Dynamic cerebral autoregulation during exhaustive exercise in humans

2005 ◽  
Vol 288 (3) ◽  
pp. H1461-H1467 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Mads K. Dalsgaard ◽  
Chie C. Yoshiga ◽  
Ellen A. Dawson ◽  
David M. Keller ◽  
...  
Keyword(s):  
Blood Flow ◽  
Phase Shift ◽  
Cerebral Autoregulation ◽  
Low Frequency ◽  
Exhaustive Exercise ◽  
Leg Cycle Ergometry ◽  
Venous Oxygen Saturation ◽  
Transfer Function Gain ◽  
Dynamic Cerebral Autoregulation

We investigated whether dynamic cerebral autoregulation is affected by exhaustive exercise using transfer-function gain and phase shift between oscillations in mean arterial pressure (MAP) and middle cerebral artery (MCA) mean blood flow velocity ( Vmean). Seven subjects were instrumented with a brachial artery catheter for measurement of MAP and determination of arterial Pco2 (PaCO2) while jugular venous oxygen saturation (SvO2) was determined to assess changes in whole brain blood flow. After a 10-min resting period, the subjects performed dynamic leg-cycle ergometry at 168 ± 5 W (mean ± SE) that was continued to exhaustion with a group average time of 26.8 ± 5.8 min. Despite no significant change in MAP during exercise, MCA Vmean decreased from 70.2 ± 3.6 to 57.4 ± 5.4 cm/s, SvO2 decreased from 68 ± 1 to 58 ± 2% at exhaustion, and both correlated to PaCO2 (5.5 ± 0.2 to 3.9 ± 0.2 kPa; r = 0.47; P = 0.04 and r = 0.74; P < 0.001, respectively). An effect on brain metabolism was indicated by a decrease in the cerebral metabolic ratio of O2 to [glucose + one-half lactate] from 5.6 to 3.8 ( P < 0.05). At the same time, the normalized low-frequency gain between MAP and MCA Vmean was increased ( P < 0.05), whereas the phase shift tended to decrease. These findings suggest that dynamic cerebral autoregulation was impaired by exhaustive exercise despite a hyperventilation-induced reduction in PaCO2.

Differential effects of acute hypoxia and high altitude on cerebral blood flow velocity and dynamic cerebral autoregulation: alterations with hyperoxia

2008 ◽  
Vol 104 (2) ◽  
pp. 490-498 ◽  
Author(s):  
Philip N. Ainslie ◽  
Shigehiko Ogoh ◽  
Katie Burgess ◽  
Leo Celi ◽  
Ken McGrattan ◽  
...  
Keyword(s):  
Blood Flow ◽  
Transfer Function ◽  
High Altitude ◽  
Blood Flow Velocity ◽  
Cerebral Autoregulation ◽  
Acute Hypoxia ◽  
Low Frequency ◽  
Frequency Range ◽  
Transfer Function Gain ◽  
Dynamic Cerebral Autoregulation

We hypothesized that 1) acute severe hypoxia, but not hyperoxia, at sea level would impair dynamic cerebral autoregulation (CA); 2) impairment in CA at high altitude (HA) would be partly restored with hyperoxia; and 3) hyperoxia at HA and would have more influence on blood pressure (BP) and less influence on middle cerebral artery blood flow velocity (MCAv). In healthy volunteers, BP and MCAv were measured continuously during normoxia and in acute hypoxia (inspired O2 fraction = 0.12 and 0.10, respectively; n = 10) or hyperoxia (inspired O2 fraction, 1.0; n = 12). Dynamic CA was assessed using transfer-function gain, phase, and coherence between mean BP and MCAv. Arterial blood gases were also obtained. In matched volunteers, the same variables were measured during air breathing and hyperoxia at low altitude (LA; 1,400 m) and after 1–2 days after arrival at HA (∼5,400 m, n = 10). In acute hypoxia and hyperoxia, BP was unchanged whereas it was decreased during hyperoxia at HA (−11 ± 4%; P < 0.05 vs. LA). MCAv was unchanged during acute hypoxia and at HA; however, acute hyperoxia caused MCAv to fall to a greater extent than at HA (−12 ± 3 vs. −5 ± 4%, respectively; P < 0.05). Whereas CA was unchanged in hyperoxia, gain in the low-frequency range was reduced during acute hypoxia, indicating improvement in CA. In contrast, HA was associated with elevations in transfer-function gain in the very low- and low-frequency range, indicating CA impairment; hyperoxia lowered these elevations by ∼50% ( P < 0.05). Findings indicate that hyperoxia at HA can partially improve CA and lower BP, with little effect on MCAv.

