Workload and spirometry associated with untethered swimming in horses.

BACKGROUND: Swimming has been used empirically for rehabilitation and conditioning of horses. However, due to challenges imposed by recording physiological parameters in water, the intensity of free swimming effort is unknown. OBJECTIVES: Measure the physiological workload associated with untethered swimming in horses. Five fit Arabian endurance horses were assessed while swimming in a 100 m-long indoor pool. Horses were equipped with a modified ergospirometry facemask to measure oxygen consumption (V̇O2) and ventilatory parameters (inspired/expired volumes, VI, VE; peak inspiratory/expiratory flows, PkVI, PkVE; respiratory frequency, Rf; minute ventilation, VE; inspiratory/expiratory durations and ratios, tI, tE, tI/ttot, tE/ttot); and an underwater electrocardiogram that recorded heart rate (HR). Postexercise venous blood lactate and ammonia concentrations were measured. Data are reported as median (interquartile ranges). RESULTS: Horses showed bradypnea (12 breaths/min (10-16)) for the first 30 s of swimming. V̇O2 during swimming was 43.2 ml/(kg.min) (36.0-56.6). Ventilatory parameters were: VI = 16.7 L (15.3-21.8), VE = 14.7 L (12.4-18.9), PkVI = 47.8 L/s (45.8-56.5), PkVE = 55.8 L/s (38.3-72.5), Rf = 31.4 breaths/min (20.0-33.8), VE = 522.9 L/min (414.7-580.0), tI = 0.5 s (0.5-0.6), tE = 1.2 s (1.1-1.6), tI/ttot = 0.3 (0.2-0.4), tE/ttot = 0.7 (0.6-0.8). Expiratory flow tracings showed marked oscillations that coincided with a vibrating expiratory sound. HR was 178.0 bpm (148.5-182.0), lactate = 1.5 mmol/L (1.0-1.9) and ammonia = 41.0 µmol/L (36.5-43.5). CONCLUSIONS: Free (untethered) swimming represents a submaximal, primarily aerobic exercise in horses. The breathing pattern during swimming is unique, with a relatively longer apneic period at the beginning of the exercise and an inspiratory time less than half that of expiration.

Pharmacokinetics of furosemide in thoroughbred horses subjected to supramaximal treadmill exercise with and without controlled access to water.

BACKGROUND: The primary objective of this study was to assess the disposition of furosemide in Thoroughbred horses treated intravenously with 1 mg/kg of furosemide 4 and 24 h before supramaximal treadmill exercise without and with controlled access to water, respectively. Another objective was to determine whether furosemide was detectable in the plasma of horses after exposure to supramaximal treadmill exercise. Thoroughbred horses (n = 4-6) were administered single intravenous doses of 1 mg/kg of furosemide at 4 and 24 h before supramaximal exercise on a high-speed treadmill, with controlled and free access to water, respectively. Plasma furosemide concentrations were determined using liquid chromatography. RESULTS: Furosemide was detected in all the horses, regardless of whether they were treated 24 h or 4 h before excersice. In both treatment sequence groups of 2 horses, the concentration time profiles of furosemide during the first 4 h after its administration were relatively similar. The average maximum observed concentrations, AUC0-1.5h, and AUC0-3h, of both groups of horses were not different (p > 0.05). There were no significant differences in systemic clearance based on the geometric mean (95% confidence interval) (409 (347-482) mL/h/kg) for 4 h and 320 (177-580) mL/h/kg) for 24 h) between horses that were exercised 4- and 24-h post-furosemide administration. The plasma concentration of furosemide in all the horses fell below the limit of quantification (25 ng/mL) within 12 h after drug administration. In the group treated 24 h before exercise, none of the horses had detectable furosemide at the time of supramaximal treadmill exercise. In the group treated 4 h before exercise, furosemide was detected 1 h before and 2 h after supramaximal treadmill exercise in 4/4 and 3/4 horses, respectively. The mean AUC3-last h of both groups of horses were not different (p > 0.05). CONCLUSIONS: Water restriction did not exert any apparent effect on the disposition of furosemide. It remains to be determined, however, whether the attained plasma concentration of furosemide in combination with other controlled water access protocols have any direct or indirect pharmacological effect that may affect the athletic performance of the horse.

