), i.e., an index of left ventricular longitudinal systolic function, was similar between groups for both thermal conditions at baseline. While normothermic, the increase in S′ between groups was similar with dobutamine administration. However, while hyperthermic, the increase in S′ was attenuated in the older participants with dobutamine ( P < 0.001). Healthy, older individuals show attenuated inotropic, but maintained chronotropic responsiveness to dobutamine administration during hyperthermia. These data suggest that older individuals have a reduced capacity to increase cardiomyocyte contractility, estimated by changes in S′, via β1-adrenergic mechanisms while hyperthermic.

Exercise is a beneficial intervention to prevent cognitive dysfunction. However, an optimal exercise prescription for preventing dementia has not been established because the physiological mechanism(s) of exercise-induced improvements in cognitive function remains unclear. Interestingly, our recent study demonstrated that individuals with a higher exercise pressor response exhibit less exercise-induced cognitive improvement, suggesting that individual differences in cardiovascular responses to exercise or its associated physiological factors, may be related to exercise-induced alterations in cognitive function. Therefore, consideration of individual cardiovascular responses is warranted to develop appropriate exercise prescriptions for a given individual to prevent cognitive dysfunction.

Cerebral autoregulation (CA) refers to the control of cerebral tissue blood flow (CBF) in response to changes in perfusion pressure. Due to the challenges of measuring intracranial pressure, CA is often described as the relationship between mean arterial pressure (MAP) and CBF. Dynamic CA (dCA) can be assessed using multiple techniques, with transfer function analysis (TFA) being the most common. A 2016 white paper by members of an international Cerebrovascular Research Network (CARNet) that is focused on CA strove to improve TFA standardization by way of introducing data acquisition, analysis, and reporting guidelines. Since then, additional evidence has allowed for the improvement and refinement of the original recommendations, as well as for the inclusion of new guidelines to reflect recent advances in the field. This second edition of the white paper contains more robust, evidence-based recommendations, which have been expanded to address current streams of inquiry, including optimizing MAP variability, acquiring CBF estimates from alternative methods, estimating alternative dCA metrics, and incorporating dCA quantification into clinical trials. Implementation of these new and revised recommendations is important to improve the reliability and reproducibility of dCA studies, and to facilitate inter-institutional collaboration and the comparison of results between studies.

Transcranial Doppler ultrasonography (TCD) is used widely to evaluate dynamic cerebral autoregulation (dCA). However, the validity of TCD-determined dCA remains unknown because TCD is only capable of measuring blood velocity and thus only provides an index as opposed to true blood flow. To test the validity of TCD-determined dCA, in nine healthy subjects, dCA was evaluated by transfer function analysis (TFA) using cerebral blood flow (CBF) or TCD-measured cerebral blood velocity during a perturbation that induces reductions in TCD-determined dCA, lower body negative pressure (LBNP) at two different stages: LBNP - 15 mmHg and - 50 mmHg. Internal carotid artery blood flow (ICA Q) was assessed as an index of CBF using duplex Doppler ultrasound. The TFA low frequency (LF) normalized gain (ngain) calculated using ICA Q increased during LBNP at - 50 mmHg (LBNP50) from rest (P = 0.005) and LBNP at - 15 mmHg (LBNP15) (P = 0.015), indicating an impaired dCA. These responses were the same as those obtained using TCD-measured cerebral blood velocity (from rest and LBNP15; P = 0.001 and P = 0.015). In addition, the ICA Q-determined TFA LF ngain from rest to LBNP50 was significantly correlated with TCD-determined TFA LF ngain (r = 0.460, P = 0.016) despite a low intraclass correlation coefficient. Moreover, in the Bland-Altman analysis, the difference in the TFA LF ngains determined by blood flow and velocity was within the margin of error, indicating that the two measurement methods can be interpreted as equivalent. These findings suggest that TCD-determined dCA can be representative of actual dCA evaluated with CBF.

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.

Excessive arterial pressure elevation induced by resistance exercise (RE) attenuates peripheral vasodilatory function, but its effect on cerebrovascular function is unknown. We aimed to evaluate the effect of different pressor responses to RE on hypercapnia-induced vasodilation of the internal carotid artery (ICA), an index of cerebrovascular function. To manipulate pressor responses to RE, 15 healthy young adults (11M/4F) performed two RE: high intensity with low repetitions (HL) and low intensity with high repetitions (LH) dynamic knee extension. ICA dilation, induced by 3 min of hypercapnia, was measured before and 10 min after RE using Doppler ultrasound. HL exercise elicited a greater pressor response than LH exercise. In relaxation phases of RE, ICA blood velocity increased in both HL and LH trials. However, ICA shear rate did not significantly increase in either trial (P = 0.06). Consequently, neither exercise altered post-exercise hypercapnia-induced ICA dilation (HL, 3.9 ± 1.9% to 5.1 ± 1.7%; LH, 4.6 ± 1.4% to 4.8 ± 1.8%; P 0.05 for all). When viewed individually, the changes in ICA shear rate were positively correlated with changes in end-tidal partial pressure of carbon dioxide (P

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.

