Meeting Abstract
Temperature increases in ectothermic vertebrates lead to increases in arterial PCO2 (PaCO2) and declines in arterial pH (pHa) of about 0.017 pH units/°C increase in temperature. This pattern acid-base regulation occurs because minute ventilation does not keep pace with metabolism (VO2), resulting in a relative hypoventilation and the observed changes in PaCO2 and pH. The regulation of ventilation with temperature and the alphastat pattern of pH has been interpreted as being adaptive for maintaining 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 show different degrees of PaCO2 increases and pH declines with temperature between the classes with reptiles > amphibians > fish. The slopes (units/°C) of the relationship between pHa and temperature for reptiles, amphibians, and fish were -0.014, -0.013 and -0.010, respectively, all below the -0.017 units/°C slope characteristic of alphastat regulation. The PaCO2 at the temperature where maximal aerobic metabolism (VO2max) is achieved was significantly and positively correlated with temperature for all vertebrate classes. For ectotherms, the PaCO2 where VO2max is greatest is also correlated with VO2max indicating there is an increased driving force (ΔPCO2) for CO2 efflux that is lowest in fish, intermediate in amphibians and highest in reptiles. We hypothesize that the pattern of increased PaCO2 and the resultant reduction of pHa to increased body temperature primarily serves to increase CO2 efflux, O2 delivery, blood buffering capacity and maintain ventilatory scope with changes in temperature or activity. This represents a new hypothesis for the selective advantage of PaCO2 and pHa regulation in ectothermic vertebrates.
