BUFFERING AND RESPIRATORY COMPENSATION OF LACTIC ACIDOSIS AFTER THE WINGATE TEST

Abstract

742 The “pH-defense” in the extracellular space after rapid addition of lactic acid by performing 30 s anaerobic exercise was studied in 13 subjects. Acid-base status and lactate concentration in earlobe blood were determined before and up to 30 min after the test. After this time [lactate] was still increased and pH as well as pCO2 decreased.-Δ[lactate]plasma/ΔpH as a measure of total pH defense(bicarbonate and nonbicarbonate buffering, respiratory compensation) increased steadily from 61 ± 14 (SE) to 120 ± 9 mmol/l.Δ[HCO3-]plasma/ΔpH (bicarbonate buffering and respiratory compensation) rose in a parallel manner from 42 ± 10 to 96± 7 mmol/l. The difference between-Δ[lactate]plasma/ΔpH andΔ[HCO3-]plasma/ΔpH amounted to 17 ± 3 mmol/l. The nonbicarbonate buffer value can be used to estimate the effect of hyperventilation and to calculate buffer capacities for constant pCO2 and thus nonrespiratory (nr) pH changes.-Δ[lactate]plasma/ΔpHnr was initially higher than-Δ[lactate]plasma/ΔpH (71 + 8 mmol/l) because of temporarily increasing pCO2, reached a minimum of 57 ± 1 mmol/l after 6 min and than increased again up to the initial values.Δ[HCO3-]plasma/ΔpHnr followed an equal time course but at a lower level (difference 17 mmol/l). Calculation ofΔ[HCO3-]plasma/ΔpHnr from initial values by use of the Henderson-Hasselbalch equation yielded only slightly different values demonstrating that no considerable bicarbonate exchange occurred with the cells. The apparently increasing total pH defense after the Wingate test resulted from a consistently decreased pCO2. The relative importance of this respiratory compensation increases with decreasing lactic acid concentration and thus decreasing total pH changes.