Intrapericardial denervation: radial artery blood flow and heart rate responses to LBNP.

Eight rhesus monkeys were used to study responses of radial artery blood flow velocity (RABFV) and heart rate (HR) to low (0 to -20 mmHg) and high (0 to -60 mmHg) ramp exposures during supine lower body negative pressure (LBNP). These levels were chosen to separate peripheral vascular responses associated with stimulation of low- and high-pressure baroreceptors. Four monkeys had efferent and afferent cardiac denervation by use of the Randall procedure with pharmacological (phenylephrine and atropine) verification. Animals were studied 3 wk after surgery to avoid reinnervation. Findings were compared with those of four identically treated intact animals. Denervated animals showed no change in RABFV or HR during low-level LBNP; however, HR increased significantly (P less than 0.05) when LBNP reached -50 mmHg and blood flow velocity also fell (P less than 0.05) starting at -30 mmHg pressure. In contrast, intact animals showed steady decreases in RABFV during both high- and low-pressure protocols, with HR showing a 6-beat/min increase (P less than 0.05) starting at -20 mmHg pressure. As with denervated animals, intact animals showed a more pronounced increase in HR after reaching a level of -60 mmHg suction. Cardiac output (electromagnetic flowmeter, ascending aorta) fell significantly in both groups starting at -30 mmHg pressure. Left ventricular pressure (Konigsberg pressure cell) in three intact animals showed a progressive fall in systolic pressure starting at -10 mmHg suction, which became significant at -55 mmHg pressure. These results demonstrate that cardiac denervation by use of the Randall technique significantly affects RABFV and HR responses to LBNP in rhesus monkeys. The lack of RABFV change during LBNP in denervated animals suggests that these changes coupled with HR response can be used as an effective method to verify the completeness of denervation of low-pressure baroreceptors in animals that have undergone intrapericardial denervation.

Effects of cocaine on incremental treadmill exercise in horses.

Four mature horses were used to test the effects of two doses (50 and 200 mg) of intravenously administered cocaine on hemodynamics and selected indexes of performance [maximal heart rate (HRmax), treadmill velocity at HRmax, treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l, maximal mixed venous blood lactate concentration, maximal treadmill work intensity, and test duration] measured during an incremental treadmill test. Both doses of cocaine increased HRmax approximately 7% (P < 0.05). Mean arterial pressure was 30 mmHg greater (P < 0.05) during the 4- to 7-m/s steps of the exercise test in the 200-mg trial. Neither dose of cocaine had an effect on the responses to exertion of right atrial pressure, right ventricular pressure, or maximal change in right ventricular pressure over time. Maximal mixed venous blood lactate concentration increased 41% (P < 0.05) with the 50-mg dose and 75% (P < 0.05) with the 200-mg dose during exercise. Administration of cocaine resulted in decreases (P < 0.05) in the treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l from 6.9 +/- 0.5 and 6.8 +/- 0.9 m/s during the control trials to 4.4 +/- 0.1 m/s during the 200-mg cocaine trial. Cocaine did not alter maximal treadmill work intensity (P > 0.05); however, time to exhaustion increased by approximately 92 s (15%; P < 0.05) during the 200-mg trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic administration of therapeutic levels of clenbuterol acts as a repartitioning agent.

The purpose of this study was to examine the effect of therapeutic levels of clenbuterol, with and without exercise training, on body composition. Twenty-three unfit Standardbred mares were divided into four experimental groups: clenbuterol (2.4 microg/kg body wt twice daily) plus exercise (ClenEx; 20 min at 50% maximal oxygen consumption 3 days/wk; n = 6), clenbuterol only (Clen; n = 6), exercise only (Ex; n = 5), and control (Con; n = 6). Rump fat thickness was measured at 2-wk intervals by using B-mode ultrasound, and percent body fat (%fat) was calculated by using previously published methods. For Ex, body fat decreased (P < 0.05) at week 4 (-9.3%), %fat at week 6 (-6.9%), and fat-free mass (FFM) increased (P < 0.05) at week 8 (+3.2%). On the other hand, Clen had significant changes in %fat (-15.4%), fat mass (-14.7%), and FFM (+4.3%) at week 2. ClenEx had significant decreases in %fat (-17.6%) and fat mass (-19.5%) at week 2, which was similar to Clen; however, this group had a different FFM response, which significantly increased (+4.4%) at week 6. Con showed no changes (P > 0.05) in any variable at any time. These results suggest that exercise training and clenbuterol have additive effects with respect to %fat and fat mass but antagonistic effects in terms of FFM. Furthermore, chronic clenbuterol administration causes significant repartitioning in the horse, even when administered in therapeutic doses.

