Exaggerated Blood Pressure Response to Exercise Is a Risk of Future Hypertension Even in Healthy, Normotensive Young Individuals-Potential Preventive Strategies for This Phenomenon?

Physical activity and regular exercise are well known to reduce the risks of cerebrovascular and cardiovascular diseases, leading the American College of Sports Medicine to endorse the concept that "exercise is medicine". However, a single bout of exercise temporarily raises arterial blood pressure (BP) to meet the metabolic demands of working muscle, and this BP response is particularly exaggerated in older adults and patients with cardiovascular conditions, such as hypertension, resulting in an exaggerated BP response during exercise. This presents a paradox: while regular exercise is crucial for preventing these diseases, excessively high BP responses during exercise could increase the risk of vascular damage. The mechanisms underlying this exaggerated BP response during exercise remain unclear, and effective exercise regimens for these populations have yet to be established. Currently, low-intensity exercise is recommended; however, its efficacy in disease prevention is uncertain. Notably, even among healthy individuals, there is significant variation in the BP response to exercise. Some healthy individuals, despite having normal resting BP, exhibit an exaggerated BP response during physical activity. Importantly, these individuals are often unaware that their BP becomes excessively elevated during physical activity. Repeated exposure to these heightened BP responses through regular physical activity may increase their long-term risk of cardiovascular disease. How can we prevent disease development in these individuals while still ensuring the effectiveness of exercise? Some studies have shown that individuals with a family history of hypertension may experience this phenomenon even in children and adolescents. Additionally, left ventricular hypertrophy contributes to an exaggerated BP response to exercise, suggesting a possible genetic influence. Conversely, other reports indicate that factors such as arterial stiffness, obesity, and low exercise capacity also contribute to this exaggerated response. Our recent preliminary data suggest that the cognitive benefits of exercise may be diminished in individuals who exhibit an exaggerated BP response during exercise. This implies that individuals with an exaggerated BP response, despite having normal resting BP, may not fully benefit from exercise. In this perspective paper, we review the physiological aspects of this phenomenon and explore strategies to address it. Additionally, we discuss BP responses in athletes within this content. Our goal is to prevent disease while maximizing the benefits of exercise for healthy individuals with an exaggerated BP response, as well as for elderly and cardiovascular patients.

Effect of prolonged sitting on dynamic cerebral autoregulation in the anterior and posterior cerebral circulations.

Individuals who experience prolonged sitting daily are reported to be at risk of developing cerebrovascular disease, which is associated, in part, with attenuation in cerebral blood flow regulation. However, the effect of prolonged sitting on dynamic cerebral autoregulation (dCA), a crucial mechanism of cerebral blood flow regulation, remains unclear. Additionally, cerebrovascular disease occurs heterogeneously within cerebral arteries. The purpose of the present study was to examine the hypothesis that prolonged sitting attenuates dCA in the cerebral circulation heterogeneously. Twelve young, healthy participants were instructed to maintain a seated position for 4 h without moving their lower limbs. Mean arterial pressure and mean blood velocities of the middle cerebral artery (MCA Vm) and the posterior cerebral artery (PCA Vm) were measured continuously throughout the experiment. The dCA was assessed using transfer function analysis (TFA) with mean arterial pressure and either MCA Vm or PCA Vm. In the MCA, very low-frequency TFA-normalized gain decreased significantly during 4 h of prolonged sitting (P = 0.029), indicating an improvement rather than attenuation in dCA, despite a significant reduction in MCA Vm after 4 h of continuous sitting (P = 0.039). In the PCA, PCA Vm remained stable throughout the 4 h sitting period (P = 0.923), and all TFA parameters remained unchanged throughout the 4 h of sitting. Contrary to our hypothesis, these results suggest that the dCA in both the MCA and the PCA was well stabilized in healthy young individuals during acute prolonged sitting.

Do changes in cerebral blood flow modulate the amplitudes of P300 during cognitive task?

