Cardiac remodeling after six weeks of high-intensity interval training to exhaustion in endurance-trained men.

High-intensity interval training (HIIT) improves physical performance of endurance athletes, although studies examining its cardiovascular effects are sparse. We evaluated the impact of HIIT on blood pressure, heart rate, and cardiac cavities' size and function in endurance-trained adults. Seventeen endurance-trained men underwent 24-h ambulatory blood pressure monitoring and Doppler echocardiography at baseline and after 6 wk of HIIT. Participants were divided into 2 groups [85% maximal aerobic power (HIIT85), n = 8 and 115% maximal aerobic power (HIIT115), n = 9] to compare the impact of different HIIT intensities. Ambulatory blood pressure monitoring and cardiac chambers' size and function were similar between groups at baseline. HIIT reduced heart rate (55 ± 8 vs. 51 ± 7 beats/min; P = 0.003), systolic blood pressure (121 ± 11 vs. 118 ± 9 mmHg; P = 0.01), mean arterial pressure (90 ± 8 vs. 89 ± 6 mmHg; P = 0.03), and pulse pressure (52 ± 6 vs. 49 ± 5 mmHg; P = 0.01) irrespective of training intensity. Left atrium volumes increased after HIIT (maximal: 50 ± 14 vs. 54 ± 14 mL; P = 0.02; minimal: 15 ± 5 vs. 20 ± 8 mL; P = 0.01) in both groups. Right ventricle global longitudinal strain lowered after training in the HIIT85 group only (20 ± 4 vs. 17 ± 3%, P = 0.04). In endurance-trained men, 6 wk of HIIT reduced systolic blood pressure and mean arterial pressure and increased left atrium volumes irrespective of training intensity, whereas submaximal HIIT deteriorated right ventricle systolic function.NEW & NOTEWORTHY The novel findings of this study are that 6 wk of high-intensity interval training increases left atrial volumes irrespective of training intensity (85 or 115% maximal aerobic power), whereas the submaximal training decreases right ventricular systolic function in endurance-trained men. These results may help identify the exercise threshold for potential toxicity of intense exercise training for at-risk individuals and ideal exercise training regimens conferring optimal cardiovascular protection and adapted endurance training for athletes.

Acute isometric and dynamic exercise do not alter cerebral sympathetic nerve activity in healthy humans.

The impact of physiological stressors on cerebral sympathetic nervous activity (SNA) remains controversial. We hypothesized that cerebral noradrenaline (NA) spillover, an index of cerebral SNA, would not change during both submaximal isometric handgrip (HG) exercise followed by a post-exercise circulatory occlusion (PECO), and supine dynamic cycling exercise. Twelve healthy participants (5 females) underwent simultaneous blood sampling from the right radial artery and right internal jugular vein. Right internal jugular vein blood flow was measured using Duplex ultrasound, and tritiated NA was infused through the participants' right superficial forearm vein. Heart rate was recorded via electrocardiogram and blood pressure was monitored using the right radial artery. Total NA spillover increased during HG (P = 0.049), PECO (P = 0.006), and moderate cycling exercise (P = 0.03) compared to rest. Cerebral NA spillover remained unchanged during isometric HG exercise (P = 0.36), PECO after the isometric HG exercise (P = 0.45), and during moderate cycling exercise (P = 0.94) compared to rest. These results indicate that transient increases in blood pressure during acute exercise involving both small and large muscle mass do not engage cerebral SNA in healthy humans. Our findings suggest that cerebral SNA may be non-obligatory for exercise-related cerebrovascular adjustments.

Cerebral blood flow pulsatility and cerebral artery stiffness acutely decrease during hemodialysis.

