{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T07:56:18Z","timestamp":1793692578281,"version":"4.5.1"},"reference-count":79,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2013,7,1]]},"abstract":"<jats:p>\n                    To determine how the obstructive sleep apnea (OSA) patient's pathophysiological traits predict the success of the treatment aimed at stabilization or increase in respiratory motor outputs, we studied 26 newly diagnosed OSA patients [apnea-hypopnea index (AHI) 42 \u00b1 5 events\/h with 92% of apneas obstructive] who were treated with O\n                    <jats:sub>2<\/jats:sub>\n                    supplementation, an isocapnic rebreathing system in which CO\n                    <jats:sub>2<\/jats:sub>\n                    was added only during hyperpnea to prevent transient hypocapnia, and a continuous rebreathing system. We also measured each patient's controller gain below eupnea [change in minute volume\/change in end-tidal Pco\n                    <jats:sub>2<\/jats:sub>\n                    (\u0394V\u0307e\/\u0394Pet\n                    <jats:sub>\n                      CO\n                      <jats:sub>2<\/jats:sub>\n                    <\/jats:sub>\n                    )], CO\n                    <jats:sub>2<\/jats:sub>\n                    reserve (eupnea-apnea threshold Pet\n                    <jats:sub>\n                      CO\n                      <jats:sub>2<\/jats:sub>\n                    <\/jats:sub>\n                    ), and plant gain (\u0394Pet\n                    <jats:sub>\n                      CO\n                      <jats:sub>2<\/jats:sub>\n                    <\/jats:sub>\n                    \/\u0394V\u0307e), as well as passive upper airway closing pressure (Pcrit). With isocapnic rebreathing, 14\/26 reduced their AHI to 31 \u00b1 6% of control ( P &lt; 0.01) (responder); 12\/26 did not show significant change (nonresponder). The responders vs. nonresponders had a greater controller gain (6.5 \u00b1 1.7 vs. 2.1 \u00b1 0.2 l\u00b7min\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7mmHg\n                    <jats:sup>\u22121<\/jats:sup>\n                    , P &lt; 0.01) and a smaller CO\n                    <jats:sub>2<\/jats:sub>\n                    reserve (1.9 \u00b1 0.3 vs. 4.3 \u00b1 0.4 mmHg, P &lt; 0.01) with no differences in Pcrit (\u22120.1 \u00b1 1.2 vs. 0.2 \u00b1 0.9 cmH\n                    <jats:sub>2<\/jats:sub>\n                    O, P &gt; 0.05). Hypercapnic rebreathing (+4.2 \u00b1 1 mmHg Pet\n                    <jats:sub>\n                      CO\n                      <jats:sub>2<\/jats:sub>\n                    <\/jats:sub>\n                    ) reduced AHI to 15 \u00b1 4% of control ( P &lt; 0.001) in 17\/21 subjects with a wide range of CO\n                    <jats:sub>2<\/jats:sub>\n                    reserve. Hyperoxia (SaO\n                    <jats:sub>2<\/jats:sub>\n                    \u223c95\u201398%) reduced AHI to 36 \u00b1 11% of control in 7\/19 OSA patients tested. We concluded that stabilizing central respiratory motor output via prevention of transient hypocapnia prevents most OSA in selected patients with a high chemosensitivity and a collapsible upper airway, whereas increasing respiratory motor output via moderate hypercapnia eliminates OSA in most patients with a wider range of chemosensitivity and CO\n                    <jats:sub>2<\/jats:sub>\n                    reserve. Reducing chemosensitivity via hyperoxia had a limited and unpredictable effect on OSA.\n                  <\/jats:p>","DOI":"10.1152\/japplphysiol.00064.2013","type":"journal-article","created":{"date-parts":[[2013,4,18]],"date-time":"2013-04-18T22:25:18Z","timestamp":1366323918000},"page":"22-33","source":"Crossref","is-referenced-by-count":67,"title":["Effects of stabilizing or increasing respiratory motor outputs on obstructive sleep apnea"],"prefix":"10.1152","volume":"115","author":[{"given":"Ailiang","family":"Xie","sequence":"first","affiliation":[{"name":"James B. Skatrud Laboratory of Pulmonary and Sleep Medicine, William S. Middleton Memorial Veterans Affairs Hospital, Madison, Wisconsin;"},{"name":"Department of Population Health Sciences, University of Wisconsin, Madison, Wisconsin; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mihaela","family":"Teodorescu","sequence":"additional","affiliation":[{"name":"James B. Skatrud Laboratory of Pulmonary and Sleep Medicine, William S. Middleton Memorial Veterans Affairs Hospital, Madison, Wisconsin;"},{"name":"Department of Medicine, University of Wisconsin, Madison, Wisconsin;"},{"name":"Middleton Memorial Veterans Hospital, Madison, Wisconsin"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David F.","family":"Pegelow","sequence":"additional","affiliation":[{"name":"James B. Skatrud Laboratory of Pulmonary and Sleep Medicine, William S. Middleton Memorial Veterans Affairs Hospital, Madison, Wisconsin;"},{"name":"Department of Population Health Sciences, University of Wisconsin, Madison, Wisconsin; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mihai C.","family":"Teodorescu","sequence":"additional","affiliation":[{"name":"James B. Skatrud Laboratory of Pulmonary and Sleep Medicine, William S. Middleton Memorial Veterans Affairs Hospital, Madison, Wisconsin;"},{"name":"Middleton Memorial Veterans Hospital, Madison, Wisconsin"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuansheng","family":"Gong","sequence":"additional","affiliation":[{"name":"James B. Skatrud Laboratory of Pulmonary and Sleep Medicine, William S. Middleton Memorial Veterans Affairs Hospital, Madison, Wisconsin;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica E.","family":"Fedie","sequence":"additional","affiliation":[{"name":"James B. Skatrud Laboratory of Pulmonary and Sleep Medicine, William S. Middleton Memorial Veterans Affairs Hospital, Madison, Wisconsin;"},{"name":"Department of Population Health Sciences, University of Wisconsin, Madison, Wisconsin; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jerome A.","family":"Dempsey","sequence":"additional","affiliation":[{"name":"James B. 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