The influence of impeding muscle perfusion on the time course of ventilatory decline during recovery from electrically induced hindlimb contractions has been studied in 14 anesthetized dogs. When intravascular balloons, placed in abdominal aorta and inferior vena cava just rostral to the iliac bifurcation, were inflated at the cessation of contraction bout, minute ventilation (VE) was significantly reduced during recovery compared with control. The subsequent restoration of iliac circulation rapidly augmented VE, which peaked at the fifth breath after release, by an average of +4.97 L.min-1; VE then returned exponentially to resting (pre-contraction) level. Breathing 100% O2 did not affect the VE recovery pattern neither during iliac occlusion nor immediately after its release (the peak average delta VE = +4.42 L.min-1). When a local anesthetic (5% Lidocaine) was applied bilaterally to the regions of carotid bifurcation, systemic blood pressure was significantly increased and the VE response to both iliac occlusion and release were nearly abolished. The VE response to inhalation of 5% CO2 in air was not affected by this procedure, whereas the stimulation of VE with 2 mg i.v. bolus of NaCN was attenuated. When the local anesthetic was thoroughly washed out (and systemic blood pressure had returned to control level) the previously observed VE responses to iliac occlusion and release were restored. These results and analysis of the VE response timing (transits and latencies) suggest that the vascular rather than humoral effects or tissue 'metaboreception' modulate ventilatory recovery from muscular contractions; baroreception appears to be important in this process.