The horse is a superb athlete, achieving a maximal O2 uptake (approximately 160 ml . min-1 . kg-1) approaching twice that of the fittest humans. Although equine O2 uptake (VO2) kinetics are reportedly fast, they have not been precisely characterized, nor has their exercise intensity dependence been elucidated. To address these issues, adult male horses underwent incremental treadmill testing to determine their lactate threshold (Tlac) and peak VO2 (VO2 peak), and kinetic features of their VO2 response to "square-wave" work forcings were resolved using exercise transitions from 3 m/s to a below-Tlac speed of 7 m/s or an above-Tlac speed of 12.3 +/- 0.7 m/s (i.e., between Tlac and VO2 peak) sustained for 6 min. VO2 and CO2 output were measured using an open-flow system: pulmonary artery temperature was monitored, and mixed venous blood was sampled for plasma lactate. VO2 kinetics at work levels below Tlac were well fit by a two-phase exponential model, with a phase 2 time constant (tau1 = 10.0 +/- 0.9 s) that followed a time delay (TD1 = 18.9 +/- 1.9 s). TD1 was similar to that found in humans performing leg cycling exercise, but the time constant was substantially faster. For speeds above Tlac, TD1 was unchanged (20.3 +/- 1.2 s); however, the phase 2 time constant was significantly slower (tau1 = 20.7 +/- 3.4 s, P < 0.05) than for exercise below Tlac. Furthermore, in four of five horses, a secondary, delayed increase in VO2 became evident 135.7 +/- 28.5 s after the exercise transition. This "slow component" accounted for approximately 12% (5.8 +/- 2.7 l/min) of the net increase in exercise VO2. We conclude that, at exercise intensities below and above Tlac, qualitative features of VO2 kinetics in the horse are similar to those in humans. However, at speeds below Tlac the fast component of the response is more rapid than that reported for humans, likely reflecting different energetics of O2 utilization within equine muscle fibers.

Fast-growing broiler chickens not uncommonly exhibit elevated pulmonary vascular resistance that leads to pulmonary hypertension and right ventricular failure. We tested the hypothesis that a distended gastrointestinal tract in these full-fed birds results in an abnormally low tidal volume and minute ventilation that could lead to pulmonary hypoxia, pulmonary arterial vasoconstriction, right ventricular failure, and ascites. Tidal volume, respiratory frequency, heart rate, percentage saturation of hemoglobin with oxygen (HbO2), O2 consumption, and carbon dioxide elimination were measured on fast-growing broiler chickens when full-fed and after 3, 6, and 9 h of feed deprivation. Tidal volume of full-fed birds was not abnormally low despite HbO2 values varying from above 80% to nearly 60%. Importantly, HbO2 was found to be markedly increased in the hypoxemic birds at and beyond a 3-h period without feed, despite a reduction in minute ventilation. This response was not caused by a decrease in O2 consumption. Thus, limitation of gas intake at the mouth was not the cause of the hypoxemia. The data suggest that feed deprivation results in an increase in parabronchial ventilation, possibly from improvement in aerodynamic valving, which would reduce pulmonary hypoxic vasoconstriction and right ventricular failure.

We evaluated the influence of the percentage saturation of hemoglobin with oxygen (HbO2) on the pulmonary arterial pressure in normal and preascitic (hypoxemic) broilers breathing ambient air or 100% O2. In Experiment 1, unanesthetized preascitic broilers (right:total ventricular weight ratios [RV:TV] = 0.32+/-0.02) breathing ambient air had initial values of 67% for HbO2 and 32 mm Hg for pulmonary arterial pressure. The HbO2 increased to > or =96.6% during inhalation of 100% O2; however, pulmonary arterial pressure was not reduced. In Experiment 2, anesthetized normal (RV:TV = 0.23; HbO2 = 88%) and preascitic broilers (RV:TV = 0.28; HbO2 = 76%) were compared. The groups did not differ in body weight or respiratory rate, but preascitic broilers had lower values for mean arterial pressure, total peripheral resistance, and partial pressure of O2 in arterial blood and had higher values for pulmonary arterial pressure. Inhaling 100% O2 increased HbO2 to 99.9% in both groups; however, pulmonary arterial pressure remained higher in preascitic than in normal broilers, and the pulmonary vascular resistance was not reduced during 100% O2 inhalation. Cardiac output was higher in preascitic than in normal broilers before and after, but not during, 100% O2 inhalation. Mean arterial pressure and total peripheral resistance increased in the preascitic but not in the normal group during 100% O2 inhalation. Low coefficients of determination (R2) were obtained for linear regression comparisons of HbO2 vs. pulmonary arterial pressure in both experiments. Overall, acute reversal of the systemic hypoxemia in preascitic broilers had little direct impact on pulmonary hypertension, providing no evidence of hypoxemic or hypoxic pulmonary vasoconstriction. Instead, acute reversal of the systemic hypoxemia primarily increased the total peripheral resistance and normalized the mean arterial pressure and cardiac output. A sustained reduction in cardiac output theoretically should attenuate pulmonary hypertension, but this was not observed because of the overriding influence of sustained pulmonary vascular resistance.

Summary The objective of this study was to develop and test a technique to allow dynamic cardiac function to be studied during exercise in the horse. Blood pressure waveforms in the exercising horse are difficult to interpret because of the large influence of stride and respiration. A method has been devised to study dynamic right ventricular variables during high‐speed exercise in the horse. A Fast Fourier Transform was performed on the digitised pressure waveforms and the frequency components associated with stride and respiration were removed. An inverse Fourier Transform was then performed to generate a time‐domain pressure signal. Several dynamic right ventricular variables were calculated using the derived signal. Various parameters associated with removing frequencies from the frequency‐domain pressure signal were changed to determine their influence on the variables. Most of the variables were not sensitive to these parameters. When compared during separate exercise bouts, some variables differed among runs, while others were not significantly different. Using the signal separation technique described here, right ventricular function of an exercising horse can be critically analysed.

SummaryExercising horses have extremely high right and left atrial pressures. Limitation in ventricular function (i.e. relaxation) may play a role in these high pressures. We studied relaxation characteristics of the right ventricular myocardium and the impact of frusemide (2.0 mgkg bwt i.v.) on these characteristics in horses exercising at 8, 10, 12 and 14 mls. Exercise tests were performed 4 h after administration of frusemide. Right ventricular (RV) pressure was analysed using Fast Fourier Transform techniques to remove non cardiac components of the pressure signal. Mean right atrial (RA) pressure increased with exercise and was significantly attenuated at all speeds by frusemide. RV maximum and minimum rates of pressure change with respect to time (RV+dP/dt,,,,,, RV-dP/dt,,,,,) increased with exercise and RV relaxation time constant (RVT) and time of RV relaxation from 65-20% of the difference between maximum and minimum ventricular pressure (1165-20) decreased with exercise. Frusemide produced no significant differences in +dP/dt,,,,,, -dP/dt,,,,,, RVT or A65-20 except at 12 m l s where RVT was longer after frusemide (23.4 ms for frusemide vs. 19.7 ms for control). Significant reductions in stroke volume were seen at 8,lO and 14 m l s after frusemide. These results suggest that the reduction of atrial pressure by frusemide is not due to changes in ventricular relaxation rate.