The purpose of this study was to examine the effect of an acute bout of prolonged sitting with and without exercise breaks on cerebrovascular function in 7‐ to 13‐year‐old children. Forty‐two ...children and adolescents were recruited to a crossover trial, with 15 girls (mean age 10.1 ± 2.5 years) and 16 boys (mean age 10.5 ± 1.3 years) completing the two trial conditions: SIT, uninterrupted sitting for 3 h and CYCLE, 3 h of sitting interrupted hourly with a 10‐min moderate intensity exercise break. Cerebrovascular function was measured Pre and Post SIT and CYCLE from blood flow (Q̇${\dot{Q}}$), diameter, and shear rate of the internal carotid artery (ICA) at rest and in response to CO2. Blood velocity in the middle (MCA) and posterior (PCA) cerebral arteries was assessed at rest, during a neurovascular coupling task (NVC) and in response to CO2. We demonstrate that SIT but not CYCLE reduced ICA cerebrovascular reactivity to CO2 (%Δ ICA Q̇${\dot{Q}}$/Δ end‐tidal CO2: SIT: Pre 5.0 ± 2.4%/mmHg to Post 3.3 ± 2.8%/mmHg vs. CYCLE: Pre 4.4 ± 2.3%/mmHg to Post 5.3 ± 3.4%/mmHg, P = 0.05) and slowed the MCA blood velocity onset response time to hypercapnia (SIT: Pre 57.2 ± 32.6 s to Post 76.6 ± 55.2 s, vs. CYCLE: Pre 64.1 ± 40.4 s to Post 52.3 ± 28.8 s, P = 0.05). There were no changes in NVC. Importantly, breaking up prolonged sitting with hourly exercise breaks prevented the reductions in cerebrovascular reactivity to CO2 and the slowed intracranial blood velocity onset response time to hypercapnia apparent with uninterrupted sitting in children.
New Findings
What is the central question of this study?
What are the effects of interrupting prolonged sitting on cerebrovascular function in children?
What is the main finding and its importance?
Prolonged sitting results in declines in cerebrovascular reactivity, a valuable index of cerebrovascular health. Breaking up prolonged sitting with hourly 10 min exercise breaks prevented these changes. These initial findings suggest excessive sedentary behaviour does impact cerebrovascular function in childhood, but taking exercise breaks prevents declines.
With an ageing population and increasing incidence of cerebrovascular disease, an increasing number of patients presenting for routine and emergency surgery have a prior history of stroke. This ...presents a challenge for pre-, intra-, and postoperative management as the neurological risk is considerably higher. Evidence is lacking around anaesthetic practice for patients with vascular neurological vulnerability. Through understanding the pathophysiological changes that occur after stroke, insight into the susceptibilities of the cerebral vasculature to intrinsic and extrinsic factors can be developed. Increasing understanding of post-stroke systemic and cerebral haemodynamics has provided improved outcomes from stroke and more robust secondary prevention, although this knowledge has yet to be applied to our delivery of anaesthesia in those with prior stroke. This review describes the key pathophysiological and clinical considerations that inform clinicians providing perioperative care for patients with a prior diagnosis of stroke.
Exercise has been shown to induce cerebrovascular adaptations. However, the underlying temporal dynamics are poorly understood, and regional variation in the vascular response to exercise has been ...observed in the large cerebral arteries. Here, we sought to measure the cerebrovascular effects of a single 20-min session of moderate-intensity exercise in the one hour period immediately following exercise cessation. We employed transcranial Doppler (TCD) ultrasonography to measure cerebral blood flow velocity (CBFV) in the middle cerebral artery (MCAv) and posterior cerebral artery (PCAv) before, during, and following exercise. Additionally, we simultaneously measured cerebral blood flow (CBF) in the internal carotid artery (ICA) and vertebral artery (VA) before and up to one hour following exercise cessation using Duplex ultrasound. A hypercapnia challenge was used before and after exercise to examine exercise-induced changes in cerebrovascular reactivity (CVR). We found that MCAv and PCAv were significantly elevated during exercise (
= 4.81 × 10
and 2.40 × 10
, respectively). A general linear model revealed that these changes were largely explained by the partial pressure of end-tidal CO
and not a direct vascular effect of exercise. After exercise cessation, there was no effect of exercise on CBFV or CVR in the intracranial or extracranial arteries (all
> 0.05). Taken together, these data confirm that CBF is rapidly and uniformly regulated following exercise cessation in healthy young males.
