The effect that cardiorespiratory fitness has on the dynamic cerebral autoregulatory capacity during changes in mean arterial pressure (MAP) remains equivocal. Using a multiple‐metrics approach, challenging MAP across the spectrum of physiological extremes (i.e., spontaneous through forced MAP oscillations), we characterized dynamic cerebral autoregulatory capacity in 19 male endurance athletes and eight controls via three methods: (1) onset of regulation (i.e., time delay before an increase in middle cerebral artery (MCA) conductance [MCA blood velocity (MCAv)/MAP] and rate of regulation, after transient hypotension induced by sit‐to‐stand, and transfer function analysis (TFA) of MAP and MCAv responses during (2) spontaneous and (3) forced oscillations (5‐min of squat‐stand maneuvers performed at 0.05 and 0.10 Hz). Reductions in MAP and mean MCAv (MCAV mean) during initial orthostatic stress (0‐30 sec after sit‐to‐stand) and the prevalence of orthostatic hypotension were also determined. Onset of regulation was delayed after sit‐to‐stand in athletes (3.1 ± 1.7 vs. 1.5 ± 1.0 sec; P = 0.03), but rate of regulation was not different between groups (0.24 ± 0.05 vs. 0.21 ± 0.09 sec−1; P = 0.82). While both groups had comparable TFA metrics during spontaneous oscillations, athletes had higher TFA gain during 0.10 Hz squat‐stand versus recreational controls (P = 0.01). Reductions in MAP (P = 0.15) and MCAV mean (P = 0.11) during orthostatic stress and the prevalence of initial orthostatic hypotension (P = 0.65) were comparable between groups. These results indicate an intact ability of the cerebral vasculature to react to spontaneous oscillations but an attenuated capability to counter rapid and large changes in MAP in individuals with elevated cardiorespiratory fitness.

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.

Objective. The aim of this study was to identify whether the addition of an individualised Active Rehabilitation Intervention to standard care influences recovery of young patients who are slow-to-recover following a mTBI. Methods. Fifteen participants aged 15 ± 2 years received standard care and an individualised Active Rehabilitation Intervention which included (1) low- to high-intensity aerobic training; (2) sport-specific coordination exercises; and (3) therapeutic balance exercises. The following criteria were used to measure the resolution of signs and symptoms of mTBI: (1) absence of postconcussion symptoms for more than 7 consecutive days; (2) cognitive function corresponding to normative data; and (3) absence of deficits in coordination and balance. Results. The Active Rehabilitation Intervention lasted 49 ± 17 days. The duration of the intervention was correlated with self-reported participation (truex-=84.64±19.63%, r = −0.792, p < 0.001). The average postconcussion symptom inventory (PCSI) score went from a total of 36.85 ± 23.21 points to 4.31 ± 5.04 points after the intervention (Z = −3.18, p = 0.001). Conclusion. A progressive submaximal Active Rehabilitation Intervention may represent an important asset in the recovery of young patients who are slow-to-recover following a mTBI.

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.

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).

Driving simulators represent a promising avenue for the assessment and rehabilitation of driving skills in TBI individuals as it allows control of stimuli in a safe, challenging and ecologically valid environment and offer the opportunity to measure and record driving performance. Additional studies, however, are needed to document strengths and limitations of this method.

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.