Comparison of ventilatory and oxygen consumption measurements of yearling Thoroughbred colts and fillies exercising unridden on an all-weather track.

Sex effects on ventilatory and oxygen consumption (V̇O2) measurements during exercise have been identified in humans. This study's aim was to evaluate the hypothesis that there are sex effects on ventilatory and V̇O2 measurements in exercising, untrained yearling Thoroughbreds (Tb). Forty-one Tbs (16 colts, 25 fillies; 19.8 ± 1.4 months old) were recruited. Physiological, ventilatory and exercise data were gathered from horses exercising unridden at high intensity on an all-weather track from a global positioning-heart rate unit and a portable ergospirometry system. Data were analysed with an unpaired Student's t-test and the Benjamini-Hochberg correction for multiple testing (P ≤ 0.05 significant). Mean bodyweight (BW, P = 0.002) and wither height (P = 0.04) were greater for colts than fillies. There were no differences in physiological and exercise data and absolute peak V̇O2 between groups. However, fillies had a higher mass specific peak V̇O2 (P = 0.03) than colts (121.5 ± 21.6 mL/kg.min vs. 111.9 ± 27.4 mL/kg.min). The peak breathing frequency was greater for fillies (P < 0.001) while the peak inspiratory (P < 0.001) and expiratory air flow (P < 0.001), peak expiratory tidal volume (VTE; P < 0.001) and peak minute ventilation (V̇E; P = 0.01) were greater for colts; there were no differences for peak VTE and V̇E when adjusted for BW. Differences in BW explain the differences in mass specific peak V̇O2 between groups. Given their morphological differences, it is likely that lung volumes and airway diameters are smaller for fillies, resulting in greater resistance and lower air flows and volumes. Further research is required to investigate the ventilatory differences and how they may change with maturation and impact performance.

The lipidome of Thoroughbred racehorses before and after supramaximal exercise.

BACKGROUND: A comprehensive study of the effect of supramaximal exercise in lipid homeostasis of Thoroughbreds provides the basis for future research on the role of lipids on energy metabolism in racehorses. OBJECTIVE: To compare the plasma lipidome of Thoroughbreds before and after supramaximal exercise using an untargeted lipidomics approach. STUDY DESIGN: Pilot experimental study. METHODS: Four Thoroughbred horses were used. The maximal oxygen consumption (VO2 max ) was calculated for each horse. Horses then underwent treadmill exercise at the speed for which the oxygen requirements had been calculated to be 115% VO2 max . Plasma samples were obtained before (T0) and immediately (T1), 15 (T2) and 30 (T3) minutes post-exercise, and evaluated using liquid chromatography/mass spectrometry. Data analysis consisted of principal component analysis and one-way repeated measures analysis of variance. RESULTS: A total of 933 plasma lipids were detected. Supramaximal exercise-induced significant changes in the signal intensity of 13 lipids; all ubiquitous in the organism as major components of biological membranes or energy substrates. MAIN LIMITATIONS: A treadmill was used to replicate track conditions. Also, sample size involved only four horses and the statistical analyses failed to achieve the desired power of 80%. CONCLUSIONS: The findings in this pilot study suggest that supramaximal exercise induces changes in specific plasma lipids in Thoroughbred racehorses. While the biological significance of these findings remains to be determined, these results provide baseline information for future studies in lipidomics applied to equine exercise physiology. Further research is warranted to better understand the role of lipids on energy metabolism in Thoroughbred racehorses.

Validation of masks for determination of V̇O2 max in horses exercising at high intensity.

