The steady-state responses of upper-airway dilating muscles and diaphragm activity to elevation of lung volume induced by positive end-expiratory pressure loading were studied in 9 pentobarbital-anesthetized dogs with vagus nerves intact. The early and late effects of 5 min of expiratory threshold loads upon upper airway dilating muscle activity (the alae nasi, the genioglossus and the posterior cricoarytenoid) were compared to their effects on diaphragm activity. During resting O2 breathing, application of 5 and 10 cm H2 0.05). No qualitative differences were found in the upper-airway dilating muscles and diaphragm responses to expiratory threshold loads when the animals breathed 3 or 7% CO2 in O2, compared to when they inspired 100% O2. Furthermore, no differences were found in the electrical activity of the upper-airway dilating muscles and diaphragm at any given end-tidal CO2 when unloaded responses were compared with loaded responses during progressive hypercapnia. However, positive end-expiratory pressure loading caused significant prolongation of expiratory duration, which gradually returned toward control levels when the loads were maintained. In animals who developed periodic breathing by increasing levels of anesthesia, positive end-expiratory pressure loading eliminated the periodicity and made the pattern of breathing regular. Based on these results, it can be concluded that under the conditions of these experiments, increases in lung volume produced by expiratory threshold loads do not reduce the activity of upper-airway dilating muscles. The maintenance of the electrical activity of the upper-airway dilating muscles might be caused by excitatory reflex mechanisms or central habituation.