Shane A Landry1,2, Christopher Andara1,2, Philip I Terrill3, Simon A Joosten4,5,6, Paul Leong4, Dwayne L Mann3, Scott A Sands7,8, Garun S Hamilton4,5,6, Bradley A Edwards1,2. 1. Sleep and Circadian Medicine Laboratory, Department of Physiology, Monash University, Melbourne, VIC, Australia. 2. School of Psychological Sciences and Monash Institute of Cognitive and Clinical Neurosciences, Monash University, Melbourne, VIC, Australia. 3. School of Information Technology and Electrical Engineering, The University of Queensland, Brisbane, Australia. 4. Monash Lung and Sleep, Monash Medical Centre, Clayton, VIC, Australia. 5. School of Clinical Sciences, Monash University, Melbourne, VIC, Australia. 6. Monash Partners - Epworth, Victoria, Australia. 7. Division of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA. 8. The Alfred and Monash University, Melbourne, VIC, Australia.
Abstract
Study Objectives: The severity of obstructive sleep apnea (OSA) is known to vary according to sleep stage; however, the pathophysiology responsible for this robust observation is incompletely understood. The objective of the present work was to examine how ventilatory control system sensitivity (i.e. loop gain) varies during sleep in patients with OSA. Methods: Loop gain was estimated using signals collected from standard diagnostic polysomnographic recordings performed in 44 patients with OSA. Loop gain measurements associated with nonrapid eye movement (NREM) stage 2 (N2), stage 3 (N3), and REM sleep were calculated and compared. The sleep period was also split into three equal duration tertiles to investigate how loop gain changes over the course of sleep. Results: Loop gain was significantly lower (i.e. ventilatory control more stable) in REM (Mean ± SEM: 0.51 ± 0.04) compared with N2 sleep (0.63 ± 0.04; p = 0.001). Differences in loop gain between REM and N3 (p = 0.095), and N2 and N3 (p = 0.247) sleep were not significant. Furthermore, N2 loop gain was significantly lower in the first third (0.57 ± 0.03) of the sleep period compared with later second (0.64 ± 0.03, p = 0.012) and third (0.64 ± 0.03, p = 0.015) tertiles. REM loop gain also tended to increase across the night; however, this trend was not statistically significant [F(2, 12) = 3.49, p = 0.09]. Conclusions: These data suggest that loop gain varies between REM and NREM sleep and modestly increases over the course of sleep. Lower loop gain in REM is unlikely to contribute to the worsened OSA severity typically observed in REM sleep, but may explain the reduced propensity for central sleep apnea in this sleep stage.
Study Objectives: The severity of obstructive sleep apnea (OSA) is known to vary according to sleep stage; however, the pathophysiology responsible for this robust observation is incompletely understood. The objective of the present work was to examine how ventilatory control system sensitivity (i.e. loop gain) varies during sleep in patients with OSA. Methods: Loop gain was estimated using signals collected from standard diagnostic polysomnographic recordings performed in 44 patients with OSA. Loop gain measurements associated with nonrapid eye movement (NREM) stage 2 (N2), stage 3 (N3), and REM sleep were calculated and compared. The sleep period was also split into three equal duration tertiles to investigate how loop gain changes over the course of sleep. Results: Loop gain was significantly lower (i.e. ventilatory control more stable) in REM (Mean ± SEM: 0.51 ± 0.04) compared with N2 sleep (0.63 ± 0.04; p = 0.001). Differences in loop gain between REM and N3 (p = 0.095), and N2 and N3 (p = 0.247) sleep were not significant. Furthermore, N2 loop gain was significantly lower in the first third (0.57 ± 0.03) of the sleep period compared with later second (0.64 ± 0.03, p = 0.012) and third (0.64 ± 0.03, p = 0.015) tertiles. REM loop gain also tended to increase across the night; however, this trend was not statistically significant [F(2, 12) = 3.49, p = 0.09]. Conclusions: These data suggest that loop gain varies between REM and NREM sleep and modestly increases over the course of sleep. Lower loop gain in REM is unlikely to contribute to the worsened OSA severity typically observed in REM sleep, but may explain the reduced propensity for central sleep apnea in this sleep stage.
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