BACKGROUND: The need for a horse to be ridden while wearing a measurement device that allows unrestricted ventilation and gas exchange has hampered accurate measurement of its maximal oxygen consumption (V̇O2 max) under field conditions. OBJECTIVES: Design and validate a facemask with the potential to measure V̇O2 max accurately in the field. STUDY DESIGN: Experiment with 6 × 6 Latin square design. METHODS: Two variations of a mask and associated electronic control module (ECM) were designed to enable breath-by-breath measurement of airflows through two 7.8 cm diameter pneumotachometers located 7.5 cm in front of each narus. The ECM was comprised of an analogue-to-digital converter and a lithium-ion battery that provided power and signal filtering to the pneumotachometers and an oxygen sensing cell, and powered a pump connected to gas sampling ports between the nares and pneumotachometers. Airflow and oxygen content of inspired and expired gases were recorded through the ECM and electronically transferred to a notebook. V̇O2 was determined from these recordings using a customised software program. Mask B encased the lower jaw. Mask R left the jaw free so the horse could wear a bit if ridden. V̇O2 max and arterial blood gases were measured in 6 horses during multiple treadmill tests. Each mask was worn twice and results compared to those from an established open flow-through system (O) by ANOVA-RM (P<0.05). System utility was evaluated using the intraclass correlation coefficient of 4 independent raters. RESULTS: Blood gases and V̇O2 max (151.9±7.0 [mean±s.d.; O], 151.5±9.6 [B], 149.5±7.5 [R] ml/[kg.min]) were not different between masks. V̇O2 max measures were reproducible for each mask. Intraclass correlation coefficient between raters = 0.99. MAIN LIMITATIONS: Some rebreathing of expired air from mask dead space. CONCLUSION: Masks capable of measuring V̇O2 max during treadmill exercise were developed, tested and found to be accurate. Mask R has potential application to measurement of V̇O2 max under field conditions.

Interaction of saddle girth construction and tension on respiratory mechanics and gas exchange during supramaximal treadmill exercise in horses.

OBJECTIVE: To determine the effect of girth construction and tension on respiratory mechanics and gas exchange during supramaximal treadmill exercise in horses. METHODS: Six healthy detrained Thoroughbred horses were exercised on a treadmill inclined at 10% at 110% VO2max. Horses were instrumented for respiratory mechanics and gas exchange studies, and data were recorded during incremental exercise tests. The animals were exercised for 2 min at 40% VO2max, and samples and measurements were collected at 1 min 45 sec. After 2 min, speed was increased to that estimated at 110% VO2max and data was collected at 45 sec, 90 sec and every 30 sec thereafter at this speed until the horses fatigued. Horses were run on three occasions with the same racing saddle and saddle packing but using two different girths, either an elastic girth (EG) or a standard canvas girth (SCG) which is nonelastic. A run with 5 kg tension applied to a standard canvas girth was the control for each horse, with additional runs at 15 kg using either the standard canvas girth or using the elastic girth. The runs were randomised and tensions applied were measured at end exhalation whilst at rest. RESULTS: Increasing girth tension was not associated with changes in respiratory mechanical or gas exchange properties. Although girths tightened to 15 kg tension had short run to fatigue times this was not found to be significantly different to girths set at 5 kg resting tension. Girth tensions declined at end exhalation in horses nearing fatigue. CONCLUSIONS: Loss in performance associated with high girth tensions is not due to alteration of respiratory mechanics. Loss in performance may be related to inspiratory muscles working at suboptimal lengths due to thoracic compression or compression of musculature around the chest. However, these changes are not reflected in altered respiratory mechanical or gas exchange properties measured during tidal breathing during supramaximal exercise. Other factors may hasten the onset of fatigue when horses exercise with tight girths and further studies are required to determine why excessively tight girths affect performance.

Exercise-induced hypercapnia in the horse.

The effects of exercise intensity and duration on blood gases in thoroughbred horses were studied to characterize the apparent exercise-induced failure in pulmonary gas exchange that occurs in these animals. In response to 2 min of exercise, arterial CO2 tension (PaCO2) decreased in mild and moderate exercise, returned to normocapnic levels in moderate to heavy exercise, and rose 5-10 Torr above resting values during very heavy exercise when CO2 production (VCO2) exceeded 20 times the resting value, and mixed venous CO2 tension approximated 140 Torr. Exercise-induced hypoxemia occurred at the onset of heavy exercise and was associated with the absence of a hyperventilatory response and an alveolar-arterial PO2 difference that increased four to six times above rest with very heavy exercise. PaCO2 was related to VCO2 but not fb, as changes in breathing frequency (fb) of 8-20 breaths/min at comparable VCO2 did not affect PaCO2. Prolonging very heavy exercise from 2 to 4 min caused a severe metabolic acidosis (arterial pH less than 7.15) and hypoxemia was maintained; however, CO2 was no longer retained, as PaCO2 gradually fell to below resting levels, due to an increased tidal volume at constant fb. We conclude that a truly compensatory hyperventilation to very heavy exercise in the horse is not achieved because of the excessive volumes and flow rates required by their extraordinarily high VCO2 and VO2. On the other hand, the frank CO2 retention during short-term high-intensity exercise occurs even though the horse is not apparently mechanically obligated to tolerate it.

