Ventilation-perfusion relationships during exercise in standardbred trotters with red cell hypervolaemia.
ABSTRACT In order to evaluate the pulmonary gas exchange during exercise in Standardbred trotters with red cell hypervolaemia (RCHV), 12 horses with RCHV were compared with 9 normovolaemic (NV) horses. VO2 and VCO2 were determined with an open bias flow system. Cardiovascular and haemodynamic data were recorded during exercise at 4 different speeds on a treadmill. Pulmonary gas exchange was assessed by conventional blood gas variables (arterial and mixed venous blood gas tensions), and the ventilation-perfusion distribution VA/Q was estimated by the multiple inert gas elimination technique. VA and AaDO2 were calculated. Dispersions of perfusion and ventilation distribution (SDQ, SDV) were determined. HR, RR, Qt, VO2, VA, log SDV, C(a-åv)O2 and lactate did not differ between groups. The degree of hypoxaemia was more pronounced in the RCHV than in the NV (PaO2 = 54 and 59 mmHg; AaDO2 = 41 and 34 mmHg in RCHV and NV, respectively, at highest workload). Further, pH was lower in the RCHV and PaCO2 and VCO2 was significantly higher in the RCHV during the course of exercise (pH = 7.24 and 7.29; PaCO2 = 56 and 51 mmHg; VCO2 = 156 and 135 ml/kg x min in RCHV and NV, respectively, at highest workload). The PaO2 predicted from the VA/Q distribution was higher than actually measured in blood during heavy exercise which may suggest a certain diffusion limitation over the alveolar-capillary membranes in both groups but there was no difference between the 2 groups. The more pronounced hypoxaemia observed in RCHV trotters was mainly caused by increased VA/Q mismatch expressed as a significantly increased log SDQ (0.78 and 0.45 in RCHV and NV, respectively, at highest workload).
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ABSTRACT: Exercise in normal human subjects causes deterioration of matching of ventilation to blood flow in the lungs, but only in about 50% of those examined. A previous study (Wagner et al. 1989) of 5 horses showed no significant worsening of ventilation/blood flow (VA/Q) relationships during heavy exercise as determined by multiple inert gas elimination technique (MIGET). Because of the small number of horses in that study and the 50% human incidence of exercise induced VA/Q mismatch, we studied an additional 6 Thoroughbreds, comparing VA/Q relationships at the walk (1.4 m/s, 0 degrees incline) and during galloping (9.6 +/- 0.3 m/s, 7% incline). Such data were collected under 4 different conditions wherein inspired gas was 1) air, 2) 21% O2 in helium, 3) 15% O2 in N2 and 4) 15% O2 in helium. Each horse exercised 4 times (morning and afternoon of 2 days, with inspired gas conditions randomised). There was a small but significant increase in VA/Q mismatch (similar under all 4 conditions). The second moment of the VA/Q distribution (determined by the MIGET) increased significantly (P < 0.01) from 0.31 +/- 0.01 at the walk to 0.38 +/- 0.02 during gallop. This increase however is small: 0.38 is well within the range of this parameter for normal human subjects (where the 95% upper confidence limit is 0.60). This study shows that a small amount of exercise induced VA/Q mismatch can occur in the horse as in man, but the mechanism remains to be elucidated and its clinical significance remains to be established.(ABSTRACT TRUNCATED AT 250 WORDS)Equine Veterinary Journal 04/1995; 27(2):104-9. · 2.29 Impact Factor
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ABSTRACT: The aim of this study was to evaluate pulmonary function in Standardbred trotters during graded exercise. The exercise test consisted of 4 work loads corresponding to 10%, 42%, 70% and 96% of the individual V̇O2max. Oxygen uptake was detected from an open bias flow system without valves. Cardiovascular and haemodynamic data were recorded at walk and during steady state exercise in 7 horses. Pulmonary gas exchange was assessed by conventional blood gas variables (arterial and mixed venous blood gas tensions) and the ventilation-perfusion distribution V̇A|Q̇ as estimated by the multiple inert gas elimination technique. The dispersion of perfusion and ventilation distribution respectively (SDQ) and the difference between measured PaO2 and that predicted on the basis of amount of ventilation-perfusion mismatching and shunt that was observed (predicted-measured), were determined. The latter reflects mostly diffusion limitation. At the highest work load the PaCO2 increased to 50.3 torr. V̇A|Q̇ inequality increased significantly with exercise [mean log = 0.32 ± 0.03 (walk) and 0.46 ± 0.06 (heavy exercise), P < 0.01]. Alveolar-capillary diffusion limitation of oxygen was evident at and above exercise at 70% of V̇O2max. The arterial hypoxaemia seen during the highest work load was a result of a) hypoventilation, accounting for 4%, b) increase in V̇A|Q̇ mismatch, accounting for 41% and c) considerable diffusion limitation of oxygen, accounting for 55%.Equine Veterinary Journal 06/2010; 27(S18):63 - 69. · 2.29 Impact Factor
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ABSTRACT: During maximal exercise, ventilation-perfusion inequality increases, especially in athletes. The mechanism remains speculative. We hypothesized that, if interstitial pulmonary edema is involved, prolonged exercise would result in increasing ventilation-perfusion inequality over time by exposing the pulmonary vascular bed to high pressures for a long duration. The response to short-term exercise was first characterized in six male athletes [maximal O2 uptake (V(O2)max) = 63 ml x kg-1 x min-1] by using 5 min of cycling exercise at 30, 65, and 90% V(O2) max. Multiple inert-gas, blood-gas, hemodynamic, metabolic rate, and ventilatory data were obtained. Resting log SD of the perfusion distribution (log SDQ) was normal [0.50 +/- 0.03 (SE)] and increased with exercise (log SDQ = 0.65 +/- 0.04, P < 0.005), alveolar-arterial O2 difference increased (to 24 +/- 3 Torr), and end-capillary pulmonary diffusion limitation occurred at 90% V(O2)max. The subjects recovered for 30 min, then, after resting measurements were taken, exercised for 60 min at approximately 65% V(O2)max. O2 uptake, ventilation, cardiac output, and alveolar-arterial O2 difference were unchanged after the first 5 min of this test, but log SDQ increased from 0.59 +/- 0.03 at 5 min to 0. 66 +/- 0.05 at 60 min (P < 0.05), without pulmonary diffusion limitation. Log SDQ was negatively related to total lung capacity normalized for body surface area (r = -0.97, P < 0.005 at 60 min). These data are compatible with interstitial edema as a mechanism and suggest that lung size is an important determinant of the efficiency of gas exchange during exercise.Journal of Applied Physiology 11/1998; 85(4):1523-32. · 3.48 Impact Factor