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J Appl Physiol 96: 2187-2193, 2004. First published February 6, 2004; doi:10.1152/japplphysiol.00998.2003
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Ventilatory dynamics and control of blood gases after maximal exercise in the Thoroughbred horse

Danielle J. Padilla,1 Paul McDonough,1 Casey A. Kindig,2 Howard H. Erickson,1 and David C. Poole1,3

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: 251–256, 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; 14–15 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



Address for reprint requests and other correspondence: D. C. Poole, Dept. of Anatomy and Physiology, 228 Coles Hall, Kansas State Univ., Manhattan, KS 66506 (E-mail: poole{at}vet.k-state.edu).







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