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.

Keywords:

• Blood Lactate
• Mixed Venous Co₂ Pressure
• Arterial Co₂ Pressure
• Incremental Exercise.