Equine plasma and blood volumes decrease with dehydration but subsequently increase with exercise.

The effects of dehydration and 40 min of exercise at approximately 40% of maximal O2 consumption on plasma volume (PV) and blood volume (BV) were studied in six horses. Horses were exercised while euhydrated (C); 4 h after administration of furosemide (1.0 mg/kg i.v.; FDH), which induced isotonic dehydration; and after 30 h without water (DDH), which caused hypertonic dehydration. Dehydration resulted in decreases of 6.3 and 9.9% for PV and BV, respectively, with FDH and 10.7 and 8.5%, respectively, with DDH. During exercise in C, PV and BV increased by 12.7 and 20.0%, respectively; during exercise with FDH, they increased by 11.7 and 26.1%, respectively; and during exercise with DDH, PV decreased by 1.3% from predehydration values, while BV increased by 18.7%. Hematocrit and total plasma protein concentration rose to higher values throughout exercise in FDH and DDH than in C; plasma [Na+] was higher in DDH than in FDH and C, [Cl-] was higher in DDH and lower in FDH than in C, and [K+] was lower in FDH and DDH than in C through exercise and recovery. From these results, we conclude that increases in PV and BV are normal features of low-intensity exercise in the horse. The increases in BV not only augment O2 carriage but also help maintain circulating volume. These increases can be modified by preexercise dehydration, the nature of which affects the extent of modification.

Effects of dehydration on thermoregulatory responses of horses during low-intensity exercise.

Effects of dehydration on thermoregulatory and metabolic responses were studied in six horses during 40 min of exercise eliciting approximately 40% of maximal O2 consumption and for 30 min after exercise. Horses were exercised while euhydrated (C), 4 h after administration of furosemide (FDH; 1.0 mg/kg i.v.) to induce isotonic dehydration, and after 30 h without water (DDH) to induce hypertonic dehydration. Cardiac output was significantly lower in FDH (144.1 +/- 8.0 l/min) and in DDH (156.6 +/- 6.9 l/min) than in C (173.1 +/- 6.2 l/min) after 30 min of exercise. When DDH, FDH, and C values were compared, dehydration resulted in higher temperatures in the middle gluteal muscle (41.9 +/- 0.3, 41.1 +/- 0.2, and 40.6 +/- 0.2 degrees C, respectively) and pulmonary artery (40.8 +/- 0.3, 40.1 +/- 0.2, and 39.7 +/- 0.2 degrees C, respectively). Temperatures in the superficial thoracic vein and subcutaneous sites on the neck and back and peak sweating rates on the neck and back were not significantly different in DDH and C. In view of higher core temperatures during exercise after dehydration and decrease in cardiac output without concomitant increases in peripheral temperatures or reduced sweating rates, we conclude that the impairment of thermoregulation was primarily due to decreased transfer of heat from core to periphery.

Ventilatory responses of the horse to exercise: effect of gas collection systems.

Experiments were undertaken to determine whether respiratory masks worn by horses exercising strenuously on a treadmill may interfere with normal gas exchange. Four collection systems, two flow-through systems and two incorporating one-way valve systems with subject-generated airflow were studied. Six horses performed standard treadmill exercise tests consisting of a 2-min warm up followed by galloping 1 min each at 8,9, and 10 m/s. Each horse exercised six times while wearing each of the four respiratory masks. Each flow-through system was used twice with flow rates of 2,360 and 3,840 l/min for one system, and 3,840 and 6,300 l/min for the other. Arterial blood gas tensions were measured during exercise at each speed for each system and were compared with values measured when the horses performed the same test without wearing a mask. Hypercapnia developed during exercise with each of the respiratory masks except with the 6,300-l/min flow-through system. All horses became hypoxemic during every exercise test, but it was most severe when systems incorporating one-way valves were used. This, plus the degree of hypercapnia observed and a suboptimal heart rate-O2 uptake relationship, indicated that such systems severely impede ventilation and suggest that experiments performed while utilizing them do not represent the normal exercise condition.

