Stimulation of central and peripheral chemoreceptors increases inspiratory and expiratory motor outputs significantly. With respect to the expiratory component, studies demonstrated that a group of neurons in the parafacial respiratory group (pFRG) are critical for the processing of abdominal expiratory response to these metabolic challenges. Besides, it has been suggested that excitatory and inhibitory mechanisms determine the level of excitation of the pFRG expiratory neurons and then the strength of abdominal muscle contraction. In this regard, we hypothesized that vagal afferent information may modulate the magnitude of expiratory response to hypercapnia and hypoxia. To elucidate this hypothesis, we used anesthetized (urethane, 1.2 g/kg), tracheostomized, spontaneously-breathing male Wistar rats (290-320 g), in which we recorded the electromyographic activity of diaphragm (DIA) and oblique abdominal (ABD) muscles as well as the air flow in response to hypercapnia (5 min 10% CO2) or hypoxia (1 min 7% O2) before and after bilateral vagotomy. Before vagotomy, hypercapnia (n=12) and hypoxia (n=6) produced increases of DIA amplitude contraction (69.1±11.5 and 31.4±9.8 %) combined with a minor increase in ABD activity (4.4±2.2 vs 19.3±5.8 %). After vagotomy, the magnitude of DIA responses to hypercapnia and hypoxia (94.8±20.4 and 50.9±7.8 %) did not differ from those before vagotomy (P>0.05). In contrast, we verified a substantial increase in ABD responses to hypercapnia and hypoxia (47.1±7.9 and 63.3±15 %) in relation to the responses observed prior to vagotomy (P<0.01). These amplified expiratory responses to hypercapnia and hypoxia after vagotomy were associated with enhanced expiratory air flow (P<0.01) and augmented tidal volume responses (P<0.01). Our data indicates that, in anesthetized conditions, peripheral afferent inputs, potentially from pulmonary stretch receptors, exerts an inhibitory effect on the processing expiratory motor activity in response hypercapnia and hypoxia, and the removal of this information potentiates the processing of active expiration.