Submitted on September 15, 2003
Accepted on February 4, 2004
Ventilatory dynamics and control of blood gases following maximal exercise in the Thoroughbred horse
Danielle J Padilla1, Paul McDonough1, Casey A Kindig2, Howard H Erickson1, and David C Poole3*
1 Department of Anatomy & Physiology, Kansas State University, Manhattan, Kansas, USA
2 Department of Medicine, University of California, San Diego, La Jolla, California, USA
3 Department of Anatomy & Physiology, Kansas State University, Manhattan, Kansas, USA; Department of Kinesiology, Kansas State University, Manhattan, Kansas, USA
* To whom correspondence should be addressed. E-mail: poole{at}vet.k-state.edu.
Despite enormous rates of ventilation (VE) in the galloping Thoroughbred (TB), the energetic demands of exercise conspire to raise arterial CO2 pressure (PaCO2: i.e. induce hypercapnia). If locomotory-respiratory coupling (LRC) is an obligatory facilitator of high VE's in the such as those found during galloping (Bramble and Carrier, Science 219: 251-256, 1983), VE should drop precipitously when LRC ceases at the gallop-trot transition, thus exacerbating the hypercapnia. TBs (n=5) were run to volitional fatigue on a motor-driven treadmill (1 m/s increments; 14 - 15 m/s) in order to study the dynamic control of breath-by-breath VE, O2 uptake (VO2), and CO2 output (VCO2) 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, VE did not drop instantaneously. Rather, VE remained at the peak exercising levels (1391±88 L/min) for ~13 s, via the combination of an increased tidal volume (VT: 12.6±1.2 L at gallop; 13.9±1.6 L over 13 s of trotting recovery; P < 0.05) and a reduced breathing frequency (113.8±5.2 br/min (at gallop); 97.7±5.9 br/min over 13 s of trotting recovery (P < 0.05)). Subsequently, VE declined in a bi-phasic fashion with a slower mean response time (MRT; 85.4±9.0 s) than that of the monoexponential decline of VCO2 (39.9±4.7 s; P < 0.05) which rapidly reversed the post-exercise arterial hypercapnia (PaCO2 at gallop: 2.8±3.2; 2 min recovery: 25.0±1.4 mmHg; P < 0.05). We conclude that LRC is not a prerequisite for achievement of VE's commensurate with maximal exercise or the pronounced hyperventilation during recovery.
