{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T08:02:44Z","timestamp":1789545764504,"version":"build-2803163510"},"reference-count":29,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2015,9,30]],"date-time":"2015-09-30T00:00:00Z","timestamp":1443571200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL61388"],"award-info":[{"award-number":["HL61388"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2015,11]]},"abstract":"<jats:sec><jats:title>New Findings<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item>\n<jats:p><jats:bold>What is the central question of this study?<\/jats:bold><\/jats:p>\n<jats:p>Does baroreceptor unloading during passive hyperthermia contribute to increases in ventilation and decreases in end\u2010tidal carbon dioxide during that exposure?<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p><jats:bold>What is the main finding and its importance?<\/jats:bold><\/jats:p>\n<jats:p>Hyperthermic hyperventilation is not mitigated by expanding central blood volume and reloading the cardiopulmonary baroreceptors via rapid saline infusion or by reloading the arterial baroreceptors via phenylephrine administration. The absence of a reduction in ventilation upon reloading the baroreceptors to pre\u2010hyperthermic levels indicates that cardiopulmonary and arterial baroreceptor unloading with hyperthermia is unlikely to contribute to hyperthermic hyperventilation in humans.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>This study tested the hypothesis that baroreceptor unloading during passive hyperthermia contributes to increases in ventilation and decreases in end\u2010tidal partial pressure of carbon dioxide (<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/eph1695-math-0001.png\" xlink:title=\"urn:x-wiley:09580670:media:eph1695:eph1695-math-0001\"\/>) during that exposure. Two protocols were performed, in which healthy subjects underwent passive hyperthermia (increasing intestinal temperature by \u223c1.8\u00b0C) to cause a sustained increase in ventilation and reduction in <jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/eph1695-math-0002.png\" xlink:title=\"urn:x-wiley:09580670:media:eph1695:eph1695-math-0002\"\/>. Upon attaining hyperthermic hyperventilation, in protocol\u00a01 (<jats:italic>n<\/jats:italic>\u00a0=\u00a010; three females) a bolus (19\u00a0\u00b1\u00a02\u00a0ml\u00a0kg<jats:sup>\u22121<\/jats:sup>) of warm (\u223c38\u00b0C) isotonic saline was rapidly (5\u201310\u00a0min) infused intravenously to restore reductions in central venous pressure, whereas in protocol\u00a02 (<jats:italic>n<\/jats:italic>\u00a0=\u00a011; five females) phenylephrine was infused intravenously (60\u2013120\u00a0\u03bcg\u00a0min<jats:sup>\u22121<\/jats:sup>) to return mean arterial pressure to normothermic levels. In protocol\u00a01, hyperthermia increased ventilation (by 2.2\u00a0\u00b1\u00a01.7\u00a0l\u00a0min<jats:sup>\u22121<\/jats:sup>, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01), while reducing <jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/eph1695-math-0003.png\" xlink:title=\"urn:x-wiley:09580670:media:eph1695:eph1695-math-0003\"\/> (by 4\u00a0\u00b1\u00a03\u00a0mmHg, <jats:italic>P<\/jats:italic> = 0.04) and central venous pressure (by 5\u00a0\u00b1\u00a01\u00a0mmHg, <jats:italic>P<\/jats:italic> &lt;0.01). Saline infusion increased central venous pressure by 5\u00a0\u00b1\u00a01 mmHg (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01), restoring it to normothermic values, but did not change ventilation or <jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/eph1695-math-0004.png\" xlink:title=\"urn:x-wiley:09580670:media:eph1695:eph1695-math-0004\"\/> (<jats:italic>P<\/jats:italic>\u00a0&gt;\u00a00.05). In protocol\u00a02, hyperthermia increased ventilation (by 5.0\u00a0\u00b1\u00a02.7\u00a0l\u00a0min<jats:sup>\u22121<\/jats:sup>, <jats:italic>P<\/jats:italic> &lt;0.01) and reduced <jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/eph1695-math-0005.png\" xlink:title=\"urn:x-wiley:09580670:media:eph1695:eph1695-math-0005\"\/> (by 5\u00a0\u00b1\u00a02 mmHg, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01) and mean arterial pressure (by 9\u00a0\u00b1\u00a07\u00a0mmHg, <jats:italic>P<\/jats:italic> &lt;0.01). Phenylephrine infusion increased mean arterial pressure by 12\u00a0\u00b1\u00a03\u00a0mmHg (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01), restoring it to normothermic values, but did not change ventilation or <jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/eph1695-math-0006.png\" xlink:title=\"urn:x-wiley:09580670:media:eph1695:eph1695-math-0006\"\/> (<jats:italic>P<\/jats:italic>\u00a0&gt;\u00a00.05). The absence of a reduction in ventilation upon reloading the cardiopulmonary and arterial baroreceptors to pre\u2010hyperthermic levels indicates that baroreceptor unloading with hyperthermia is unlikely to contribute to hyperthermic hyperventilation in humans.<\/jats:p><\/jats:sec>","DOI":"10.1113\/ep085259","type":"journal-article","created":{"date-parts":[[2015,8,24]],"date-time":"2015-08-24T08:30:58Z","timestamp":1440405058000},"page":"1309-1318","source":"Crossref","is-referenced-by-count":8,"title":["Cardiopulmonary and arterial baroreceptor unloading during passive hyperthermia does not contribute to hyperthermia\u2010induced hyperventilation"],"prefix":"10.1113","volume":"100","author":[{"given":"Rebekah A. I.","family":"Lucas","sequence":"first","affiliation":[{"name":"Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital of Dallas  TX USA"},{"name":"School of Sport, Exercise and Rehabilitation Sciences University of Birmingham  Birmingham UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James","family":"Pearson","sequence":"additional","affiliation":[{"name":"Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital of Dallas  TX USA"},{"name":"Department of Biology University of Colorado at Colorado Springs  Colorado Springs CO USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zachary J.","family":"Schlader","sequence":"additional","affiliation":[{"name":"Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital of Dallas  TX USA"},{"name":"Department of Exercise and Nutrition Sciences University at Buffalo  Buffalo NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Craig G.","family":"Crandall","sequence":"additional","affiliation":[{"name":"Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital of Dallas  TX 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