Abstract
Control of hyperpnea during recovery from diving in unanesthetized White Pekin ducks, Anas platyrhynchos, was examined. Postdive minute ventilation (VE) increased five times regardless of the length of the preceding dive (1–4 min), although longer dives resulted in slower return of VE towards predive levels. Manipulation of arterial blood gases showed that both hypoxia and hypercapnia contributed to hyperpnea on emergence. Although chronic bilateral carotid body denervation depressed VE before and after diving, VE still increased four times after 1-min dives. Postdive hyperpnea was accompanied by dramatic elevations in heart rate, cardiac output, and the ventilation/perfusion ratio. However, artificially maintaining heart rate at abnormally low levels did not affect the postdive hyperpnea. In addition, postdive hyperpnea was unaffected by systemic arterial baroreceptor denervation. Postdive hyperpnea in ducks depends on blood gas changes occurring during a dive, yet a substantial part of the response is independent of input from carotid body chemoreceptors and the accompanying rises in heart rate and cardiac output.