Acute Gravitational Stress Selectively Impairs Dynamic Cerebrovascular Reactivity in the Anterior Circulation Independent of Changes to the Central Respiratory Chemoreflex

Cerebrovascular reactivity (CVR) to changes in the partial pressure of arterial carbon dioxide (PaCO(2)) is an important mechanism that maintains CO(2) or pH homeostasis in the brain. To what extent this is influenced by gravitational stress and corresponding implications for the regulation of cerebral blood flow (CBF) remain unclear. The present study examined the onset responses of pulmonary ventilation (V̇(E)) and anterior middle (MCA) and posterior (PCA) cerebral artery mean blood velocity (V(mean)) responses to acute hypercapnia (5% CO(2)) to infer dynamic changes in the central respiratory chemoreflex and cerebrovascular reactivity (CVR), in supine and 50° head-up tilt (HUT) positions. Each onset response was evaluated using a single-exponential regression model consisting of the response time latency [CO(2)-response delay (t(0))] and time constant (τ). Onset response of V̇(E) and PCA V(mean) to changes in CO(2) was unchanged during 50° HUT compared with supine (τ: V̇(E), p = 0.707; PCA V(mean), p = 0.071 vs. supine) but the MCA V(mean) onset response was faster during supine than during 50° HUT (τ: p = 0.003 vs. supine). These data indicate that gravitational stress selectively impaired dynamic CVR in the anterior cerebral circulation, whereas the posterior circulation was preserved, independent of any changes to the central respiratory chemoreflex. Collectively, our findings highlight the regional heterogeneity underlying CBF regulation that may have translational implications for the microgravity (and hypercapnia) associated with deep-space flight notwithstanding terrestrial orthostatic diseases that have been linked to accelerated cognitive decline and neurodegeneration

Dynamic cerebral autoregulation during cognitive task:Effect of hypoxia

Changes in cerebral blood flow (CBF) subsequent to alterations in the partial pressures of oxygen and carbon dioxide can modify dynamic cerebral autoregulation (CA). While cognitive activity increases CBF, the extent to which it impacts CA remains to be established. In the present study we determined whether dynamic CA would decrease during a cognitive task and whether hypoxia would further compound impairment. Fourteen young healthy subjects performed a simple Go/No-go task during normoxia and hypoxia (inspired O2 fraction = 12%), and the corresponding relationship between mean arterial pressure (MAP) and mean middle cerebral artery blood velocity (MCA Vmean) was examined. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated with transfer function analysis. While MCA Vmean increased during the cognitive activity ( P &lt; 0.001), hypoxia did not cause any additional changes ( P = 0.804 vs. normoxia). Cognitive performance was also unaffected by hypoxia (reaction time, P = 0.712; error, P = 0.653). A decrease in the very low- and low-frequency phase shift (VLF and LF; P = 0.021 and P = 0.01) and an increase in LF gain were observed ( P = 0.037) during cognitive activity, implying impaired dynamic CA. While hypoxia also increased VLF gain ( P &lt; 0.001), it failed to cause any additional modifications in dynamic CA. Collectively, our findings suggest that dynamic CA is impaired during cognitive activity independent of altered systemic O2 availability, although we acknowledge the interpretive complications associated with additional competing, albeit undefined, inputs that could potentially distort the MAP-MCA Vmean relationship. NEW &amp; NOTEWORTHY During normoxia, cognitive activity while increasing cerebral perfusion was shown to attenuate dynamic cerebral autoregulation (CA) yet failed to alter reaction time, thereby questioning its functional significance. No further changes were observed during hypoxia, suggesting that impaired dynamic CA occurs independently of altered systemic O2 availability. However, impaired dynamic CA may reflect a technical artifact, given the confounding influence of additional inputs that could potentially distort the mean arterial pressure-mean middle cerebral artery blood velocity relationship. </jats:p

Relationship between Aortic Compliance and Impact of Cerebral Blood Flow Fluctuation to Dynamic Orthostatic Challenge in Endurance Athletes

Aorta effectively buffers cardiac pulsatile fluctuation generated from the left ventricular (LV) which could be a mechanical force to high blood flow and low-resistance end-organs such as the brain. A dynamic orthostatic challenge may evoke substantial cardiac pulsatile fluctuation via the transient increases in venous return and stroke volume (SV). Particularly, this response may be greater in endurance-trained athletes (ET) who exhibit LV eccentric remodeling. The aim of this study was to determine the contribution of aortic compliance to the response of cerebral blood flow fluctuation to dynamic orthostatic challenge in ET and age-matched sedentary (SED) young healthy men. ET (n = 10) and SED (n = 10) underwent lower body negative pressure (LBNP) (−30 mmHg for 4 min) stimulation and release the pressure that initiates a rapid regain of limited venous return and consequent increase in SV. The recovery responses of central and middle cerebral arterial (MCA) hemodynamics from the release of LBNP (~15 s) were evaluated. SV (via Modeflow method) and pulsatile and systolic MCA (via transcranial Doppler) normalized by mean MCA velocity (MCAv) significantly increased after the cessation of LBNP in both groups. ET exhibited the higher ratio of SV to aortic pulse pressure (SV/AoPP), an index of aortic compliance, at the baseline compared with SED (P < 0.01). Following the LBNP release, SV was significantly increased in SED by 14 ± 7% (mean ± SD) and more in ET by 30 ± 15%; nevertheless, normalized pulsatile, systolic, and diastolic MCAv remained constant in both groups. These results might be attributed to the concomitant with the increase in aortic compliance assessed by SV/AoPP. Importantly, the increase in SV/AoPP following the LBNP release was greater in ET than in SED (P < 0.01), and significantly correlated with the baseline SV/AoPP (r = 0.636, P < 0.01). These results suggest that the aortic compliance in the endurance athletes is able to accommodate the additional SV and buffer the potential increase in pulsatility at end-organs such as the brain

