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.

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 HIIT 85 (85% of maximal aerobic power, 1–7 min effort bouts, n = 8) and HIIT 115 (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 (MCAv mean ) 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 MCAv mean (both P > 0.05). TFA phase during 0.10 Hz squat‐stands decreased after HIIT irrespective of intensity (HIIT 85 : 0.77 ± 0.22 vs. 0.67 ± 0.18 radians; HIIT 115 : 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.

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 trueV˙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 (PETCO2; 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). PETCO2 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 PETCO2 (+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 PETCO2.

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.

The influence of high‐intensity exercise training (HIIT) on cerebral blood flow (CBF) regulation remains unclear. HIIT induces surges in mean arterial pressure (MAP), which could be transmitted to the brain, especially early after exercise onset. The aims of this study were to 1) describe regional CBF changes during and following 30 s of high‐intensity exercise and; 2) examine whether dynamic cerebral autoregulation (dCA) is associated with CBF changes. Ten women (age: 26 ± 6 yrs; VO2max: 48.6 ± 3.8 ml×kg×min−1) cycled for 30 s at the workload reached at VO2max followed by 3 min of passive recovery. dCA was characterized using transfer function analysis of forced oscillations induced by repeated squat‐stands (0.05 and 0.10 Hz). Middle (MCAvmean) and posterior cerebral artery mean blood velocities (PCAvmean; transcranial Doppler), MAP (finger photoplethysmography) and end‐tidal carbon dioxide partial pressure (PETCO2; gaz analyzer) were measured. MCAvmean (+19 ± 10%) and PCAvmean (+21 ± 14%) increased early after exercise onset, returning toward baseline values afterwards. MAP increased throughout exercise (p<0.0001). PETCO2 initially decreased by 3 ±2 mmHg (p<0.0001) before returning to baseline values at end‐exercise. During recovery, MCAvmean (+43 ±15%), PCAvmean (+42 ± 15%) and PETCO2 (+11 ± 3 mmHg; p<0.0001) increased. TFA gain was higher in the MCA (p < 0.0001). Other dCA metrics were comparable between arteries and unrelated to exercise‐induced cerebral blood velocity changes. In young fit women, blood velocity changes during and following a 30‐s high‐intensity exercise are comparable between MCA and PCA and unrelated to dCA. Support or Funding Information L.L. and S.I. are supported by a doctoral training scholarship from the Fonds de recherche du Québec – Santé (FRQS).

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-trainedwomen (age: 25 ± 4 y; 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 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). RelativeCVRCO2 was 39% lower in the MCA (2.16±1.02 vs. 3.00±1.09%/Torr, p<0.01). These findings indicate cerebral pressure-flow relationship appears to be similar between the MCA and 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.

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.

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).