Physiological model of CO2 output during incremental exercise

Abstract

In this study, a physiological model to explain the pathway of CO2 output during incremental exercise was examined by referring to experimental data. Since CO2 output (V˙CO2) shows multiple correlations with mixed venous CO2 pressure (Pv˙CO2) and arterial CO2 pressure (PaCO2), the increase in the difference between Pv˙CO2 and PaCO2 was considered to be involved in the increase in V˙CO2. In order to better understand the influence of CO2 pressure, V˙CO2 was divided into the expiratory CO2 phase (non-lactic V˙CO2), which was unrelated to lactic acid increase and the expiratory CO2 phase (excess V˙CO2), which was related to lactic acid increase. As a result, the non-lactic V˙CO2 significantly correlated to Pv˙CO2. When non-lactic V˙CO2 was zero, the value of Pv˙CO2 was 43·7 mmHg. This was higher than the resting PaCO2 value. On the other hand, as PaCO2 showed an almost constant value in the low load phase and showed a low value in the high load phase, it was believed that the low value of PaCO2 was related to the excess V˙CO2 that appeared in the high load phase. The CO2 excess, which was obtained by adding excess V˙CO2 in terms of the lapse of exercise time, correlated significantly with an increase in lactate in the blood. Based on the results, a model was constructed to illustrate the pathway of CO2 output. The key points of the model were as follows: (1) the use of the blood CO2 dissociation curve as the vector to transport CO2 from tissue to lungs, (2) the standard value of PaCO2 was established in order to divide non-lactic V˙CO2 and excess V˙CO2, (3) the dextroversion of the blood CO2 dissociation curve due to lactic acid was connected to excess V˙CO2, and (4) a decrease in PaCO2 was related to excess V˙CO2 derived from tissue.