Introduction: from water to air breathing

Transition from water to land has freed animals from the constraints of water breathing: due to the low O2 concentration in water, a waterbreather is obliged to achieve a high ventilatory flow rate of a medium with a high capacitance both for CO2 and for heat (Dejours, 1981). The animal thus has very little control over any of these. By contrast, the high O2 concentration in air has enabled PCO2 to be set at a higher level and air-breathers can therefore partly devote the ventilatory system to its control. Two major benefits accrue from this in terms of acid–base regulation. The first is a much higher open system CO2 buffer value, and thereby a more efficient ventilatory control of pH (this buffer value is proportional to PCO2 at a given pH). The second stems from the high diffusivity of CO2. Krogh's diffusion coefficient for CO2 in frog muscle at 21°C is 37-fold higher than the same coefficient for O2 (Dejours, 1981). In a mammal breathing air at sea level, the maximal possible PO2 difference between arterial blood and mitochondria is 13.3 kPa. The corresponding difference for CO2 is 0.36 kPa, less than 7 per cent of arterial PCO2. This percentage would be much higher in a waterbreather. As a consequence, the ventilatory control sets the value of PCO2, not only in the arterial blood, but in all intracellular compartments (except for a few ill-perfused areas in which CO2 may accumulate).