Arterial stiffness is a disease of the arterial media, and it is well known that it is accelerated by aging [...]

The present study aimed to examine the validity of a novel method to assess cerebrovascular carbon dioxide (CO2) reactivity (CVR) that does not require a CO2 inhalation challenge, e.g., for use in patients with respiratory disease or the elderly, etc. In twenty-one healthy participants, CVR responses to orthostatic stress (50° head-up tilt, HUT) were assessed using two methods: (1) the traditional CO2 inhalation method, and (2) transfer function analysis (TFA) between middle cerebral artery blood velocity (MCA V) and predicted arterial partial pressure of CO2 (PaCO2) during spontaneous respiration. During HUT, MCA V steady-state (i.e., magnitude) and MCA V onset (i.e., time constant) responses to CO2 inhalation were decreased (p < 0.001) and increased (p = 0.001), respectively, indicative of attenuated CVR. In contrast, TFA gain in the very low-frequency range (VLF, 0.005–0.024 Hz) was unchanged, while the TFA phase in the VLF approached zero during HUT (−0.38 ± 0.59 vs. 0.31 ± 0.78 radians, supine vs. HUT; p = 0.003), indicative of a shorter time (i.e., improved) response of CVR. These findings indicate that CVR metrics determined by TFA without a CO2 inhalation do not track HUT-evoked reductions in CVR identified using CO2 inhalation, suggesting that enhanced cerebral blood flow response to a change in CO2 using CO2 inhalation is necessary to assess CVR adequately.

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.

Head-up tilt (HUT)-induced gravitational stress causes collapse of the internal jugular vein (IJV) by decreasing central blood volume and through mass-effect from the surrounding tissues. Besides HUT, lower body negative pressure (LBNP) is used to stimulate orthostatic stress as an experimental model. Compared to HUT, LBNP has less of a gravitational effect because of the supine position; therefore, we hypothesized that LBNP causes less of a decrease in the cross-sectional area of the IJV compared to HUT. We tested the hypothesis by measuring the cross-sectional area of the IJV using B-mode ultrasonography while inducing orthostatic stress at levels of -40 mmHg LBNP and 60° HUT. The cross-sectional area of IJV decreased from the resting baseline during both LBNP and HUT trials, but the LBNP-induced decrease in the cross-sectional area of IJV was smaller than that of HUT (right, -45% ± 49% vs. -78% ± 27%, p = 0.008; left, -49% ± 27% vs. -78% ± 20%, p = 0.004). Since changes in venous outflow may affect cerebral arterial circulation, the findings of the present study suggest that orthostatic stress induced by different techniques modulates cerebral blood flow regulation through its effect on venous outflow.

What is the central question of this study? Sympathetic vasomotor outflow is reduced during low-intensity dynamic leg exercise in younger individuals: does ageing influence the sympathoinhibitory effect during low-intensity leg cycling? What is the main finding and its importance? Muscle sympathetic nerve activity during low-intensity cycling decreased in older males, as seen in young males. It is possible that cardiopulmonary baroreflex-mediated inhibition of sympathetic vasomotor outflow during dynamic leg exercise is preserved in healthy older males.Muscle sympathetic nerve activity (MSNA) is reduced during low-intensity dynamic leg exercise in young males. It is suggested that this inhibition is mediated by loading of the cardiopulmonary baroreceptors. The purpose of this study was to clarify the impact of age on MSNA during dynamic leg exercise. Nine younger males (YM, mean ± SD, 20 ± 1 years) and nine older males (OM, 72 ± 3 years) completed the study. The subjects performed two 4-min cycling exercises at 10% of their heart rate reserve using a cycle ergometer in a semirecumbent position (MSNA and estimated central venous pressure (eCVP) trials). MSNA was recorded via microneurography of the left radial nerve. The CVP was estimated based on peripheral venous pressure, which was monitored using a cannula in the right large antecubital vein. The magnitude of the increase in mean arterial blood pressure during leg cycling was larger in OM (+9.3 ± 5.5 mmHg) compared with YM (+2.8 ± 4.7 mmHg). MSNA burst frequency was decreased during cycling in both YM (-8.1 ± 3.8 bursts/min) and OM (-10.6 ± 3.3 bursts/min), but no significant difference was found between the two groups. The eCVP increased during exercise in both groups, and there was no difference in the changes in eCVP between YM (+1.1 ± 0.4 mmHg) and OM (+1.2 ± 0.7 mmHg). These data indicate that inhibition of sympathetic vasomotor outflow during low-intensity cycling appears in OM as seen in YM. It is possible that the muscle pump-induced loading of the cardiopulmonary baroreflex is preserved during cycling in healthy older males.

