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In order to clarify the kinetics of excess CO2 output during and after intensive exercise, six male subjects were each instructed to perform 40-, 60- and 80-s cycle ergometer exercises (282 +/- 9 W, 90 rpm). Ventilation and gas exchange parameters were recorded breath-by-breath, and lactate concentration (La) was repeatedly measured with blood samples from a finger tip. The increase in La from the resting value to peak value and the duration of exercise showed a significant linear relationship (r = 0.91, p

Cerretelli et al. (1982) proposed a model to estimate pH changes due to lactate production in exercise. This model was modified in the present study so as to express the relationship between CO2 excess and lactate production. The modified model fitted to the data reported on endurance-trained men.

The purpose of this study was to investigate the differences in kinetics of CO2 output (VCO2) during incremental exercise in sprinters (S), middle (MD), and long distance runners (LD). In the steady state exercise, the VCO2 was linearly related to the O2 uptake (VO2). In the incremental exercise below anaerobic threshold (AT), the VCO2 was also linearly related to the VO2. The difference between the VCO2 estimates from the regression lines obtained in steady state and incremental exercise was added from the start of exercise up to a given time. The added values were defined as CO2 stores. The CO2 stores per body weight were significantly related to mixed venous CO2 pressure (PVCO2) determined by the CO2 rebreathing method. The slopes of the regression lines between PVCO2 and CO2 stores per body weight were not different among three groups. If VCO2 above AT is estimated from the VO2 using the regression line obtained in incremental exercise below AT, the estimated VCO2 is lower than the measured VCO2. The sum of the differences in VCO2 up to a given time was defined as CO2 excess. The CO2 excess per body weight was significantly related to delta LA (the difference between blood lactates at 5 min after exercise and at rest). The ratios of CO2 excess per body weight to delta LA were 3.30 +/- 1.49, 4.16 +/- 2.33, and 5.55 +/- 2.05 for sprinters, middle, and long distance runners, respectively. This ratio obtained in sprinters was significantly lower than that in long distance runners (p less than 0.01).

The purpose of the present study was to obtain the immediate CO2 storage capacity at the onset of exercise. The CO2 stores at the onset of the exercise were calculated from the difference between the respiratory gas exchange ratio (R) and the metabolic gas exchange ratio (RQ: R obtained at 5.5 min of exercise). The CO2 stores per body weight (CO2 stores/w) were linearly related to the CO2 pressure (P'vCO2) determined by the CO2 rebreathing method (r = 0.713, p less than 0.001), the slope being 0.330 ml/(mmHg X kg). The CO2 stores were then corrected for change in O2 stores with exercise, that defined as total CO2 stores. P'vCO2 was also corrected for the effect of lung-bag volume shrinkage and Haldane effect during CO2 rebreathing, that defined as true PvCO2. The total CO2 stores/w were also related linearly to the true PvCO2 (r = 0.725, p less than 0.001), the slope of the regression line defined as the immediate CO2 storage capacity being 0.650 ml/(mmHg X kg).

The differences between VO2 at the 5th min in steady state exercise and VO2 in incremental exercise were consecutively added from start of incremental exercise to a given time. These added values were defined as oxygen deficit. Anaerobic threshold was determined as the breakpoint of blood lactate during incremental exercise. The oxygen deficit at the anaerobic threshold in normoxia was almost identical to that in hypoxia.

The purpose of this study was to elucidate the effect of lung-bag volume shrinkage on P'VCO2 estimated by the CO2 rebreathing method and to correct its effect in calculation of cardiac output. The P'VCO2 was extrapolated with the linear relationship between dPACO2/dt and PACO2 during rebreathing. The P'VCO2 was higher than real mixed PCO2 by 0.82 mmHg at rest, by 1.35 mmHg at 50W, 1.57 mmHg at 100W, and 3.06 mmHg at 150W considering the effect of lung-bag volume shrinkage detected by argon concentration. The cardiac output obtained by the CO2 rebreathing method with correction of above differences was in good agreement with that determined by the acetylene method (r = 0.930, p less than 0.001). When the cardiac output was plotted against O2 uptake, our results and the regression line were fairly close to the reported regression lines.