Acid-base status of arterial and femoral-venous blood during and after intense cycle exercise
Keywords: acid-base balance, anion gap, arterio-venous difference, blood, buffering, chloride, chloride shift, electrolytes, exercise, lactate, pH, plasma
AbstractIntense exercise depends on energy from both aerobic and anaerobic processes. These processes produce CO2 and lactate, respectively, and both metabolites affect blood's acid-base status. To examine how the acid-base status of arterial and femoral-venous blood is affected and regulated, seven healthy young men cycled for 2 min at constant power to exhaustion. Blood samples were drawn from indwelling catheters in the femoral artery and vein during exercise and for 1 h after, and the samples were analysed for lactate (La–), acid-base parameters, and plasma electrolytes (Na+, K+, Cl–, La–, HCO3–). The chloride concentration in red blood cells (cClRBC) was also determined to quantify the chloride shift. Arterial (femoral-venous, fv, mean values) blood lactate concentration rose to 13.8 mmol L–1 (fv 15.7), pH fell to 7.18 (fv 7.00), pCO2 changed to 41 hPa (fv 114), and blood bicarbonate concentration was more than halved after exercise. cClRBC rose by 5 (a) and 8 mmol L–1 blood (fv) during exercise. pCO2 and pH fell linearly by the lactate concentration. Consequently, blood bicarbonate concentration fell by 81% of the increase in blood lactate concentration, while blood base deficit rose 30% more than lactate did. Bicarbonate thus neutralised 62% of the total acid load. cClRBC rose in proportion to the amount of hydrogen ions buffered by haemoglobin, and chloride shift amounted to 31% of the total acid load. pH was lower and pCO2 and bicarbonate concentration were higher in femoral-venous than in arterial blood with the same lactate concentrations. The relationship between base deficit and blood lactate concentration did not differ between arterial and femoral-venous blood. In conclusion, after intense exercise pH falls more in femoral-venous than in arterial blood because of a lack of respiratory compensation of the metabolic acidosis.