Time-dependent ventilatory responses to hypoxic and hypercapnic challenges, such as post-hypoxic frequency decline (PHxFD) and post-hypercapnic frequency decline (PHcFD), could profoundly affect breathing stability. However, little is known about the mechanisms that mediate these phenomena. To determine the contribution of specific carotid body chemo-stimuli to PHxFD and PHcFD, we developed a novel in situ arterially perfused, vagotomized, decerebrate rat preparation in which central and peripheral chemoreceptors are perfused separately (i.e., a non-anaesthetized in situ dual perfused preparation, DPP). We confirmed that (a) perfusion of central and peripheral chemoreceptor compartments was independent by applying specific carotid body hypoxia and hypercapnia before and after carotid sinus nerve transection, (b) the PCO₂ chemo-response of the DPP was similar to other decerebrate preparations and (c) the phrenic output was stable enough to allow investigation of time-dependent phenomena. We then applied four 5 min bouts (separated by 5 min) of specific carotid body hypoxia (40 Torr PO₂ and 40 Torr PCO₂) or hypercapnia (100 Torr PO₂ and 60 Torr PCO₂) while holding the brainstem PO₂ and PCO₂ constant. We report the novel finding that specific carotid body chemo-stimuli were sufficient to elicit several phrenic time-dependent phenomena in the rat. Hypoxic challenges elicited PHxFD which increased with bout, leading to progressive augmentation of the phrenic response. Conversely, hypercapnia elicited short-term depression and PHcFD, neither of which were bout dependent. These results, placed in the context of previous findings, suggest multiple physiological mechanisms are responsible for PHxFD and PHcFD: a redundancy that may illustrate these phenomena have significant adaptive advantage.