A single session of aerobic or resistance training transiently enhances cognitive function, making it a valuable strategy for dementia prevention in the older people. Despite its acknowledged benefits, the precise mechanism behind exercise-induced cognitive improvement remains controversial. In the present study, we investigated the impact of altered cerebral blood flow (CBF) on brain neural activity originating from motor executive and inhibitory processing using electroencephalographic event-related potentials (EEG-ERPs). Sixteen healthy subjects participated in four sessions, with EEG-ERPs measured during somatosensory Go/No-go tasks. The sessions were conducted under four distinct respiratory conditions presented in random order: normal breathing (NB) and rapid breathing (RB) with room air, normal breathing with hypercapnic gas (5% CO2, 21% O2, and balanced N2) (NB + Gas), and rapid breathing with the same gas (RB + Gas). Changes in CBF were evaluated based on the middle cerebral artery mean blood velocity (MCA Vmean) using transcranial Doppler. [Formula: see text] was decreased under the RB condition but increased under the NB + Gas condition, thereby decreasing and increasing MCA Vmean, respectively. Under the NB + Gas condition, MCA Vmean significantly increased, but it had no effect on either the executive or inhibitory function. In contrast, the reduction in MCA Vmean induced by RB decreased the peak amplitudes of Go-P300 and No-go-P300. However, even under the RB + Gas condition while MCA Vmean increased, the peak amplitudes of both also decreased. These findings suggest that neither increases nor decreases in CBF affected cognitive function.NEW & NOTEWORTHY A single session of aerobic or resistance training transiently enhances cognitive function, but the precise mechanism behind this exercise-induced cognitive improvement remains unknown. We investigated the effect of altered cerebral blood flow (CBF) on brain neural activity originating from motor executive and inhibitory processing using electroencephalographic event-related potentials. Exercise-induced improvement in cognitive function could not be explained by an increase in CBF, whereas a decrease in CBF did not affect cognitive function.

Sympathoinhibition during cardiopulmonary baroreceptor loading is attenuated in older females.

The purpose of the present study was to clarify the impact of age on the sympathoinhibitory response to cardiopulmonary baroreceptor loading in females. Nine older females (mean ± SD, 70 ± 6 yr) and 11 younger females (20 ± 1 yr) completed the study. A passive leg raising (PLR) test was performed wherein the participants were positioned supine (baseline, 0°), and their lower limbs were passively lifted at 10°, 20°, 30°, and 40° (3 min at each angle). Muscle sympathetic nerve activity (MSNA) was recorded via microneurography of the left radial nerve. The central venous pressure was estimated based on peripheral venous pressure (eCVP), which was monitored using a cannula in the right large antecubital vein. Baseline MSNA was higher in older females than in younger females. MSNA burst frequency (BF) decreased during the PLR test in both older and younger females, but the magnitude of the decrease in MSNA BF was smaller in older females than in younger females (older, -3.5 ± 1.5 vs. younger, -6.3 ± 1.5 bursts/min at 40° from baseline, P = 0.014). The eCVP increased during the PLR in both groups, and there was no difference in the changes in eCVP between the two groups (older, +1.07 ± 0.37 vs. younger, +1.12 ± 0.33 mmHg at 40° from baseline, P = 0.941). These results suggest that inhibition of sympathetic vasomotor outflow during cardiopulmonary baroreceptor loading could be blunted with advancing age in females.NEW & NOTEWORTHY There were no available data concerning the effect of age on the sympathoinhibitory response to cardiopulmonary baroreceptor loading in females. The magnitude of the decrease in muscle sympathetic nerve activity during passive leg raising (10°-40°) was smaller in older females than in young females. In females, inhibition of sympathetic vasomotor outflow during cardiopulmonary baroreceptor loading could be blunted with advancing age.

Acute effects of static stretching exercise-induced decrease in arterial stiffness on maximal aerobic capacity.

