Extracellular and intracellular acid-base effects of submergence anoxia and nitrogen breathing in turtles.

We compared extracellular and intracellular acid-base state in turtles (Chrysemys picta bellii) subjected to anoxic submergence to turtles made anoxic by N2-breathing. Measurements made on control animals and on animals after 1, 2, 4, or 6 h of anoxia included blood pH, PO2, PCO2, and lactate as well as liver, heart, skeletal muscle, and brain pHi (using DMO equilibration), lactate, and glycogen concentrations. We hypothesized that the anaerobic metabolic rate of submerged turtles would be depressed by the more severe extra- and intracellular acidosis, and that this would be indicated by reduced lactate accumulation and glycogen depletion. Submerged turtles became extremely acidemic due to a combined metabolic and respiratory acidosis and had significantly lower arterial pH than N2-breathing animals (6.98 and 7.34, respectively, after 6 h). In spite of this disparity in pHa, 6 h pHi values for liver, heart, and brain were similar. Likewise, our data on glycogen depletion and lactate accumulation at h 6 in these tissues suggest no dramatic differences in anaerobic metabolic rate. While skeletal muscle pHi was somewhat lower at h 6 in the submerged group (6.73 vs 6.91 for N2-breathers), we observed no differences in either glycogen depletion or lactate accumulation in this tissue between our two treatments. Thus, at h 6, in spite of a 0.37 pH unit difference in pHa and a nearly 70 mm Hg difference in arterial and presumably cytosolic PCO2, pHi and tissue lactate and glycogen concentrations were similar. These results can be explained if the in vivo intracellular buffer values (beta) of turtle tissues are very high. We conclude that extracellular acid-base state is not necessarily reflected intracellularly in vivo in turtles and care must be taken in extrapolating from one compartment to another when attempting to make inferences about metabolic depression or acid-base regulation in this species.