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Biomedical subjects

K W Hinchcliff

Publications and source records attributed to K W Hinchcliff.

At least 19 recordsLinked to original sources
PubMed2000

Analysis of risk factors for the development of equine protozoal myeloencephalitis in horses.

OBJECTIVE: To investigate risk factors for development of equine protozoal myeloencephalitis (EPM) in horses. DESIGN: Case-control study. ANIMALS: 251 horses admitted to The Ohio State University Veterinary Teaching Hospital from 1992 to 1995. PROCEDURE: On the basis of clinical signs of neurologic disease and detection of antibody to Sarcocystis neurona or S neurona DNA in cerebrospinal fluid, a diagnosis of EPM was made for 251 horses. Two contemporaneous series of control horses were selected from horses admitted to the hospital. One control series (n = 225) consisted of horses with diseases of the neurologic system other than EPM (neurologic control horses), and the other consisted of 251 horses admitted for reasons other than nervous system diseases (nonneurologic control horses). Data were obtained from hospital records and telephone conversations. Risk factors associated with disease status were analyzed, using multivariable logistic regression. RESULTS: Horses ranged from 1 day to 30 years old (mean +/- SD, 5.7 +/- 5.2 years). Risk factors associated with an increased risk of developing EPM included age, season of admission, prior diagnosis of EPM on the premises, opossums on premises, health events prior to admission, and racing or showing as a primary use. Factors associated with a reduced risk of developing EPM included protection of feed from wildlife and proximity of a creek or river to the premises where the horse resided. CONCLUSIONS AND CLINICAL RELEVANCE: Development of EPM was associated with a number of management-related factors that can be altered to decrease the risk for the disease.

Animals↗
PubMed2000

Evaluation of risk factors associated with clinical improvement and survival of horses with equine protozoal myeloencephalitis.

OBJECTIVE: To investigate risk factors for use in predicting clinical improvement and survival of horses with equine protozoal myeloencephalitis (EPM). DESIGN: Longitudinal epidemiologic study. ANIMALS: 251 horses with EPM. PROCEDURE: Between 1992 and 1995, 251 horses with EPM were admitted to our facility. A diagnosis of EPM was made on the basis of neurologic abnormalities and detection of antibody to Sarcocystis neurona or S neurona DNA in CSF. Data were obtained from hospital records and through telephone follow-up interviews. Factors associated with clinical improvement and survival were analyzed, using multivariable logistic regression. RESULTS: The likelihood of clinical improvement after diagnosis of EPM was lower in horses used for breeding and pleasure activities. Treatment for EPM increased the probability that a horse would have clinical improvement. The likelihood of survival among horses with EPM was lower among horses with more severe clinical signs and higher among horses that improved after EPM was diagnosed. CONCLUSIONS AND CLINICAL RELEVANCE: Treatment of horses with EPM is indicated in most situations; however, severity of clinical signs should be taken into consideration when making treatment decisions. Response to treatment is an important indicator of survival.

Animals↗
PubMed2000

Glucose infusion attenuates endogenous glucose production and enhances glucose use of horses during exercise.

We examined the effects of increased glucose availability on glucose kinetics and substrate utilization in horses during exercise. Six conditioned horses ran on a treadmill for 90 min at 34 +/- 1% of maximum oxygen uptake. In one trial [glucose (Glu)], glucose was infused at a mean rate of 34.9 +/- 1.1 micromol. kg(-1). min(-1), whereas in the other trial [control (Con)] an equivalent volume of isotonic saline was infused. Plasma glucose increased during exercise in Glu (90 min: 8.3 +/- 1.7 mM) but was largely unchanged in Con (90 min: 5.1 +/- 0.4 mM). In Con, hepatic glucose production (HGP) increased during exercise, reaching a peak of 38.6 +/- 2.7 micromol. kg(-1). min(-1) after 90 min. Glucose infusion partially suppressed (P < 0.05) the rise in HGP (peak value 25.8 +/- 3.3 micromol. kg(-1). min(-1)). In Con, glucose rate of disappearance (R(d)) rose to a peak of 40.4 +/- 2.9 micromol. kg(-1). min(-1) after 90 min; in Glu, augmented glucose utilization was reflected by values for glucose R(d) that were twofold higher (P < 0.001) than in Con between 30 and 90 min. Total carbohydrate oxidation was higher (P < 0.05) in Glu (187.5 +/- 8.5 micromol. kg(-1). min(-1)) than in Con (159.2 +/- 7.3 micromol. kg(-1).min(-1)), but muscle glycogen utilization was similar between trials. We conclude that an increase in glucose availability in horses during low-intensity exercise 1) only partially suppresses HGP, 2) attenuates the decrease in carbohydrate oxidation during such exercise, but 3) does not affect muscle glycogen utilization.