BACKGROUND: We recently have reported that individual day-to-day arterial stiffness variations are associated with maximal aerobic capacity. However, the evidence of this phenomenon was not provided sufficiently. The present study aimed to examine whether a decrease in arterial stiffness through static stretching exercise could enhance maximal aerobic capacity. METHODS: Twelve healthy young men (age 22±2 years, mean and standard deviation) participated in this study and underwent two separate sessions in a randomized controlled crossover design: a single session of a whole-body static stretching exercise protocol that involved the trunk, upper limb, and lower limb (stretch condition), and sedentary control where they rested in the exercise room. Brachial-ankle pulse wave velocity (baPWV) was measured as an index of systemic arterial stiffness before, immediately after and at 30 min after both conditions. Maximal oxygen uptake (V̇O2max) was assessed using a graded power test on an electronically braked cycle ergometer after these measurements. RESULTS: As we expected, there was a significant decrease in the baPWV at 30 min after the stretch trial compared to baseline values (P=0.01). The baPWV in the stretch condition was lower than that of the control condition, while V̇O2max in the stretch condition was higher than that of the control condition (P=0.03). CONCLUSIONS: Based on these findings, it can be inferred that an acute reduction in arterial stiffness may contribute to change in maximal aerobic capacity.

Influence of sex on sympathetic vasomotor outflow responses to passive leg raising in young individuals.

The purpose of this study was to clarify sex differences in the inhibition of sympathetic vasomotor outflow which is caused by the loading of cardiopulmonary baroreceptors. Ten young males and ten age-matched females participated. The participants underwent a passive leg raising (PLR) test wherein they were positioned supine (baseline, 0º), and their lower limbs were lifted passively at 10º, 20º, 30º, and 40º. Each angle lasted for 3 min. Muscle sympathetic nerve activity (MSNA) was recorded via microneurography of the left radial nerve. Baseline MSNA was lower in females compared to males. MSNA burst frequency was decreased during the PLR in both males (- 6.2 ± 0.4 bursts/min at 40º) and females (- 6.5 ± 0.4 bursts/min at 40º), but no significant difference was detected between the two groups (P = 0.61). These results suggest that sex has minimal influence on the inhibition of sympathetic vasomotor outflow during the loading of cardiopulmonary baroreceptors in young individuals.

Cardiac output-mediated regulation of cerebral blood flow during exercise: Clinical perspectives on the indirect impact of muscle metaboreflex.

The muscle metaboreflex stimulates the elevation of arterial blood pressure, aiming to rectify the oxygen deficit by enhancing oxygen delivery to support muscle activity. Moreover, activating the muscle metaboreflex significantly increases cardiac output (CO) by increasing factors such as heart rate, ventricular contractility, preload, stroke volume and mobilization of central blood volume. Previous studies indicate that ageing and cardiovascular diseases modify the muscle metaboreflex during exercise, limiting the ability to increase CO during physical activity. Alongside reduced exercise capacity, the attenuated rise in CO due to abnormal muscle metaboreflex in these patients impedes the increase in cerebral blood flow during exercise. Considering that CO plays a pivotal role in regulating cerebral blood flow adequately during exercise, this occurrence might contribute to an elevated risk of cerebral diseases, and it could also, at least, reduce the effective role of exercise in preventing cerebral disease and dementia among elderly individuals and patients with cardiovascular conditions. Therefore, it is important to consider this phenomenon when optimizing the effectiveness of exercise rehabilitation in patients with cardiovascular disease to prevent cerebral diseases and dementia.

Observing an expert's action swapped with an observer's face increases corticospinal excitability during combined action observation and motor imagery.

