The Acid-base Equilibrium of the Blood in Exercise

and the associated extra output of CO2 through the lungs acts as one of the principal buffering mechanisms of the body. However observations upon the relation of the magnitude of changes in lactate and CO2 capacity have been contradictory. Mellanby and Thomas (1920) and Evans (1922), by addition of lactic acid to drawn blood, found that the decline in CO2 content was less than the increase in blood lactate. Results of similar experiments performed in this laboratory have shown close agreement yet the picture is not identical with that seen in blood drawn after exercise. In six observations on blood drawn after exercise, Barr, Himwich and Green (1923) obtained wide variations and found a greater change in blood lactate than in CO2 capacity in only two cases. Dill, Talbott and Edwards (1930) found in general a greater decline in CO2 capacity of the blood. Dennig et al. (1931) found approximately equal changes when the blood lactate rose to 10 mEq. per liter. Robinson and Harmon (1941) found that the decreases in COz capacity, at physiologically high concentrations of blood lactate, were smaller than the corresponding increases in lactate. By further study of this problem we have attempted to relate changes in blood lactate, CO2 capacity, and serum pH and to determine the role of the various mechanisms in buffering acid as it is accumulated during exercise. Samples of blood were drawn from human subjects in the basal state and after exercise on the same day. Various intensities of exercise, which consisted of running on a motor driven treadmill or in competitive races, were used to produce different concentrations of blood lactic acid in the men. For comparison of changes in pH, CO2 capacity, lactate, and related changes in available base, arterial blood samples were drawn under oil and treated with heparin. Several samples of venous blood were used in t,he comparison of the variations in lactate concentration with those of CO2 capacity. Blood lactate was determined by the method of Edwards (1938), and plasma protein by micro-Kjeldahl analysis. HbOs and CO2 capacity were determined by equilibration of blood with O2 and COz pressures of 200 and 40 mm. Hg respectively at 37OC. as described by Dill in Henderson’s book (1928). Analyses of blood samples for both content and capacity of HbOz and CO8 were done on the Van Slyke apparatus. The pH values of arterial blood samples were calculated by means of the Henderson-Hasselbalch equation and some over the entire range of values