Rationale: Ventilatory motor output is an important determinant of upper airway patency during sleep.
Objectives: We hypothesized that central hypocapnic hypopnea would lead to increased expiratory upper airway resistance and pharyngeal narrowing during non-REM sleep.
Methods: Noninvasive positive pressure ventilation was used to induce hypocapnic hypopnea in 20 healthy subjects. Expiratory pressure was set at the lowest pressure (2 cm H(2)O), and inspiratory pressure was increased gradually during each 3-minute noninvasive positive pressure ventilation trial by increments of 2 cm H(2)O. Analysis 1 (n = 9) included measured retropalatal cross-sectional area (CSA) using nasopharyngoscope to compare CSA at five points of the respiratory cycle between control (eupneic) and hypopneic breaths. The pharyngeal pressure (P(ph)) was measured using a catheter positioned at the palatal rim. Analysis 2 (n = 11) included measured supraglottic pressure and airflow to compare inspiratory and expiratory upper airway resistance (R(UA)) at peak flow between eupneic and hypopneic breaths.
Measurements and main results: Expiratory CSA during hypopneic breaths was decreased relative to eupnea (CSA at beginning of expiration [BI]: 101.5 +/- 6.3 vs. 121.6 +/- 8.9%; P < 0.05); P(ph)-BI was lower than that generated during eupnea (1.5 +/- 0.3 vs. 3.3 +/- 0.9 cm H(2)O; P < 0.05). Body mass index was an independent predictor of retropalatal narrowing during hypopnea. Hypopnea-R(UA) increased during expiration relative to eupnea (14.0 +/- 5.7 vs. 10.6 +/- 2.5 cm H(2)O/L/s; P = 0.01), with no change in inspiratory resistance.
Conclusions: Expiratory pharyngeal narrowing occurs during central hypocapnic hypopnea. Reduced ventilatory drive leads to increased expiratory, but not inspiratory, upper airway resistance. Central hypopneas are obstructive events because they cause pharyngeal narrowing.