BUFFERING AGAINST LACTIC ACID DURING EXERCISE 531

Abstract

The acidosis caused by lactic acid during exercise is attenuated by bicarbonate and nonbicarbonate buffers and by reduction of PCO2 via hyperventilation. An estimate of the total effect in the extracellular space can be obtained from Δ[Lac]/ΔpHtot in arterial blood. If the respiratory (r) changes in PCO2, pH and [HCO3] are known, a nonrespiratory buffer value (Δ[Lac]/ΔpHnr) can be calculated. For this correction an in vivo CO2-equilibration curve of blood has to be measured. In 12 well-trained subjects (10 males, 2 females: 30.8±5.4 (SD) years, ˙VO2max 61.2 ± 8.2 ml/kg·min) we determined Δ[Lac]/Δ pHtot during a graded bicycle ergometer test. Lactic acid concentration and acid-base status were measured in arterialized ear lobe blood. During hypocapnia and hypercapnia the same quantities were determined in arterialized venous blood. The relation between Δ[HCO5]r and ΔpHr as well as between ΔLac and ΔpHtot in the exercise experiments was approximately linear. The mean of the individual regression coefficients for Δ[Lac]/Δptot amounted to - 71 ± 24 mmol/l. MeanΔ[HCO3]/ΔpHr was much lower (- 19.2±4.2 mmol/l) and scattered less. Δ[Lac]/ΔpHnr showed a decreased mean value with a reduced standard deviation (-54 ± 13 mmol/l) compared to the total effect. This quantity seems to be relatively stable and can be considered as a measure of buffers available to the extracellular space(mainly bicarbonates and proteins in red cells, plasma and interstitial fluid). In contrast the contribution of ventilation to acid-base stability during exercise is rather variable.