Emergent evidence suggests that cyclic intermittent hypoxia increases cerebral arterial shear rate and endothelial function, whereas continuous exposure decreases anterior cerebral oxygen (O

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

New findings What is the central question of this study? What are the dynamic characteristics of cerebrovascular carbon dioxide reactivity and the central respiratory chemoreflex? What is the main finding and its importance? The transfer function gain from the end-tidal partial pressure of carbon dioxide to cerebral blood flow or ventilation decreased in the high frequency range at rest and during exercise. These findings indicate that the dynamic characteristics of both systems were not constant in all frequency ranges, and this trend was not modified by exercise. Abstract The purpose of this study was to examine the dynamic characteristics of cerebrovascular reactivity and ventilatory response to change in arterial CO2 in all frequency ranges at rest using frequency domain analysis, and also to examine whether this is modified by dynamic exercise as with the traditionally determined cerebrovascular CO2 reactivity. In nine healthy young subjects, at rest and during exercise (cycling exercise at constant predetermined work rate corresponding to a V O 2 level of 0.90 l min-1 ), the dynamic characteristics of cerebrovascular CO2 reactivity and the central respiratory chemoreflex were assessed by transfer function analysis using a binary white-noise sequence (0-7% inspired CO2 fraction) from the end-tidal partial pressure of CO2 ( P ETC O 2 ) to the mean middle cerebral artery mean blood velocity (MCA Vm ) or minute ventilation ( V E ), respectively. In the high frequency range, both transfer function gains decreased but, interestingly, the cut-off frequency in the transfer function gain from P ETC O 2 to MCA Vm response was higher than that from P ETC O 2 to V E response at rest (0.024 vs. 0.015 Hz) and during exercise (0.030 vs. 0.011 Hz), indicating that cerebrovascular CO2 reactivity or central respiratory chemoreflex was not constant in all frequency ranges, and this trend was not modified by exercise. These findings suggest that dynamic characteristics of the cerebrovascular CO2 reactivity or central chemoreflex need to be assessed to identify the whole system because the traditional method cannot identify the property of time response of these systems.

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.

Cerebrovascular reactivity (CVR) to changes in the partial pressure of arterial carbon dioxide (PaCO2) is an important mechanism that maintains CO2 or pH homeostasis in the brain. To what extent this is influenced by gravitational stress and corresponding implications for the regulation of cerebral blood flow (CBF) remain unclear. The present study examined the onset responses of pulmonary ventilation (V̇E) and anterior middle (MCA) and posterior (PCA) cerebral artery mean blood velocity (Vmean) responses to acute hypercapnia (5% CO2) to infer dynamic changes in the central respiratory chemoreflex and cerebrovascular reactivity (CVR), in supine and 50° head-up tilt (HUT) positions. Each onset response was evaluated using a single-exponential regression model consisting of the response time latency [CO2-response delay (t0)] and time constant (τ). Onset response of V̇E and PCA Vmean to changes in CO2 was unchanged during 50° HUT compared with supine (τ: V̇E, p = 0.707; PCA Vmean, p = 0.071 vs. supine) but the MCA Vmean onset response was faster during supine than during 50° HUT (τ: p = 0.003 vs. supine). These data indicate that gravitational stress selectively impaired dynamic CVR in the anterior cerebral circulation, whereas the posterior circulation was preserved, independent of any changes to the central respiratory chemoreflex. Collectively, our findings highlight the regional heterogeneity underlying CBF regulation that may have translational implications for the microgravity (and hypercapnia) associated with deep-space flight notwithstanding terrestrial orthostatic diseases that have been linked to accelerated cognitive decline and neurodegeneration.

Change in cardiac output (Q) contributes to cerebral blood flow (CBF) regulation at rest and even during steady-state exercise. At the onset of cycling exercise, Q increases acutely and largely via muscle pump. The purpose of the present study was to examine whether onset exercise-induced a large increase in Q contributes to CBF regulation at the onset of exercise.In 20 young healthy participants (10 males and 10 females), Q, mean arterial pressure (MAP), and mean blood velocities of middle and posterior cerebral arteries (MCA Vm and PCA Vm) were continuously measured during light cycling exercise for 3 min.At the onset of exercise, Q increased acutely to the peak (P 0.001), while the CBF peak responses were not significantly higher than the values during the steady-state exercise (MCA Vm and PCA Vm; P = 0.183 and P = 0.101, respectively). The change in Q was correlated with that of MCA Vm or PCA Vm from resting baseline to the steady-state exercise (r = 0.404, P 0.001 and r = 0.393, P 0.001, respectively). However, the change in Q was not correlated with that of MCA Vm or PCA Vm at the onset of exercise (P = 0.853 and P = 0.893, respectively). Any sex differences in the onset response of peripheral and cerebral hemodynamics to exercise were not observed.These findings suggest that the acute change in Q does not contribute to CBF regulation at the onset of exercise for protecting cerebral vasculature against a large and acute elevation in Q at the onset of exercise.

