Elevated CO₂ increases energetic cost and ion movement in the marine fish intestine

Energetic costs associated with ion and acid-base regulation in response to ocean acidification have been predicted to decrease the energy available to fish for basic life processes. However, the low cost of ion regulation (6-15% of standard metabolic rate) and inherent variation associated with whole-animal metabolic rate measurements have made it difficult to consistently demonstrate such a cost. Here we aimed to gain resolution in assessing the energetic demand associated with acid-base regulation by examining ion movement and O₂ consumption rates of isolated intestinal tissue from Gulf toadfish acclimated to control or 1900 μatm CO₂ (projected for year 2300). The active marine fish intestine absorbs ions from ingested seawater in exchange for HCO₃^- to maintain water balance. We demonstrate that CO₂ exposure causes a 13% increase of intestinal HCO₃^- secretion that the animal does not appear to regulate. Isolated tissue from CO₂-exposed toadfish also exhibited an 8% higher O₂ consumption rate than tissue from controls. These findings show that compensation for CO₂ leads to a seemingly maladaptive persistent base (HCO₃^-) loss that incurs an energetic expense at the tissue level. Sustained increases to baseline metabolic rate could lead to energetic reallocations away from other life processes at the whole-animal level.