• T Yano.
• Laboratory of Human Movement Sciences, Faculty of Education, Hokkaido University, Sapporo, Japan.
• Ergonomics. 1997 May 1; 40 (5): 522-30.

AbstractIn 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 (VCO2) shows multiple correlations with mixed venous CO2 pressure (PvCO2) and arterial CO2 pressure (PaCO2), the increase in the difference between PvCO2 and PaCO2 was considered to be involved in the increase in VCO2. In order to better understand the influence of CO2 pressure, VCO2 was divided into the expiratory CO2 phase (non-lactic VCO2), which was unrelated to lactic acid increase and the expiratory CO2 phase (excess VCO2), which was related to lactic acid increase. As a result, the non-lactic VCO2 significantly correlated to PvCO2. When non-lactic VCO2 was zero, the value of PvCO2 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 VCO2 that appeared in the high load phase. The CO2 excess, which was obtained by adding excess VCO2 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 VCO2 and excess VCO2, (3) the dextroversion of the blood CO2 dissociation curve due to lactic acid was connected to excess VCO2, and (4) a decrease in PaCO2 was related to excess VCO2 derived from tissue.

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