Swimming rats for up to 2 h in water at 34 ± 1°C increased the rate of breathing by 60% and tidal volume by 200-300%. In each case we infused 20 μCi.kg-1 [methyl-3H]choline chloride, via a caudal vein, 3 h prior to the end of swimming. Maximum specific activity of tissue phospholipid (PL) and alveolar PL (PL(alv)) occurred in 1 and 12 h, respectively. Total PL(alv), specific activity of PL(alv) and the percentage of total PL released (%A/T) increased within 10 min of start of swimming and were sustained for at least 2 h of swimming [PL(alv) in mg.g dry lung-1:5 s swim, 7.3 ± 0.96 (mean ± SD; n = 15 rats); 1-h swim, 10.1 ± 1.1 (n = 23 rats)]. After a 1-h swim, PL(alv) returned to control within 4 h. Pretreatment with propranolol hydrochloride (10 mg.kg-1) (P), atropine methyl nitrate (3 mg.kg-1) (A), indomethacin (15 mg.kg-1), and cyproheptadine (1 mg.kg-1) did not alter the increase in PL(alv) with swimming, however, both P and A reduced the increase in specific activity of PL(alv) and %A/T. We suggest that the exercise releases surfactant from two pools: a readily released pool that responds to direct distortion of the alveolar type II cell and a pool that is under sympathetic nervous control.