Aerobically generated CO₂stored 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${HCO}_3^{-}$ concentrations increase without an increase in $P{\text{CO}}_2$ . Thus CO₂ from aerobic metabolism is converted to ${HCO}_3^{-}$ 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-I Alk). To avoid masking the increase in CO₂ stores by CO₂ released as${HCO}_3^{-}$ 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 airway starting at ∼15 s; the increase reached a peak at ∼60 s and was complete by ∼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 $P{\text{CO}}_2$ , and the E-I Alk. The Haldane effect was calculated to be ∼5%. Physically dissolved CO₂ in the tissues was ∼30% of the store increase. The remaining E-I Alk CO₂ stores averaged 61 and 68% for 60 and 80% LAT WRs, respectively. The kinetics of O₂ uptake correlated with the time course of the increase in CO₂stores; the size of the O₂ 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${HCO}_3^{-}$ generated as phosphocreatine is converted to creatine.