Traditional concepts of gas transport in the lung cannot explain the adequate alveolar ventilation observed during high-frequency ventilation (HFV) with tidal volumes (VT) less than the anatomic dead space (VD). Different physical mechanisms enhance and limit gas exchange during HFV. Mechanisms enhancing transport include: diffusion, the spontaneous intermingling of the molecules of 2 gases due to Brownian motion; convective mechanisms which depend on bulk flow, such as direct alveolar ventilation, pendelluft, and streaming; and the combined effects of convection and diffusion, often termed augmented transport. Equations describing some of these mechanisms have been incorporated into theorectical models of gas transport which predict that the efficiency of HFV is proportional to faVTb, where f is frequency and b is greater than a. These predictions generally agree with experimental results obtained in healthy animals and humans. However, experimental results in subjects with lung disease show that, at a fixed VT, gas transport efficiency plateaus as f increases. One explanation for this plateau is that in subjects with increased peripheral airway resistance, the upper airways act as a shunt compliance, absorbing a fraction of the delivered VT. Experimental results to date have not confirmed or refuted any specific theory, but it seems likely that gas mixing during HFV is enhanced by a number of the mechanisms mentioned above and that the mechanical properties of the lungs might limit gas transport, especially in patients with peripheral airway obstruction.