Animals↗
PubMed2000

Epinephrine inhibits exogenous glucose utilization in exercising horses.

This study examined the effects of preexercise glucose administration, with and without epinephrine infusion, on carbohydrate metabolism in horses during exercise. Six horses completed 60 min of treadmill exercise at 55 +/- 1% maximum O(2) uptake 1) 1 h after oral administration of glucose (2 g/kg; G trial); 2) 1 h after oral glucose and with an intravenous infusion of epinephrine (0.2 micromol. kg(-1). min(-1); GE trial) during exercise, and 3) 1 h after water only (F trial). Glucose administration (G and GE) caused hyperinsulinemia and hyperglycemia ( approximately 8 mM). In GE, plasma epinephrine concentrations were three- to fourfold higher than in the other trials. Compared with F, the glucose rate of appearance was approximately 50% and approximately 33% higher in G and GE, respectively, during exercise. The glucose rate of disappearance was approximately 100% higher in G than in F, but epinephrine infusion completely inhibited the increase in glucose uptake associated with glucose administration. Muscle glycogen utilization was higher in GE [349 +/- 44 mmol/kg dry muscle (dm)] than in F (218 +/- 28 mmol/kg dm) and G (201 +/- 35 mmol/kg dm). We conclude that 1) preexercise glucose augments utilization of plasma glucose in horses during moderate-intensity exercise but does not alter muscle glycogen usage and 2) increased circulating epinephrine inhibits the increase in glucose rate of disappearance associated with preexercise glucose administration and increases reliance on muscle glycogen for energy transduction.

Adrenergic Agonists↗
PubMed2000

beta-adrenergic blockade augments glucose utilization in horses during graded exercise.

To examine the role of beta-adrenergic mechanisms in the regulation of endogenous glucose (Glu) production [rate of appearance (R(a))] and utilization [rate of disappearance (R(d))] and carbohydrate (CHO) metabolism, six horses completed consecutive 30-min bouts of exercise at approximately 30% (Lo) and approximately 60% (Hi) of estimated maximum O(2) uptake with (P) and without (C) prior administration of the beta-blocker propranolol (0.22 mg/kg iv). All horses completed exercise in C; exercise duration in P was 49.9 +/- 1.2 (SE) min. Plasma Glu was unchanged in C during Lo but increased progressively in Hi. In P, plasma Glu rose steadily during Lo and Hi and was higher (P < 0.05) than in C throughout exercise. Plasma insulin declined during exercise in P but not in C; beta-blockade attenuated (P < 0.05) the rise in plasma glucagon and free fatty acids and exaggerated the increases in epinephrine and norepinephrine. Glu R(a) was 8.1 +/- 0.8 and 8.4 +/- 1.0 micromol. kg(-1). min(-1) at rest and 30.5 +/- 3.6 and 42.8 +/- 4.1 micromol. kg(-1). min(-1) at the end of Lo in C and P, respectively. During Hi, Glu R(a) increased to 54.4 +/- 4.4 and 73.8 +/- 4.7 micromol. kg(-1). min(-1) in C and P, respectively. Similarly, Glu R(d) was approximately 40% higher in P than in C during Lo (27.3 +/- 2.0 and 39.5 +/- 3.3 micromol. kg(-1). min(-1) in C and P, respectively) and Hi (37.4 +/- 2.6 and 61.5 +/- 5.3 micromol. kg(-1). min(-1) in C and P, respectively). beta-Blockade augmented CHO oxidation (CHO(ox)) with a concomitant reduction in fat oxidation. Inasmuch as estimated muscle glycogen utilization was similar between trials, the increase in CHO(ox) in P was due to increased use of plasma Glu. We conclude that beta-blockade increases Glu R(a) and R(d) and CHO(ox) in horses during exercise. The increase in Glu R(d) under beta-blockade suggests that beta-adrenergic mechanisms restrain Glu R(d) during exercise.

