Abstract The mechanisms that determine the temperature tolerances of fish are poorly understood, creating barriers to disentangle how additional environmental challenges—such as CO 2}-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 CO 2} impact acute temperature tolerance limits in a freshwater fish, rainbow trout ( Oncorhynchus mykiss ). We separated the potential effects of acute high CO 2} exposure on critical thermal maximum (CT max}), caused via either respiratory acidosis (reduced internal pH) or O 2} supply capacity (aerobic scope), by exposing rainbow trout to ~1 kPa CO 2} (~1% or 10 000 μatm) in combination with normoxia or hyperoxia (~21 or 42 kPa O 2}, respectively). In normoxia, acute exposure to high CO 2} caused a large acidosis in trout (blood pH decreased by 0.43 units), while a combination of hyperoxia and ~1 kPa CO 2} 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 O 2} to tissues.
【저자키워드】 CO2, hypercapnia, hyperoxia, OCLTT,