Effect of tryptophan and of glucose on exercise capacity of horses.

We hypothesized that central fatigue may have a role in limiting the endurance capacity of horses. Therefore, we tested the effect of infusing tryptophan and/or glucose on endurance time and plasma concentrations of free tryptophan and other substrates thought to affect tryptophan uptake into the brain of seven mares (3-4 yr of age, 353-435 kg) that ran on a treadmill at 50% of maximal O2 consumption to fatigue. With use of a counterbalanced crossover design, the horses were infused with tryptophan (100 mg/kg in saline solution) or a similar volume of saline solution (placebo) before exercise. During exercise, horses received infusions of glucose (2 g/min, 50% wt/vol) or a similar volume of saline. Thus the treatments were 1) tryptophan and glucose (T & G), 2) tryptophan and placebo (T & P), 3) placebo and glucose (P & G), and 4) placebo and placebo (P & P). Mean heart rate, hematocrit, and concentration of plasma total solids before and during exercise were similar for all trials. Mean time to exhaustion was reduced (P < 0.05) for T & P and T & G compared with P & P [86.1 +/- 6.9 and 87.1 +/- 6.8 vs. 102.3 +/- 10.3 (SE) min], whereas endurance for P & G (122.4 +/- 11.9 min) was greater than for all other trials (P < 0.05). Compared with nontryptophan trials, during the tryptophan trials plasma prolactin increased (P < 0.05) nearly threefold before exercise and almost twofold early in exercise. Muscle glycogen concentrations were reduced (P < 0.05) below preexercise values in the P & G and P & P trials only. However, glucose infusions (P & G) did not affect (P > 0.05) concentrations of plasma free fatty acids or ratios of branched-chain amino acids to free tryptophan. In conclusion, tryptophan infusion reduced endurance time, which was consistent with the central fatigue hypothesis. The failure of glucose infusion to alleviate the effects of tryptophan and the absence of significant muscle glycogen reduction in the tryptophan trials suggest that the early onset of fatigue in the tryptophan trials is not due to a lack of readily available substrate.

Furosemide reduces accumulated oxygen deficit in horses during brief intense exertion.

We theorized that furosemide-induced weight reduction would reduce the contribution of anaerobic metabolism to energy expenditure of horses during intense exertion. The effects of furosemide on accumulated O2 deficit and plasma lactate concentration of horses during high-intensity exercise were examined in a three-way balance randomized crossover study. Nine horses completed each of three trials: 1) a control (C) trial, 2) a furosemide-unloaded (FU) trial in which the horse received furosemide 4 h before running, and 3) a furosemide weight-loaded (FL) trial during which the horse received furosemide and carried weight equal to the weight lost after furosemide administration. Horses ran for 2 min at approximately 120% maximal O2 consumption. Furosemide (FU) increased O2 consumption (ml.2 min-1.kg-1) compared with C (268 +/- 9 and 257 +/- 9, P < 0.05), whereas FL was not different from C (252 +/- 8). Accumulated O2 deficit (ml O2 equivalents/kg) was significantly (P < 0.05) lower during FU (81.2 +/- 12.5), but not during FL (96.9 +/- 12.4), than during C (91.4 +/- 11.5). Rate of increase in blood lactate concentration (mmol.2 min-1.kg-1) after FU (0.058 +/- 0.001), but not after FL (0.061 +/- 0.001), was significantly (P < 0.05) lower than after C (0.061 +/- 0.001). Furosemide decreased the accumulated O2 deficit and rate of increase in blood lactate concentration of horses during brief high-intensity exertion. The reduction in accumulated O2 deficit in FU-treated horses was attributable to an increase in the mass-specific rate of O2 consumption during the high-intensity exercise test.