Adrenergic beta-Antagonists↗
PubMed2000

Determinants of oxygen delivery and hemoglobin saturation during incremental exercise in horses.

OBJECTIVE: To determine components of the increase in oxygen consumption (VO2) and evaluate determinants of hemoglobin saturation (SO2) during incremental treadmill exercise in unfit horses. ANIMALS: 7 unfit adult mares. PROCEDURES: Horses performed 1 preliminary exercise test (EXT) and 2 experimental EXT. Arterial and mixed venous blood samples and hemodynamic measurements were taken during the last 30 seconds of each step of the GXT to measure PO2, hemoglobin concentration ([Hb]), SO2, and determinants of acid-base state (protein, electrolytes, and PCO2). RESULTS: Increased VO2 during exercise was facilitated by significant increases in cardiac output (CO), [Hb], and widening of the arteriovenous difference in O2. Arterial and venous pH, PaO2, and PvO2 decreased during exercise. Arterial PCO2, bicarbonate ([HCO3-])a, and [HCO3-] decreased significantly, whereas PVCO2 and increased. Arterial and venous sodium concentration, potassium concentration, strong ion difference, and venous lactate concentration all increased significantly during exercise. CONCLUSIONS AND CLINICAL RELEVANCE: Increases in CO, [Hb], and O2 extraction contributed equally to increased VO2 during exercise. Higher PCO2 did not provide an independent contribution to shift in the oxyhemoglobin dissociation curve (OCD) in venous blood. However, lower PaCO2 shifted the curve leftward, facilitating O2 loading. The shift of ODC resulted in minimal effect on O2 extraction because of convergence of the ODC at lower values of PO2. Decreased pH appeared responsible for the rightward shift of the ODC, which may be necessary to allow maximal O2 extraction at high blood flows achieved during exercise.

Acid-Base Equilibrium↗
PubMed2000

Oxidant stress in sled dogs subjected to repetitive endurance exercise.

OBJECTIVE: To determine whether repetitive endurance exercise in sled dogs was associated with substantial lipid peroxidation, decreases in antioxidant capacity of the serum, and skeletal muscle damage. ANIMALS: 24 lightly trained sled dogs. PROCEDURE: 16 dogs completed a 58-km run on each of 3 consecutive days; the other 8 dogs (control) did not exercise during the study. Blood samples were collected before the first exercise run and after the first and third exercise runs. Plasma isoprostane and serum vitamin E concentrations, total antioxidant status of plasma, and serum creatine kinase activity were measured. RESULTS: Plasma isoprostane concentrations in dogs in the exercise group were significantly increased after the first exercise run and further significantly increased after the third exercise run. Serum vitamin E concentration was significantly decreased after the first exercise run in dogs in the exercise group, and this change persisted after the third exercise run. There was a significant linear relationship between plasma isoprostane concentration and the logarithm of serum creatine kinase activity (adjusted ? = 0.84). CONCLUSIONS AND CLINICAL RELEVANCE: Results demonstrate that repetitive endurance exercise in dogs is associated with lipid peroxidation and a reduction in plasma antioxidant concentrations. We interpret these results as indicating that the antioxidant mechanisms of minimally trained dogs may, in some instances, be inadequate to meet the antioxidant requirements of repetitive endurance exercise.

