Elevated CO ₂ increases energetic cost and ion movement in the marine fish intestine

Abstract

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 O ₂ consumption rates of isolated intestinal tissue from Gulf toadfish acclimated to control or 1900 μatm CO ₂ (projected for year 2300). The active marine fish intestine absorbs ions from ingested seawater in exchange for HCO ₃ ⁻ to maintain water balance. We demonstrate that CO ₂ exposure causes a 13% increase of intestinal HCO ₃ ⁻ secretion that the animal does not appear to regulate. Isolated tissue from CO ₂-exposed toadfish also exhibited an 8% higher O ₂ consumption rate than tissue from controls. These findings show that compensation for CO ₂ leads to a seemingly maladaptive persistent base (HCO ₃ ⁻) 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.