Decreased steady-state cerebral blood flow velocity and altered dynamic cerebral autoregulation during 5-h sustained 15% O2 hypoxia

2010 ◽  
Vol 108 (5) ◽  
pp. 1154-1161 ◽  
Author(s):  
Naoko Nishimura ◽  
Ken-ichi Iwasaki ◽  
Yojiro Ogawa ◽  
Ken Aoki
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Steady State ◽  
Cerebral Circulation ◽  
Cerebral Autoregulation ◽  
Low Frequency ◽  
Very Low Frequency ◽  
Increased Risk ◽  
Dynamic Cerebral Autoregulation ◽  
Mild Hypoxia

Effects of hypoxia on cerebral circulation are important for occupational, high-altitude, and aviation medicine. Increased risk of fainting might be attributable to altered cerebral circulation by hypoxia. Dynamic cerebral autoregulation is reportedly impaired immediately by mild hypoxia. However, continuous exposure to hypoxia causes hyperventilation, resulting in hypocapnia. This hypocapnia is hypothesized to restore impaired dynamic cerebral autoregulation with reduced steady-state cerebral blood flow (CBF). However, no studies have examined hourly changes in alterations of dynamic cerebral autoregulation and steady-state CBF during sustained hypoxia. We therefore examined cerebral circulation during 5-h exposure to 15% O2 hypoxia and 21% O2 in 13 healthy volunteers in a sitting position. Waveforms of blood pressure and CBF velocity in the middle cerebral artery were measured using finger plethysmography and transcranial Doppler ultrasonography. Dynamic cerebral autoregulation was assessed by spectral and transfer function analysis. As expected, steady-state CBF velocity decreased significantly from 2 to 5 h of hypoxia, accompanying 2- to 3-Torr decreases in end-tidal CO2 (ETCO2). Furthermore, transfer function gain and coherence in the very-low-frequency range increased significantly at the beginning of hypoxia, indicating impaired dynamic cerebral autoregulation. However, contrary to the proposed hypothesis, indexes of dynamic cerebral autoregulation showed no significant restoration despite ETCO2 reductions, resulting in persistent higher values of very-low-frequency power of CBF velocity variability during hypoxia (214 ± 40% at 5 h of hypoxia vs. control) without significant increases in blood pressure variability. These results suggest that sustained mild hypoxia reduces steady-state CBF and continuously impairs dynamic cerebral autoregulation, implying an increased risk of shortage of oxygen supply to the brain.

Dynamic cerebral autoregulation is preserved during acute head-down tilt

2003 ◽  
Vol 95 (4) ◽  
pp. 1439-1445 ◽  
Author(s):  
William H. Cooke ◽  
Guy L. Pellegrini ◽  
Olga A. Kovalenko
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Autoregulation ◽  
Cerebral Blood Flow Velocity ◽  
Spectral Power ◽  
Low Frequency ◽  
Dynamic Cerebral Autoregulation

Complete ganglion blockade alters dynamic cerebral autoregulation, suggesting links between systemic autonomic traffic and regulation of cerebral blood flow velocity. We tested the hypothesis that acute head-down tilt, a physiological maneuver that decreases systemic sympathetic activity, would similarly disrupt normal dynamic cerebral autoregulation. We studied 10 healthy young subjects (5 men and 5 women; age 21 ± 0.88 yr, height 169 ± 3.1 cm, and weight 76 ± 6.1 kg). ECG, beat-by-beat arterial pressure, respiratory rate, end-tidal CO2 concentration, and middle cerebral blood flow velocity were recorded continuously while subjects breathed to a metronome. We recorded data during 5-min periods and averaged responses from three Valsalva maneuvers with subjects in both the supine and -10° head-down tilt positions (randomized). Controlled-breathing data were analyzed in the frequency domain with power spectral analysis. The magnitude of input-output relations were determined with cross-spectral techniques. Head-down tilt significantly reduced Valsalva phase IV systolic pressure overshoot from 36 ± 4.0 (supine position) to 25 ± 4.0 mmHg (head down) ( P = 0.03). Systolic arterial pressure spectral power at the low frequency decreased from 5.7 ± 1.6 (supine) to 4.4 ± 1.6 mmHg2 (head down) ( P = 0.02), and mean arterial pressure spectral power at the low frequency decreased from 3.3 ± 0.79 (supine) to 2.0 ± 0.38 mmHg2 (head down) ( P = 0.05). Head-down tilt did not affect cerebral blood flow velocity or the transfer function magnitude and phase angle between arterial pressure and cerebral blood flow velocity. Our results show that in healthy humans, mild physiological manipulation of autonomic activity with acute head-down tilt has no effect on the ability of the cerebral vasculature to regulate flow velocity.

