{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T20:15:34Z","timestamp":1774124134461,"version":"3.50.1"},"reference-count":53,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2006,1]]},"abstract":"<jats:p> To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired Po<jats:sub>2<\/jats:sub>. We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O<jats:sub>2<\/jats:sub> saturation = 78\u201380%), and hyperoxia (inspired O<jats:sub>2<\/jats:sub> fraction = 50\u201352%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sighlike breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 \u00b1 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 \u00b1 0.8 s; P &lt; 0.05), whereas hyperoxia prolonged it (71.5 \u00b1 13.8 s; P &lt; 0.01). The apneic threshold end-tidal Pco<jats:sub>2<\/jats:sub> (Pet<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub>) was defined as the Pet<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub> at the onset of apnea. During hypoxia, the apneic threshold Pet<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub> was higher (38.9 \u00b1 1.7 Torr; P &lt; 0.01) compared with normoxia (35.8 \u00b1 1.1; Torr); during hyperoxia, it was lower (33.0 \u00b1 0.8 Torr; P &lt; 0.05). Furthermore, the difference between the eupneic Pet<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub> and apneic threshold Pet<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub> was smaller during hypoxia (3.0 \u00b1 1.0 Torr P &lt; 001) and greater during hyperoxia (10.6 \u00b1 0.8 Torr; P &lt; 0.05) compared with normoxia (8.0 \u00b1 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO<jats:sub>2<\/jats:sub> below the eupneic Pet<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub> was increased by hypoxia (3.44 \u00b1 0.63 l\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7Torr<jats:sup>\u22121<\/jats:sup>; P &lt; 0.05) and decreased by hyperoxia (0.63 \u00b1 0.04 l\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7Torr<jats:sup>\u22121<\/jats:sup>; P &lt; 0.05) compared with normoxia (0.79 \u00b1 0.05 l\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7Torr<jats:sup>\u22121<\/jats:sup>). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors. <\/jats:p>","DOI":"10.1152\/japplphysiol.00440.2005","type":"journal-article","created":{"date-parts":[[2005,9,23]],"date-time":"2005-09-23T00:23:56Z","timestamp":1127435036000},"page":"171-177","source":"Crossref","is-referenced-by-count":47,"title":["Influence of arterial O<sub>2<\/sub> on the susceptibility to posthyperventilation apnea during sleep"],"prefix":"10.1152","volume":"100","author":[{"given":"Ailiang","family":"Xie","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James B.","family":"Skatrud","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dominic S.","family":"Puleo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jerome A.","family":"Dempsey","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.266.6.R1951"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1979.46.4.843"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1983.sp014906"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1164\/ajrccm.153.6.8665047"},{"key":"R5","unstructured":"Bouverot P, Flandrois R, Puccinelli R, and Dejours P. 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