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Intermittent hypoxia-induced inflammation is postulated to promote AHVR enhancement in OSA, although the role of inflammation in intermittent hypoxia-induced respiratory changes in humans has not been examined. Thus, this study assessed the role of inflammation in intermittent hypoxia-induced respiratory plasticity in healthy humans.<\/jats:p><jats:p>In a double-blind, placebo-controlled, randomised crossover study design, 12 males were exposed to 6\u2005h of intermittent hypoxia on three occasions. Prior to intermittent hypoxia exposures, participants ingested (for 4\u200a\u2005days) either placebo or the nonsteroidal anti-inflammatory drugs indomethacin (nonselective cyclooxygenase (COX) inhibitor) and celecoxib (selective COX-2 inhibitor). Pre- and post-intermittent hypoxia resting ventilation, AHVR, AHCVR and serum concentration of the pro-inflammatory cytokine tumour necrosis factor (TNF)-\u03b1 were assessed.<\/jats:p><jats:p>Pre-intermittent hypoxia resting ventilation, AHVR, AHCVR and TNF-\u03b1 concentrations were similar across all three conditions (p\u22650.093). Intermittent hypoxia increased resting ventilation and the AHVR similarly across all conditions (p=0.827), while the AHCVR was increased (p=0.003) and TNF-\u03b1 was decreased (p=0.006) with only selective COX-2 inhibition.<\/jats:p><jats:p>These findings indicate that inflammation does not contribute to human intermittent hypoxia-induced respiratory plasticity. Moreover, selective COX-2 inhibition augmented the AHCVR following intermittent hypoxia exposure, suggesting that selective COX-2 inhibition could exacerbate OSA severity by increasing ventilatory instability.<\/jats:p>","DOI":"10.1183\/09031936.00007415","type":"journal-article","created":{"date-parts":[[2015,6,12]],"date-time":"2015-06-12T03:06:55Z","timestamp":1434078415000},"page":"1072-1083","update-policy":"https:\/\/doi.org\/10.1183\/ers-crossmark-policy","source":"Crossref","is-referenced-by-count":13,"title":["Human intermittent hypoxia-induced respiratory plasticity is not caused by inflammation"],"prefix":"10.1183","volume":"46","author":[{"given":"Andrew 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