{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T17:54:37Z","timestamp":1787507677994,"version":"build-2736575974"},"reference-count":75,"publisher":"Wiley","license":[{"start":{"date-parts":[[2025,10,19]],"date-time":"2025-10-19T00:00:00Z","timestamp":1760832000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"abstract":"\n Abstract<\/jats:title>\n \n Hyperventilation\u2010induced alterations in acid\u2010base buffering play a crucial role in resetting the cerebrovascular and ventilatory control during high\u2010altitude acclimatisation. This study examines the relationship between cerebrovascular CO\n 2<\/jats:sub>\n reactivity, ventilatory CO\n 2<\/jats:sub>\n sensitivity and acid\u2010base balance during a 10 h hypoxic exposure. We assessed resting venous pH and bicarbonate concentrations [HCO\n 3<\/jats:sub>\n \u2212<\/jats:sup>\n ], middle cerebral artery velocity (MCAv; transcranial Doppler ultrasound) and ventilatory () responses during hyperoxic rebreathing in 27 healthy individuals (13 females) at 0, 2, 4 and 8\u00a0h of 10 h exposures to normobaric normoxia (fraction of inspired O\n 2<\/jats:sub>\n (): 0.21) and normobaric hypoxia (: 0.117, simulated altitude of 5000\u00a0m) in a randomised, single\u2010blinded manner. The MCAv\u2010 and \u2010CO\n 2<\/jats:sub>\n relationships were analysed using sigmoidal and segmental linear regression fitting, respectively. Compared to normoxia hypoxia progressively increased venous pH and decreased venous [HCO\n 3<\/jats:sub>\n \u2212<\/jats:sup>\n ] throughout the 10\u00a0h exposure (\n P<\/jats:italic>\n < 0.001 for both). We observed a progressive decrease in the ventilatory recruitment threshold (VRT) with hypoxia across the day (\n d\u00a0=\u00a0<\/jats:italic>\n 0.9,\n P<\/jats:italic>\n < 0.001\n vs<\/jats:italic>\n . normoxia), along with an increased \u2010CO\n 2<\/jats:sub>\n slope by \u223c0.4 l\/min\/mmHg (\n d\u00a0=\u00a0<\/jats:italic>\n 0.3,\n P\u00a0=\u00a0<\/jats:italic>\n 0.039). The slope of the MCAv\u2010CO\n 2<\/jats:sub>\n response was moderately increased with hypoxia by 0.5 cm\/s\/mmHg across all time points (\n d\u00a0=\u00a0<\/jats:italic>\n 0.5,\n P\u00a0=\u00a0<\/jats:italic>\n 0.006), whereas the midpoint of the MCAv\u2010CO\n 2<\/jats:sub>\n response was unchanged (\n P\u00a0=\u00a0<\/jats:italic>\n 0.401). Our data support the role of altered blood acid\u2010base buffering in the resetting of the ventilatory CO\n 2<\/jats:sub>\n sensitivity to a lower operating point. Because we did not observe a concurrent leftward shift in the MCAv\u2010CO\n 2<\/jats:sub>\n response, we attribute this to the lagging compensation of respiratory alkalosis within the cerebrospinal fluid compartment.\n \n \n image<\/jats:alt-text>\n <\/jats:graphic>\n <\/jats:boxed-text>\n <\/jats:p>\n <\/jats:sec>\n \n Key points<\/jats:title>\n \n \n \n Acid\u2010base balance plays an important role in the control of cerebral blood flow and ventilation, but the compensation of hypoxia\u2010induced respiratory alkalosis in cerebrospinal fluid is slower than that within the arterial compartment.<\/jats:p>\n <\/jats:list-item>\n \n \n In this study we hypothesized that the rates of resetting between the cerebrovascular and ventilatory responsiveness to CO\n 2<\/jats:sub>\n would be different during 10 h exposure to normobaric hypoxia.\n <\/jats:p>\n <\/jats:list-item>\n \n \n We found a progressive leftward shift in the ventilatory response to hyperoxic rebreathing, which appears to be linked to changes in blood acid\u2010base balance during early hypoxic exposure. In contrast we did not observe a resetting of cerebrovascular response to CO\n 2<\/jats:sub>\n during the 10 h exposure period.\n <\/jats:p>\n <\/jats:list-item>\n \n \n Our data demonstrate a dissociation in the rate of resetting between the cerebrovascular and ventilatory responsiveness to CO\n 2<\/jats:sub>\n during early hypoxic exposure. We speculate that these differences are due to the slower compensatory metabolic acidosis in the cerebrospinal fluid compared to the arterial\/venous compartments.\n <\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1113\/jp288240","type":"journal-article","created":{"date-parts":[[2025,10,20]],"date-time":"2025-10-20T00:54:04Z","timestamp":1760921644000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["The role of acid\u2010base balance in cerebrovascular and ventilatory responses to CO\n 2<\/sub>\n during 10 h normobaric hypoxia"],"prefix":"10.1113","author":[{"given":"Holly","family":"Barclay","sequence":"first","affiliation":[{"name":"Department of paediatrics, Nelson Hospital Te Whatu Ora \u2013 Health New Zealand New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saptarshi","family":"Mukerji","sequence":"additional","affiliation":[{"name":"Emergency Department, Hutt Hospital Te Whatu Ora \u2013 Health New Zealand New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9776-7501","authenticated-orcid":false,"given":"Bengt","family":"Kayser","sequence":"additional","affiliation":[{"name":"Institute of Sport Sciences University of Lausanne Lausanne Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4413-5615","authenticated-orcid":false,"given":"Jui\u2010Lin","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Physiology, Manaaki Manawa \u2013 The Centre for Heart Research Faculty of Medical & Health Sciences University of Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2025,10,19]]},"reference":[{"issue":"1","key":"e_1_2_7_2_1","doi-asserted-by":"crossref","first-page":"175","DOI":"10.1113\/EP088938","article-title":"Respiratory alkalinization and posterior cerebral artery dilatation predict acute mountain sickness severity during 10 h normobaric hypoxia","volume":"106","author":"Barclay H.","year":"2021","journal-title":"Experimental Physiology"},{"issue":"12","key":"e_1_2_7_3_1","doi-asserted-by":"crossref","first-page":"3039","DOI":"10.1113\/jphysiol.2011.206052","article-title":"The cerebrovascular response to carbon dioxide in humans","volume":"589","author":"Battisti\u2010Charbonney A.","year":"2011","journal-title":"The Journal of Physiology"},{"issue":"1","key":"e_1_2_7_4_1","doi-asserted-by":"crossref","first-page":"367","DOI":"10.1113\/jphysiol.1989.sp017578","article-title":"The ventilatory CO2 sensitivities from Read's rebreathing method and the steady\u2010state method are not equal in man","volume":"411","author":"Berkenbosch A.","year":"1989","journal-title":"The Journal of Physiology"},{"key":"e_1_2_7_5_1","volume-title":"Barometic Pressure","author":"Bert P.","year":"1943"},{"issue":"13","key":"e_1_2_7_6_1","doi-asserted-by":"crossref","first-page":"2455","DOI":"10.1113\/jphysiol.2010.187211","article-title":"Peripheral chemoreceptors determine the respiratory sensitivity of central chemoreceptors to CO(2)","volume":"588","author":"Blain G. 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