This study aimed to examine whether observing an expert's action swapped with an observer's face increases corticospinal excitability during combined action observation and motor imagery (AOMI). Twelve young males performed motor imagery of motor tasks with different difficulties while observing the actions of an expert performer and an expert performer with a swapped face. Motor tasks included bilateral wrist dorsiflexion (EASY) and unilateral two-ball rotating motions (DIFF). During the AOMI of EASY and DIFF, single-pulse transcranial magnetic stimulation was delivered to the left primary motor cortex, and motor-evoked potentials (MEPs) were obtained from the extensor carpi ulnaris and first dorsal interosseous muscles of the right upper limb, respectively. Visual analogue scale (VAS) assessed the subjective similarity of the expert performer with the swapped face in the EASY and DIFF to the participants themselves. The MEP amplitude in DIFF was larger in the observation of the expert performer with the swapped face than that of the expert performer (P = 0.012); however, the corresponding difference was not observed in EASY (P = 1.000). The relative change in the MEP amplitude from observing the action of the expert performer to that of the expert performer with the swapped face was positively correlated with VAS only in DIFF (r = 0.644, P = 0.024). These results indicate that observing the action of an expert performer with the observer's face enhances corticospinal excitability during AOMI, depending on the task difficulty and subjective similarity between the expert performer being observed and the observer.

Circulating Plasma Oxytocin Level Is Elevated by High-Intensity Interval Exercise in Men.

PURPOSE: We evaluated whether repeated high-intensity interval exercise (HIIE) influences plasma oxytocin (OT) concentration in healthy men, and, given that OT is mainly synthesized in the hypothalamus, we assessed the concentration difference between the arterial (OT ART ) versus the internal jugular venous OT concentration (OT IJV ). Additionally, we hypothesized that an increase in cerebral OT release and the circulating concentration would be augmented by repeated HIIE. METHODS: Fourteen healthy men (age = 24 ± 2 yr; mean ± SD) performed two identical bouts of HIIE. These HIIE bouts included a warm-up at 50%-60% maximal workload ( Wmax ) for 5 min followed by four bouts of exercise at 80%-90% Wmax for 4 min interspersed by exercise at 50%-60% Wmax for 3 min. The HIIE bouts were separated by 60 min of rest. OT was evaluated in blood through radial artery and internal jugular vein catheterization. RESULTS: Both HIIE bouts increased both OT ART (median [IQR], from 3.9 [3.4-5.4] to 5.3 [4.4-6.3] ng·mL -1 in the first HIIE, P < 0.01) and OT IJV (from 4.6 [3.4-4.8] to 5.9 [4.3-8.2] ng·mL -1 , P < 0.01), but OT ART-IJV was unaffected (from -0.24 [-1.16 to 1.08] to 0.04 [-0.88 to 0.78] ng·mL -1 , P = 1.00). The increased OT levels were similar in the first and second HIIE bouts (OT ARTP = 0.25, OT IJVP = 0.36). CONCLUSIONS: Despite no change in the cerebral OT release via the internal jugular vein, circulating OT increases during HIIE regardless of the accumulated exercise volume, indicating that OT may play role as one of the exerkines.

Acute aerobic exercise enhances cerebrovascular shear-mediated dilation in young adults: the role of cerebral shear.

