Limits and patterns of acid-base regulation during elevated environmental CO in fish.

Aquatic CO tensions may exceed 30-60 Torr (ca. 30,000-79,000 μatm, respectively; hypercarbia) in some environments inducing severe acid-base challenges in fish. Typically, during exposure to hypercarbia blood pH (pH) is initially reduced and then compensated in association with an increase in plasma HCO in exchange for Cl. Typically, intracellular pH (pH) is reduced and recovery is to some degree coupled to pH recovery (coupled pH regulation). However, during acute hypercarbia, pH recovery has been proposed to be limited by an "apparent upper bicarbonate threshold", restricting complete pH recovery to below 15 Torr PCO. At PCO values beyond that which fish can compensate pH, some fish are able to fully protect pH despite large sustained reductions in pH (preferential pH regulation) and can tolerate PCO > 45 Torr. This review discusses pH and pH regulation during exposure to hypercarbia starting with modeling the capacity and theoretical limit to pH compensation in 19 studies. Next, we discuss how fish compensate severe acute hypercarbia exposures beyond the putative limit of pH compensation using preferential pH regulation which has recently been observed to be common among fish subjected to severe hypercarbia. Finally, we consider the evolution of pH regulatory strategies in vertebrates, including how the presence of preferential pH regulation in embryonic reptiles may indicate that it is an embryonic trait that is either lost or retained in adult vertebrates and may have served as an exaptation for key evolutionary transitions during vertebrate evolution.