UPPER AIRWAY MUSCLE-ACTIVITY AND THE THORACIC VOLUME DEPENDENCE OF UPPER AIRWAY-RESISTANCE

Although a thoracic volume dependence of upper airway resistance and caliber is known to exist in seated subjects, the mechanisms mediating this phenomenon are unknown. To test the hypothesis that actively altered end-expiratory lung volume (EELV) affects upper airway resistance in the supine position and to explore the mechanisms of any EELV-induced resistance changes, we studied five normal males during wakefulness. Supraglottic upper airway resistance (Ruaw) was calculated at an inspiratory flow of 0.1 l/s. The genioglossal electromyogram was obtained with indwelling wire electrodes and processed as moving time average. End-tidal CO2 was monitored by infrared analyzer. Observations were made during four 20-breath voluntary maneuvers: two at high and two at low EELV in each subject. Each maneuver was preceded by a control period at functional residual capacity. At high lung volume the EELV was increased by 2.23 +/- 0.54 (SD) liters; Ruaw decreased to 67.8 +/- 35.1 % of control, while tonic and phasic genioglossal activities declined to 79.0 +/- 23.1 and 72.4 +/- 29.8%, respectively. At low lung volume the EELV was decreased by 0.86 +/- 0.23 liters. Ruaw increased to 178.2 +/- 186.8 %, while tonic and phasic genioglossal activities increased to 243.0 +/- 139.3 and 249.1 +/- 146.3 %, respectively (P < 0.0001 for all). The findings were not explained by CO2 perturbations or respiratory pattern. Multiple linear regression analysis indicated that the genioglossal responses blunted the EELV-induced changes in upper airway patency. We conclude that actively mediated increases in EELV in the supine position are associated with reduced Ruaw, decreases in EELV are associated with increased Ruaw, and genioglossal activity is not the means by which these relationships occur. The generation of tension in muscles linking the thorax to the upper airway and/or the transmission of force via the trachea may explain the observations. These findings suggest that fluctuations in EELV attendant to respiratory instability during sleep may predispose to upper airway occlusion.