scholarly journals Comparing Different Recording Lengths of Dynamic Cerebral Autoregulation: 5 versus 10 Minutes

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Nai-Fang Chi ◽  
Cheng-Yen Wang ◽  
Lung Chan ◽  
Han-Hwa Hu
Keyword(s):  
Phase Shift ◽  
High Frequency ◽  
Cerebral Autoregulation ◽  
Function Analysis ◽  
Low Frequency ◽  
Mean Difference ◽  
Frequency Bands ◽  
Very Low Frequency ◽  
Transfer Function Analysis ◽  
Dynamic Cerebral Autoregulation

We compared the dynamic cerebral autoregulation (dCA) indices between 5- and 10-minute data lengths by analyzing 37 patients with ischemic stroke and 51 controls in this study. Correlation coefficient (Mx) and transfer function analysis were applied for dCA analysis. Mx and phase shift in all frequency bands were not significantly different between 5- and 10-minute recordings [mean difference: Mx = 0.02; phase shift of very low frequency (0.02–0.07 Hz) = 0.3°, low frequency (0.07–0.20 Hz) = 0.6°, and high frequency (0.20–0.50 Hz) = 0.1°]. However, the gains in all frequency bands of a 5-minute recording were slightly but significantly higher than those of a 10-minute recording (mean difference of gain: very low frequency = 0.05 cm/s/mmHg, low frequency = 0.11 cm/s/mmHg, and high frequency = 0.14 cm/s/mmHg). The intraclass correlation coefficients between all dCA indices of 5- and 10-minute recordings were favorable, especially in Mx (0.93), phase shift in very low frequency (0.87), and gain in very low frequency (0.94). The areas under the receiver operating characteristic curve for stroke diagnosis between 5- and 10-minute recordings were not different. We concluded that dCA assessed by using a 5-minute recording is not significantly different from that using a 10-minute recording in the clinical application.

Dynamic cerebral autoregulation remains stable during physical challenge in healthy persons

2003 ◽  
Vol 285 (3) ◽  
pp. H1048-H1054 ◽  
Author(s):  
Miroslaw Brys ◽  
Clive M. Brown ◽  
Harald Marthol ◽  
Renate Franta ◽  
Max J. Hilz
Keyword(s):  
Blood Flow ◽  
Phase Shift ◽  
Physical Exercise ◽  
Cerebral Autoregulation ◽  
Transcranial Doppler Sonography ◽  
Low Frequency ◽  
Stable Phase ◽  
Cerebrovascular Resistance ◽  
Phase Shift Angle ◽  
Shift Angle

The effects of physical activity on cerebral blood flow (CBF) and cerebral autoregulation (CA) have not yet been fully evaluated. There is controversy as to whether increasing heart rate (HR), blood pressure (BP), and sympathetic and metabolic activity with altered levels of CO2 might compromise CBF and CA. To evaluate these effects, we studied middle cerebral artery blood flow velocity (CBFV) and CA in 40 healthy young adults at rest and during increasing levels of physical exercise. We continuously monitored HR, BP, end-expiratory CO2, and CBFV with transcranial Doppler sonography at rest and during stepwise ergometric challenge at 50, 100, and 150 W. The modulation of BP and CBFV in the low-frequency (LF) range (0.04–0.14 Hz) was calculated with an autoregression algorithm. CA was evaluated by calculating the phase shift angle and gain between BP and CBFV oscillations in the LF range. The LF BP-CBFV gain was then normalized by conductance. Cerebrovascular resistance (CVR) was calculated as mean BP adjusted to brain level divided by mean CBFV. HR, BP, CO2, and CBFV increased significantly with exercise. Phase shift angle, absolute and normalized LF BP-CBFV gain, and CVR, however, remained stable. Stable phase shift, LF BP-CBFV gain, and CVR demonstrate that progressive physical exercise does not alter CA despite increasing HR, BP, and CO2. CA seems to compensate for the hemodynamic effects and increasing CO2 levels during exercise.

Abstract WP437: Sleep Apnea and Cerebral Blood Flow: the Role of Autoregulation

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Sara K Rostanski ◽  
Andrew J Westwood ◽  
Mehran Baboli ◽  
Randolph S Marshall
Keyword(s):  
Risk Factor ◽  
Sleep Apnea ◽  
Phase Shift ◽  
Cerebral Autoregulation ◽  
Apnea Hypopnea Index ◽  
Stroke Risk Factor ◽  
Vasomotor Reactivity ◽  
Obstructive Sleep ◽  
Increased Risk ◽  
Dynamic Cerebral Autoregulation