Animal Feed↗
PubMed2000

Effects of endurance training on standard and signal-averaged electrocardiograms of sled dogs.

OBJECTIVE: To determine the effect of endurance training on QRS duration, QRS-wave amplitude, and QT interval. ANIMALS: 100 sled dogs in Alaska. PROCEDURE: Dogs were examined in early September (before training) and late March (after training). During the interim, dogs trained by pulling a sled with a musher (mean, 20 km/d). Standard and signal-averaged ECG were obtained before and after training. RESULTS: Endurance training significantly increased mean QRS duration by 4.4 milliseconds for standard ECG (mean +/- SEM; 62.3 +/- 0.7 to 66.7 +/- 0.6 milliseconds) and 4.3 milliseconds for signal-averaged ECG (51.5 +/- 0.7 to 55.8 +/- 0.6 milliseconds) without changing body weight. Increase in QRS duration corresponded to a calculated increase in heart weight (standard ECG, 23%; signal-averaged ECG, 27%). Signal-averaged QRS duration was correlated with echocardiographically determined left ventricular diastolic diameter for the X orthogonal lead (r = +0.41), Y orthogonal lead (r = +0.33), and vector (r = +0.35). Training also increased QT interval (234 +/- 2 to 249 +/- 2 milliseconds) and R-wave amplitude in leads II and rV2, increased peak-to-peak voltage and S-wave amplitude in the Y orthogonal lead, and decreased Q-wave amplitude in the Y orthogonal lead. CONCLUSIONS AND CLINICAL RELEVANCE: Electrocardiographic changes reflected physiologic cardiac hypertrophy in these canine athletes in response to repetitive endurance exercise. The QRS duration increases in response to endurance exercise training and, therefore, may be of use in predicting performance in endurance activities.

Animals↗
PubMed2000

Effects of warm-up intensity on kinetics of oxygen consumption and carbon dioxide production during high-intensity exercise in horses.

OBJECTIVE: To compare effects of low and high intensity warm-up exercise on oxygen consumption (VO2) and carbon dioxide production (VCO2) in horses. ANIMALS: 6 moderately conditioned adult Standard-breds. PROCEDURES: Horses ran for 2 minutes at 115% of maximum oxygen consumption (VO2max), 5 minutes after each of the following periods: no warm-up (NoWU); 10 minutes at 50% of VO2max (LoWU); or 7 minutes at 50% VO2max followed by 45-second intervals at 80, 90, and 100% VO2max (HiWU). Oxygen consumption and VCO2 were measured during exercise, and kinetics of VO2 and VCO2 were calculated. Accumulated O2 deficit was also calculated. RESULTS: For both warm-up trials, the time constant for the rapid exponential increase in VO2 was 30% lower than for NoWU. Similarly, the rate of increase in VCO2 was 23% faster in LoWU and HiWU than in NoWU. Peak values for VO2 achieved during the high-speed test were not significantly different among trials (LoWU, 150.2 +/- 3.2 ml/kg/min; HiWU, 151.2 +/- 4.2 ml/kg/min; NoWU, 145.1 +/- 4.1 ml/kg/min). However, accumulated O2 deficit (ml of O2 equivalents/kg) was significantly lower during LoWU (65.3 +/- 5.1) and HiWU (63.4 +/- 3.9) than during NoWU (82.1 +/- 7.3). CONCLUSIONS AND CLINICAL RELEVANCE: Both the low- and high-intensity warm-up, completed 5 minutes before the start of high-intensity exercise, accelerated the kinetics of VO2 and VCO2 and decreased accumulated O2 deficit during 2 minutes of intense exertion in horses that were moderately conditioned.

Animals↗
PubMed2000

Effects of dietary antioxidant supplementation on oxidative damage and resistance to oxidative damage during prolonged exercise in sled dogs.