Does an acute COPD crisis modify the cardiorespiratory and ventilatory adjustments to exercise in horses?

The present study was conducted to understand better the mechanisms leading to the decrease in exercise capacity observed in horses suffering from chronic obstructive pulmonary disease (COPD). Five COPD horses were submitted to a standardized submaximal treadmill exercise test while they were in clinical remission or in acute crisis. Respiratory airflow, O2 and CO2 fractions in the respired gas, pleural pressure changes and heart rate were recorded, and arterial and mixed venous blood were analyzed for gas tensions, hemoglobin, and plasma lactate concentrations. O2 consumption, CO2 production, expired minute ventilation, tidal volume, alveolar ventilation, cardiac output, total pulmonary resistance, and mechanical work of breathing were calculated. The results showed that, when submaximally exercised, COPD horses in crisis were significantly more hypoxemic and hypercapnic and that their total pulmonary resistance and mechanical work of breathing were significantly higher and their expired minute ventilation significantly lower than when they were in remission. However, their O2 consumption remained unchanged, which was probably due to the occurrence of compensatory mechanisms, i.e., higher heart rate, cardiac output, and hemoglobin concentration. Last, their net anaerobic metabolism seemed to be more important.

Effect of prolonged heavy exercise on pulmonary gas exchange in horses.

During short-term maximal exercise, horses have impaired pulmonary gas exchange, manifested by diffusion limitation and arterial hypoxemia, without marked ventilation-perfusion (VA/Q) inequality. Whether gas exchange deteriorates progressively during prolonged submaximal exercise has not been investigated. Six thoroughbred horses performed treadmill exercise at approximately 60% of maximal oxygen uptake until exhaustion (28-39 min). Multiple inert gas, blood-gas, hemodynamic, metabolic rate, and ventilatory data were obtained at rest and 5-min intervals during exercise. Oxygen uptake, cardiac output, and alveolar-arterial PO2 gradient were unchanged after the first 5 min of exercise. Alveolar ventilation increased progressively during exercise, from increased tidal volume and respiratory frequency, resulting in an increase in arterial PO2 and decrease in arterial PCO2. At rest there was minimal VA/Q inequality, log SD of the perfusion distribution (log SDQ) = 0.20. This doubled by 5 min of exercise (log SDQ = 0.40) but did not increase further. There was no evidence of alveolar-end-capillary diffusion limitation during exercise. However, there was evidence for gas-phase diffusion limitation at all time points, and enflurane was preferentially overretained. Horses maintain excellent pulmonary gas exchange during exhaustive, submaximal exercise. Although VA/Q inequality is greater than at rest, it is less than observed in most mammals and the effect on gas exchange is minimal.

Maximum O2 uptake, O2 debt and deficit, and muscle metabolites in Thoroughbred horses.

This study determined maximal O2 uptake (VO2max), maximal O2 deficit, and O2 debt in the Thoroughbred racehorse exercising on an inclined treadmill. In eight horses the O2 uptake (VO2) vs. speed relationship was linear until 10 m/s and VO2max values ranged from 131 to 153 ml.kg-1.min-1. Six of these horses then exercised at 120% of their VO2max until exhaustion. VO2, CO2 production (VCO2), and plasma lactate (La) were measured before and during exercise and through 60 min of recovery. Muscle biopsies were collected before and at 0.25, 0.5, 1, 1.5, 2, 5, 10, 15, 20, 40, and 60 min after exercise. Muscle concentrations of adenosine 5'-triphosphate (ATP), phosphocreatine (PC), La, glucose 6-phosphate (G-6-P), and creatine were determined, and pH was measured. The O2 deficit was 128 +/- 32 (SD) ml/kg (64 +/- 13 liters). The O2 debt was 324 +/- 62 ml/kg (159 +/- 37 liters), approximately two to three times comparative values for human beings. Muscle [ATP] was unchanged, but [PC] was lower (P less than 0.01) than preexercise values at less than or equal to 10 min of recovery. [PC] and VO2 were negatively correlated during both the fast and slow phases of VO2 during recovery. Muscle [La] and [G-6-P] were elevated for 10 min postexercise. Mean muscle pH decreased from 7.05 (preexercise) to 6.75 at 1.5 min recovery, and the mean peak plasma La value was 34.5 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of acetazolamide on metabolic and respiratory responses to exercise at maximal O2 uptake.

