The purpose of this study was to compare the integrated intracranial cerebrovascular reactivity (CVR) and hypercapnic ventilatory response between children and adults and to explore the dynamic response of the middle cerebral artery mean velocity (MCA V ). Children (n = 20; 9.9 ± 0.7 years of age) and adults (n = 21; 24.4 ± 2.0 years of age) completed assessment of CVR over 240 s using a fixed fraction of inspired CO 2 (0.06). Baseline MCA V was higher in the adult females compared with the males (P ≤ 0.05). The MCA V was greater in female children compared with male children (P ≤ 0.05) and in female adults compared with male adults (P ≤ 0.05) with hypercapnia. Relative CVR was similar in children and adults (3.71 ± 1.06 versus 4.12 ± 1.32% mmHg −1 ; P = 0.098), with absolute CVR being higher in adult females than males (3.27 ± 0.86 versus 2.53 ± 0.70 cm s −1 mmHg −1 ; P ≤ 0.001). Likewise, the hypercapnic ventilatory response did not differ between the children and adults (1.89 ± 1.00 versus 1.77 ± 1.34 l min −1 mmHg −1 ; P = 0.597), but was lower in adult females than males (1.815 ± 0.37 versus 2.33 ± 1.66 l min −1 mmHg −1 ; P ≤ 0.05). The heart rate response to hypercapnia was greater in children than in adults (P = 0.001).A monoexponential regression model was used to characterize the dynamic onset, consisting of a delay term, amplitude and time constant ( ). The results revealed that MCA V was faster in adults than in children (34 ± 18 versus 74 ± 28 s; P = 0.001). Our study provides new insight into the impact of age and sex on CVR and the dynamic response of the MCA V to hypercapnia.

Purpose: To understand the extent different types of acute exercise influence cerebral blood flow during and following exercise in children. Methods: Eight children (7–11 y; 4 girls) completed 2 conditions: high-intensity interval exercise (HIIE; 6 × 1-min sprints at 90% watt maximum) and moderate-intensity steady-state exercise (MISS; 15 min at 44% watt maximum). Blood velocity in the middle cerebral artery (MCAV) and heart rate were assessed continuously. The partial pressure of end-tidal carbon dioxide and mean arterial pressure were assessed at baseline and following exercise. Results: Percentage of maximum heart rate during HIIE was 82% (4%), compared with 69% (4%) during MISS. MCAV was increased above baseline in MISS after 75 seconds (5.8% [3.9%], P × .004) but was unchanged during HIIE. MCAV was reduced below baseline (−10.7% [4.1%], P × .004) during the sixth sprint of HIIE. In both conditions, MCAV remained below baseline postexercise, but returned to baseline values 30-minute postexercise (P < .001). A postexercise increase in mean arterial pressure was apparent following HIIE and MISS, and persisted 30-minute postexercise. Partial pressure of end-tidal carbon dioxide declined post HIIE (−3.4 mm Hg, P < .05), but not following MISS. Conclusion: These preliminary findings show HIIE and MISS elicit differing intracranial vascular responses; however, research is needed to elucidate the implications and underlying regulatory mechanisms of these responses.

Little is known about the response of the cerebrovasculature to acute exercise in children and how these responses might differ with adults. Therefore, we compared changes in middle cerebral artery blood velocity (MCAV), end-tidal Pco ([Formula: see text]), blood pressure, and minute ventilation (V̇e) in response to incremental exercise between children and adults. Thirteen children [age: 9 ± 1 (SD) yr] and thirteen sex-matched adults (age: 25 ± 4 yr) completed a maximal exercise test, during which MCAV, [Formula: see text], and V̇e were measured continuously. These variables were measured at rest, at exercise intensities specific to individual ventilatory thresholds, and at maximum. Although MCAV was higher at rest in children compared with adults, there were smaller increases in children (1-12%) compared with adults (12-25%) at all exercise intensities. There were alterations in [Formula: see text] with exercise intensity in an age-dependent manner [(2.5,54.5) = 7.983, < 0.001; η = 0.266], remaining stable in children with increasing exercise intensity (37-39 mmHg; > 0.05) until hyperventilation-induced reductions following the respiratory compensation point. In adults, [Formula: see text] increased with exercise intensity (36-45 mmHg, < 0.05) until the ventilatory threshold. From the ventilatory threshold to maximum, adults showed a greater hyperventilation-induced hypocapnia than children. These findings show that the relative increase in MCAV during exercise was attenuated in children compared with adults. There was also a weaker relationship between MCAV and [Formula: see text] during exercise in children, suggesting that cerebral perfusion may be regulated by different mechanisms during exercise in the child. These findings provide the first direct evidence that exercise increases cerebral blood flow in children to a lesser extent than in adults. Changes in end-tidal CO parallel changes in cerebral perfusion in adults but not in children, suggesting age-dependent regulatory mechanisms of cerebral blood flow during exercise.

