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

Abstract

Despite enormous rates of minute ventilation (V̇e) 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 V̇e in the horse such as those found during galloping (Bramble and Carrier. Science 219: 251–256, 1983), V̇e should drop precipitously when LRC ceases at the galloptrot 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 V̇e, O2uptake, and CO2output 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, V̇e did not drop instantaneously. Rather, V̇e 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; 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, V̇e declined in a biphasic fashion with a slower mean response time (85.4 ± 9.0 s) than that of the monoexponential decline of CO2output (39.9 ± 4.7 s; P < 0.05), which rapidly reversed the postexercise arterial hypercapnia (arterial Pco2at 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 V̇e commensurate with maximal exercise or the pronounced hyperventilation during recovery.