Open AccessThe effects of acute incremental hypocapnia on the magnitude of neurovascular coupling in healthy participants
Author(s) -
Bader Taylor J.,
Leacy Jack K.,
Keough Joanna R. G.,
CiorogariuIvan AnnaMaria,
Donald Joshua R.,
Marullo Anthony L.,
O’Halloran Ken D.,
Jendzjowsky Nicholas G.,
Wilson Richard J. A.,
Day Trevor A.
Publication year - 2021
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.14952
Subject(s) - hypocapnia , hyperventilation , cardiology , respiratory alkalosis , anesthesia , medicine , cerebral blood flow , respiratory compensation , chemistry , hypercapnia , respiratory system , physical therapy , anaerobic exercise , metabolic acidosis
Abstract The high metabolic demand of cerebral tissue requires that local perfusion is tightly coupled with local metabolic rate (neurovascular coupling; NVC). During chronic altitude exposure, where individuals are exposed to the antagonistic cerebrovascular effects of hypoxia and hypocapnia, pH is maintained through renal compensation and NVC remains stable. However, the potential independent effect of acute hypocapnia and respiratory alkalosis on NVC remains to be determined. We hypothesized that acute steady‐state hypocapnia via voluntary hyperventilation would attenuate the magnitude of NVC. We recruited 17 healthy participants and insonated the posterior cerebral artery (PCA) with transcranial Doppler ultrasound. NVC was elicited using a standardized strobe light stimulus (6 Hz; 5 × 30 s on/off) where absolute delta responses from baseline (BL) in peak, mean, and total area under the curve (tAUC) were quantified. From a BL end‐tidal (P ET )CO 2 level of 36.7 ± 3.2 Torr, participants were coached to hyperventilate to reach steady‐state hypocapnic steps of Δ‐5 Torr (31.6 ± 3.9) and Δ‐10 Torr (26.0 ± 4.0; p < 0.001), which were maintained during the presentation of the visual stimuli. We observed a small but significant reduction in NVC peak (ΔPCAv) from BL during controlled hypocapnia at both Δ‐5 (−1.58 cm/s) and Δ‐10 (−1.37 cm/s), but no significant decrease in mean or tAUC NVC response was observed. These data demonstrate that acute respiratory alkalosis attenuates peak NVC magnitude at Δ‐5 and Δ‐10 Torr P ET CO 2 , equally. Although peak NVC magnitude was mildly attenuated, our data illustrate that mean and tAUC NVC are remarkably stable during acute respiratory alkalosis, suggesting multiple mechanisms underlying NVC.