Intracranial blood velocity reactivity to a steady‐state hypercapnic stimulus has been shown to be similar in children and adults, but the onset response to hypercapnia is slower in the child. Given the vasodilatory effect of hypercapnia on the cerebrovasculature, assessment of vessel diameter, and blood flow are vital to fully elucidate whether the temporal hypercapnic response differs in children versus adults. Assessment of internal carotid artery (ICA) vessel diameter (ICAd), blood velocity (ICAv), volumetric blood flow (QICA), and shear rate (ICASR) in response to a 4 min hypercapnic challenge was completed in children (n = 14, 8 girls; 9.8 ± 0.7 years) and adults (n = 17, 7 females; 24.7 ± 1.8 years). The dynamic onset responses of partial pressure of end‐tidal CO2 (PETCO2), QICA, ICAv, and ICASR to hypercapnia were modeled, and mean response time (MRT) was computed. Following 4 min of hypercapnia, ICA reactivity and ICAd were comparable between the groups. Despite a similar MRT in PETCO2 in children and adults, children had slower QICA (children 108 ± 60 s vs. adults 66 ± 37 s; p = 0.023), ICAv (children 120 ± 52 s vs. adults 52 ± 31 s; p = 0.001), and ICASR (children 90 ± 27 s vs. adults 47 ± 36 s; p = 0.001) MRTs compared with adults. This is the first study to show slower hypercapnic hyperemic kinetic responses of the ICA in children. The mechanisms determining these differences and the need to consider the duration of hypercapnic exposure when assessing CVR in children should be considered in future studies.

Developmental cerebral hemodynamic adaptations to chronic high-altitude exposure, such as in the Sherpa population, are largely unknown. To examine hemodynamic adaptations in the developing human brain, we assessed common carotid (CCA), internal carotid (ICA), and vertebral artery (VA) flow and middle cerebral artery (MCA) velocity in 25 (9.6 ± 1.0 yr old, 129 ± 9 cm, 27 ± 8 kg, 14 girls) Sherpa children (3,800 m, Nepal) and 25 (9.9 ± 0.7 yr old, 143 ± 7 cm, 34 ± 6 kg, 14 girls) age-matched sea level children (344 m, Canada) during supine rest. Resting gas exchange, blood pressure, oxygen saturation and heart rate were assessed. Despite comparable age, height and weight were lower (both < 0.01) in Sherpa compared with sea level children. Mean arterial pressure, heart rate, and ventilation were similar, whereas oxygen saturation (95 ± 2 vs. 99 ± 1%, < 0.01) and end-tidal Pco (24 ± 3 vs. 36 ± 3 Torr, < 0.01) were lower in Sherpa children. Global cerebral blood flow was ∼30% lower in Sherpa compared with sea level children. This was reflected in a lower ICA flow (283 ± 108 vs. 333 ± 56 ml/min, = 0.05), VA flow (78 ± 26 vs. 118 ± 35 ml/min, < 0.05), and MCA velocity (72 ± 14 vs. 88 ± 14 cm/s, < 0.01). CCA flow was similar between Sherpa and sea level children (425 ± 92 vs. 441 ± 81 ml/min, = 0.52). Scaling flow and oxygen uptake for differences in vessel diameter and body size, respectively, led to the same findings. A lower cerebral blood flow in Sherpa children may reflect specific cerebral hemodynamic adaptations to chronic hypoxia. Cerebral blood flow is lower in Sherpa children compared with children residing at sea level; this may reflect a cerebral hemodynamic pattern, potentially due to adaptation to a hypoxic environment.