Exercise-induced increases in shear rate (SR) acutely improve peripheral endothelial function, but the presence of this mechanism in cerebral arteries remains unclear. Thus, we evaluated shear-mediated dilation of the internal carotid artery (ICA), which is an index of cerebrovascular endothelial function, before and after exercise. Shear-mediated dilation was measured with 30 s of hypercapnia in 16 young adults before and 10 min after 30 min of sitting rest (CON) or three cycling exercises on four separate days. The target exercise intensity was 80% of oxygen uptake at the ventilatory threshold. To manipulate the ICA SR during exercise, participants breathed spontaneously (ExSB, SR increase) or hyperventilated without (ExHV, no increase in SR) or with ([Formula: see text], restoration of SR increase) addition of CO2 to inspiratory air. Shear-mediated dilation was calculated as a percent increase in diameter from baseline. Doppler ultrasound measures ICA velocity and diameter. The CON trial revealed that 30 min of sitting did not alter shear-mediated dilation (4.34 ± 1.37% to 3.44 ± 1.23%, P = 0.052). ICA dilation after exercise compared with preexercise levels increased in the ExSB trial (3.32 ± 1.37% to 4.74 ± 1.84%, P < 0.01), remained unchanged in the ExHV trial (4.07 ± 1.55% to 3.21 ± 1.48%, P = 0.07), but was elevated in the [Formula: see text] trial (3.35 ± 1.15% to 4.33 ± 2.12%, P = 0.04). Our results indicate that exercise-induced increases in cerebral shear may play a crucial role in improving cerebrovascular endothelial function after acute exercise in young adults.NEW & NOTEWORTHY We found that 30-min cycling (target intensity was 80% of the ventilatory threshold) with increasing shear of the internal carotid artery (ICA) enhanced transient hypercapnia-induced shear-mediated dilation of the ICA, reflecting improved cerebrovascular endothelial function. This enhancement of ICA dilation was diminished by suppressing the exercise-induced increase in ICA shear via hyperventilation. Our results indicate that increases in cerebral shear may be a key stimulus for improving cerebrovascular endothelial function after exercise in young adults.

Acute hypoxia impairs posterior cerebral bioenergetics and memory in man.

Hypoxia has the potential to impair cognitive function; however, it is still uncertain which cognitive domains are adversely affected. We examined the effects of acute hypoxia (∼7 h) on central executive (Go/No-Go) and non-executive (memory) tasks and the extent to which impairment was potentially related to regional cerebral blood flow and oxygen delivery (CDO2 ). Twelve male participants performed cognitive tasks following 0, 2, 4 and 6 h of passive exposure to both normoxia and hypoxia (12% O2 ), in a randomized block cross-over single-blinded design. Middle cerebral artery (MCA) and posterior cerebral artery (PCA) blood velocities and corresponding CDO2 were determined using bilateral transcranial Doppler ultrasound. In hypoxia, MCA DO2 was reduced during the Go/No-Go task (P = 0.010 vs. normoxia, main effect), and PCA DO2 was attenuated during memorization (P = 0.005 vs. normoxia) and recall components (P = 0.002 vs. normoxia) in the memory task. The accuracy of the memory task was also impaired in hypoxia (P = 0.049 vs. normoxia). In contrast, hypoxia failed to alter reaction time (P = 0.19 vs. normoxia) or accuracy (P = 0.20 vs. normoxia) during the Go/No-Go task, indicating that selective attention and response inhibition were preserved. Hypoxia did not affect cerebral blood flow or corresponding CDO2 responses to cognitive activity (P > 0.05 vs. normoxia). Collectively, these findings highlight the differential sensitivity of cognitive domains, with memory being selectively vulnerable in hypoxia. NEW FINDINGS: What is the central question of this study? We sought to examine the effects of acute hypoxia on central executive (selective attention and response inhibition) and non-executive (memory) performance and the extent to which impairments are potentially related to reductions in regional cerebral blood flow and oxygen delivery. What is the main finding and its importance? Memory was impaired in acute hypoxia, and this was accompanied by a selective reduction in posterior cerebral artery oxygen delivery. In contrast, selective attention and response inhibition remained well preserved. These findings suggest that memory is selectively vulnerable to hypoxia.

Selective elevation in external carotid artery flow during acute gravitational transition to microgravity during parabolic flight.