Objective: Obstructive sleep apnea (OSA) is a stroke risk factor and is increasingly recognized as a risk factor for cognitive impairment. Altered cerebral autoregulation may play a role in these relationships. We measured the association between OSA and two forms of cerebral autoregulation: (1) dynamic cerebral autoregulation (DCA), which plays a homeostatic role; and (2) vasomotor reactivity (VMR), which is a measure of cerebrovascular reserve. We hypothesized that both VMR and DCA would be impaired in subjects with OSA. Methods: We recruited subjects with untreated OSA. VMR and DCA were measured with continuous transcranial Doppler (TCD) of the middle cerebral arteries (MCA). DCA was measured with phase shift analysis where lower degrees of phase shift indicate greater impairment; values <24 degrees are abnormal. VMR was measured as % change in MCA velocity in response to 5% CO2 inhalation; values <2% change are abnormal. We assessed the relationship between apnea-hypopnea index (AHI) and autoregulation using bivariate correlations (Pearson coefficient). We also assessed the association between moderate to severe OSA (AHI≥15) and abnormal autoregulation (Fisher’s exact test). Results: Twelve subjects were enrolled; 11 had TCD data. Mean age was 53 (SD 11) and the majority had moderate to severe OSA (median AHI 27, IQR 16-37). Mean VMR (% change in MCA velocity) was 3.1 (SD 0.7); mean phase shift was 34 degrees (SD 15). There was a moderate association between AHI and phase shift (r=-0.40); the correlation with VMR was weaker (r=-0.25). The proportion of subjects with abnormal DCA was greater among those with moderate-severe OSA compared to those with mild OSA (66.7% vs. 0%, p=0.2). No enrolled subjects had abnormal VMR. Conclusion: Moderate to severe OSA is associated with abnormal dynamic cerebral autoregulation and normal vasomotor reactivity. The mechanism underlying this dissociation may involve OSA-mediated inflammation and endothelial dysfunction. Further study may clarify how this dissociation relates to increased risk of cerebral ischemia among patients with OSA.

scholarly journals Dynamic cerebral autoregulation during passive heat stress in humans

2009 ◽  
Vol 296 (5) ◽  
pp. R1598-R1605 ◽  
Author(s):  
David A. Low ◽  
Jonathan E. Wingo ◽  
David M. Keller ◽  
Scott L. Davis ◽  
Jian Cui ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Transfer Function ◽  
High Frequency ◽  
Cerebral Autoregulation ◽  
Low Frequency ◽  
Passive Heating ◽  
Frequency Range ◽  
Very Low Frequency ◽  
Dynamic Cerebral Autoregulation

This study tested the hypothesis that passive heating impairs cerebral autoregulation. Transfer function analyses of resting arterial blood pressure and middle cerebral artery blood velocity (MCA Vmean), as well as MCA Vmean and blood pressure responses to rapid deflation of previously inflated thigh cuffs, were examined in nine healthy subjects under normothermic and passive heat stress (increase core temperature 1.1 ± 0.2°C, P < 0.001) conditions. Passive heating reduced MCA Vmean [change (Δ) of 8 ± 8 cm/s, P = 0.01], while blood pressure was maintained (Δ −1 ± 4 mmHg, P = 0.36). Coherence was decreased in the very-low-frequency range during heat stress (0.57 ± 0.13 to 0.26 ± 0.10, P = 0.001), but was >0.5 and similar between normothermia and heat stress in the low- (0.07–0.20 Hz, P = 0.40) and high-frequency (0.20–0.35 Hz, P = 0.12) ranges. Transfer gain was reduced during heat stress in the very-low-frequency (0.88 ± 0.38 to 0.59 ± 0.19 cm·s−1·mmHg−1, P = 0.02) range, but was unaffected in the low- and high-frequency ranges. The magnitude of the decrease in blood pressure (normothermia: 20 ± 4 mmHg, heat stress: 19 ± 6 mmHg, P = 0.88) and MCA Vmean (13 ± 4 to 12 ± 6 cm/s, P = 0.59) in response to cuff deflation was not affected by the thermal condition. Similarly, the rate of regulation of cerebrovascular conductance (CBVC) after cuff release (0.44 ± 0.22 to 0.38 ± 0.13 ΔCBVC units/s, P = 0.16) and the time for MCA Vmean to recover to precuff deflation baseline (10.0 ± 7.9 to 8.7 ± 4.9 s, P = 0.77) were not affected by heat stress. Counter to the proposed hypothesis, similar rate of regulation responses suggests that heat stress does not impair the ability to control cerebral perfusion after a rapid reduction in perfusion pressure, while reduced transfer function gain and coherence in the very-low-frequency range during heat stress suggest that dynamic cerebral autoregulation is improved during spontaneous oscillations in blood pressure within this frequency range.

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