Aerobically generated CO2 stored during early exercise

Previous studies have shown that a metabolic alkalosis develops in the musc le during early exercise. This has been linked to phosphocreatine hydrolysi s. Over a similar time frame, the femoral vein blood pH and plasma K+ and H CO3- concentrations increase without an increase in PCO2 Thus CO2 from aero bic metabolism is converted to HCO3- rather than being eliminated by the lu ngs. The purpose of this study was to quantify the increase in early CO2 st ores and the component due to the exercise-induced metabolic alkalosis (E-I Alk). 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 increa se in CO2 stores was evident at the ail-way starting at similar to 15 s; th e 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 kinetic s were unaffected at the higher WR. Three components of the change in aerob ically generated CO2 stores were considered relevant: the carbamate compone nt of the Haldane effect, the increase in CO2 stores due to increase in tis sue PCO2, and the E-IAlk. The Haldane effect was calculated to be similar t o 5%. Physically dissolved CO2 in the tissues was similar to 30% of the sto re 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 corr elated with the size of the E-I Alk component of the CO2 stores. We conclud e that a major component of the aerobically generated increase in CO2 store s is the new HCO3- generated as phosphocreatine is converted to creatine.