Airway opening pressure, esophageal pressure, and flow were obtained during relaxed expirations in two normal anesthetized paralyzed dogs. The signal-to-noise ratio in the flow signals was greatly increased by averaging 10 different signals obtained with the same lung inflation volume. Numerical integration of an averaged flow signal then yielded the time course of the volume of the respiratory system above functional residual capacity (the elastic equilibrium volume). Comparison of volume signals obtained with different inflation volumes suggests that the resistance of the respiratory system increases with flow. The flow-volume and semilog volume curves show that expiration is induced by two apparently separate mechanisms: one causes emptying of most of the expired volume over a time interval of much less than 1 s, whereas the other contributes a relatively small amount to the expired volume over a significantly longer time (greater than or equal to 1 s). We postulate the first mechanism to be due to that of the respiratory system behaving like a single unit, with an elastance that is slightly volume dependent, emptying through a single airway which has a resistance that increases with flow. From the nature of airway opening pressure and esophageal pressure measured after occlusion in midexpiration, we conclude that the second mechanism is due to the viscoelastic properties (i.e., creep) of the respiratory system. The properties are manifest mainly in the chest wall.