Hyperhydration prior to a simulated second day of the 3-day moderate intensity equestrian competition does not cause arterial hypoxemia in Thoroughbred horses

Dehydration and the associated impairment of cardiovascular and thermoregulatory function comprise major veterinary problems in horses performing prolonged exercise, particularly under hot and humid conditions. For these reasons, there is considerable interest in using pre-exercise hyperhydration to help maintain blood volume in the face of the excessive fluid loss associated with sweat production during prolonged exertion. However, recently it was reported that pre-exercise hyperhydration causes arterial hypoxemia in horses performing moderate intensity exercise simulating the second day of an equestrian 3-day event competition (E3DEC) which may adversely affect performance (Sosa Leon et al. in Equine Vet J Suppl 34:425–429, 2002). These findings are contrary to data from horses performing short-term maximal exertion, wherein hyperhydration did not affect arterial O₂ tension/saturation. Thus, our objective in the present study was to examine the impact of pre-exercise hyperhydration on arterial oxygenation of Thoroughbred horses performing an exercise test simulating the second day of an E3DEC. Control and hyperhydration studies were carried out on seven healthy Thoroughbred horses in random order, 7 days apart. In the control study, horses received no medications. In the hyperhydration experiments, nasogastric administration of NaCl (0.425 g/kg) 5 h pre-exercise induced a plasma volume expansion of 10.9% at the initiation of exercise. This methodology for inducing hypervolemia was different from that of Sosa Leon et al. (2002). Blood-gas tensions/pH as well as plasma protein, hemoglobin and blood lactate concentrations were measured pre-exercise and during the exercise test. Our data revealed that pre-exercise hyperhydration neither adversely affected arterial O₂ tension nor hemoglobin-O₂ saturation at any time during the exercise test simulating the second day of an E3DEC. Further, it was observed that arterial blood CO₂ tension, pH, and blood lactate concentrations also were not affected by pre-exercise hyperhydration. However, hemodilution in hyperhydrated horses caused an attenuation of the expansion in the arterial to mixed-venous blood O₂ content gradient during phases B and D of the exercise protocol, which was likely offset by an increase in cardiac output. It is concluded that pre-exercise hyperhydration of horses induced in the manner described above is not detrimental to arterial oxygenation of horses performing an exercise test simulating the second day of an E3DEC.     

Arterial hypoxemia in exercising thoroughbreds is not affected by pre-exercise nedocromil sodium inhalation

It has been reported that pulmonary injury (i.e. capillary stress failure) evoked histamine release from airway inflammatory/mast cells contributes to exercise-induced arterial hypoxemia (EIAH) and that pre-exercise inhalation of nedocromil sodium mitigated EIAH in human subjects 'Med. Sci. Sports Exercise 29, (1997) 10-16'. Because exercise-induced pulmonary hemorrhage due to capillary stress failure is routinely observed in racehorses, we examined whether nedocromil inhalation would similarly benefit EIAH and desaturation of hemoglobin in horses. Two sets of experiments, namely, placebo studies followed in 7 days by pre-exercise nedocromil sodium (30 puffs=60 mg) inhalation experiments were carried out on 7 healthy, sound, exercise-trained thoroughbred horses. In both treatments, arterial and mixed-venous blood-gas/pH measurements were made at rest pre- and post-placebo/drug inhalation, as well as during incremental exercise leading to galloping at 14 m/sec on a 3.5% uphill grade-a workload that elicited maximal heart rate and caused pulmonary hemorrhage in all horses in both treatments, thereby indicating capillary stress failure had occurred. In both treatments, significant (P<0.0001) EIAH of a similar magnitude had developed by 30 sec of maximal exertion, and further significant changes in arterial O(2) tension did not occur as exercise duration progressed to 120 sec. Thus, pre-exercise inhalation of nedocromil sodium was ineffective in modifying the development and/or severity of EIAH in the present study. These findings argue against the airway inflammatory mediator(s) release hypothesis for causing arterial hypoxemia in racehorses.     

