Impact of long-term moderate hypercapnia and elevated temperature on the energy budget of isolated gills of Atlantic cod (Gadus morhua)

Effects of severe hypercapnia have been extensively studied in marine fishes,while knowledge on the impacts of moderately elevated CO₂ levels and their combination with warming is scarce. Here we investigate ion regulation mechanisms and energy budget in gills from Atlantic cod acclimated long-term to elevated PCO₂ levels (2500 ~katm) and temperature (18 °C). Isolated perfused gill preparations were established to determine gill thermal plasticity during acute exposures (10–22 °C) and in vivo costs of Na⁺/K⁺-ATPase activity, protein and RNA synthesis. Maximum enzyme capacities of F₁F_o-ATPase, H⁺-ATPase and Na⁺/K⁺-ATPase were measured in vitro in crude gill homogenates. After whole animal acclimation to elevated PCO₂ and/or warming, branchial oxygen consumption responded more strongly to acute temperature change. The fractions of gill respiration allocated to protein and RNA synthesis remained unchanged. In gills of fish CO₂-exposed at both temperatures, energy turnover associated with Na⁺/K⁺-ATPase activity was reduced by 30% below rates of control fish. This contrasted in vitro capacities of Na⁺/K⁺-ATPase, which remained unchanged under elevated CO₂ at 10 °C, and earlier studies which had found a strong upregulation under severe hypercapnia. F₁F_o-ATPase capacities increased in hypercapnic gills at both temperatures, whereas Na⁺/K⁺ATPase and H⁺-ATPase capacities only increased in response to elevated CO₂ and warming indicating the absence of thermal compensation under CO₂. We conclude that in vivo ion regulatory energy demand is lowered undermoderately elevated CO₂ levels despite the stronger thermal response of total gill respiration and the upregulation of F₁F_o-ATPase. This effect is maintained at elevated temperature.