Exercise training-induced hypervolemia in the horse.

The purpose of this study was to determine if a chronic hypervolemia would accompany endurance exercise training in the horse. Six mature previously inactive horses were utilized for this study. During the 5-wk experiment, five of the horses were trained for 14 d on a treadmill ergometer at a constant treadmill speed of 5.6 km X hr-1 and a constant grade of 12.5% for graduated lengths of time. One horse was trained by lunging at a trotting pace in a round pen. Following training, plasma volume increased by 4.7 1 (29.1%, P less than 0.05). Although the rate of daily water intake did not change during the training period, 24-h urine output decreased by an average of 3.5 1 X d-1 (-24.5%, P less than 0.05). Resting glomerular filtration rate and the rate of sodium clearance were not altered by training. However, urea, potassium, and osmotic clearance were decreased by training (P less than 0.05) while free water clearance was increased (P less than 0.05). Resting plasma aldosterone and arginine vasopressin concentrations were not altered by training. Plasma potassium concentration was significantly decreased (P less than 0.05) following the 2 wk of training. These data would appear to suggest that renal control mechanisms affecting water reabsorption via the re-absorption of urea and osmotically active substances other than sodium provide the primary route for the training-induced hypervolemia seen in horses.

Resistance training-induced increases in muscle mass and performance in ponies.

The purpose of this study was to determine whether 8 wk of progressive resistance exercise training would produce increases in strength and changes in foreleg muscle characteristics indicative of hypertrophy in ponies. Two mature 3- to 6-yr-old, male ponies (188 +/- 16 kg) were taught to carry sheets of lead over their saddle region (wither) while walking on a level treadmill at 1.9 m.s-1. This initial familiarization period was followed by 8 wk of training (3 d per wk), in which the ponies performed a series of progressive sets of weight carrying to fatigue. Each workout started with a 2-min walk at 1.9 m.s-1 followed by sets of weight carrying. The ponies carried 44.5 kg for the first set with increases of 22.3 kg per set until fatigue. Weights were applied and then removed for 60-90 s between sets using a chain hoist and sling apparatus. Measurements of forelimb girth, body weight, and total weight carried were recorded at each workout session. Ultrasound measurement of the diameters of the superdigital flexor muscles and muscle biopsies were performed before and after the 8-wk training period. Eight weeks of resistance training resulted in significant increases in peak weight carried (260%, P < 0.05) and total weight carried (1525%, P < 0.05) during each workout. Forelimb girth increased 12 +/- 1% (P < 0.05) with a corresponding 19 +/- 3% (P < 0.05) increase in muscle cross-sectional diameter. There were no changes (P > 0.05) in Type I muscle fiber area; however, there was a nonsignificant 26% increase in Type IIA+IIB fiber area. These data suggest that 8 wk of progressive resistance exercise training increase strength and cause changes in muscle size and characteristics consistent with hypertrophy.

Effect of phenylbutazone on the haemodynamic, acid-base and eicosanoid responses of horses to sustained submaximal exertion.

The systemic haemodynamic and acid-base effects of the administration of phenylbutazone (4.4 mg kg-1 intravenously) to standing and running horses were investigated. Phenylbutazone, or a placebo, was administered to each of six mares either 15 minutes before, or after 30 minutes of a 60-minute submaximal exercise test which elicited heart rates approximately 55 per cent of maximal, and to the same horses at rest. The variables examined included the cardiac output, heart rate, systemic and pulmonary arterial pressures, right atrial and right ventricular pressures, and arterial and mixed venous blood gases and pH. Serum sodium, potassium and chloride concentrations, and plasma thromboxane B2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and prostaglandin E2 (PGE2) concentrations were measured in separate studies using similar protocols in the same horses. Running produced increases in heart rate, cardiac output, mean arterial and right ventricular pressure, and decreases in total peripheral resistance. The acid:base responses to exertion were characterised by respiratory alkalosis. Exertion did not significantly influence plasma 6-keto-PGF1 alpha or PGE2 concentrations but plasma thromboxane B2 concentrations were increased significantly by 60 minutes of exertion in the untreated horses. This exercise-induced increase in plasma thromboxane B2 concentration was inhibited by the previous administration of phenylbutazone, but phenylbutazone did not produce detectable changes in systemic haemodynamic or acid-base variables in either standing or running horses.

