Athletes have changes in the lung epithelial cells caused by inhalation of cold and dry air. The exhaled breath condensate contains a number of mediators from the respiratory system and H(2)O(2) is described as a marker of airways inflammation. The aim of this study was to determine the influence of exercise combined with cold air on the H(2)O(2) release in the exhaled breath. Twelve males (23.1 ± 1.5 years) were randomly assigned at 2 different days (1 day rest) to perform a 50 min run (75-80% of their max. heart rate) under normal (N) laboratory (18.1 ± 1.1°C) or cold (C) field condition (-15.2 ± 3.1°C). Before and immediately after each run, the EBC was collected under laboratory conditions and was analyzed amperometrically. Prior to the two runs, H(2)O(2) concentrations were 145.0 ± 31.0 (N) and 160.0 ± 49.1 nmol/L (C) and theoretical release was 70.3 ± 37.1 (N) and 82.6 ± 27.1 pmol/min (C) (p > 0.05). After each run, H(2)O(2) concentration increased significantly to 388.0 ± 22.8 nmol/L (N) and 622.1 ± 44.2 nmol/L (C) (p < 0.05), along with an increase in the theoretical release: 249.2 ± 35.7 pmol/min (N) and 400.9 ± 35.7 pmol/min (C) (p < 0.05). We conclude that release of H(2)O(2) into the EBC takes place under both resting conditions and after exercise. The concentration and release of H(2)O(2) increased after exercise in cold air compared to resting and laboratory conditions, which points to an increase in inflammatory and oxidative stress.