{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T07:21:35Z","timestamp":1788247295075,"version":"build-2803163510"},"reference-count":55,"publisher":"Wiley","issue":"20","license":[{"start":{"date-parts":[[2012,9,13]],"date-time":"2012-09-13T00:00:00Z","timestamp":1347494400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:title>Key points<\/jats:title>\n                  <jats:p>\n                    <jats:list list-type=\"explicit-label\">\n                      <jats:list-item>\n                        <jats:p>\n                          In awake humans, when CO\n                          <jats:sub>2<\/jats:sub>\n                          is maintained above normal levels, exposure to acute intermittent hypoxia causes a sustained elevation in ventilation that persists when normoxic breathing is resumed.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          In this study we have demonstrated that when CO\n                          <jats:sub>2<\/jats:sub>\n                          is maintained above normal levels, exposure to acute continuous hypoxia also causes a sustained elevation in ventilation when normoxic breathing is resumed.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>This sustained elevation in ventilation following both acute intermittent hypoxia and acute continuous hypoxia is maintained by mechanisms other than increased activity of the carotid body.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>These results help develop our understanding of respiratory control in humans and may aid future development of treatments for respiratory control disorders, such as obstructive sleep apnoea.<\/jats:p>\n                      <\/jats:list-item>\n                    <\/jats:list>\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Abstract\u2002<\/jats:bold>\n                    In awake humans, long\u2010term facilitation of ventilation (vLTF) following acute intermittent hypoxia (AIH) is only expressed if CO\n                    <jats:sub>2<\/jats:sub>\n                    is maintained above normocapnic levels. vLTF has not been reported following acute continuous hypoxia (ACH) and it is not known whether this might be unmasked by elevated CO\n                    <jats:sub>2<\/jats:sub>\n                    . Twelve healthy participants completed three trials. In all trials end\u2010tidal pressure of CO\n                    <jats:sub>2<\/jats:sub>\n                    was elevated 4\u20135 mmHg above normocapnic levels. During Trial 1 (AIH) participants were exposed to eight 4 min episodes of hypoxia. During Trial 2 (ACH) participants were exposed to continuous hypoxia for 32 min. In Trial 3 (Control) participants were exposed to euoxia throughout. To assess the contribution of the carotid body (CB) in observed ventilatory responses, CB afferent discharge before and after each trial was transiently inhibited with hyperoxia. Minute ventilation (\n                    <jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/TJP_5288_mu1.gif\" xlink:title=\"inline image\"\/>\n                    ) increased following all trials, but was significantly greater in Trials 1 and 2 when compared with Trial 3 (Trial 1: 4.96 \u00b1 0.87, Trial 2: 5.07 \u00b1 0.7, Trial 3: 2.55 \u00b1 0.98 l min\n                    <jats:sup>\u22121<\/jats:sup>\n                    ,\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.05). Hyperoxia attenuated\n                    <jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/TJP_5288_mu2.gif\" xlink:title=\"inline image\"\/>\n                    to a similar extent in baseline and recovery in all trials (Trial 1: 3.0 \u00b1 0.57\n                    <jats:italic>vs<\/jats:italic>\n                    . 3.27 \u00b1 0.68, Trial 2: 1.97 \u00b1 0.62\n                    <jats:italic>vs<\/jats:italic>\n                    . 2.56 \u00b1 0.62, Trial 3: 2.23 \u00b1 0.49\n                    <jats:italic>vs<\/jats:italic>\n                    . 2.15 \u00b1 0.55 l min\n                    <jats:sup>\u22121<\/jats:sup>\n                    ,\n                    <jats:italic>P<\/jats:italic>\n                    &gt; 0.05). Data are means \u00b1 SEM. In awake humans with elevated CO\n                    <jats:sub>2<\/jats:sub>\n                    , ACH evokes a sustained increase in ventilation that is comparable to that evoked by AIH. However, a gradual positive drift in ventilation in response to elevated CO\n                    <jats:sub>2<\/jats:sub>\n                    accounts for approximately half of this apparent vLTF. Additionally, our data support the view that the CB is not directly involved in maintaining vLTF.\n                  <\/jats:p>","DOI":"10.1113\/jphysiol.2012.236109","type":"journal-article","created":{"date-parts":[[2012,7,23]],"date-time":"2012-07-23T23:00:24Z","timestamp":1343084424000},"page":"5151-5165","source":"Crossref","is-referenced-by-count":39,"title":["Long\u2010term facilitation of ventilation following acute continuous hypoxia in awake humans during sustained hypercapnia"],"prefix":"10.1113","volume":"590","author":[{"given":"Harry S.","family":"Griffin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keith","family":"Pugh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Prem","family":"Kumar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George 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