Cerebrovascular regulation is not blunted during mental stress

Abstract

In this study, we examined the effects of acute mental stress on cerebrovascular function.Sixteen participants (aged 23 ± 4 years; five female) were exposed to low and high mental stress using simple arithmetic (counting backwards from 1000) and more complex arithmetic (serial subtraction of 13 from a rapidly changing four-digit number), respectively. During consecutive conditions of baseline, low stress and high stress, end-tidal partial pressure of CO 2 (P ET,CO 2 ) was recorded at normocapnia (37 ± 3 mmHg) and clamped at two elevated levels (P < 0.01): 41 ± 1 and 46 ± 1 mmHg. Mean right middle cerebral artery blood velocity (MCAv mean ; transcranial Doppler ultrasound), right prefrontal cortex haemodynamics (near-infrared spectroscopy) and mean arterial blood pressure (MAP; finger photoplethysmography) were measured continuously.Cerebrovascular hypercapnic reactivity (ΔMCAv mean /ΔP ET,CO 2 ), cerebrovascular conductance (CVC; MCAv mean /MAP), CVC CO 2 reactivity (ΔCVC/ΔP ET,CO 2 ) and total peripheral resistance (MAP/cardiac output) were calculated. Acute high mental stress increased MCAv mean by 7 ± 7%, and more so at higher P ET,CO 2 (32 ± 10%; interaction, P = 0.03), illustrating increased sensitivity to CO 2 (i.e. its major regulator). High mental stress also increased MAP (17 ± 9%; P ≤ 0.01), coinciding with increased near-infrared spectroscopy-derived prefrontal haemoglobin volume and saturation measures. High mental stress elevated both cerebrovascular hypercapnic and conductance reactivities (main effect of stress, P ≤ 0.04). These findings indicate that the cerebrovascular response to acute high mental stress results in a coordinated regulation between multiple processes.

Indomethacin markedly blunts cerebral perfusion and reactivity, with little cognitive consequence in healthy young and older adults

“…Participants breathed through a leak‐free respiratory mask (Hans‐Rudolf 8980; Hans‐Rudolf Inc., Kansas City, MO, USA) attached to a turbine and two‐way valve, as described in Shoemaker et al . (2019a). Partial pressure of end‐tidal CO 2 () was measured continuously using an online gas analyser (Model CD‐3A Carbon Dioxide Analyser; AEI Technologies, Pittsburgh, PA, USA).…”

Impact of Age on Cognitive Testing Practice Effects and Cardiorespiratory Responses

“…Studies with larger sample size and including assessments of blood flow responses to cognitive testing in different age groups with impaired or normal cognition are needed to define further the relationships between cognitive training effects and cardiorespiratory responses. Physiologically, mental challenges during cognitive testing may stimulate blood flows to muscle ( Barcroft et al, 1960 ; Widegren et al, 2010 ), skin ( Fencl et al, 1959 ) and brain ( Shoemaker et al, 2019 ). Resting cardiac output ( Guo et al, 2005 ), cerebral tissue oxygenation ( Liu et al, 2020 ) and middle cerebral artery flow velocity ( Liu et al, 2020 ) are lower in older than younger adults despite similar resting heart rates.…”

The Clamping of End-Tidal Carbon Dioxide Does Not Influence Cognitive Function Performance During Moderate Hyperthermia With or Without Skin Temperature Manipulation

“…Lastly, this study is limited by not having a measure of intracranial pressure or cerebral perfusion, which are influenced by changes in MAP and vascular resistance (for review see: Numan et al, 2014 ). Recently, Shoemaker et al, (2019) determined that, under hypercapnia in thermoneutral conditions, CO 2 is the primary driver for changes in MCA v as opposed to MAP changes that occur during acute mental stress caused by performing a subtraction task. In the current study, it is unlikely that there were differences in cerebral perfusion as MAP remained relatively unchanged throughout heating, as well as participants remained in the semi-recumbent posture throughout heating to reduce the impact of positional changes on MAP and cerebral perfusion ( Nelson et al, 2011 ; Numan et al, 2014 ).…”