Arterio‐venous differences of blood acid–base status and plasma sodium caused by intense bicycling

After intense exercise muscle may give off hydrogen ions independently of lactate, perhaps by a mechanism involving sodium ions. To examine this possibility further five healthy young men cycled for 2 min to exhaustion. Blood was drawn from catheters in the femoral artery and vein during exercise and at 1‐h intervals after exercise. The blood samples were analysed for pH, blood gases, lactate, haemoglobin, and plasma proteins and electrolytes. Base deficit was calculated directly without using common approximations. The leg blood flow was also measured, thus allowing calculations of the leg’s exchange of metabolites. The arterial blood lactate concentration rose to 14.2 ± 1.0 mmol L^–1, the plasma pH fell to 7.18 ± 0.02, and the base deficit rose 22% more than the blood lactate concentration did. The femoral‐venous minus arterial differences peaked at 1.8 ± 0.2 mmol L^–1 (lactate), –0.24 ± 0.01 (pH), and 4.5 ± 0.4 mmol L^–1 (base deficit), and –2.5 ± 0.7 mmol L^–1 (plasma sodium concentration corrected for volume changes). Thus, near the end of the exercise and for the first 10 min of the recovery period the leg gave off more hydrogen ions than lactate ions to the blood, and sodium left plasma in proportion to the extra hydrogen ions appearing. The leg’s integrated excess release of hydrogen ions of 0.88 ± 0.45 mmol kg^–1 body mass was 67% of the integrated lactate release. Base deficit calculated by the traditional approximate equations underestimated the true value, but the error was less than 10%. We conclude that intense exercise and lactic acidosis may lead to a muscle release of hydrogen ions independent of lactate release, possibly by a Na⁺,H⁺ exchange. Hydrogen ions were largely buffered in the red blood cells.