This study sought to determine to what extent acute exposure to microgravity (0 G) and related increases in central blood volume (CBV) during parabolic flight influence the regional redistribution of intra and extra cranial cerebral blood flow (CBF). Eleven healthy participants performed during two parabolic flights campaigns aboard the Airbus A310-ZERO G aircraft. The response of select variables for each of the 15 parabolas involving exposure to both 0 G and hypergravity (1.8 G) were assessed in the seated position. Mean arterial blood pressure (MAP) and heart rate (HR) were continuously monitored and used to calculate stroke volume (SV), cardiac output ([Formula: see text]), and systemic vascular resistance (SVR). Changes in CBV were measured using an impedance monitor. Extracranial flow through the internal carotid, external carotid, and vertebral artery ([Formula: see text]ICA, [Formula: see text]ECA, and [Formula: see text]VA), and intracranial blood velocity was measured by duplex ultrasound. When compared with 1-G baseline condition, 0 G increased CBV (+375 ± 98 mL, P = 0.004) and [Formula: see text] (+16 ± 14%, P = 0.024) and decreased SVR (-7.3 ± 5 mmHg·min·L-1, P = 0.002) and MAP (-13 ± 4 mmHg, P = 0.001). [Formula: see text]ECA increased by 43 ± 46% in 0 G (P = 0.030), whereas no change was observed for CBF, [Formula: see text]ICA, or [Formula: see text]VA (P = 0.102, P = 0.637, and P = 0.095, respectively).NEW & NOTEWORTHY Our findings demonstrate that in microgravity there is a selective increase in external carotid artery blood flow whereas global and regional cerebral blood flow remained preserved. To what extent this reflects an adaptive, neuroprotective response to counter overperfusion remains to be established.

Handgrip exercise does not alter CO2 -mediated cerebrovascular flow-mediated dilation.

Handgrip exercise (HG), a small muscle exercise, improves cognitive function and is expected to provide a useful exercise mode to maintain cerebral health. However, the effect of HG on cerebral blood flow regulation is not fully understood. The present study aimed to examine the effect of acute HG on cerebral endothelial function as one of the essential cerebral blood flow regulatory functions. Thirteen healthy young participants performed interval HG, consisting of 4 sets of 2 min HG at 25% of maximum voluntary contraction with 3 min recovery between each set. Cognitive performance was evaluated before and at 5 and 60 min after interval HG using the Go/No-Go task (reaction time and accuracy). The diameter and blood velocity of the internal carotid artery (ICA) were measured using a duplex Doppler ultrasound system. To assess cerebral endothelial function, hypercapnia (30 s of hypercapnia stimulation, end-tidal partial pressure of CO2 : +9 mmHg)-induced cerebrovascular flow-mediated dilatation (cFMD) was induced, calculated as relative peak dilatation from baseline diameter. The shear rate (SR) was calculated using the diameter and blood velocity of the ICA. As a result, cognitive performance improved only at 5 min after interval HG (reaction time, P = 0.008; accuracy, P = 0.186), whereas ICA SR during interval HG and cFMD after interval HG were unchanged (P = 0.313 and P = 0.440, respectively). These results suggest that enhancement in cerebral endothelial function is not an essential mechanism responsible for acute HG-induced cognitive improvement. NEW FINDINGS: What is the central question of this study? Does handgrip exercise, a small muscle exercise, improve cerebral endothelial function? What is the main finding and its importance? Acute interval isometric handgrip exercise (2 min of exercise at 25% maximum voluntary contraction, followed by 3 min of recovery, repeated for a total of 4 sets) did not improve cerebral endothelial function. Since the cerebrovascular shear rate did not change during exercise, it is possible that acute handgrip exercise is not sufficient stimulation to improve cerebral endothelial function.

Attenuated pulsatile transition to the cerebral vasculature during high-intensity interval exercise in young healthy men.

