Aerobically generated CO2 stored during early exercise

Previous studies have shown that a metabolic alkalosis develops in the muscle during early exercise. This has been linked to phosphocreatine hydrolysis. Over a similar time frame, the femoral vein blood pH and plasma K+ and HCO3- concentrations increase without an increase in PCO2 Thus CO2 from aerobic metabolism is converted to HCO3- rather than being eliminated by the lungs. The purpose of this study was to quantify the increase in early CO2 stores and the component due to the exercise-induced metabolic alkalosis (E-IAlk). To avoid masking the increase in CO2 stores by CO2 released as HCO3- buffers lactic acid, the transient increase in CO2 stores was measured only for work rates (WRs) below the lactic acidosis threshold (LAT). The increase in CO2 stores was evident at the ail-way starting at similar to 15 s; the increase reached a peak at similar to 60 s and was complete by similar to 3 min of exercise. The increase in CO2 stores was greater, but the kinetics were unaffected at the higher WR. Three components of the change in aerobically generated CO2 stores were considered relevant: the carbamate component of the Haldane effect, the increase in CO2 stores due to increase in tissue PCO2, and the E-IAlk. The Haldane effect was calculated to be similar to 5%. Physically dissolved CO2 in the tissues was similar to 30% of the store increase. The remaining E-IAlk CO2 stores averaged 61 and 68% for 60 and 80% LAT WRs, respectively. The kinetics of O-2 uptake correlated with the time course of the increase in CO2 stores; the size of the O-2 deficit correlated with the size of the E-I Alk component of the CO2 stores. We conclude that a major component of the aerobically generated increase in CO2 stores is the new HCO3- generated as phosphocreatine is converted to creatine.