Stimulation of chemo-, irritant, and pulmonary C-fiber receptors reflexly constricts airway smooth muscle and alters ventilation in mature animals. These reflex responses of airway smooth muscle have, however, not been clearly characterized during early development. In this study we compared the maturation of reflex pathways regulating airway smooth muscle tone and ventilation in anesthetized, paralyzed, and artificially ventilated 2- to 3- and 10-wk-old piglets. Tracheal smooth muscle tension was measured from an open tracheal segment by use of a force transducer, and phrenic nerve activity was measured from a proximal cut end of the phrenic nerve. Inhalation of 7% CO2 caused a transient increase in tracheal tension in both age groups, whereas hypoxia caused no airway smooth muscle response in either group. The phrenic responses to 7% CO2 and 12% O2 were comparable in both age groups. Lung deflation and capsaicin (20 μg/kg iv) administration did not alter tracheal tension in the younger piglets but caused tracheal tension to increase by 87 ± 28 and 31 ± 10%, respectively, in the older animals (both P < 0.05). In contrast, phrenic response to both stimuli was comparable between ages: defiation increased phrenic activity while capsaicin induced neural apnea. Laryngeal stimulation did not increase tracheal tension but induced neural apnea in both age groups. These data demonstrate that between 2 and 10 wk of life, piglets exhibit developmental changes in the reflex responses of airway smooth muscle situated in the larger airways in response to irritant and C-fiber but not chemoreceptor stimulation. Reflex airway smooth muscle responses to stimulation of irritant and C-fiber receptors are absent in the younger animals, despite the presence of appropriate phrenic responses. We speculate that weak or absent reflex responses of airway smooth muscle during early development minimize the risk of bronchospasm in response to mechanoreceptor stimulation.