Impact of Short-Term Training Camp on Aortic Blood Pressure in Collegiate Endurance Runners

To investigate the influence of short-term vigorous endurance training on aortic blood pressure (BP), pulse wave analysis was performed in 36 highly trained elite collegiate endurance runners before and after a 7-day intense training camp. Subjects participated three training sessions per day, which mainly consisted of long distance running and sprint training to reach the daily target distance of 26 km. After the camp, they were divided into two groups based on whether the target training was achieved. Aortic systolic BP, pulse pressure, and tension-time index (TTI, a surrogate index of the myocardial oxygen demand) were significantly elevated after the camp in the accomplished group but not in the unaccomplished group, whereas the brachial BP remained unchanged in both groups. The average daily training distance was significantly correlated with the changes in aortic systolic BP (r = 0.608, p = 0.0002), pulse pressure (r = 0.415, p = 0.016), and TTI (r = 0.438, p = 0.011). These results suggest that aortic BP is affected by a short-term vigorous training camp even in highly trained elite endurance athletes presumably due to a greater training volume compared to usual

Does respiratory drive modify the cerebral vascular response to changes in end‐tidal carbon dioxide?

What is the central question of this study? An interaction exists between the regulatory systems of respiration and cerebral blood flow (CBF), because of the same mediator (carbon dioxide, CO ) for both physiological systems. The present study examined whether the traditional method for determining cerebrovascular reactivity to CO (cerebrovascular reactivity; CVR) is modified by changes in respiration. What is the main finding and its importance? CVR was modified by voluntary changes in respiration during hypercapnia. This finding suggests that an alteration in the respiratory system may under- or over-estimate CVR determined by traditional methods in healthy adults.The cerebral vasculature is sensitive to changes in the arterial partial pressure of carbon dioxide (CO ). This physiological mechanism has been well established as a cerebrovascular reactivity to CO (CVR). However, arterial CO may not be an independent variable in the traditional method to assess CVR since the cerebral blood flow (CBF) response is partly affected by the activation of respiratory drive or higher centers in the brain. We hypothesized that CVR is modified by changes in respiration. To test our hypothesis, in the present study, ten young healthy subjects performed hyper- or hypo-ventilation to change end-tidal CO (P CO ) under different concentrations of CO gas inhalation (0, 2.0, 3.5%). We measured middle cerebral artery mean blood flow velocity (MCAVm) by transcranial Doppler to identify the CBF response to change in P CO during each condition. At each F CO condition, P CO was significantly altered by changes in ventilation, and MCA Vm changed accordingly. However, the relationship between changes in MCV Vm and P CO as a response curve of CVR was reset upwards and downwards by hypo- and hyper-ventilation, respectively, compared with CVR during normal-ventilation. The findings of the present study may provide the possibility that an alteration in respiration under- or over-estimates CVR determined by the traditional methods

Effects of Mild Orthostatic Stimulation on Cerebral Pulsatile Hemodynamics

The augmented cerebral hemodynamic pulsatility could lead to the elevated risk of cerebrovascular disease. To determine the impact of an acute orthostatic challenge on a pulsatile component of cerebral hemodynamics, mild lower body negative pressure (LBNP, -30 mmHg) was applied to 29 men. Middle cerebral artery blood flow velocity (MCAv) was measured by transcranial Doppler technique. Stroke volume (SV) was estimated by the Modelflow method with adjustment by the Doppler ultrasound-measured SV at rest. SV, peak and pulsatile MCAv, and pulsatility index were significantly lower during the LBNP stimulation than those at the baseline (e.g., supine resting) (P &lt; 0.05 for all), whereas mean arterial pressure and mean MCAv remained unchanged. The change in SV with the LBNP stimulation significantly correlated with corresponding changes in peak and pulsatile MCAv (r = 0.617, P &lt; 0.001; r = 0.413, P = 0.026, respectively). These results suggest that pulsatile components of cerebrovascular hemodynamics are dampened during the transient period of orthostatic challenge (as simulated using LBNP) when compared to supine rest, and which is partly due to the modified SV