Acid-base balance and the control of respiration during anaxic and anoxic-hypercapnic gas breathing in turtles

We studied the ventilatory and blood acid-base response of turtles to 6 of breathing eithe 100% N₂(anoxic) or 95% N₂-5% CO₂ (anoxic-hypercapnic). In both groups, minute ventilation (V̇E) increased promptly with anoxia, with peak ventilation occurring between 1 and 3 h. V̇E then decreased but was still significantly above control at 6h. The increase in V̇E resulted from increases in both respiratory frequency (f) and tidal volume (VT) but after ventilation peaked, f declined to control while VT remained elevated. We observed no significant differences in V̇E between the two groups in spite of significantly lower arterial pH and higher arterial P_CO2 in the anoxic-hypercapnic turtles. During normoxic recovery, V̇E quickly increased to the peak anoxic values due primarily to a greatly increased f. In both groups, plasma [lactate⁻] increased during anoxia. Plasma cation concentrations also increased, partially compensating for the elevated blood lactate. We conclude that the anoxic hyperventilation did not depend on arterial pH and central chemoreceptor control but rather on peripheral hypoxic chemoreceptor control. We believe that the decline in V̇E during prolonged anoxic breathing results from a metabolic arrest response and/or a depression in central nervous function.