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1Departments of Anatomy and Physiology, 3Kinesiology, Kansas State University, Manhattan, Kansas 66506; and 2Department of Medicine, University of California, San Diego, La Jolla, California 92093
Submitted 15 September 2003 ; accepted in final form 4 February 2004
Despite enormous rates of minute ventilation (
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
E in the horse such as those found during galloping (Bramble and Carrier. Science 219: 251256, 1983),
E 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; 1415 m/s) to study the dynamic control of breath-by-breath
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,
E did not drop instantaneously. Rather,
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; 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,
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
E commensurate with maximal exercise or the pronounced hyperventilation during recovery.
exercise recovery; locomotory-respiratory coupling; blood acid-base; equid
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