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 ( [Formula: see text] ) 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 6h (the earliest time period investigated) following exposure to severe (sub-lethal) hypercarbia (45 and 90 mm Hg PCO(2)). Sturgeon exposed to 15 and 30 mm Hg PCO(2) exhibited pHe compensation and significant increases in [Formula: see text] (up to 80% greater than control values). In contrast, severe hypercarbia (≥45 mm Hg 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 [Formula: see text] , respectively. While behavioral, respiratory and cellular responses to hypercarbia were observed, none corresponded well with the pattern or magnitude of changes in [Formula: see text] . 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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