Changes in lung volume and diaphragm muscle activity at sleep onset in obese obstructive sleep apnea patients vs. healthy-weight controls.
Obese obstructive sleep apnea (OSA) patients potentially defend end-expiratory lung volume (EELV) during wakefulness via increased expiratory diaphragmatic activity (eEMG(dia)). A reduction in eEMG(dia) and EELV at sleep onset could, therefore, increase upper airway collapsibility via reduced tracheal traction. The aim of this study was to establish if eEMG(dia) is greater in obese OSA patients vs. healthy-weight controls during wakefulness, and to compare eEMG(dia) and EELV changes at sleep onset between groups as a function of stable breathing, hypopnea vs. apnea events developing within the first few breaths after sleep onset. Eight obese men with OSA and eight healthy-weight men without OSA were studied in the supine position while instrumented with an intraesophageal catheter to measure eEMG(dia) and magnetometer coils to assess changes in EELV. While eEMG(dia) expressed as %maximal activity was not significantly different between groups during wakefulness, OSA patients experienced a greater fall in eEMG(dia) following sleep onset (group × breath, P < 0.001) and a greater decrease when respiratory events accompanied sleep onsets (category × breath, P < 0.001). The decrease in EELV by the third postsleep onset breath was small (OSA, 61.4 ± 8.0 ml, P < 0.001; controls, 34.0 ± 4.2 ml, P < 0.001), with the decrease significantly greater in OSA patients over time (group × breath, P = 0.007). There was a greater decrease with more severe events (category × breath, P < 0.001), with EELV decreasing by 89.6 ± 14.2 ml (P < 0.001) at the onset of apneas in the OSA group. These data support that diaphragm tone and EELV frequently decrease following sleep onset, with greater falls at transitions accompanied by respiratory events. In addition to decrements in upper airway dilator muscle activity, decreasing lung volume potentially contributes to an increased propensity for upper airway collapse in OSA patients at sleep onset.
Stadler
Daniel L
DL
Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, South Australia 5041, Australia. daniel.stadler@health.sa.gov.au
McEvoy
R Doug
RD
Bradley
Jana
J
Paul
Denzil
D
Catcheside
Peter G
PG
D000328:Adult; D016022:Case-Control Studies; D003964:Diaphragm / Q000503:physiopathology*; D006801:Humans; D008168:Lung / Q000503:physiopathology*; D008176:Lung Volume Measurements; D008280:Magnetics; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000503:physiopathology*; D017286:Polysomnography; D011312:Pressure; D015656:Respiratory Mechanics; D012890:Sleep; D012891:Sleep Apnea Syndromes / Q000503:physiopathology*; D016683:Supine Position; D013997:Time Factors