A metabolic hypothesis for the evolution of temperature effects on the arterial PCO2 and pH of vertebrate ectotherms.

Abstract

Body temperature increases in ectothermic vertebrates characteristically lead to both increases in arterial PCO2 (PaCO2 ) and declines in resting arterial pH (pHa) of about 0.017 pH units per 1°C increase in temperature. This 'alphastat' pH pattern has previously been interpreted as being evolutionarily driven by the maintenance of a constant protonation state on the imidazole moiety of histidine protein residues, hence stabilizing protein structure-function. Analysis of the existing data for interclass responses of ectothermic vertebrates shows different degrees of PaCO2 increases and pH declines with temperature between the classes, with reptiles>amphibians>fish. The PaCO2 at the temperature where maximal aerobic metabolism (V̇O2,max) is achieved is significantly and positively correlated with temperature for all vertebrate classes. For ectotherms, the PaCO2 where V̇O2,max is greatest is also correlated with V̇O2,max, indicating there is an increased driving force for CO2 efflux that is lowest in fish, intermediate in amphibians and highest in reptiles. The pattern of increased PaCO2 and the resultant reduction of pHa in response to increased body temperature would serve to increase CO2 efflux, O2 delivery and blood buffering capacity and maintain ventilatory scope. This represents a new hypothesis for the selective advantage of arterial pH regulation from a systems physiology perspective in addition to the advantages of maintenance of protein structure-function.