Mechanistic basis for the gas exchange threshold in Thoroughbred horses.

The exercising Thoroughbred horse (TB) is capable of exceptional cardiopulmonary performance. However, because the ventilatory equivalent for O2 (VE/VO2) does not increase above the gas exchange threshold (Tge), hypercapnia and hypoxemia accompany intense exercise in the TB compared with humans, in whom VE/VO2 increases during supra-Tge work, which both removes the CO2 produced by the HCO buffering of lactic acid and prevents arterial partial pressure of CO2 (PaCO2) from rising. We used breath-by-breath techniques to analyze the relationship between CO2 output (VCO2) and VO2 [V-slope lactate threshold (LT) estimation] during an incremental test to fatigue (7 to approximately 15 m/s; 1 m x s(-1) x min(-1)) in six TB. Peak blood lactate increased to 29.2 +/- 1.9 mM/l. However, as neither VE/VO2 nor VE/VCO2 increased, PaCO2 increased to 56.6 +/- 2.3 Torr at peak VO2 (VO2 max). Despite the presence of a relative hypoventilation (i.e., no increase in VE/VO2 or VE/VCO2), a distinct Tge was evidenced at 62.6 +/- 2.7% VO2 max. Tge occurred at a significantly higher (P < 0.05) percentage of VO2 max than the lactate (45.1 +/- 5.0%) or pH (47.4 +/- 6.6%) but not the bicarbonate (65.3 +/- 6.6%) threshold. In addition, PaCO2 was elevated significantly only at a workload > Tge. Thus, in marked contrast to healthy humans, pronounced V-slope (increase VCO2/VO2) behavior occurs in TB concomitant with elevated PaCO2 and without evidence of a ventilatory threshold.