OBJECTIVES: To determine effects of dietary antioxidant supplementation on plasma concentrations of antioxidants, exercise-induced oxidative damage, and resistance to oxidative damage during exercise in Alaskan sled dogs. ANIMALS: 62 Alaskan sled dogs. PROCEDURE: Dogs were matched for age, sex, and ability and assigned to 1 of 3 groups: sedentary and nonsupplemented (control [C]; n = 21), exercised and supplemented (S; 22), and exercised and nonsupplemented (N; 19). Dogs in group S were given 400 units of alpha-tocopherol acetate, 3 mg of beta-carotene, and 20 mg of lutein orally per day for 1 month, then dogs in groups S and N completed 3 days of exercise. Blood samples were collected before and after 1 and 3 days of exercise and after 3 days of rest. Plasma antioxidant concentrations were determined, and oxidative damage to DNA (plasma 7,8 dihydro-8-oxo-2'deoxyguanosine [8-oxodG] concentration) and membrane lipids (plasma hydroperoxide concentration) and resistance of plasma lipoproteins to oxidation were assessed. RESULTS: Supplementation increased plasma concentrations of alpha-tocopherol, beta-carotene, and lutein. Plasma concentration of alpha-tocopherol increased and concentration of lutein decreased in group S with exercise. Concentration of 8-oxodG decreased in group S but increased in group N during and after exercise. Lag time of in vitro oxidation of lipoprotein particles increased with exercise in group S only. CONCLUSIONS AND CLINICAL RELEVANCE: Dietary supplementation with antioxidants resulted in increased plasma concentrations of antioxidants. Moreover, supplementation decreased DNA oxidation and increased resistance of lipoprotein particles to in vitro oxidation. Antioxidant supplementation of sled dogs may attenuate exercise-induced oxidative damage.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1999

Effect of furosemide on performance of Thoroughbreds racing in the United States and Canada.

OBJECTIVE: To determine the effect of furosemide on performance of Thoroughbreds racing on dirt surfaces at tracks in the United States and Canada. DESIGN: Cross-sectional study. ANIMALS: All Thoroughbreds (n = 22,589) that finished a race on dirt surfaces at tracks in the United States and Canada between June 28 and July 13, 1997 in jurisdictions that allowed the use of furosemide. PROCEDURE: Race records were analyzed by use of multivariable ANOVA procedures and logistic regression analyses to determine the effect of furosemide on estimated 6-furlong race time, estimated racing speed, race earnings, and finish position. Principal component analysis was used to create orthogonal scores from multiple collinear variables for inclusion in the models. RESULTS: Furosemide was administered to 16,761 (74.2%) horses. Horses that received furosemide raced faster, earned more money, and were more likely to win or finish in the top 3 positions than horses that did not. The magnitude of the effect of furosemide on estimated 6-furlong race time varied with sex, with the greatest effect in males. When comparing horses of the same sex, horses receiving furosemide had an estimated 6-furlong race time that ranged from 0.56 +/- 0.04 seconds (least-squares mean +/- SE) to 1.09 +/- 0.07 seconds less than that for horses not receiving furosemide, a difference equivalent to 3 to 5.5 lengths. CONCLUSIONS AND CLINICAL RELEVANCE: Because of the pervasive use of furosemide and its apparent association with superior performance in Thoroughbred racehorses, further consideration of the use of furosemide and investigation of its effects in horses is warranted.

Age Factors↗
PubMed1999

Renal pharmacology.

Pharmacologic treatment of diseases of the urinary tract of horses is limited to administration of antibiotics for treatment of urinary tract infections (UTIs), administration of drugs that alter urine pH, administration of drugs that alter bladder smooth muscle function or urethral sphincter tone, and treatment of acute renal failure. The indications, mechanisms of action, pharmacokinetic characteristics, and adverse effects of these agents in each of these groups are discussed in this article. The use of the agents is discussed within the context of the pathophysiology of the disease being treated.

Acute Kidney Injury↗
PubMed1999

Attenuation by phenylbutazone of the renal effects and excretion of frusemide in horses.