Changes in blood gases, ions, lactate, pH, hemoglobin, blood temperature, total body metabolism, and muscle metabolites were measured before and during exercise (except muscle), at fatigue, and during recovery in normal and acetazolamide-treated horses to test the hypothesis that an acetazolamide-induced acidosis would compromise the metabolism of the horse exercising at maximal O2 uptake. Acetazolamide-treated horses had a 13-mmol/l base deficit at rest, higher arterial Po2 at rest and during exercise, higher arterial and mixed venous Pco2 during exercise, and a 48-s reduction in run time. Arterial pH was lower during exercise but not in recovery after acetazolamide. Blood temperature responses were unaffected by acetazolamide administration. O2 uptake was similar during exercise and recovery after acetazolamide treatment, whereas CO2 production was lower during exercise. Muscle [glycogen] and pH were lower at rest, whereas heart rate, muscle pH and [lactate], and plasma [lactate] and [K+] were lower and plasma [Cl-] higher following exercise after acetazolamide treatment. These data demonstrate that acetazolamide treatment aggravates the CO2 retention and acidosis occurring in the horse during heavy exercise. This could negatively affect muscle metabolism and exercise capacity.

Dissipation of metabolic heat in the horse during exercise.

Horses were exercised at 40, 65, and 90% of their maximum O2 uptake (VO2max) until moderately fatigued (approximately 38, 15, and 9 min, respectively) to assess heat loss through different routes. Approximately 4,232, 3,195, and 2,333 kcal of heat were generated in response to exercise at these intensities. Of this, approximately 7, 16, and 20% remained as stored heat 30 min postexercise. Respiratory heat loss, estimated from the temperature difference between blood in the pulmonary and carotid arteries and the cardiac output, was estimated to be 30, 19, and 23% of the heat produced during exercise at the three intensities. The kinetics of the increases in muscle and blood temperature were similar, with the greatest change in temperature occurring in muscle (+3.8, 5.2, and 6.1 degrees C after exercise at 40, 65, and 90% of VO2max, respectively). The temperature of blood in the superficial thoracic vein was approximately 2 degrees C below that of arterial blood at rest. This difference had increased to approximately 3 degrees C during the last minute of exercise. The rate of sweating at sites on the back and neck increased with exercise intensity to a common peak of approximately 40 ml.m-2.min-1. If complete evaporation had occurred, water loss in response to exercise (estimated to be 12, 10, and 7.7 liters for the different intensities of exercise) greatly surpassed that required for dissipation of the metabolic heat load.

Exercise intensity, training, diet, and lactate concentration in muscle and blood.

With some, but not all, types and intensities of exercise, lactate accumulates in the blood and in the muscles engaged in the exercise. A great deal of attention has been directed towards attempting to understand the dynamics of lactate production and removal at the onset of exercise, during exercise, and during the recovery process following exercise. It has been hoped that an unravelling of these events would provide a key to understanding cellular metabolism and its regulation during exercise. The purpose of this introductory paper to a symposium on lactate is to present a brief overview of some of the conditions that influence the rate and magnitude of lactate accumulation during exercise. It is pointed out that many conditions influence the rate and magnitude of the accumulation of lactate in blood and muscles. Included are diet, state of physical fitness, and the type and duration of the exercise. We have cautioned against trying to evaluate the state of oxygen delivery to muscle and the state of tissue oxygenation from the appearance of lactate in blood. We have pointed out the positive aspects of lactate production based on how it augments the cellular supply of ATP, thereby allowing for high intensity exercise, and also the negative aspects that develop as a result the reduction in pH which adversely influences many cellular processes essential for muscular activity.

Airflow mechanics in models of equine obstructive airway disease under conditions simulating exercise.

