We have used previously characterized models to investigate the reuptake of surfactant from the alveolus. In model 1, rats were swum in a water bath at 33°C for 30 min, which increased tidal volume (VT) ~ 300% and frequency 60%; they were then allowed to rest for up to 4 h. In model 2, rats were exposed to 5% CO2-13% O2-82% N2 for 24 h, which increased both VT and frequency ~ 200%; these rats were then rested for up to 24 h. In both models we harvested a tissue fraction (lamellar bodies, lb) and two alveolar fractions - tubular myelin rich (alv-1) and tubular myelin poor (alv-2). Immediately after swimming, lb-dipalmitoylphosphatidylcholine (DPPClb) was 18% below the control of 0.94 ± 0.037 (SE) mg/g wet lung (n = 24 rats; P < 0.05); this returned to control by 2 h. Whereas DPPCalv-1 was constant at all time points, DPPCalv-2 was increased 50% above the control of 2.68 ± 0.085 mg/g dry lung (n = 27 rats; P < 0.001) immediately and up to 1 h after swimming. It returned to control levels between 2 an 3 h. After gas exposure, DPPC in lb, alv-1 and alv-2 was 33, 64, and 89%, respectively, above controls. All three fractions had normalized after 24 h. Our results demonstrate marked differences in the response of the surfactant system to acute and more prolonged stimuli. Of particular interest was the constancy of alv-1 with swimming, suggesting that it may be the controlled variable. However, the system appeared to be reset by prolonged hyperpnea, a process that may involve an increase in synthesis of surfactant.