Abstract

CO 2 tolerance in white sturgeon is associated with the ability to tightly regulate intracellular pH (pHi) despite a large reduction in extracellular pH (pHe) termed preferential pHi regulation. How this regulatory response affects whole animal metabolic rate is unknown. Accordingly, we characterized oxygen consumption rate ( M ˙ O 2 ) and metabolically-relevant organismal and cellular responses in white sturgeon during exposure to hypercarbia. White sturgeon were able to protect intracellular pH (pHi) in liver and white muscle as early as 6 h (the earliest time period investigated) following exposure to severe (sub-lethal) hypercarbia (45 and 90 mmHg PCO 2). Sturgeon exposed to 15 and 30 mmHg PCO 2 exhibited pHe compensation and significant increases in M ˙ O 2 (up to 80% greater than control values). In contrast, severe hypercarbia (≥ 45 mmHg PCO 2) elicited an uncompensated reduction in pHe (up to ~ 1.0 pH units) and red blood cells (as great as ~ 0.5 pH units), and was accompanied by 30 and 60% reductions in M ˙ O 2 , respectively. While behavioral, respiratory and cellular responses to hypercarbia were observed, none corresponded well with the pattern or magnitude of changes in M ˙ O 2 . The findings of this research provide empirical support for the hypothesis that preferential pHi regulation is not metabolically costly, and thus may have been a strategy strongly selected for in fishes encountering short-term hypercarbia.

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