Effects of respiratory tract obstructions on ventilatory mechanics in horses exercising at high speeds were tested with a fibreglass replica of the airways (nares to mainstem bronchi) of an adult horse. Segmental pressures were recorded at six sites along the model at four different unidirectional flows (1300-4100 litre min-1), and the respective resistances (R) to airflow were calculated. The external nares and the larynx made the greatest contributions to the total resistance (RTOT) when no obstruction was present. Modifying the model to simulate severe pharyngeal lymphoid hyperplasia (PLH) had no effect on R at the larynx or at any point in the trachea under these flow conditions. Two 16 litre anaesthetic rebreathing bags were attached to the bronchial end of the model, and tidal ventilation generated by a piston pump. Upper (nares to pharynx) and lower tract R (RU and RL) and RTOT, and dynamic compliance were determined for pump volumes (Vp) of six and 12 litres, at pumping frequencies (fp) of 20-100 min-1 while the airway was clear, and after modifying it to simulate either PLH or partial bronchial obstruction. Model condition had no effect on RU. However, RL and RTOT were higher in the PLH simulated condition when fp > or = 90 and Vp = 12 litres (P < 0.05). This suggested that severe PLH may significantly interfere with airflow distal to the site of the lesions during high frequency high volume ventilation of the type seen in galloping horses. With partial bronchial obstruction RL and RTOT were increased when fp > 34 with each Vp. The applicability of the model was verified by comparing results from the unobstructed state with those from normal horses exercising on a treadmill.

Arterial blood gas tensions during exercise in a horse with laryngeal hemiplegia, before and after corrective surgery.

Arterial blood samples were collected during maximal exercise over 1.6 km in a thoroughbred horse with left laryngeal hemiplegia. Acid-base and blood gas measurements were performed on each sample and compared to the results from samples which were similarly collected 48 hours after laryngoplasty surgery was performed. Before surgery, the PaO2 was 53.2 mm Hg and the PaCO2 was 58.1 mm Hg after 1.6 km. After surgery, the corresponding results were 83.6 mm Hg (PaO2) and 39.0 mm Hg (PaCO2). There was no significant difference in the times taken for each gallop. The exercise intolerance associated with laryngeal paralysis may be caused by an increase in the oxygen cost of breathing.

Arterial blood gas tension and acid base balance during exercise in horses with pharyngeal lymphoid hyperplasia.

Arterial blood gas and acid-base values during maximal exercise over a 1.2 km distance were recorded in four Thoroughbred horses before and after the chemical induction of pharyngeal lymphoid hyperplasia (PLH). Samples were collected after galloping 0.8 km and 1.2 km, immediately upon stopping and 5 mins after exercising. In only one horse was any difference noted in the pre and post PLH induction results. The horse was more hypercapnoeic at the 1.2 km mark and also took much longer to complete the gallop when it had PLH. However, it also had signs of lower respiratory disease. In the other horses, the only changes which could be attributed to PLH were seen immediately upon stopping. It seems that PLH does not inhibit gas exchange during exercise unless the lesions are extremely severe.

Haematuria, pigmenturia and proteinuria in exercising horses.

The effects of exercise on urinary excretion of red blood cells, pigments (haemoglobin and myoglobin) and protein were studied in 8 mares performing treadmill exercise at speeds eliciting 40, 60 and 95% of the maximal oxygen consumption (VO2max). Gross haematuria and pigmenturia were observed in all horses during exercise at the 2 higher intensities, while these findings were detected in only one of 8 mares during exercise at 40% of the VO2max. For the remaining 7 mares exercised at 40% of the VO2max, increased urinary excretion of red blood cells (RBCs) and pigments was evident after centrifugation of urine samples and reagent strip analysis of the supernatant fractions. An increase in urine flow (UF) during exercise at 40% of the VO2max may have contributed to the infrequent observation of gross haematuria and pigmenturia during exercise at this intensity. A transient increase in UF following exercise at 60 and 95% of the VO2max resulted in rapid resolution of gross haematuria and pigmenturia, but increased urinary excretion of RBCs and pigments remained evident by reagent strip analysis for up to 60 min following exercise. Mean +/- s.e. urinary protein excretion increased from a resting value of 2.2 +/- 0.2 mg/min to 5.6 +/- 0.9, 14.5 +/- 4.7 and 78.4 +/- 18.6 mg/min after exercise at 40, 60 and 95% of the VO2max, respectively. These results demonstrate that exercise induced haematuria and pigmenturia and post exercise proteinuria are common in horses. Their occurrence is transient and does not appear to be associated with any lasting changes in renal function.