End-stage kidney disease (ESKD) is associated with increased arterial stiffness and cognitive impairment. Cognitive decline is accelerated in ESKD patients on hemodialysis and may result from repeatedly inappropriate cerebral blood flow (CBF). The aim of this study was to examine the acute effect of hemodialysis on pulsatile components of CBF and their relation to acute changes in arterial stiffness. In eight participants (age: 63 ± 18 years, men: 5), CBF was estimated using middle cerebral artery blood velocity (MCAv) assessed with transcranial Doppler ultrasound before, during, and after a single hemodialysis session. Brachial and central blood pressure, along with estimated aortic stiffness (eAoPWV) were measured using an oscillometric device. Arterial stiffness from heart to MCA was measured as the pulse arrival time (PAT) between electrocardiogram (ECG) and transcranial Doppler ultrasound waveforms (cerebral PAT). During hemodialysis, there was a significant reduction in mean MCAv (-3.2 cm/s, p < 0.001), and systolic MCAv (-13.0 cm/s, p < 0.001). While baseline eAoPWV (9.25 ± 0.80 m/s) did not significantly change during hemodialysis, cerebral PAT increased significantly (+0.027 , p < 0.001) and was associated with reduced pulsatile components of MCAv. This study shows that hemodialysis acutely reduces stiffness of arteries perfusing the brain along with pulsatile components of blood velocity.

Impact of sex on the cerebrovascular response to incremental aerobic exercise in moderately trained endurance athletes.

The cerebrovascular response to incremental aerobic exercise is comparable between males and females. Whether this response can be found in moderately trained athletes remains unknown. We aimed to examine the effect of sex on the cerebrovascular response to incremental aerobic exercise until volitional exhaustion in this population. Twenty-two moderately trained athletes (11 M/11 F; age: 25 ± 5 vs. 26 ± 6 yr, P = 0.6478; peak oxygen consumption: 55.8 ± 5.2 vs. 48.3 ± 4 mL/kg/min; P = 0.0011; training volume: 532 ± 173 vs. 466 ± 151 min/wk, P = 0.3554) performed a maximal ergocycle exercise test. Systemic and cerebrovascular hemodynamics were measured. At rest, middle cerebral artery mean blood velocity (MCAvmean; 64.1 ± 12.7 vs. 72.2 ± 15.3 cm·s-1; P = 0.2713) was not different between groups, whereas partial pressure of end-tidal carbon dioxide ([Formula: see text], 42 ± 3 vs. 37 ± 2 mmHg, P = 0.0002) was higher in males. During the MCAvmean ascending phase, changes in MCAvmean (intensity: P < 0.0001, sex: P = 0.3184, interaction: P = 0.9567) were not different between groups. Changes in cardiac output ([Formula: see text]) (intensity: P < 0.0001, sex: P < 0.0001, interaction: P < 0.0001) and [Formula: see text] (intensity: P < 0.0001, sex: P < 0.0001, interaction: P < 0.0001) were higher in males. During the MCAvmean descending phase, changes in MCAvmean (intensity: P < 0.0001, sex: P = 0.5522, interaction: P = 0.4828) and [Formula: see text] (intensity: P = 0.0550, sex: P = 0.0003, interaction: P = 0.2715) were not different between groups. Changes in [Formula: see text] (intensity P < 0.0001, sex: P < 0.0001, interaction: P = 0.0280) were higher in males. These results suggest the MCAvmean response during exercise is comparable between moderately trained males and females notwithstanding differences in the response of key cerebral blood flow determinants.NEW & NOTEWORTHY The results of this study suggest the cerebrovascular response between moderately endurance-trained males and females is comparable in spite of a higher arterial carbon dioxide and cardiac output in males compared with females during incremental aerobic exercise until volitional exhaustion. This could help in providing a better understanding of the key differences in cerebral blood flow regulation between males and females during aerobic exercise.

Influence of high-intensity interval training to exhaustion on the directional sensitivity of the cerebral pressure-flow relationship in young endurance-trained men.

