The objective of the present study was to examine the effects of preexercise NaHCO3 administration to induce metabolic alkalosis on the arterial oxygenation in racehorses performing maximal exercise. Two sets of experiments, intravenous physiological saline and NaHCO3 (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. NaHCO3 administration caused alkalosis and hemodilution in standing horses, but arterial O2 tension and hemoglobin-O2 saturation were unaffected. Thus NaHCO3 administration caused a reduction in arterial O2 content at rest, although the arterial-to-mixed venous blood O2 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 NaHCO3-treated horses, which had higher arterial pH. Despite these observations, the arterial blood O2 content of exercising horses was less in the NaHCO3 experiments because of the hemodilution, and an attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O2 content gradient was observed. It was concluded that preexercise NaHCO3 administration does not affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing short-term, high-intensity exercise.
Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans