NaHCO 3 does not affect arterial O 2 tension but attenuates desaturation of hemoglobin in maximally exercising Thoroughbreds

The objective of the present study was to examine the effects of preexercise NaHCO 3 administration to induce metabolic alkalosis on the arterial oxygenation in racehorses performing maximal exercise. Two sets of experiments, intravenous physiological saline and NaHCO 3 (250 mg/kg iv), were carried out on 13 healthy, sound Thoroughbred horses in random order, 7 days apart. Blood-gas variables were examined at rest and during incremental exercise, leading to 120 s of galloping at 14 m/s on a 3.5% uphill grade, which elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. NaHCO 3 administration caused alkalosis and hemodilution in standing horses, but arterial O 2 tension and hemoglobin-O 2 saturation were unaffected. Thus NaHCO 3 administration caused a reduction in arterial O 2 content at rest, although the arterial-to-mixed venous blood O 2 content gradient was unaffected. During maximal exercise in both treatments, arterial hypoxemia, desaturation, hypercapnia, acidosis, hyperthermia, and hemoconcentration developed. Although the extent of exercise-induced arterial hypoxemia was similar, there was an attenuation of the desaturation of arterial hemoglobin in the NaHCO 3 -treated horses, which had higher arterial pH. Despite these observations, the arterial blood O 2 content of exercising horses was less in the NaHCO 3 experiments because of the hemodilution, and an attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O 2 content gradient was observed. It was concluded that preexercise NaHCO 3 administration does not affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing short-term, high-intensity exercise.