Furosemide magnifies the exercise-induced elevation of plasma vasopressin concentration in horses.

The purpose of this study was to test the hypothesis that furosemide administration before exercise would cause greater increases in plasma arginine vasopressin (AVP) concentration in exercising horses than exercise alone. Six adult, clinically normal, unfit mares underwent three randomly ordered 60 minute standard exercise tests on an equine treadmill to examine the effect of furosemide administration on plasma AVP concentration. In one trial, furosemide (1 mg kg-1) was infused four hours before exercise (FUR-4) and a placebo (10 ml saline) was infused two minutes before exercise; in another trial the placebo was infused four hours before exercise and drug was infused two minutes before exercise (FUR-2); in a third trial a placebo was infused four hours and two minutes before exercise (CON). During the treadmill test each mare ran up a fixed 4 degrees incline for one hour at a speed previously determined to produce a heart rate of 65 per cent of each horse's maximum heart rate. Venous blood samples were collected at rest in the stall, immediately before exercise while standing on the treadmill, and at 15 minute intervals during the treadmill test. Plasma AVP concentration was measured by radioimmunoassay. In the CON trial, plasma AVP concentration increased 561 per cent (P < 0.05) from 6.3 +/- 1.0 pg ml-1 (mean +/- SE) at rest to 38.8 +/- 12.8 pg ml-1 at the end of the 60 minute run. During the FUR-2 trial, AVP increased 1185 per cent (P < 0.05) from 5.9 +/- 1.7 pg ml-1 to 75.8 +/- 17.7 pg ml-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Fluid administration attenuates the haemodynamic effect of frusemide in running horses.

The effect of blood volume repletion after frusemide administration on the right atrial and pulmonary artery pressure responses of horses to exercise has not been reported. We examined right atrial and pulmonary artery pressure and plasma atrial natriuretic peptide concentration (ANP) responses to an incremental exercise test in 6 Standardbred mares. Horses were treated, in a 3 way cross over design, with isotonic saline, frusemide (1 mg/kg bwt, i.v.), and frusemide followed 3 h later by lactated Ringer's solution (12 ml/kg bwt, i.v.). Three and a half hours after saline or frusemide administration the horses completed a standard exercise test. Frusemide significantly affected the right atrial and pulmonary artery pressure and ANP responses to exercise. Fluid administration decreased plasma total protein concentrations at rest and during running and abolished the effects of frusemide on the haemodynamic and ANP responses to exercise. These results suggest that the haemodynamic effect of frusemide in running horses is mediated, in large part, by a reduction in plasma and blood volume.

Overview of horse body composition and muscle architecture: implications for performance.

Locomotion requires skeletal muscle to sustain and generate force. A muscle's force potential is proportional to its weight. Since the larger the muscle the larger its potential power output, a better understanding of the proportion of skeletal muscle a horse possesses may lead to a better understanding of horse performance. Several techniques exist to assess body composition, which include dual energy X-ray absorption, underwater (hydrostatic) weighing, derivation from total body water, bio-electric impedance, air displacement, body condition scoring, cadaver dissection and ultrasound. The relevance of each method to the equine industry will be discussed as will the practical information that the existing horse body composition studies have provided. Attention will be given to the data regarding the implications of body composition on the performance horse. The limited number of studies discussing different varieties of muscle architectures and the functional importance of these muscles will also be addressed. These body composition data may provide a better understanding of important issues in horse care that can lead to more optimal horse care techniques and a healthier and safer environment for horses.

Fat-free mass is related to one-mile race performance in elite standardbred horses.

