Ventilatory dynamics and control of blood gases after maximal exercise in the Thoroughbred horse

Despite enormous rates of minute ventilation ((V)over dot E) in the galloping Thoroughbred (TB) horse, the energetic demands of exercise conspire to raise arterial PCO2 (i.e., induce hypercapnia). If locomotory-respiratory coupling (LRC) is an obligatory facilitator of high (V)over dot E in the horse such as those found during galloping (Bramble and Carrier. Science 219: 251-256, 1983), (V)over dot E should drop precipitously when LRC ceases at the gallop-trot transition, thus exacerbating the hypercapnia. TB horses (n=5) were run to volitional fatigue on a motor-driven treadmill (1 m/s increments; 14-15 m/s) to study the dynamic control of breath-by-breath (V)over dot E, O-2 uptake, and CO2 output at the transition from maximal exercise to active recovery (i.e., trotting at 3 m/s for 800 m). At the transition from the gallop to the trot, (V)over dot E did not drop instantaneously. Rather, V. E remained at the peak exercising levels (1,391+/-88 l/min) for similar to13 s via the combination of an increased tidal volume (12.6+/-1.2 liters at gallop; 13.9+/-1.6 liters over 13 s of trotting recovery; P<0.05) and a reduced breathing frequency [113.8 +/- 5.2 breaths/min (at gallop); 97.7 +/- 5.9 breaths/min over 13 s of trotting recovery (P<0.05)]. Subsequently, V. E declined in a biphasic fashion with a slower mean response time (85.4+/-9.0 s) than that of the monoexponential decline of CO2 output (39.9+/-4.7 s; P<0.05), which rapidly reversed the postexercise arterial hypercapnia (arterial PCO2 at gallop: 52.8 +/- 3.2 Torr; at 2 min of recovery: 25.0 +/- 1.4 Torr; P<0.05). We conclude that LRC is not a prerequisite for achievement of (V)over dot E commensurate with maximal exercise or the pronounced hyperventilation during recovery.