Loughborough University
Leicestershire, UK
LE11 3TU
+44 (0)1509 263171
Loughborough University

Loughborough University Institutional Repository

Please use this identifier to cite or link to this item: https://dspace.lboro.ac.uk/2134/26919

Title: Effect of hypocapnia on the sensitivity of hyperthermic hyperventilation and the cerebrovascular response in resting heated humans
Authors: Tsuji, Bun
Filingeri, Davide
Honda, Yasushi
Eguchi, Tsubasa
Fujii, Naoto
Kondo, N.
Nishiyasu, Takeshi
Keywords: Hyperpnea
Cerebral blood flow
Issue Date: 2017
Publisher: © American Physiological Society
Citation: TSUJI, B. ... et al, 2017. Effect of hypocapnia on the sensitivity of hyperthermic hyperventilation and the cerebrovascular response in resting heated humans. Journal of Applied Physiology, 124 (1), pp.225-233.
Abstract: Elevating core temperature at rest causes increases in minute ventilation (V̇e), which lead to reductions in both arterial CO2 partial pressure (hypocapnia) and cerebral blood flow. We tested the hypothesis that in resting heated humans this hypocapnia diminishes the ventilatory sensitivity to rising core temperature but does not explain a large portion of the decrease in cerebral blood flow. Fourteen healthy men were passively heated using hot-water immersion (41°C) combined with a water-perfused suit, which caused esophageal temperature (Tes) to reach 39°C. During heating in two separate trials, end-tidal CO2 partial pressure decreased from the level before heating (39.4 ± 2.0 mmHg) to the end of heating (30.5 ± 6.3 mmHg) (P = 0.005) in the Control trial. This decrease was prevented by breathing CO2-enriched air throughout the heating such that end-tidal CO2 partial pressure did not differ between the beginning (39.8 ± 1.5 mmHg) and end (40.9 ± 2.7 mmHg) of heating (P = 1.00). The sensitivity to rising Tes (i.e., slope of the Tes − V̇E relation) did not differ between the Control and CO2-breathing trials (37.1 ± 43.1 vs. 16.5 ± 11.1 l·min−1·°C−1, P = 0.31). In both trials, middle cerebral artery blood velocity (MCAV) decreased early during heating (all P < 0.01), despite the absence of hyperventilation-induced hypocapnia. CO2 breathing increased MCAV relative to Control at the end of heating (P = 0.005) and explained 36.6% of the heat-induced reduction in MCAV. These results indicate that during passive heating at rest ventilatory sensitivity to rising core temperature is not suppressed by hypocapnia and that most of the decrease in cerebral blood flow occurs independently of hypocapnia.
Description: This paper is closed access until 24th January 2019.
Sponsor: This study was supported by the grants from Ministry of Education, Culture, Sports, Science and Technology in Japan and Japan Society for the Promotion of Science.
Version: Accepted for publication
DOI: 10.1152/japplphysiol.00232.2017
URI: https://dspace.lboro.ac.uk/2134/26919
Publisher Link: https://doi.org/10.1152/japplphysiol.00232.2017
ISSN: 8750-7587
Appears in Collections:Closed Access (Design School)

Files associated with this item:

File Description SizeFormat
2017_Hyperventilation_JAP.pdfAccepted version512.98 kBAdobe PDFView/Open


SFX Query

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.