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.