This study examined whether body composition was predictive of competitive success in elite standardbreds (STB). Rump fat and muscle thickness (MTH) (vastus lateralis/intermedius [VL], extensor carpi radialis [ECR]) were measured in vivo in male n=6; female n=8 by B-mode ultrasound. Percentage body fat (%fat) was calculated from rump fat. There were no gender differences for age, body mass (males 432+/-11 kg; females 443+/-13 kg), fat-free mass (FFM) (males 400+/-12 kg; females 400+/-11 kg), ECR MTH (males 61+/-2 cm; females 60+/-2 cm) or race time (RT) (males 113+/-3 s; females 114+/-2 s). Males had less (P<0.05) fat mass (males 32+4 kg; females 44+/-3 kg) and %fat (males 7.4+/-0.9%; females 9.9+/-0.5%) and larger (P<0.05) VL MTH (males 88+/-7 cm; females 81+/-3 cm). RT was correlated to %fat and fat mass in males (r=0.89; r=0.82, P<0.05) not females (r=0.51; r=0.14). FFM tended to relate to RT in males (r=-0.76, P=0.07) and females (r=-0.59, P=0.12). Combined %fat and FFM data were correlated to RT (%fat r=0.70, P<0.01; FFM r=-0.65, P<0.01). RT was not correlated to MTH (VL r=-0.28; ECR r=-0.31). In conclusion, FFM was related to RT in elite STB with %fat negatively related to RT in males.

Chronic recombinant equine somatotropin (eST) administration does not affect aerobic capacity or exercise performance in geriatric mares.

The purpose of this experiment was to test the hypothesis that chronic (89 days) administration of recombinant equine somatotropin (eST) would increase aerobic capacity and improve exercise performance in old mares. Fifteen, healthy, unfit, aged (20-26 year old) mares were randomly assigned to a treatment (eST, 12.5 mg day-1 in 3 ml glycine/manitol buffer, s.c., n = 7) or control (vehicle, 3 ml day-1, s.c., n = 8) group. Aerobic capacity and exercise performance were measured using a standardized exercise test (SET) performed on a high speed treadmill. Tests were conducted before (-21 days), during (+43 days and +89 days) and after (+127 days) treatment. During the SET, resting data were collected and the horses then ran up a fixed 6% grade, starting at 4 m s-1, with a 1 m s-1 increase every 60 s (omitting 5 m s-1) until fatigue. Oxygen uptake (VO2) was measured using an open flow calorimeter and blood lactate concentration (LA) via a lactate analyser. Venous blood samples (10 ml) were collected at rest, during the last 10 s of each step of the SET, and after exercise and used to measure LA, plasma protein concentration (PP), hematocrit (HCT), and the plasma concentrations of creatine kinase (CK) and aspartamine transferase (AST). There were no differences (P > 0.05) in resting VO2, LA, TPP, or HCT due to treatment or test time. Furthermore, there were no differences (P > 0.05) in maximal oxygen uptake (VO2max), top run velocity, run time, watts at VO2max, velocity to produce a lactate of 4 mmoll-1 (VLA4), watts at VLA4, peak HCT or peak LA. Finally, there were no differences (P > 0.05) in resting or post-exercise CK or AST. These data indicate that chronic eST administration does not affect aerobic capacity or indices of exercise performance in unfit aged mares.

Plasma constituents during incremental treadmill exercise in intact and splenectomised horses.

Six intact and 6 splenectomised mares were given an incremental exercise test on a treadmill to examine the fluid and electrolyte changes associated with exercise and the role of the spleen in these changes. Blood samples were obtained at rest and at the end of each 1-min step of the test. Exercise at 7 m/sec caused significant (P < 0.05) increases in plasma osmolality (intact, +9.9%; splenectomised, +6.2%), plasma protein concentration (intact, +15.8%; splenectomised, +11.4%), and plasma K+ concentration (intact 46%; splenectomised, +57%). Plasma Na+ concentration did not increase significantly (P > 0.05) in either group (intact = 2.7%; splenectomised, = 3.5%). This appears to be the first record of substantial changes of these constituents during short-term exercise, even before the onset of visible sweat losses. The changes in the concentration of plasma protein suggest that short-term exercise causes a decrease in plasma volume. The changes in the concentration and content of sodium suggest that this is an isotonic shift of fluid. The increase in plasma potassium concentration appears to be due to haemoconcentration as well as an increase in the content of potassium within the vascular compartment.

Chronic clenbuterol administration alters myosin heavy chain composition in standardbred mares.

