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Dynamic cerebral carbon dioxide reactivity at rest and during exercise

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The cerebral vasculature is highly sensitive to direct arterial carbon dioxide tension (PaCO2) changes. Hypocapnia causes cerebral vasoconstriction, while hypercapnia causes cerebral vasodilation to maintain the brain tissue PCO2 within narrow limits. The cerebral blood flow (CBF) responses to PaCO2 changes should be quick, but the cerebral vasculature sensitivity as cerebral CO2 is measured during steady‐state vascular responses. Therefore, the CBF time response to PaCO2 changes remains unknown. The purpose of this study was to examine dynamic cerebral CO2 reactivity at rest and during exercise using the frequency domain analysis.Seven healthy young subjects participated in the study. At rest and during exercise (30% VO2max and cycling exercise), the dynamic CO2 reactivity was calculated based on the transfer function analysis between the end‐tidal CO2 (PETCO2) and the middle cerebral artery mean blood velocity (MCAvm), using a binary white‐noise sequence (0%–7% inspired CO2 fraction). Dynamic characteristics of the respiratory controller showed a low‐pass filter characteristic for regulating ventilation, and the dynamic gain was decreased gradually to 0.7 at 0.02 Hz. However, the gain from PETCO2 to MCAvm (dynamic CO2 reactivity) remained reasonably constant up to 0.02 Hz. Moreover, it did not change during exercise.These findings suggest that the dynamic cerebral CO2 reactivity is reflected in slow to fast PaCO2 changes, and does not change during exercise. In terms of CO2 homeostasis, the cerebral CO2 reactivity may be a more important physiological mechanism to adapt to fast CO2 changes than the ventilatory response to PaCO2 changes.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Title: Dynamic cerebral carbon dioxide reactivity at rest and during exercise
Description:
The cerebral vasculature is highly sensitive to direct arterial carbon dioxide tension (PaCO2) changes.
Hypocapnia causes cerebral vasoconstriction, while hypercapnia causes cerebral vasodilation to maintain the brain tissue PCO2 within narrow limits.
The cerebral blood flow (CBF) responses to PaCO2 changes should be quick, but the cerebral vasculature sensitivity as cerebral CO2 is measured during steady‐state vascular responses.
Therefore, the CBF time response to PaCO2 changes remains unknown.
The purpose of this study was to examine dynamic cerebral CO2 reactivity at rest and during exercise using the frequency domain analysis.
Seven healthy young subjects participated in the study.
At rest and during exercise (30% VO2max and cycling exercise), the dynamic CO2 reactivity was calculated based on the transfer function analysis between the end‐tidal CO2 (PETCO2) and the middle cerebral artery mean blood velocity (MCAvm), using a binary white‐noise sequence (0%–7% inspired CO2 fraction).
Dynamic characteristics of the respiratory controller showed a low‐pass filter characteristic for regulating ventilation, and the dynamic gain was decreased gradually to 0.
7 at 0.
02 Hz.
However, the gain from PETCO2 to MCAvm (dynamic CO2 reactivity) remained reasonably constant up to 0.
02 Hz.
Moreover, it did not change during exercise.
These findings suggest that the dynamic cerebral CO2 reactivity is reflected in slow to fast PaCO2 changes, and does not change during exercise.
In terms of CO2 homeostasis, the cerebral CO2 reactivity may be a more important physiological mechanism to adapt to fast CO2 changes than the ventilatory response to PaCO2 changes.
This abstract is from the Experimental Biology 2019 Meeting.
There is no full text article associated with this abstract published in The FASEB Journal.

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