title: Mechanisms used to restore ventilation after partial upper airway collapse during sleep in humans.
abstract: BACKGROUND
  Most patients with obstructive sleep apnoea (OSA) can restore airflow after an obstructive respiratory event without arousal at least some of the time. The mechanisms that enable this ventilatory recovery are unclear but probably include increased upper airway dilator muscle activity and/or changes in respiratory timing. The aims of this study were to compare the ability to recover ventilation and the mechanisms of compensation following a sudden reduction of continuous positive airway pressure (CPAP) in subjects with and without OSA.
  
  
  METHODS
  Ten obese patients with OSA (mean (SD) apnoea-hypopnoea index 62.6 (12.4) events/h) and 15 healthy non-obese non-snorers were instrumented with intramuscular genioglossus electrodes and a mask/pneumotachograph which was connected to a modified CPAP device that could deliver either continuous positive or negative pressure. During stable non-rapid eye movement sleep the CPAP was repeatedly reduced 2-10 cm H2O below the level required to eliminate flow limitation and was held at this level for 5 min or until arousal from sleep occurred.
  
  
  RESULTS
  During reduced CPAP the increases in genioglossus activity (311.5 (49.4)% of baseline in subjects with OSA and 315.4 (76.2)% of baseline in non-snorers, p = 0.9) and duty cycle (123.8 (3.9)% of baseline in subjects with OSA and 118.2 (2.8)% of baseline in non-snorers, p = 0.4) were similar in both groups, yet patients with OSA could restore ventilation without cortical arousal less often than non-snorers (54.1% vs 65.7% of pressure drops, p = 0.04). When ventilatory recovery did not occur, genioglossus muscle and respiratory timing changes still occurred but these did not yield adequate pharyngeal patency/ventilation.
  
  
  CONCLUSIONS
  Compensatory mechanisms (increased genioglossus muscle activity and/or duty cycle) often restore ventilation during sleep but may be less effective in obese patients with OSA than in non-snorers.
authors.affiliation: Sleep Disorders Program @ BIDMC, 75 Francis St, Boston, Massachusetts 02115, USA. ajordan@rics.bwh.harvard.edu
authors.forename: Amy S
authors.initials: AS
authors.lastname: Jordan
authors.forename: Andrew
authors.initials: A
authors.lastname: Wellman
authors.forename: Raphael C
authors.initials: RC
authors.lastname: Heinzer
authors.forename: Yu-Lun
authors.initials: YL
authors.lastname: Lo
authors.forename: Karen
authors.initials: K
authors.lastname: Schory
authors.forename: Louise
authors.initials: L
authors.lastname: Dover
authors.forename: Shiva
authors.initials: S
authors.lastname: Gautam
authors.forename: Atul
authors.initials: A
authors.lastname: Malhotra
authors.forename: David P
authors.initials: DP
authors.lastname: White
mesh_terms: D000328:Adult; D000368:Aged; D045422:Continuous Positive Airway Pressure; D006801:Humans; D008875:Middle Aged; D009765:Obesity / Q000503:physiopathology*; D012132:Respiratory Muscles / Q000502:physiology; D012143:Respiratory Physiological Phenomena; D020181:Sleep Apnea, Obstructive / Q000503:physiopathology* / Q000628:therapy