A small atmospheric bubble was introduced into a surfactant suspension in a captive bubble surfactometer. After film formation to the equilibrium surface tension at the bubble air-liquid interface, the bulk phase surfactant was depleted by replacing the chamber contents several times with a saline-CaCl2 solution. The remaining film adsorbed at the bubble surface was then compressed stepwise in quasi-static fashion to near zero minimum surface tension. This was followed by a series of quasi-static expansion steps to surface tensions slightly above equilibrium. The surface tension of films from lipid extract surfactants and phospholipid mixtures did not increase in a manner consistent with the presence of a single surface monolayer. After the initial, rapid rise in surface tension at each expansion step, a decrease in surface tension to a new value was observed. This decrease in surface tension is likely due to the adsorption of 'surplus' material from a 'surface-associated reservoir' into the surface active film. The presence of surplus non-monolayer surfactant material in situ at the alveolar surface was also demonstrated by electron microscopy. SP-A acted as a potent promoter for the movement of excess material (equivalent to 2-3 monolayers) at the interface into the surface active film. In contrast, inhibitory serum proteins prevented the formation of a surface-associated reservoir or the adsorption of excess material into a surface active film.