Abolition of reflex bradycardia by cardiac vagotomy has no effect on the regulation of oxygen uptake by Atlantic cod in progressive hypoxia

The functional significance of chemoreflexive hypoxic bradycardia was explored in Atlantic cod Gadus morhua L. (mean mass ∼ 800 g, acclimated to a seawater temperature of 11 °C) by investigating responses to progressive hypoxia following section of the cardiac branches of cranial nerve X. Cardiac denervation had no effect on oxygen uptake rate (MO2), gill ventilation rate (fG) or opercular pressure amplitude (POP) under normoxic conditions, but caused a significant increase in heart rate (fH), to 50 ± 1 beats min− 1 by comparison to 40 ± 2 beats min− 1 in sham-operated cod (mean ± s.e.m., n = 9). Sham-operated cod exhibited transient profound bradycardia following oxygen chemoreceptor stimulation by bolus injection of sodium cyanide into the buccal cavity (2 mg in 2 ml seawater), but this cardiac chemoreflex was abolished in denervated cod. Both groups, however, exhibited similar marked transient chemoreflexive hyperventilation following NaCN. When exposed from normoxia (PO2 ∼ 18 kPa) to progressive hypoxia at nominal water PO2's of 8, 6, 5, 4 and 3 kPa, both groups exhibited the same pattern of homeostatic regulation of MO2, with no significant difference in their mean critical PO2 (Pcrit) values, which were 7.40 ± 0.81 kPa and 8.73 ± 0.71 kPa, respectively (n = 9). Both groups exhibited significant bradycardia during progressive hypoxia, although denervated fish always had higher mean fH. The incipient threshold for bradycardia coincided with Pcrit in sham-operated cod whereas, in denervates, the threshold was below their Pcrit and bradycardia presumably reflected direct effects of hypoxia on the myocardium. The sham-operated group displayed a significantly more pronounced ventilatory response than denervates in hypoxia, in particular for POP. In sham-operated cod, peak ventilatory responses occurred in deep hypoxia below Pcrit whereas, in denervates, more modest peak responses coincided with Pcrit and, in deep hypoxia, they exhibited a significant decline in fG below their normoxic rate. Only a minority of shams lost equilibrium in hypoxia whereas a majority of denervates did, some of which failed to recover. The results indicate that chemoreflexive bradycardia plays no role in the homeostatic regulation of oxygen uptake by cod in hypoxia, but does contribute to maintenance of overall functional integrity below Pcrit.