The objectives of this study were to determine the effect of phenylbutazone premedication on the pharmacokinetics and urinary excretion of frusemide in horses; and on frusemide-induced changes in urinary electrolyte excretion. Six Standardbred mares were used in a 3-way crossover design. The pharmacokinetics and renal effects of frusemide (1 mg/kg bwt i.v.) were studied with and without phenylbutazone premedication (8.8 mg/kg bwt per os 24 h before, followed by 4.4 mg/kg bwt i.v. 30 min before frusemide administration). A control (saline) treatment was also studied. Administration of frusemide without phenylbutazone led to diuresis, natriuresis, kaliuresis and chloruresis, and altered the ratio of sodium:chloride excretion from 0.4 to 1.0 in the first hour of diuresis. When frusemide and phenylbutazone were administered, sodium and chloride excretion in the first hour were significantly (P<0.05) reduced by 40 and 32%, respectively, when compared to frusemide administrationwithout phenylbutazone. The fractional clearance of sodium and chloride was also significantly reduced. Potassium excretion, potassium fractional clearance and the ratio of sodium to chloride excretion were not affected by administration of phenylbutazone. During peak diuresis, phenylbutazone did not affect the efficiency of frusemide with respect to electrolyte excretion. The plasma disposition of frusemide was not affected by phenylbutazone. However, the renal excretion of frusemide decreased by approximately 25%. We conclude that the decreased urinary excretion of frusemide by phenylbutazone led to an attenuation of frusemide-induced increases in urinary excretion of sodium and chloride. Since the efficiency of frusemide was not affected by phenylbutazone, we conclude that phenylbutazone attenuates the renal excretion of frusemide without inhibiting the intrarenal activity of frusemide in horses.

Animals↗
PubMed1999

Exercise that induces substantial muscle glycogen depletion impairs subsequent anaerobic capacity.

The purpose of this study was to develop a model of muscle glycogen depletion and to study the effect of this model on aerobic and anaerobic capacity of horses. The maximal rate of oxygen consumption (VO2max), maximal accumulated oxygen deficit (MAOD), muscle glycogen concentration and blood lactate concentration of 6 fit Standardbred horses were measured on 3 occasions 7 days apart (Trials 1, 2 and 3). Between Trials 2 and 3, strenuous exercise intended to deplete muscle glycogen was performed by exercising horses on the treadmill on 3 consecutive days. Strenuous exercise resulted in reduction of muscle glycogen concentration by at least 55% (from mean +/- s.e. 155.1 +/- 5.6 mmol/kg, wet weight, before Trial 2 to 55.4 +/- 5.5 mmol/kg before Trial 3; P < 0.05). VO2max was similar in Trials 2 and 3 (140.4 +/- 5.4 ml O2/kg bwt and 141.8 ml +/- 6.2 ml O2/kg, respectively). Run time to fatigue during a single high-speed exercise test (253.9 +/- 33.3 s and 153.8 +/- 16.4 s, P < 0.05), accumulated oxygen deficit (95 +/- 13.2 ml O2/kg and 35 +/- 13.9 ml O2/kg, P < 0.05) and blood lactate concentration at the end of the sprint (17 +/- 1.2 mmol/l and 10.5 +/- 1.1 mmol/l, P < 0.05) were less during Trial 3 than Trial 2. These data suggested that repeated strenuous exercise that causes muscle glycogen depletion results in impairment of anaerobic, but not aerobic, metabolism.

Aerobiosis↗
PubMed1999

Frusemide and weight carriage alter the acid:base responses of horses to incremental and to brief intense exertion.