NEW FINDINGS: What is the central question of this study? High-intensity interval exercise (HIIE) is recommended for its favourable haemodynamic stimulation, but excessive haemodynamic fluctuations may stress the brain: is the cerebral vasculature protected against exaggerated systemic blood flow fluctuation during HIIE? What is the main finding and its importance? Time- and frequency-domain indices of aortic-cerebral pulsatile transition were lowered during HIIE. The findings suggest that the arterial system to the cerebral vasculature may attenuate pulsatile transition during HIIE as a defence mechanism against pulsatile fluctuation for the cerebral vasculature. ABSTRACT: High-intensity interval exercise (HIIE) is recommended because it provides favourable haemodynamic stimulation, but excessive haemodynamic fluctuations may be an adverse impact on the brain. We tested whether the cerebral vasculature is protected against systemic blood flow fluctuation during HIIE. Fourteen healthy men (age 24 ± 2 years) underwent four 4-min exercises at 80-90% of maximal workload (Wmax ) interspaced by 3-min active rest at 50-60% Wmax . Transcranial Doppler measured middle cerebral artery blood velocity (CBV). Systemic haemodynamics (Modelflow) and aortic pressure (AoP, general transfer function) were estimated from an invasively recorded brachial arterial pressure waveform. Using transfer function analysis, gain and phase between AoP and CBV (0.39-10.0 Hz) were calculated. Stroke volume, aortic pulse pressure and pulsatile CBV increased during exercise (time effect: P < 0.0001 for all), but a time-domain index of aortic-cerebral pulsatile transition (pulsatile CBV/pulsatile AoP) decreased throughout the exercise bouts (time effect: P < 0.0001). Furthermore, transfer function gain reduced, and phase increased throughout the exercise bouts (time effect: P < 0.0001 for both), suggesting the attenuation and delay of pulsatile transition. The cerebral vascular conductance index (mean CBV/mean arterial pressure; time effect: P = 0.296), an inverse index of cerebral vascular tone, did not change even though systemic vascular conductance increased during exercise (time effect: P < 0.0001). The arterial system to the cerebral vasculature may attenuate pulsatile transition during HIIE as a defence mechanism against pulsatile fluctuation for the cerebral vasculature.

Greater task difficulty during unilateral motor tasks changes intracortical inhibition and facilitation in the ipsilateral primary motor cortex in young men.

This study aimed to clarify the changes in short-interval intracortical inhibition (SICI) and facilitation (ICF) in the ipsilateral primary motor cortex (iM1) when the task difficulty during unilateral force-matching tasks was manipulated. Twelve young male adults matched their left index finger abduction force to a displayed target force. Task difficulty was manipulated by varying the acceptable force range of the mean target force (5% MVC). Briefly, unilateral force-matching tasks with lesser and greater task difficulty (EASY and DIFF, respectively) were assigned acceptable force ranges of ± 7% and ± 0% of the target force, respectively. To evaluate SICI and ICF in iM1, paired-pulse transcranial magnetic stimulation with 2-ms and 10-ms interstimulus intervals was applied to correct motor-evoked potentials (MEPs) from the first dorsal interosseous muscle during each task. Test stimulus intensity to evoke the MEP with a peak-to-peak amplitude of approximately 0.5-1.5 mV for each task was lower in DIFF than in EASY (P = 0.001), indicating that DIFF increased corticospinal excitability of the ipsilateral hemisphere compared with EASY. The MEPs in SICI and ICF were significantly larger in DIFF than in EASY (P < 0.050). These results suggest that greater corticospinal excitability in the ipsilateral hemisphere during DIFF is associated with reduced SICI and increased ICF.

Acute and Chronic Effect of Physiological Factors on Arterial Stiffness.

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

Can Alterations in Cerebrovascular CO2 Reactivity Be Identified Using Transfer Function Analysis without the Requirement for Carbon Dioxide Inhalation?

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.

Point/counterpoint: Arterial blood pressure response to exercise does relate to exercise-induced improvement in cognitive function.

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.

Dynamic resistance exercise-induced pressor response does not alter hypercapnia-induced cerebral vasodilation in young adults.

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 (PETCO2) (r = 0.46, P < 0.01) than with mean arterial pressure (r = 0.32, P = 0.02). These findings suggest that the effects of RE-induced pressor response on cerebrovascular function may be different from peripheral arteries. An increase in PETCO2 during the relaxation phase may play a more crucial role than elevated pressure in increasing cerebral shear during dynamic RE.