Deacon-Diaz, N.L.Sands, S.A.McEvoy, R.D.Catcheside, P.G.2019-01-222019-01-222018Journal of applied physiology, 2018; 125(5):1490-14978750-75871522-1601http://hdl.handle.net/2440/117373Reduced ventilatory control stability (elevated loop gain) is a key non-anatomical pathological trait contributing to obstructive sleep apnea (OSA), yet the mechanisms responsible remain unclear. We sought to identify the key factors contributing to elevated loop gain in OSA (controller versus plant contributions) and to examine if abnormalities in these factors persist after OSA treatment. In 15 males (8 OSA, 7 height, weight- and age-matched controls) we measured loop gain, controller gain and plant gain using a pseudorandom binary CO₂ stimulation method during wakefulness. Factors potentially influencing plant gain were also assessed (supine lung volume via helium dilution and spirometry). Measures were repeated 2 and 6 weeks after initiating CPAP. Loop gain was higher in OSA versus controls (LG at 1 cycle/min 0.28 ± 0.04 versus 0.16 ± 0.04, p = 0.046) and the controller exhibited a greater peak response to CO2 and faster roll-off in OSA. OSA patients also exhibited reduced FEV1 and FVC compared to controls (92.2 ± 1.7 versus 102.9 ± 3.5% predicted, p = 0.021; 93.4 ± 3.1 versus 106.6 ± 3.6% predicted, p = 0.015, respectively). There was no effect of treatment on any variable. These findings confirm loop gain is higher in untreated OSA patients than in matched controls, however this was not affected by treatment.enCopyright © 2018 the American Physiological SocietyContinuous positive airway pressure; loop gain; obstructive sleep apneaJournal article003010562010.1152/japplphysiol.00175.20180004514459000152-s2.0-85056278166441367McEvoy, R.D. [0000-0002-5759-0094]Catcheside, P.G. [0000-0002-9372-6788]