The purpose of this study was to examine changes in myosin heavy chain (MHC) composition due to chronic clenbuterol administration with or without exercise in mares. Unfit Standardbred mares (aged 10+/-3 years) were divided into four groups: clenbuterol (2.4 micro/kg BW twice daily) plus exercise (3 days/week for 20 min at 50% VO(2max); CLENEX; n=6), clenbuterol only (CLEN; n=6), exercise only (EX; n=5), and control (CON; n=6). Muscle biopsies were obtained from gluteus medius muscle before and after the eight-week training/administration period. MHC composition was determined via SDS gel electrophoresis and quantified using a scanning and densometric system. CLENEX and CLEN exhibited significant (P<0.05) MHC changes while EX and CON did not. MHC type IIA decreased (29.8+/-6.1 to 19.3+/-4.0%, CLENEX; and 36.8+/-12.4 to 26.4+/-7.9%, CLEN) and MHC type IIX increased (59.4+/-7.2 to 71.8+/-5.8%, CLENEX; and 50.5+/-12.5 to 62.0+/-9.3%, CLEN). Chronic clenbuterol administration with and without exercise resulted in a significant shift in MHC profile in Standardbred mares.

Hemodynamic effects of atropine, dobutamine, nitroprusside, phenylephrine, and propranolol in conscious horses.

The authors investigated the cardiovascular effects of low doses of nitroprusside, dobutamine, and phenylephrine and a beta-adrenergic blocking dose of propranolol in conscious, healthy horses with and without prior atropine administration. A parasympathetic blocking dose of atropine produced significant increases in heart rate and arterial pressures, and decreased stroke volume, ejection fraction, pulse pressure, and right-ventricular end-diastolic pressure and volume. Cardiac output was not changed by atropine administration. Nitroprusside reduced arterial pressures to a greater extent in atropinized horses but increased heart rate in both atropinized and non-atropinized horses. Dobutamine increased mean arterial pressure in both non-atropinized and atropinized horses but increased heart rate, diastolic arterial pressure, and systemic vascular resistance only in atropinized horses. Propranolol did not affect any of the hemodynamic variables that were measured. Phenylephrine, in the presence of beta-adrenergic blockade, increased mean arterial pressure and reduced cardiac output. This study showed that low doses of nitroprusside, dobutamine, and phenylephrine produce significant hemodynamic effects in conscious, healthy horses and that these effects are modified by prevailing parasympathetic tone.

Exercise capacity in young and old mares.

OBJECTIVE: To test the hypothesis that, compared with unfit young horses, unfit older horses have lower aerobic capacity and reduction in other indices of exercise capacity. ANIMALS: 6 young (mean +/- SEM, 5.3 +/- 0.8 years and 445 +/- 13 kg) and 6 aged (22.0 +/- 0.4 years and 473 +/- 18 kg) healthy Standardbred and Thoroughbred mares. PROCEDURES: The mares, accustomed to running on a treadmill, were tested by use of an incremental exercise test. None of the mares had received exercise training for at least 4 months prior to the study. During testing, mares ran up a fixed 6% grade, starting at a speed of 4 m/s, with 1 m/s increase every 60 seconds (omitting 5 m/s) until they reached fatigue. Maximal oxygen uptake (VO2max) was measured by use of an open-flow calorimeter. Venous blood samples (10 ml) were collected during the last 10 seconds of each step and were used to measure blood lactate concentration and PCV. Calculated performance indices included velocity at VO2max, maximal velocity, and velocity at lactate concentration of 4 mmol/L; work rate (watts) at those velocities also was determined. RESULTS: There were differences (P < 0.05) between old and young mares for maximal run velocity attained during the test (8.7 +/- 0.5 versus 10.8 +/- 0.5 m/s, respectively), VO2max (89.4 +/- 4.3 versus 117.3 +/- 9.5 ml/kg of body weight/min, respectively), and velocity at VO2max (8.0 +/- 0.4 versus 9.8 +/- 0.7 m/s, respectively). Also, velocity required to reach blood lactate concentration of 4 mmol/L was lower (P < 0.05) in old (7.5 +/- 0.4 m/s), compared with young (10.2 +/- 0.7 m/s), mares. CONCLUSION: Older mares have substantially (-24%) lower maximal aerobic capacity than do young mares. CLINICAL RELEVANCE: Many horses participate in athletic activities into their late teens and some do so beyond the age of 20 years; thus, the need exists to explore ways to adjust training programs for older horses.

