Intense exercise depends on energy from both aerobic and anaerobic processes. These processes produce CO 2 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. The chloride concentration in red blood cells (cCl RBC ) 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), pCO 2 changed to 41 hPa (fv 114), and blood bicarbonate concentration was more than halved after exercise. cCl RBC rose by 5 (a) and 8 mmol L -1 blood (fv) during exercise. pCO 2 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. cCl RBC 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 pCO 2 and bicarbonate concentration were higher in femoral-venous than in arterial blood with the same lactate Acid-base status of arterial and femoral-venous blood … 67 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 femoralvenous than in arterial blood because of a lack of respiratory compensation of the metabolic acidosis.