{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T05:35:35Z","timestamp":1789623335783,"version":"build-2803163510"},"reference-count":77,"publisher":"Wiley","issue":"15","license":[{"start":{"date-parts":[[2022,7,12]],"date-time":"2022-07-12T00:00:00Z","timestamp":1657584000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2022,8]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Humans hyperventilate under heat and cold strain. This hyperventilatory response has detrimental consequences including acid\u2013base dysregulation, dyspnoea, decreased cerebral blood flow and accelerated brain heating. The ventilatory response to hypoxia is exaggerated under whole\u2010body heating and cooling, indicating that altered carotid body function might contribute to thermally mediated hyperventilation. To address whether the carotid body might contribute to heat\u2010 and cold\u2010induced hyperventilation, we indirectly measured carotid body tonic activity via hyperoxia, and carotid body sensitivity via hypoxia, under graded heat and cold strain in 13 healthy participants in a repeated\u2010measures design. We hypothesised that carotid body tonic activity and sensitivity would be elevated in a dose\u2010dependent manner under graded heat and cold strain, thereby supporting its role in driving thermally mediated hyperventilation. Carotid body tonic activity was increased in a dose\u2010dependent manner with heating, reaching 175% above baseline (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.0005), and carotid body suppression with hyperoxia removed all of the heat\u2010induced increase in ventilation (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.9297). Core cooling increased carotid body activity by up to 250% (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.0001), but maximal values were reached with mild cooling and thereafter plateaued. Carotid body sensitivity to hypoxia was profoundly increased by up to 180% with heat stress (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.0097), whereas cooling had no detectable effect on hypoxic sensitivity. In summary, cold stress increased carotid body tonic activity and this effect was saturated with mild cooling, whereas heating had clear dose\u2010dependent effects on carotid body tonic activity and sensitivity. These dose\u2010dependent effects with heat strain indicate that the carotid body probably plays a primary role in driving heat\u2010induced hyperventilation.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp15158-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Humans over\u2010breathe (hyperventilate) when under heat and cold stress, and though this has detrimental physiological repercussions, the mechanisms underlying this response are unknown.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The carotid body, a small organ that is responsible for driving hyperventilation in hypoxia, was assessed under incremental heat and cold strain.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The carotid body drive to breathe, as indirectly assessed by transient hyperoxia, increased in a dose\u2010dependent manner with heating, reaching 175% above baseline; cold stress similarly increased the carotid body drive to breathe, but did not show dose\u2010dependency.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Carotid body sensitivity, as indirectly assessed by hypoxic ventilatory responses, was profoundly increased by 70\u2013180% with mild and severe heat strain, whereas cooling had no detectable effect.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Carotid body hyperactivity and hypersensitivity are two interrelated mechanisms that probably underlie the increased drive to breathe with heat strain, whereas carotid body hyperactivity during mild cooling may play a subsidiary role in cold\u2010induced hyperventilation.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp282918","type":"journal-article","created":{"date-parts":[[2022,6,22]],"date-time":"2022-06-22T12:56:45Z","timestamp":1655902605000},"page":"3603-3624","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Contribution of the carotid body to thermally mediated hyperventilation in humans"],"prefix":"10.1113","volume":"600","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3893-9948","authenticated-orcid":false,"given":"Travis D.","family":"Gibbons","sequence":"first","affiliation":[{"name":"School of Physical Education Sport &amp; Exercise Science University of Otago  Dunedin Otago New Zealand"},{"name":"Centre for Heart, Lung and Vascular Health School of Health and Exercise Science University of British Columbia\u2010Okanagan  Kelowna British Columbia Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jerome A.","family":"Dempsey","sequence":"additional","affiliation":[{"name":"John Rankin Laboratory for Pulmonary Medicine School of Medicine and Public Health University of Wisconsin\u2010Madison  Madison WI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1565-9169","authenticated-orcid":false,"given":"Kate N.","family":"Thomas","sequence":"additional","affiliation":[{"name":"Department of Surgical Sciences University of Otago  Dunedin Otago New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0024-5433","authenticated-orcid":false,"given":"Holly A.","family":"Campbell","sequence":"additional","affiliation":[{"name":"Department of Surgical Sciences University of Otago  Dunedin Otago New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiarna A. 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