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Previous work has shown that replacing N2 in air with He at the same inspired O2 fraction reduces the exercise-induced alveolar-arterial PO2 difference (AaPO2) in horses but has provided no mechanism explaining this effect. We sought to distinguish among possible causes by using the multiple inert gas elimination technique. Six horses were studied on a high-speed treadmill while they breathed either ambient air or normoxic He-O2. O2 uptake reached 138.0 ml.min-1.kg-1 and was not affected by He-O2. Temperature-corrected arterial PO2 was 76.7 Torr (air) and 86.9 Torr (He-O2) (P < 0.01). Corresponding AaPO2 was 22.3 and 15.9 Torr, respectively (P < 0.01). Mean AaPO2 predicted from ventilation-perfusion inequality did not change with He-O2 (12.7 Torr with air and 11.9 Torr with He-O2). Mean arterial PCO2 was 50.1 Torr with air and 44.1 Torr with He-O2 (P < 0.01); minute ventilation and tidal volume were correspondingly higher by 140 l/min and 1.0 liter, respectively, with He-O2. Pulmonary O2 diffusing capacity, cardiac output, and all ventilation-perfusion dispersion indexes did not change with He-O2. Intrapulmonary shunt was insignificant. Higher ventilation with He-O2 explained only approximately 4 Torr of the 10-Torr rise observed in arterial PO2. The remainder (and the corresponding fall in AaPO2) was due to more complete diffusion equilibration as a consequence of the higher minute ventilation and thus alveolar PO2, which reduced the average slope of the O2 dissociation curve, thereby increasing the ratio of diffusive to perfusive conductance.

We determined the weight, volume and center of gravity (CG) of 20 frozen body segments using three Thoroughbred horses. Segment weight and volume to whole body weight and volume were 4.4 and 4.1 (%) for the head, 7.0 and 6.5 neck, 59.5 and 63.0 torso, 9.2 and 8.6 scapulabrachia, 1.8 and 1.6 antebrachia, 0.5 and 0.4 metacarpi, 0.5 and 0.4 digiti, 13.8 and 12.7 thigh, 2.0 and 1.6 crura, 0.8 and 0.6 metatarsi, 0.6 and 0.4 digiti, and 0.1 and 0.1 for the tail. Segmental body density was more than 1 g/m3 except 0.90 g/cm3 for the torso. Total body density calculated from total weight and volume was 0.95 g/cm3. The location of CG for each body segment was presented on the reference line by percentage of distance from location of segment CG to proximal end which was divided by the segment length.

Summary 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 (V̇a/Q̇) 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 V̇a/Q̇ mismatch, we studied an additional 6 Thoroughbreds, comparing V̇a/Q̇ relationships at the walk (1.4 m/s, 0o 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 V̇a/Q̇ mismatch (similar under all 4 conditions). The second moment of the V̇a/Q̇ 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 V̇a/Q̇ mismatch can occur in the horse as in man, but the mechanism remains to be elucidated and its clinical significance remains to be established. It may reflect interstitial pulmonary oedema but effects on arterial oxygenation are minimal.