Effect of alae nasi activation on maximal nasal inspiratory airflow in humans.

The upper airway is a complicated structure that is usually widely patent during inspiration. However, on inspiration during certain physiological and pathophysiological states, the nares, pharynx, and larynx may collapse. Collapse at these locations occurs when the transmural pressure (Ptm) at a flow-limiting site (FLS) falls below a critical level (Ptm'). On airway collapse, inspiratory airflow is limited to a maximal level (VImax) determined by (-Ptm')/Rus, where Rus is the resistance upstream to the FLS. The airflow dynamics of the upper airway are affected by the activity of its associated muscles. In this study, we examine the modulation of VImax by muscle activity in the nasal airway under conditions of inspiratory airflow limitation. Each of six subjects performed sniffs through one patent nostril (pretreated with an alpha agonist) while flaring the nostril at varying levels of dilator muscle (alae nasi) EMG activity (EMGan). For each sniff, we located the nasal FLS with an airway catheter and determined VImax, Ptm', and Rus. Activation of the alae nasi from the lowest to the highest values of EMGan increased VImax from 422 +/- 156 to 753 +/- 291 ml/s (P < 0.01) and decreased Ptm' from -3.6 +/- 3.0 to -6.0 +/- 4.7 cmH2O (P < 0.05). Activation of the alae nasi had no consistent effect on Rus. VImax was positively correlated with EMGan, and Ptm' was negatively correlated with EMGan in all subjects. Our findings demonstrate that alae nasi activation increases VImax through the nasal airway by decreasing airway collapsibility.