We previously reported subtle dynamic cerebral autoregulation (dCA) alterations following 6 weeks of high-intensity interval training (HIIT) to exhaustion using transfer function analysis (TFA) on forced mean arterial pressure (MAP) oscillations in young endurance-trained men. However, accumulating evidence suggests the cerebrovasculature better buffers cerebral blood flow changes when MAP acutely increases compared to when MAP acutely decreases. Whether HIIT affects the directional sensitivity of the cerebral pressure-flow relationship in these athletes is unknown. In 18 endurance-trained men (age: 27 ± 6 years, VO2 max: 55.5 ± 4.7 ml·kg-1 ·min-1 ), we evaluated the impact of 6 weeks of HIIT to exhaustion on dCA directionality using induced MAP oscillations during 5-min 0.05 and 0.10 Hz repeated squat-stands. We calculated time-adjusted changes in middle cerebral artery mean blood velocity (MCAv) per change in MAP (ΔMCAvT /ΔMAPT ) for each squat transition. Then, we compared averaged ΔMCAvT /ΔMAPT during MAP increases and decreases. Before HIIT, ΔMCAvT /ΔMAPT was comparable between MAP increases and decreases during 0.05 Hz repeated squat-stands (p = 0.518). During 0.10 Hz repeated squat-stands, ΔMCAvT /ΔMAPT was lower during MAP increases versus decreases (0.87 ± 0.17 vs. 0.99 ± 0.23 cm·s-1 ·mmHg-1 , p = 0.030). Following HIIT, ΔMCAvT /ΔMAPT was superior during MAP increases over decreases during 0.05 Hz repeated squat-stands (0.97 ± 0.38 vs. 0.77 ± 0.35 cm·s-1 ·mmHg-1 , p = 0.002). During 0.10 Hz repeated squat-stands, dCA directional sensitivity disappeared (p = 0.359). These results suggest the potential for HIIT to influence the directional sensitivity of the cerebral pressure-flow relationship in young endurance-trained men.

Trans-cerebral HCO3- and PCO2 exchange during acute respiratory acidosis and exercise-induced metabolic acidosis in humans.

This study investigated trans-cerebral internal jugular venous-arterial bicarbonate ([HCO3-]) and carbon dioxide tension (PCO2) exchange utilizing two separate interventions to induce acidosis: 1) acute respiratory acidosis via elevations in arterial PCO2 (PaCO2) (n = 39); and 2) metabolic acidosis via incremental cycling exercise to exhaustion (n = 24). During respiratory acidosis, arterial [HCO3-] increased by 0.15 ± 0.05 mmol ⋅ l-1 per mmHg elevation in PaCO2 across a wide physiological range (35 to 60 mmHg PaCO2; P < 0.001). The narrowing of the venous-arterial [HCO3-] and PCO2 differences with respiratory acidosis were both related to the hypercapnia-induced elevations in cerebral blood flow (CBF) (both P < 0.001; subset n = 27); thus, trans-cerebral [HCO3-] exchange (CBF × venous-arterial [HCO3-] difference) was reduced indicating a shift from net release toward net uptake of [HCO3-] (P = 0.004). Arterial [HCO3-] was reduced by -0.48 ± 0.15 mmol ⋅ l-1 per nmol ⋅ l-1 increase in arterial [H+] with exercise-induced acidosis (P < 0.001). There was no relationship between the venous-arterial [HCO3-] difference and arterial [H+] with exercise-induced acidosis or CBF; therefore, trans-cerebral [HCO3-] exchange was unaltered throughout exercise when indexed against arterial [H+] or pH (P = 0.933 and P = 0.896, respectively). These results indicate that increases and decreases in systemic [HCO3-] - during acute respiratory/exercise-induced metabolic acidosis, respectively - differentially affect cerebrovascular acid-base balance (via trans-cerebral [HCO3-] exchange).

Dynamic cerebral autoregulation and cerebrovascular carbon dioxide reactivity in middle and posterior cerebral arteries in young endurance-trained women.

