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

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

乗用カート使用によるゴルフラウンドでの血圧，脈拍の変化

Regular aerobic physical activity increases exercise capacity and plays an important role in prevention of cardiovascular disease. Our study aimed at evaluation of level of exercise intensity during playing golf using a self-driving golf cart with monitoring both heart rates and blood pressure. Seven healthy middle-aged and older men （ 49 years old， SD: 6，1） performed playing golf with monitoring Holter-ECG and blood pressure using a golf cart and also performed doing their routine job with monitoring Holter-ECG and blood pressure. The mean heart rates （ 107 beats/min， SD:18） on playing golf moderately and significantly elevated in compared with the mean heart rates （ 82 beats/min， SD: 14） on doing routine job. The mean systolic blood pressure （ 131 mmHg， SD: 16） on playing golf significantly higher than the mean systolic blood pressure（ 123 mmHg， SD: 15） on doing routine job. However， there was no difference between the mean diastolic blood pressure （ 82 mmHg， SD: 14） on playing golf and the mean diastolic blood pressure （ 86 mmHg， SD: 11） on doing routine job. In comparison with doing routine job， systolic blood pressure at starting time of playing golf just before the tee shot was significantly elevated probably due to excitation of sympathetic nerve system. We suggest that playing golf even if using a self-driving golf cart is suitable and recommendable exercise for prevention of disease

Onset responses of ventilation and cerebral blood flow to hypercapnia in humans: rest and exercise

The respiratory and cerebrovascular reactivity to changes in arterial Pco2 (\documentclass[10pt]{article} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{pmc} \usepackage[Euler]{upgreek} \pagestyle{empty} \oddsidemargin -1.0in \begin{document} \begin{equation*}{\mathrm{Pa}}_{{\mathrm{CO}}_{2}}\end{equation*}\end{document}) is an important mechanism that maintains CO2 or pH homeostasis in the brain. It remains unclear, however, how cerebrovascular CO2 reactivity might influence the respiratory chemoreflex. The purpose of the present study was therefore to examine the interaction between onset responses of the respiratory chemoreflex and middle cerebral artery (MCA) mean blood velocity (Vmean) to hypercapnia (5.0% CO2-40% O2-balance N2) at rest and during dynamic exercise (∼1.0 l/min O2 consumption). Each onset response was evaluated using a single-exponential regression model consisting of the response time latency [CO2-response delay (t0)] and time constant (τ). At rest, t0 and τ data indicated that the MCA Vmean onset response was faster than the ventilatory (V̇e) response (P < 0.001). In contrast, during exercise, t0 of V̇e and MCA Vmean onset responses were decreased. In addition, despite the enhanced \documentclass[10pt]{article} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{pmc} \usepackage[Euler]{upgreek} \pagestyle{empty} \oddsidemargin -1.0in \begin{document} \begin{equation*}{\mathrm{Pa}}_{{\mathrm{CO}}_{2}}\end{equation*}\end{document} response to CO2 administration (P = 0.014), τ of MCA Vmean tended to increase during exercise (P = 0.054), whereas τ of V̇e decreased (P = 0.015). These findings indicate that 1) at rest, faster washout of CO2 via cerebral vasodilation results in a reduced activation of the central chemoreflex and subsequent reduced V̇e onset response, and 2) during exercise, despite higher rates of increasing \documentclass[10pt]{article} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{pmc} \usepackage[Euler]{upgreek} \pagestyle{empty} \oddsidemargin -1.0in \begin{document} \begin{equation*}{\mathrm{Pa}}_{{\mathrm{CO}}_{2}}\end{equation*}\end{document}, the lack of change in the onset response of cerebral blood flow and reduced washout of CO2 may act to augment the V̇e onset response

Linear and nonlinear identification of the carotid sinus baroreflex in the very low‐frequency range

