Effect of prior high-intensity exercise on exercise-induced arterial hypoxemia in Thoroughbred horses

Abstract

Strenuously exercising horses exhibit arterial hypoxemia and exercise-induced pulmonary hemorrhage (EIPH), the latter resulting from stress failure of pulmonary capillaries. The present study was carried out to examine whether the structural changes in the blood-gas barrier caused by a prior bout of high-intensity short-term exercise capable of inducing EIPH would affect the arterial hypoxemia induced during a successive bout of exercise performed at the same workload. Two sets of experiments, double- and single-exercise-bout experiments, were carried out on seven healthy, sound Thoroughbred horses. Experiments were carried out in random order, 7 days apart. In the double-exercise experiments, horses performed two successive bouts (each lasting 120 s) of galloping at 14 m/s on a 3.5% uphill grade, separated by an interval of 6 min. Exertion at this workload induced arterial hypoxemia within 30 s of the onset of galloping as well as desaturation of Hb, a progressive rise in arterial PCO2, and acidosis as exercise duration increased from 30 to 120 s. In the single-exercise-bout experiments, blood-gas/pH data resembled those from the first run of the double-exercise experiments, and all horses experienced EIPH. Thus, in the double-exercise experiments, before the horses performed the second bout of galloping at 14 m/s on a 3.5% uphill grade, stress failure of pulmonary capillaries had occurred. Although arterial hypoxemia developed during the second run, arterial PO2 values were significantly (P < 0.01) higher than in the first run. Thus prior exercise not only failed to accentuate the severity of arterial hypoxemia, it actually diminished the magnitude of exercise-induced arterial hypoxemia. The decreased severity of exercise-induced arterial hypoxemia in the second run was due to an associated increase in alveolar PO2, as arterial PCO2 was significantly lower than in the first run. Thus our data do not support a role for structural changes in the blood-gas barrier related to the stress failure of pulmonary capillaries in causing the exercise-induced arterial hypoxemia in horses.

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

“…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.…”

In pursuit of Irving and Scholander: a review of oxygen store management in seals and penguins

“…Oxygen stores in seals and penguins (Elsner et al, 1970;. Routine venous P O2 values and Hb saturations were as low as 2-10mmHg (0-4%), equivalent to or even lower than those measured in forced submersion studies, and even lower than the well-documented hypoxemic extremes of horses performing strenuous exercise (Bayly et al, 1989;Manohar et al, 2001). These low end-of-dive P O2 values result in near-complete depletion of blood O 2 stores during routine dives, with net O 2 content depletion values up to 91% and 100% in the arterial and venous stores, respectively.…”

Exercise-induced pulmonary haemorrhage in horses – review

“…For this reason, some authors have suggested that the use of nasal patches prevents the collapse of lateral nasal walls, which help keep the upper airway unobstructed for the passage of air and thus reduce the resistance of the upper airway to step air (Geor et al 2001). The use of the patches reduces nasal airway resistance, but this reduction is insufficient to produce changes in physiological indicators, so its use does not diminish hypoxaemia, hypercapnia, lactic acid production or incidence of EIPH (Goetz et al 2001). However, studies by Geor et al (2001) in race horses showed that the simultaneous use of nasal patches and furosemide attenuated the presentation of EIPH and diminished the presence of erythrocytes in the BALF.…”

“…These changes in pressure, accompanied by a negative pleural pressure and largevolume ventilation during maximal exercise may induce transmural capillary pressure that breaks the endothelial cell junctions in the alveolar epithelium, which ruptures the pulmonary capillaries (Manohar et al 1993;Mathieu-Costello, 1994, 1995;Deksen et al 2001). It has been shown that there is insufficient gas exchange due to the disruption of pulmonary capillaries, which suffer from arterial hypoxaemia and hypercapnia, which leads to increased anaerobic metabolism (Manohar et al 2001;Caillaud et al 2002). The fact that EIPH occurs after high-intensity exercise and prolonged low-intensity exercise suggests that this problem is due to extreme mechanical stresses on the tissue and pulmonary vessels during exercise (Art and Lekeux 1994).…”