Abstract

A method to estimate the CO2 derived from buffering lactic acid by HCO3- during constant work rate exercise is described. It utilizes the simultaneous continuous measurement of O2 uptake (VO2) and CO2 output (VCO2), and the muscle respiratory quotient (RQm). The CO2 generated from aerobic metabolism of the contracting skeletal muscles was estimated from the product of the exercise-induced increase in VO2 and RQm calculated from gas exchange. By starting exercise from unloaded cycling, the increase in CO2 stores, not accompanied by a simultaneous decrease in O2 stores, was minimized. The total CO2 and aerobic CO2 outputs and, by difference, the millimoles (mmol) of lactate buffered by HCO3- (corrected for hyperventilation) were estimated. To test this method, ten normal subjects performed cycling exercise at each of two work rates for 6 min, one below the lactic acidosis threshold (LAT) (50 W for all subjects), and the other above the LAT, midway between LAT and peak VO2 [mean (SD), 144 (48) W]. Hyperventilation had a small effect on the calculation of mmol lactate buffered by HCO3- [6.5 (2.3)% at 6 min in four subjects who hyperventilated]. The mmol of buffer CO2 at 6 min of exercise was highly correlated (r = 0.925, P < 0.001) with the increase in venous blood lactate sampled 2 min into recovery (coefficient of variation = +/- 0.9 mmol.l-1). The reproducibility between tests done on different days was good. We conclude that the rate of release of CO2 from HCO3- can be estimated from the continuous analysis of simultaneously measured VCO2, VO2, and an estimate of muscle substrate.

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