Model implications of gas exchange dynamics on blood gases in incremental exercise

Abstract

In humans, arterial PCO2 (PaCO2) has been demonstrated to be regulated at or near resting levels in the steady state of moderate exercise (i.e., for work rates not associated with a sustained lactic acidosis). To determine how PaCO2 might be expected to behave under the nonsteady-state conditions of incremental exercise testing, the influence of the dynamic characteristics of the primary variables that determine PaCO2 was explored by means of computer modeling. We constructed a dynamic model that utilized previously reported experimental estimates for the kinetic response parameters of ventilation (VE) and CO2 output (VCO2). In response to incremental work rate forcings, the model yielded an increase in PaCO2, which reflected the disparity between the VE and VCO2 time constants; this hypercapnic condition was maintained despite VE and VCO2 both increasing linearly with respect to the input work rate profile. The degree of hypercapnia increased with the rate of the incremental forcing, reaching 9 Torr for a 50-W/min forcing. In conclusion, therefore, sustained increases in PaCO2 during nonsteady-state incremental exercise should be interpreted with caution, because this is the predicted response even in subjects with normal ventilatory control and lung function.