{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T22:59:18Z","timestamp":1790463558441,"version":"4.1.0"},"reference-count":25,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2000,10,1]]},"abstract":"<jats:p>\n                    We examined the neurocirculatory and ventilatory responses to intermittent asphyxia (arterial O\n                    <jats:sub>2<\/jats:sub>\n                    saturation = 79\u201385%, end-tidal Pco\n                    <jats:sub>2<\/jats:sub>\n                    =3\u20135 Torr above eupnea) in seven healthy humans during wakefulness. The intermittent asphyxia intervention consisted of 20-s asphyxic exposures alternating with 40-s periods of room-air breathing for a total of 20 min. Minute ventilation increased during the intermittent asphyxia period (14.2 \u00b1 2.0 l\/min in the final 5 min of asphyxia vs. 7.5 \u00b1 0.4 l\/min in baseline) but returned to the baseline level within 2 min after completion of the series of asphyxic exposures. Muscle sympathetic nerve activity increased progressively, reaching 175 \u00b1 12% of baseline in the final 5 min of the intervention. Unlike ventilation, sympathetic activity remained elevated for at least 20 min after removal of the chemical stimuli (150 \u00b1 10% of baseline in the last 5 min of the recovery period). Intermittent asphyxia caused a small, but statistically significant, increase in heart rate (64 \u00b1 4 beats\/min in the final 5 min of asphyxia vs. 61 \u00b1 4 beats\/min in baseline); however, this increase was not sustained after the return to room-air breathing. These data demonstrate that relatively short-term exposure to intermittent asphyxia causes sympathetic activation that persists after removal of the chemical stimuli. This carryover effect provides a potential mechanism whereby intermittent asphyxia during sleep could lead to chronic sympathetic activation in patients with sleep apnea syndrome.\n                  <\/jats:p>","DOI":"10.1152\/jappl.2000.89.4.1333","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:57:01Z","timestamp":1513972621000},"page":"1333-1339","source":"Crossref","is-referenced-by-count":89,"title":["Neurocirculatory consequences of intermittent asphyxia in humans"],"prefix":"10.1152","volume":"89","author":[{"given":"Ailiang","family":"Xie","sequence":"first","affiliation":[{"name":"Departments of Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James B.","family":"Skatrud","sequence":"additional","affiliation":[{"name":"Departments of Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David C.","family":"Crabtree","sequence":"additional","affiliation":[{"name":"Departments of Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dominic S.","family":"Puleo","sequence":"additional","affiliation":[{"name":"Departments of Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian M.","family":"Goodman","sequence":"additional","affiliation":[{"name":"William S. 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