We speculated that frusemide would attenuate the acidosis associated with intense exertion, and that weight carriage would mitigate this effect. Therefore, in each of 2 experiments we measured pulmonary artery and systemic arterial blood pH, PCO2, PO2 and pulmonary artery temperature in 9 horses during exertion on a treadmill after each of 3 treatments. The treatments were: 1) injection of saline solution (C), 2) injection of frusemide (1 mg/kg bwt, i.v. 4 h before running) (FU) and 3) injection of frusemide (F) as for FU and the horses carried weight equal to that lost in the 4 h after frusemide administration (FL). In Experiment 1 the horses performed an incremental exercise test of 90 s at each of 4, 7 and 9 m/s (4 degrees incline). In Experiment 2, the horses ran on a treadmill inclined at 4 degrees for 3 min at 3 m/s, at approximately 120% VO2max for 2 min, and 3 m/s for 5 min. Blood samples for measurement of blood pH, PCO2 and PO2 were collected into heparinised glass syringes. Values were adjusted for changes in pulmonary artery blood temperature. Data were analysed using a 2 way repeated measures ANOVA. There was a consistent pattern in both experiments characterised by a mild alkalosis or mitigated acidosis, compared to C, at rest and during exercise and recovery after FU (P < 0.05). Weight carriage blunted or inhibited the effect of frusemide during exercise and recovery. In experiment 2, at the end of the sprint, FU treatment resulted in a less severe acidosis than did C or FI: mixed venous pH for C, FU, and FL at the end of the sprint were 6.93, 6.98 and 6.93, respectively (P interaction = 0.038), mixed venous base excess was -12.4, -9.91, and -11.8 mmol/l, respectively, and arterial base excess of -1.44, -12.7 and -14.1 mmol/l (P interaction = 0.006) respectively. These effects persisted into recovery. A similar pattern of responses occurred during the incremental exercise test, with weight carriage offsetting the alkalinizing effect of frusemide. We conclude that frusemide attenuates the acidosis of intense exertion and that carriage of weight prevents this effect.

Acid-Base Equilibrium↗
PubMed1999

Effect of ambient temperature and humidity on pulmonary artery temperature of exercising horses.

Six healthy Thoroughbred mares were trained to run on a high-speed treadmill and were conditioned for approximately 5 weeks. Each horse performed 6 identical standardised exercise tests (SET) 5 to 7 days apart. Each SET was performed under different ambient laboratory conditions: low temperature/low humidity (LL) 20.2 degrees +/- 0.6 degree C, 53.6 +/- 4.1%; low temperature/high humidity (LH) 19.7 +/- 0.6 degrees C, 86.7 +/- 4.2%; medium temperature/low humidity (ML) 24.6 +/- 0.2 degrees C, 58.7 +/- 3.7%; medium temperature/high humidity (MH) 24.7 +/- 0.3 degrees C, 87.5 +/- 1.4%; high temperature/low humidity (HL) 31.1 +/- 0.6 degrees C, 41.6 +/- 3.5%; and high temperature/high humidity (HH) 30.6 +/- 0.2 degrees C, 84.4 +/- 3.6%. Horses completed the 46 min SET, became fatigued or exercise was terminated when a pulmonary artery temperature (PAT) of 41.5 degrees C was reached. During a 30 min recovery period, horses stood quietly on the treadmill. Only one trial was terminated due to fatigue; in all other trials horses completed the 46 min SET or the trial was terminated when PAT = 41.5 degrees C. The relationships among run time (min) or PAT (degree C), ambient temperature and % relative humidity were defined by multiple linear regression analysis. Run time (min) = 90.9 - (1.39 x ambient temperature degree C) - (0.236 x relative humidity %). Approximately 54% of the variation in run times was explained by variation in environmental conditions, indicating that ambient temperature and humidity contribute substantially to the rate of rise in PAT. Run times to a PAT of 41.5 degrees C were significantly shorter (P < 0.000001) in HH than in other groups during the SET. Approximately 63% of the variation in PAT at the end of exercise was due to ambient temperature and humidity. In general, the longer the exercise time, the better the correlation among PAT, ambient temperature and relative humidity. Rectal temperature increased significantly (P < 0.0001) during the recovery period only in horses in the HH group, indicating that heat dissipation during recovery may have been impaired by environmental conditions. This study demonstrates that hot humid conditions result in more rapid rate of rise in PAT for horses undertaking identical exercise tests.

Animals↗