Preexercise hypervolemia does not affect arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise

Abstract

It is reported that preexercise hyperhydration caused arterial O(2) tension of horses performing submaximal exercise to decrease further by 15 Torr (Sosa-Leon L, Hodgson DR, Evans DL, Ray SP, Carlson GP, and Rose RJ. Equine Vet J Suppl 34: 425-429, 2002). Because hydration status is important to optimal athletic performance and thermoregulation during exercise, the present study examined whether preexercise induction of hypervolemia would similarly accentuate the arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise. Two sets of experiments (namely, control and hypervolemia studies) were carried out on seven healthy, exercise-trained Thoroughbred horses in random order, 7 days apart. In resting horses, an 18.0 +/- 1.8% increase in plasma volume was induced with NaCl (0.30-0.45 g/kg dissolved in 1,500 ml H(2)O) administered via a nasogastric tube, 285-290 min preexercise. Blood-gas and pH measurements as well as concentrations of plasma protein, hemoglobin, and blood lactate were determined at rest and during incremental exercise leading to maximal exertion (14 m/s on a 3.5% uphill grade) that induced pulmonary hemorrhage in all horses in both treatments. In both treatments, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, acidosis, and hyperthermia developed during maximal exercise, but statistically significant differences between treatments were not found. Thus preexercise 18% expansion of plasma volume failed to significantly affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing maximal exercise. Although blood lactate concentration and arterial pH were unaffected, hemodilution caused in this manner resulted in a significant (P < 0.01) attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O(2) content gradient.

Intrapulmonary arteriovenous shunts of >15 μm in diameter probably do not contribute to arterial hypoxemia in maximally exercising Thoroughbred horses

“…Our findings regarding development of significant hyperthermia, arterial hypoxemia, desaturation of hemoglobin, hypercapnia, and acidosis during galloping at 14 m/s on a 3.5% uphill grade in the present study (Table 1) are consistent with previously reported data in maximally exercising Thoroughbred horses (13)(14)(15)(16). It has also been reported that submaximal exercise performed at 8 m/s on a 3.5% uphill grade did not result in arterial hypoxemia (13)(14)(15)(16); this was also true in the present study (Table 1).…”

“…Vigorously agitated, ultrasonicated suspension of 15-m-diameter stable isotope-labeled microspheres was injected into the right atrium at 30 s of galloping at 14 m/s on a 3.5% uphill grade, when exercise-induced arterial hypoxemia is known to be well developed in Thoroughbred horses (13)(14)(15)(16). Blood withdrawal from the aorta and the pulmonary artery continued until 90 s postinjection of microspheres.…”

“…10 -12)] and 2) the exercise-induced arterial hypoxemia tends to be more pronounced in racehorses [arterial O 2 tension and hemoglobin O 2 saturation in maximally exercising racehorses usually decreasing (from near 100 mmHg and ϳ98 -99%, respectively, at rest) to ϳ75 mmHg and ϳ85%, respectively; Refs. [13][14][15][16], it was hypothesized that dormant intrapulmonary arteriovenous shunts similar to those described in exercising human subjects (5, 22a) may become functional in strenuously exercising racehorses, thereby contributing to the observed arterial hypoxemia and desaturation of hemoglobin. Thus our primary objective in the present study was to determine whether intrapulmonary arteriovenous shunts become functional in the lungs of Thoroughbred horses performing short-term, high-intensity exercise capable of eliciting maximal heart rate, stress failure of pulmonary capillaries leading to exercise-induced pulmonary hemorrhage (EIPH), and significant arterial hypoxemia and desaturation of hemoglobin.…”

“…This is because, assuming that a constant fraction of total pulmonary blood flow bypasses the gas-exchange areas of the equine lungs via intrapulmonary arteriovenous shunts during 30 -120 s of maximal exertion, the observed significant reductions in mixed venous blood oxygenation should cause a significant reduction in arterial O2 tension, which was not the case in our horses. Thus it is suggested that intrapulmonary arteriovenous shunting probably does not contribute to the exercise-induced arterial hypoxemia in racehorses.blood gas tensions during exertion; arterial desaturation during exercise; pulmonary microcirculation; microspheres IT IS WELL KNOWN THAT STRENUOUSLY EXERCISING racehorses experience significant arterial hypoxemia and desaturation of hemoglobin, and it is reported that these changes in arterial oxygenation limit athletic performance (1,3,8,(13)(14)(15)(16)24). A significant arterial hypercapnia is also observed in strenuously exercising Thoroughbred horses despite significantly increased alveolar ventilation.…”

“…blood gas tensions during exertion; arterial desaturation during exercise; pulmonary microcirculation; microspheres IT IS WELL KNOWN THAT STRENUOUSLY EXERCISING racehorses experience significant arterial hypoxemia and desaturation of hemoglobin, and it is reported that these changes in arterial oxygenation limit athletic performance (1,3,8,(13)(14)(15)(16)24). A significant arterial hypercapnia is also observed in strenuously exercising Thoroughbred horses despite significantly increased alveolar ventilation.…”