Nitric oxide (NO) is present in the exhaled breath of humans and experimental animals, but its physiologic role and cellular source(s) remain to be determined. Possible sites of origin are pulmonary endothelial cells and/or resident macrophages. Here we have tested the hypothesis that changes in cardiovascular status can alter the apparent pulmonary excretion of NO. Exercise on a stationary bicycle produced rapid and reversible increases in pulmonary NO excretion rate, and changes in NO excretion rate during exercise were well correlated with observed changes in heart rate. These results suggest that changes in expired NO during exercise are related to corresponding cardiovascular responses.