Effects of acute exercise stress on lung cellular response are not well understood. The purpose of this experiment was to determine if exercise (acute and chronic) alters cellular defense pathways and immune cell populations in the lung. Mice were exercised for 45, 90, or 180 minutes to compare acute exercise effects. Other mice exercised regularly (5 d/week, 45 min/day) for 8 weeks to examine chronic adaptations in cellular stress/defense pathways. PCR arrays examined defense pathways in lungs. Innate immune cell populations were identified in lungs and bronchoalveolar lavage fluid. Heat shock proteins were expressed more in acute exercise, but less in chronic. Inflammation regulating genes increased in acute exercise, but not in chronic. Neither condition altered Apoptosis genes expression, although Cdkn1a, which may limit proliferation, increased in acute exercise. Chronic exercise decreased CD45+ population in BALF, but increased it in lungs. Chronic training showed decreased inflammatory monocytes in BALF, but increased alveolar macrophages in the lung. Exercise training might promote an anti-inflammatory environment in the lung. Chronic training may cause lung tissue to adapt to stress and to control inflammation. A shift in immune cells from BALF to lungs may explain reduced viral titer and decreased inflammation with influenza infection in exercise-trained mice.