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

mous rates of minute ventilation (V ˙ 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 ˙ E in the horse such as those found during galloping (Bramble and Carrier. Science 219: 251–256, 1983), V ˙ 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 ˙ E, O2 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 ˙ E did not drop instantaneously. Rather, V ˙ E remained at the peak exercising levels (1,391 88 l/min) for 13 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