Abstract Since the arterial baroreflex system is classified as an immediate control system, the focus has been on analyzing its dynamic characteristics in the frequency range between 0.01 and 1 Hz. Although the dynamic characteristics in the frequency range below 0.01 Hz are not expected to be large, actual experimental data are scant. The aim was to identify the dynamic characteristics of the carotid sinus baroreflex in the frequency range down to 0.001 Hz. The carotid sinus baroreceptor regions were isolated from the systemic circulation, and carotid sinus pressure (CSP) was changed every 10 s according to Gaussian white noise with a mean of 120 mmHg and standard deviation of 20 mmHg for 90 min in anesthetized Wistar‐Kyoto rats (n = 8). The dynamic gain of the linear transfer function relating CSP to arterial pressure (AP) at 0.001 Hz tended to be greater than that at 0.01 Hz (1.060 ± 0.197 vs. 0.625 ± 0.067, p = 0.080), suggesting that baroreflex control was largely maintained at 0.001 Hz. Regarding nonlinear analysis, a second‐order Uryson model predicted AP with a higher R2 value (0.645 ± 0.053) than a linear model (R2 = 0.543 ± 0.057, p = 0.025) or a second‐order Volterra model (R2 = 0.589 ± 0.055, p = 0.045) in testing data. These pieces of information may be used to create baroreflex models that can add a component of autonomic control to a cardiovascular digital twin for predicting acute hemodynamic responses to treatments and tailoring individual treatment strategies

A novel approach for evaluating the effects of odor stimulation on dynamic cardiorespiratory functions.

We aimed to develop a novel method to quantitatively evaluate the effects of odor stimulation on cardiorespiratory functions over time, and to examine the potential usefulness of clinical aromatherapy. Eighteen subjects participated. Nine people were assigned to each of the two resting protocols. Protocol 1: After resting for 2 min in a sitting position breathing room air, the subject inhaled either air or air containing sweet marjoram essential oil from the Douglas bag for 6 min, Protocol 2: After resting for 5 min in a supine position, the subject inhaled the essential oil for 10 min, and then recovered for 10 min breathing room air. All subjects inhaled the essential oil through a face mask attached to one-way valve, and beat-to-beat heart rate (HR) and arterial blood pressure (BP) as well as breath-by-breath respiratory variables were continuously recorded. In both protocols, during fragrance inhalation of the essential oil, time-dependent decrease in mean BP and HR were observed (P<0.05). During post-inhalation recovery, the significant fragrance-induced bradycardic effect lasted at least 5 min (- 3.1 ± 3.9% vs. pre-inhalation baseline value, p<0.05). The mean BP response at the start of odor stimulation was approximated by a first-order exponential model. However, such fragrance-induced changes were not observed in the respiratory variables. We established a novel approach to quantitatively and accurately evaluate the effects of quantitative odor stimulation on dynamic cardiorespiratory functions, and the duration of the effect. This methodological approach may be useful for scientific evaluation of aromatherapy as an approach to integrated medicine, and the mechanisms of action of physiological effects in fragrance compounds

Effects of walking in water on gut hormone concentrations and appetite: comparison with walking on land

The effects of water exercise on gut hormone concentrations and appetite currently remain unclear. The aim of the present study was to investigate the effects of treadmill walking in water on gut hormone concentrations and appetite. Thirteen men (mean ± s.d. age: 21.6 ± 2.2 years, body mass index: 22.7 ± 2.8 kg/m2, peak oxygen uptake (VO2peak): 49.8 ± 7.8 mL/kg per min) participated in the walking in water and on land challenge. During the study period, ratings of subjective feelings of hunger, fullness, satiety and motivation to eat were reported on a 100-mm visual analog scale. A test meal was presented after walking, and energy intake (EI) was calculated. Blood samples were obtained during both trials to measure glucagon-like peptide-1 (GLP-1), peptide YY (PYY) and acylated ghrelin (AG) concentrations. Hunger scores (How hungry do you feel?) were significantly lower during the water trial than during the land trial (P < 0.05). No significant differences were observed in EI between water and land trials. GLP-1 concentrations were significantly higher in the water trial than in the land trial (P < 0.05). No significant differences were observed in PYY concentrations between water and land trials. AG concentrations were significantly lower in the water trial than in the land trial (P < 0.01). In conclusion, changes in gut hormone concentrations during walking in water contribute to the exercise-induced suppression of appetite and provide novel information on the influence of walking in water on the acute regulation of appetite