Acute hypervolemia lengthens red cell pulmonary transit time during exercise in endurance athletes

The purpose was to determine if acute plasma volume expansion (PVE) changed red-cell pulmonary transit time (PTT) during severe exercise. Twelve endurance athletes performed 6.5 min of severe cycling exercise on different days. Pentaspan [(500 ml, infusion condition, I] or placebo [(60 ml saline), non-infusion condition, N] were infused prior to exercise. Blood gas tensions, PTT, multigated acquisition (MUGA) derived cardiac output, and oxygen uptake were measured during exercise. PTT was measured during minute 3 of exercise by radionuclide cardiography. Arterial P(O(2)) (Pa(O(2))), and alveolar-arterial oxygen pressure difference (AaD(O(2))) at minute 3 of exercise did not differ between conditions. Mean PTT at minute 3 of exercise was 0.3 sec longer in the I condition (P=0.002). However, the change in PTT between conditions was not correlated to the change in either Pa(O(2)) or AaD(O(2)). We conclude that PVE slows (lengthens) PTT without affecting pulmonary gas exchange. Therefore, rapid PTT may not be related to hypoxemia during exercise.     

Acute hypoxic ventilatory response and exercise-induced arterial hypoxemia in men and women

Recent studies claim a higher prevalence of exercise-induced arterial hypoxemia (EIAH) in women relative to men and that diminished peripheral chemosensitivity is related to the degree of arterial desaturation during exercise in male endurance athletes. The purpose of this study was to determine the relationship between the acute ventilatory response to hypoxia (AHVR) and EIAH and the potential influence of gender in trained endurance cyclists and untrained individuals. Healthy untrained males (n = 9) and females (n = 9) and trained male (n = 11) and female (n = 10) cyclists performed an isocapnic AHVR test followed by an incremental cycle test to exhaustion. Oxyhemoglobin saturation (Sa(O(2)) was lower in trained men (91.4 +/- 0.9%) and women (91.3 +/- 0.9%) compared to their untrained counterparts (94.4 +/- 0.8% versus 94.3 +/- 0.7%) (P < 0.05). AHVR and maximal O(2) consumption were related for all subjects (r = -0.46), men (r = -0.45) and women (r = -0.53) (P < 0.05) but AHVR was unrelated to Sa(O(2)) for any groups (P > 0.05). We conclude that resting AHVR does not have a significant role in maintaining Sa(O(2)) during sea-level maximal cycle exercise in men or women.     

Bovine colostrum supplementation does not affect plasma buffer capacity or haemoglobin content in elite female rowers

It has been reported that bovine colostrum (BC) supplementation improves buffer capacity () during exercise, but whether the improvement results from changes in tissue and/or blood buffer systems has not been determined. The purpose of the present study was to examine the effect of supplementation with BC on blood buffer systems. Thirteen elite females rowers were supplemented with 60 g·day^–1 of either BC (n=6) or whey protein (WP, n=7) during 9 weeks of pre-competition training in a randomised, double-blind, placebo-controlled, parallel design. All subjects undertook the study as a group and completed the same training program. Resting haemoglobin (Hb) concentration and plasma buffer capacity (p) (determined by titration with HCl) were measured pre- and post-supplementation. There were no differences in macronutrient intakes (P>0.56) or training volumes (P>0.99) between BC and WP during the study period. There were no differences in Hb [BC 13.28 (0.28) mg·dl^–1, WP 13.70 (0.26) mg·dl^–1; P=0.45] or p [BC 14.8 (1.1) nmol HCl·ml^–1·pH^–1, WP 14.8 (0.5) nmol HCl·ml^–1·pH^–1; P=0.68] between groups at week 0. p increased in both groups during the study period (P<0.001), but the increases were not significantly different between groups (P=0.52). Hb did not change significantly in either group (P=0.35). These data indicate that supplementation with BC does not affect p or Hb. We therefore suggest that adaptations in tissue buffer systems are responsible for the previously reported increases in buffer capacity that result from BC supplementation.