The integrated responses regulating cerebral blood flow are understudied in women, particularly in relation to potential regional differences. In this study, we compared dynamic cerebral autoregulation (dCA) and cerebrovascular reactivity to carbon dioxide (CVRco2) in the middle (MCA) and posterior cerebral arteries (PCA) in 11 young endurance-trained women (age, 25 ± 4 yr; maximal oxygen uptake, 48.1 ± 4.1 mL·kg-1·min-1). dCA was characterized using a multimodal approach including a sit-to-stand and a transfer function analysis (TFA) of forced blood pressure oscillations (repeated squat-stands executed at 0.05 Hz and 0.10 Hz). The hyperoxic rebreathing test was utilized to characterize CVRco2. Upon standing, the percent reduction in blood velocity per percent reduction in mean arterial pressure during initial orthostatic stress (0-15 s after sit-to-stand), the onset of the regulatory response, and the rate of regulation did not differ between MCA and PCA (all P > 0.05). There was an ANOVA effect of anatomical location for TFA gain (P < 0.001) and a frequency effect for TFA phase (P < 0.001). However, normalized gain was not different between arteries (P = 0.18). Absolute CVRco2 was not different between MCA and PCA (1.55 ± 0.81 vs. 1.30 ± 0.49 cm·s-1/Torr, P = 0.26). Relative CVRco2 was 39% lower in the MCA (2.16 ± 1.02 vs. 3.00 ± 1.09%/Torr, P < 0.01). These findings indicate that the cerebral pressure-flow relationship appears to be similar between the MCA and the PCA in young endurance-trained women. The absence of regional differences in absolute CVRco2 could be women specific, although a direct comparison with a group of men will be necessary to address that issue.NEW & NOTEWORTHY Herein, we describe responses from two major mechanisms regulating cerebral blood flow with a special attention on regional differences in young endurance-trained women. The novel findings are that dynamic cerebral autoregulation and absolute cerebrovascular reactivity to carbon dioxide appear similar between the middle and posterior cerebral arteries of these young women.

What recording duration is required to provide physiologically valid and reliable dynamic cerebral autoregulation transfer functional analysis estimates?

Objective. Currently, a recording of 300 s is recommended to obtain accurate dynamic cerebral autoregulation estimates using transfer function analysis (TFA). Therefore, this investigation sought to explore the concurrent validity and the within- and between-day reliability of TFA estimates derived from shorter recording durations from squat-stand maneuvers.Approach. Retrospective analyses were performed on 70 young, recreationally active or endurance-trained participants (17 females; age: 26 ± 5 years, [range: 20-39 years]; body mass index: 24 ± 3 kg m-2). Participants performed 300 s of squat-stands at frequencies of 0.05 and 0.10 Hz, where shorter recordings of 60, 120, 180, and 240 s were extracted. Continuous transcranial Doppler ultrasound recordings were taken within the middle and posterior cerebral arteries. Coherence, phase, gain, and normalized gain metrics were derived. Bland-Altman plots with 95% limits of agreement (LOA), repeated measures ANOVA's, two-tailed paired t-tests, coefficient of variation, Cronbach's alpha, intraclass correlation coefficients, and linear regressions were conducted.Main results. When examining the concurrent validity across different recording durations, group differences were noted within coherence (F(4155) > 11.6,p < 0.001) but not phase (F(4155) < 0.27,p > 0.611), gain (F(4155) < 0.61,p > 0.440), or normalized gain (F(4155) < 0.85,p > 0.359) parameters. The Bland-Altman 95% LOA measuring the concurrent validity, trended to narrow as recording duration increased (60 s: < ±0.4, 120 s: < ±0.3, 180 s  < ±0.3, 240 s: < ±0.1). The validity of the 180 and 240 s recordings further increased when physiological covariates were included within regression models.Significance. Future studies examining autoregulation should seek to have participants perform 300 s of squat-stand maneuvers. However, valid and reliable TFA estimates can be drawn from 240 s or 180 s recordings if physiological covariates are controlled.

Comparable blood velocity changes in middle and posterior cerebral arteries during and following acute high-intensity exercise in young fit women.

The cerebral blood flow response to high-intensity interval training (HIIT) remains unclear. HIIT induces surges in mean arterial pressure (MAP), which could be transmitted to the brain, especially early after exercise onset. The aim of this study was to describe regional cerebral blood velocity changes during and following 30 s of high-intensity exercise. Ten women (age: 27 ± 6 years; VO2max : 48.6 ± 3.8 ml·kg·min-1 ) cycled for 30 s at the workload reached at V˙ O2max followed by 3min of passive recovery. Middle (MCAvmean ) and posterior cerebral artery mean blood velocities (PCAvmean ; transcranial Doppler ultrasound), MAP (finger photoplethysmography), and end-tidal carbon dioxide partial pressure (PET CO2 ; gaz analyzer) were measured. MCAvmean (+19 ± 10%) and PCAvmean (+21 ± 14%) increased early after exercise onset, returning toward baseline values afterward. MAP increased throughout exercise (p < .0001). PET CO2 initially decreased by 3 ± 2 mmHg (p < .0001) before returning to baseline values at end-exercise. During recovery, MCAvmean (+43 ± 15%), PCAvmean (+42 ± 15%), and PET CO2 (+11 ± 3 mmHg; p < .0001) increased. In young fit women, cerebral blood velocity quickly increases at the onset of a 30-s exercise performed at maximal workload, before returning to baseline values through the end of the exercise. During recovery, cerebral blood velocity augments in both arteries, along with PET CO2 .

