EFFECT OF ALAE NASI ACTIVATION ON MAXIMAL NASAL INSPIRATORY AIR-FLOW IN HUMANS

The upper airway is a complicated structure that is usually widely pat ent during inspiration. However, on inspiration during certain physiol ogical and pathophysiological states, the nares, pharynx, and larynx m ay collapse. Collapse at these locations occurs when the transmural pr essure (Ptm) at a flow-limiting site (FLS) falls below a critical leve l (Ptm'). On airway collapse, inspiratory airflow is limited to a maxi mal level (VImax) determined by (-Ptm')/Rus, where Rus is the resistan ce upstream to the FLS. The airflow dynamics of the upper airway are a ffected by the activity of its associated muscles. In this study, we e xamine the modulation of V(over dot)I-max by muscle activity in the na sal 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 lo cated the nasal FLS with an airway catheter and determined V(over dot) I-max, Ptm', and Rus. Activation of the alae nasi from the lowest to t he highest values of EMGan increased V(over dot)I-max from 422 +/- 156 to 753 +/- 291 ml/s (P < 0.01) and decreased Ptm' from -3.6 +/- 3.0 t o -6.0 +/- 4.7 cmH(2)O (P < 0.05). Activation of the alae nasi had no consistent effect on Rus. V(over dot)I-max was positively correlated w ith EMGan, and Ptm' was negatively correlated with EMGan in all subjec ts. Our findings demonstrate that alae nasi activation increases V(ove r dot)I-max through the nasal airway by decreasing airway collapsibili ty.