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The objective of the present study was to examine the relative roles of peripheral versus central mechanisms in producing ventilatory adjustments in pekin ducks during prolonged (5 h) hypercapnia (5% inspired CO 2 ), and to determine whether these adjustments differed between male and female ducks. After 20 min of CO 2 exposure, intact ducks increased total ventilation (V E ) 2.5-3-fold above control values, due to large increases (∼200%) in tidal volume (V T ) and slightly smaller increases (∼140%) in breathing frequency (f R ). This response was accompanied by respiratory acidosis (pHa fell from ∼7.46 to ∼7.41) and hypercapnia (Pa CO 2 increased from ∼35 to ∼40 Torr). In males,V E fell progressively thereafter due exclusively to a fall in f R , in parallel with a rapid partial recovery of pH (to 7.44) while Pa CO 2 continued to climb (to ∼42 Torr). In females,V E remained elevated during hypercapnia, and no pH recovery occurred. This suggests that a respiratory decline resulting from acid-base compensation (probably due to HCO 3 − mobilization) occurred in males but not in females. Bicarbonate mobilization, and thus pH compensation, may have been reduced in females due to the CaCO 3 requirements of eggshell formation. In males, the acute ventilatory response was reduced slightly by denervation of the carotid bodies or intrapulmonary chemoreceptors, but there was no effect of denervation of either receptor group on the responses to prolonged CO 2 . We conclude that pH compensation triggered by constant or increasing Pa CO 2 , acting at central chemoreceptors, likely mediates the respiratory adjustments seen in male pekin ducks during hypercapnia. Furthermore, we suggest that this ventilatory response be considered a gender-specific hypercapnic ventilatory roll off, in the context of the various time domains of the hypercapnic ventilatory response.

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