Effect of furosemide and weight carriage on energetic responses of horses to incremental exertion.

The effect of furosemide-induced weight loss on the energetic responses of horses to running was examined in a 3-way crossover study. Eight 2- to 3-year-old Standardbred mares received, in random order, 10 ml of saline solution 4 hours before running on a treadmill (control trial, C); or, during 2 trials, 1 mg of furosemide/kg of body weight, i.v., 4 hours before running. During one of the trials when the horses received furosemide, they carried weight equal to that lost over the 3.75 hours after furosemide administration while running (furosemide-loaded, FL), and during the other trial they did not carry weight equal to that lost after furosemide administration (furosemide-unloaded, FU). Horses performed an incremental exercise test on a treadmill during which rates of oxygen consumption (VO2) and carbon dioxide production (VCO2) were measured, respiratory exchange ratio was calculated, and blood samples were collected for determination of mixed venous plasma lactate concentration and arterial and mixed venous oxygen saturation. Furosemide treatment caused significantly (P < 0.001) greater weight loss than did saline administration; mean +/- SEM weight loss (exclusive of fecal loss) was 1.6, 8.8, and 10.2 kg (SEM = 2.0) for C, FL, and FU trials, respectively. The speed at which peak VO2 was achieved was 9.31, 9.56, and 9.50 (SEM = 0.16) m/s, respectively, time to fatigue was 547, 544, and 553 (SEM = 26) seconds, respectively, and the highest speed attained was 10.3, 10.2, and 10.2 (SEM = 0.2) m/s, respectively. Mean peak rate of oxygen consumption was 130.7, 129.6, and 129.6 (SEM = 1.9) ml/min/kg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Early insulin response to an intravenous glucose tolerance test in horses.

Plasma insulin concentration of many species has a characteristic early or acute-phase response in the minutes after IV administration of glucose. However, the plasma insulin response of horses soon after the IV administration of glucose has not been examined, whereas the more prolonged response has been evaluated. We examined the plasma insulin and glucose concentration responses of adult mares during the 30 minutes after rapid IV administration of glucose (0.33 g/kg of body weight). Plasma glucose concentration peaked at 664 +/- 54 mg/dl within 1 minute of cessation of glucose administration, whereas insulin concentration peaked at 326 +/- 24 pmol/L at 2 minutes after the end of glucose administration. Thus, these mares had an acute insulin response, consistent with that observed in other species, including dogs, human beings, and cattle.

Evaluation of washing with cold water to facilitate heat dissipation in horses exercised in hot, humid conditions.

OBJECTIVE: To determine whether body temperature of horses exercised in hot, humid conditions and then repetitively washed with cold water will decrease more rapidly than that of horses that are not washed, and to determine whether washing with cold water has deleterious effects on horses. ANIMALS: 5 physically fit Thoroughbred mares, 3 to 10 years old. PROCEDURES: Horses were exercised on a high-speed treadmill in hot (31.1+/-0.3 C), humid (relative humidity, 77.7+/-2%) conditions. Exercise was terminated when pulmonary artery temperature reached 41.5 C. Values for pulmonary artery, rectal, and left gluteal muscle temperatures were compared throughout a 30-minute recovery period after exercise during which horses stood quietly (passive cooling) or were cooled (active cooling) by repeated applications of cold (1 5.6+/-0.6 C) water. RESULTS: Pulmonary artery temperature was significantly less for actively cooled horses, compared with passively cooled horses 4 minutes into the recovery period. Left gluteal muscle temperature decreased significantly in actively cooled, but not passively cooled, horses during the recovery period. Heart rate and rectal temperature were significantly less for actively cooled horses by 15 minutes of the recovery period. Cooling technique did not effect hydration status, muscle health, or serum electrolyte concentrations. Active cooling did not cause obvious adverse effects. CONCLUSION AND CLINICAL RELEVANCE: Active cooling by washing with cold water is a safe, effective means for facilitating heat dissipation of horses after exercise in a hot, humid environment.