Six weeks of high-intensity interval training to exhaustion attenuates dynamic cerebral autoregulation without influencing resting cerebral blood velocity in young fit men.

Elevated cardiorespiratory fitness (CRF) is associated with reduced dynamic cerebral autoregulation (dCA), but the impact of exercise training per se on dCA remains equivocal. In addition, resting cerebral blood flow (CBF) and dCA after high-intensity interval training (HIIT) in individuals with already high CRF remains unknown. We examined to what extent 6 weeks of HIIT affect resting CBF and dCA in cardiorespiratory fit men and explored if potential changes are intensity-dependent. Endurance-trained men were assigned to group HIIT85 (85% of maximal aerobic power, 1-7 min effort bouts, n = 8) and HIIT115 (115% of maximal aerobic power, 30 sec to 1 min effort bouts, n = 9). Training sessions were completed until exhaustion 3 times/week over 6 weeks. Mean arterial pressure (MAP) and middle cerebral artery mean blood velocity (MCAvmean ) were measured continuously at rest and during repeated squat-stands (0.05 and 0.10 Hz). Transfer function analysis (TFA) was used to characterize dCA on driven blood pressure oscillations during repeated squat-stands. Neither training nor intensity had an effect on resting MAP and MCAvmean (both P > 0.05). TFA phase during 0.10 Hz squat-stands decreased after HIIT irrespective of intensity (HIIT85 : 0.77 ± 0.22 vs. 0.67 ± 0.18 radians; HIIT115 : pre: 0.62 ± 0.19 vs. post: 0.59 ± 0.13 radians, time effect P = 0.048). These results suggest that HIIT over 6 weeks have no apparent benefits on resting CBF, but a subtle attenuation in dCA is seen posttraining irrespective of intensity training in endurance-trained men.

Dynamic cerebral autoregulation is attenuated in young fit women.

Young women exhibit higher prevalence of orthostatic hypotension with presyncopal symptoms compared to men. These symptoms could be influenced by an attenuated ability of the cerebrovasculature to respond to rapid blood pressure (BP) changes [dynamic cerebral autoregulation (dCA)]. The influence of sex on dCA remains unclear. dCA in 11 fit women (25 ± 2 years) and 11 age-matched men (24 ± 1 years) was compared using a multimodal approach including a sit-to-stand (STS) and forced BP oscillations (repeated squat-stand performed at 0.05 and 0.10 Hz). Prevalence of initial orthostatic hypotension (IOH; decrease in systolic ≥ 40 mmHg and/or diastolic BP ≥ 20 mmHg) during the first 15 sec of STS was determined as a functional outcome. In women, the decrease in mean middle cerebral artery blood velocity (MCAvmean ) following the STS was greater (-20 ± 8 vs. -11 ± 7 cm sec-1 ; P = 0.018) and the onset of the regulatory change (time lapse between the beginning of the STS and the increase in the conductance index (MCAvmean /mean arterial pressure) was delayed (P = 0.007). Transfer function analysis gain during 0.05 Hz squat-stand was ~48% higher in women (6.4 ± 1.3 vs. 3.8 ± 2.3 cm sec-1 mmHg-1 ; P = 0.017). Prevalence of IOH was comparable between groups (women: 4/9 vs. men: 5/9, P = 0.637). These results indicate the cerebrovasculature of fit women has an attenuated ability to react to rapid changes in BP in the face of preserved orthostasis, which could be related to higher resting cerebral blood flow allowing women to better face transient hypotension.