Abstract only
The rapid hemodynamic changes induced by the initiation of dynamic exercise robustly challenge the regulatory processes which ensure that cerebral perfusion is appropriately maintained. ...We sought to determine whether age alters the cerebrovascular responses to the initiation of dynamic exercise.
Ten young (mean±SD, 23±2 years, 2 women) and eight older (65±3 years, 1 women) individuals performed a 5‐minute bout of semi‐recumbent leg cycling exercise at 75W. Blood pressure, cardiac output, total peripheral resistance (Finometer) and middle cerebral artery blood flow velocity (MCAv: transcranial Doppler ultrasound) were monitored. Gosling pulsatility index (PI) was calculated as; (systolic MCAv–diastolic MCAv)/mean MCAv. Beat‐to‐beat data during exercise were linearly interpolated at 1 Hz.
At baseline, MAP (mean±SEM, young, 87±3; older, 93±4 mmHg), MCAv (young, 57±2; older, 56±3 cm/s) and PI (young, 0.88±0.4; older, 0.92±0.4 cm/s) were not different in young and older groups (P>0.05), while TPR tended to be lower (young, 16±1; older, 21±2 mmHg/L·min
−1
, p=0.08) and CO tended to be higher (young, 5.6±0.4; older, 4.6±4 L·min
−1
; p=0.13) in the young. The initiation of exercise evoked a rapid and sustained increase in cardiac output and fall in total peripheral resistance, that was blunted in the older group. Blood pressure fell transiently at exercise onset, reaching a similar nadir (young, −9.9±2.8; older, −10.0±2.9 mmHg; p>0.05) after a similar duration (15±2; older, 13±2 s; p>0.05) in both groups. MCAv also fell transiently at the initiation of exercise (young, −5.3±1.5; older, −5.1±1.9 cm/s, p>0.05), but the nadir was reached later in the older group (young, 20±2; older, 29±2 s, p<0.05). PI increased rapidly at the onset of exercise in young individuals, but was elevated more sluggishly in older individuals.
Collectively, these findings suggest that older individuals exhibit delayed cerebrovascular adjustments at the onset of exercise.
Support or Funding Information
This research was supported by a National Sciences and Engineering Research Council Discovery Grant and Canadian Research Chair in Cerebrovascular Physiology (PNA), the Swiss National Science Foundation (DF) and the British Heart Foundation (JPF).
ObjectivesRaised intracranial pressure is proposed to be a mediator of acute mountain sickness. However, establishing this is difficult due to the invasive nature of intracranial pressure ...measurement. In this study we used a non-invasive estimate of intracranial pressure, ultrasound of the optic nerve sheath diameter (ONSD), during ascent to high altitude in both low-altitude residents and high-altitude natives.Methods42 (30 low-altitude, 12 high-altitude residents) participants ascended from 1300 to 5050m with ONSD, cerebral blood flow (CBF, duplex ultrasound), and arterial blood gas measurements at 1300, 2700, 3400, 4125 and 5050m. Lake Louise acute mountain sickness scores were collected at 5050m.ResultsAscent to high-altitude was associated with an increase in median IQR ONSD (4.61mm 4.39–5.26 at 1300m to 6.47mm 5.78–7.34 at 5050m). At 5050m, those with more symptoms of acute mountain sickness had larger optic nerve sheath diameters (r =0.47, p=0.015). The increase in ONSD was related to an increase in CBF with altitude (p=0.005). High-altitude residents ascending to altitude had higher baseline ONSD, however this did not increase with altitude as much as low-altitude residents (interaction p=0.0001).ConclusionsIncreased optic nerve sheath diameter with ascent to altitude supports the theory that intracranial pressure rises during ascent to high altitude and that this may contribute to acute mountain sickness. The increases in ONSD are mediated in part by increased cerebral blood flow. The smaller increase in ONSD in Sherpa may protect against acute mountain sickness.
Scientists and clinicians interested in cerebrovascular physiology in humans now have numerous possibilities to monitor, invasively or non-invasively, the oxygenation status of cerebral tissue. ...Monitoring cerebral oxygenation has several utilities; to improve patient outcome, to better understand the mechanisms underlying orthostatic hypotension; to provide insight into functional neurovascular coupling; to evaluate the influence of vasopressors on cerebral oxygen levels in patients under anesthesia; and to study the limitations of exercise tolerance. This themed research topic, through theoretical and experimental papers, covers new and exciting issues related to the study of cerebral oxygenation in health and disease. This e-book includes manuscripts inclusive of original research, methodologies and reviews in the field of integrative physiology, cognitive testing, orthostatic stress, exercise physiology and anesthesia.
PDF