Different cerebral blood flow (CBF) responses to exercise between the posterior cerebral artery (PCA) and vertebral artery (VA) have been previously observed, though the physiological mechanisms remain unknown. There is regional heterogeneity in sympathetic innervation between the PCA and VA, which may affect CBF regulation, especially during sympathoexcitation. Thus, in the present study, we hypothesized that different CBF regulatory mechanisms between PCA and VA contribute to heterogeneous CBF responses to isometric exercise. To test this hypothesis, in thirteen healthy young men, dynamic cerebral autoregulation (CA) and cerebrovascular CO

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.

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).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 VMAP was elevated during the IHG-BH compared with IHG (P 0.001) and BH (P = 0.001). Similarly, both MCA VThese results indicate that during isometric exercise, a breath-hold enhances an exercise-induced increase in MAP and, consequently, MCA V

The handgrip exercise, a small muscle exercise, is useful for exercise therapy, particularly in the elderly and bedridden patients. The isometric handgrip (IHG) exercise has been utilized in training programs to reduce resting blood pressure; however, the acute effects of the IHG exercise on cognitive performance are not fully understood. The present study aimed to investigate the effect of an intermittent IHG exercise protocol with short exercise duration, which minimizes the arterial blood pressure response to exercise, on cognitive performance. Twenty-two young healthy subjects performed the intermittent IHG exercise protocol, which consisted of 30-s IHG and 45-s recovery × 16 trials; the exercise intensity of the IHG exercise was 30% of the maximal voluntary contraction. Cognitive performance was evaluated before and after the exercise with the Go/No-Go and memory recognition tasks. Specifically, the reaction time (RT) and performance accuracy were measured. The intermittent IHG exercise protocol did not change the RT or performance accuracy of either the Go/No-Go task (P = 0.222 and P = 0.260, respectively) or the memory recognition task (P = 0.427 and P = 0.245, respectively). These findings suggest that the intermittent IHG exercise protocol with short exercise duration may not provide enough stimulation to improve cognitive performance despite being useful as a safe exercise therapy in the elderly and in patients with cardiovascular disease.

Additional file 1. Supplementary material. Short form of the International Physical Activity Questionnaire.

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

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 0.05) without any change in shear rate and mean blood velocity. In contrast, during the relaxation period, the mean blood velocity (baseline vs. relaxation period of the 5th set, 2.98 ± 0.54 vs. 6.25 ± 1.48 cm/s) increased, and consequently, the shear rate (baseline vs. relaxation period of the 5th set, 66.75 ± 15.39 vs. 122.85 ± 29.40 sThe stretching procedure increased the shear rate in the peripheral artery of the stretched leg during the relaxation period. This finding indicates that the local hemodynamic response (possibly through endothelial function), resulting from an increase in shear stress, may contribute to stretching-induced attenuation of local arterial stiffness.

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.

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.

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.

To clarify whether the relaxation period during stretching affects the degree of elevated shear rate and the degree of reduction of arterial stiffness, we examined relaxation duration to build an adequate stretching protocol. In Experiment 1, the changes in cardiac output, the shear rate in the posterior tibial artery, and blood volume in the calf muscle were measured during recovery (0–60 s) from a single bout of one-legged passive calf stretching in 12 healthy young men. In Experiment 2, the effects of different relaxation periods (5-, 10-, 20-, and 60-s) of passive one-legged intermittent calf stretching (30-s × 6 sets) on the femoral-ankle pulse wave velocity (faPWV) as an index of peripheral arterial stiffness were identified in 17 healthy young men. As a result, the stretched leg’s shear rate significantly increased from 0 to 10th s after stretching. The muscle blood volume in the stretched leg significantly reduced during stretching, and then significantly increased during the recovery period after stretching; however, cardiac output remained unchanged during stretching and recovery. Additionally, the reduction in faPWV from the pre-stretching value in the stretched leg was significantly larger in the protocol with 10-s and 20-s relaxation periods than that in the non-stretched leg, but this did not differ in the 5-s and 60-s relaxation periods. These findings suggest that the relaxation periods of intermittent static stretching that cause a high transient increase in shear rate (via reperfusion after microvascular compression by the stretched calf muscles) are effective to reduce arterial stiffness.

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