Respiratory acidosis and O2 supply capacity do not affect the acute temperature tolerance of rainbow trout (Oncorhynchus mykiss).

Abstract

The mechanisms that determine the temperature tolerances of fish are poorly understood, creating barriers to disentangle how additional environmental challenges-such as CO₂-induced aquatic acidification and fluctuating oxygen availability-may exacerbate vulnerability to a warming climate and extreme heat events. Here, we explored whether two acute exposures (~0.5 hours or ~72 hours) to increased CO₂ impact acute temperature tolerance limits in a freshwater fish, rainbow trout (Oncorhynchus mykiss). We separated the potential effects of acute high CO₂ exposure on critical thermal maximum (CT_max), caused via either respiratory acidosis (reduced internal pH) or O₂ supply capacity (aerobic scope), by exposing rainbow trout to ~1 kPa CO₂ (~1% or 10 000 μatm) in combination with normoxia or hyperoxia (~21 or 42 kPa O₂, respectively). In normoxia, acute exposure to high CO₂ caused a large acidosis in trout (blood pH decreased by 0.43 units), while a combination of hyperoxia and ~1 kPa CO₂ increased the aerobic scope of trout by 28%. Despite large changes in blood pH and aerobic scope between treatments, we observed no impacts on the CT_max of trout. Our results suggest that the mechanisms that determine the maximum temperature tolerance of trout are independent of blood acid-base balance or the capacity to deliver O₂ to tissues.