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Surveys indicate that up to 15% of the equine population in the United States is older than 20 years of age, with many of these animals performing various athletic activities well into their 20s. As is the case with their human counterparts, these geriatric equine athletes have the ability to continue to perform in athletic events. Unfortunately, many horse owners continue to train their active older animals using exercise training protocols that, although appropriate for a younger animal, may not be appropriate for the older equine athlete. Studies in aged human beings have led to a fine-tuning of exercise prescription for the older human athlete so as to prevent the adverse and potentially dangerous effects of excessive work. Published results have led to new and improved programs to promote fitness for the growing population of older adults. Unfortunately, limited data exist regarding the exercise capacity of the aged horse. Future studies on the effects of aging on exercise capacity in equine athletes need to take a few major directions. One question to be answered is at what age does physiologic function first begin to decline in the horse? In human beings, this age varies with training, but noticeable changes in aerobic capacity are first seen in 40- to 50-year-olds. Second, data are needed to determine what levels of exercise enhance the health and well-being of the older horse without harm. Lastly, studies are needed to determine the physiologic mechanisms associated with the onset of aging-induced decreases in physiologic function in the horse. The ultimate goal of all these studies should be to adjust exercise levels to meet the needs of the growing population of athletically active older equine athletes.

Purpose: The purpose of this 8-wk study was to examine the effect of therapeutic levels of clenbuterol on aerobic performance and hemodynamics associated with exercise., Methods: Twenty-three unfit Standardbred mares were divided into four experimental groups, clenbuterol (2.4 microg x kg(-1) body weight twice daily) plus exercise (20 min at 50% O2max; CLENEX; N = 6), clenbuterol only (CLEN; N = 6), exercise only (EX; N = 5), and control (CON; N = 6). All horses performed an incremental exercise test (GXT) to measure maximal oxygen consumption (O2max), blood lactate concentration, total plasma protein concentration, and hematocrit. Plasma volume, heart rate, right ventricular pressure (RVP), and pulmonary artery pressure (PAP) were measured before and after the treatment/training. Each horse also performed an exercise capacity test (ECT) in which they ran at their pretreatment O2max speed until exhausted., Results: There were no significant changes in blood lactate, total protein, or hematocrit for any group during either the GXT or ECT. CLENEX decreased (P < 0.05) O2max (-6.2%) and velocity to O2max (-10.0%), whereas both CLENEX and CLEN decreased (P < 0.05) in time to exhaustion (-20.5+/-4.7 and -20.9 +/- 5.6%). EX alone increased (P < 0.05) O2max (+6.5%), velocity to O2max (+10.0%), velocity to produces lactate concentration of 4 mmol (+13.5%), and time to exhaustion (+32.3 +/- 15.0%). Plasma volume was altered (P < 0.05) in CLENEX (-10%) and EX (+27%) but not in CLEN. Posttest recovery HR was higher (P < 0.05) at 2 min post-GXT in the CLENEX, CLEN, and CON compared with their pretest values; RVP remained elevated at 2 min of recovery in the CLEN and CON groups; however, in the EX, recovery HR and RVP had returned to pre-GXT levels by 2 min of recovery., Conclusions: These data suggest that the combined effect of therapeutic levels of clenbuterol and training decrease aerobic performance and that the resultant reduction in plasma volume may affect improvements in cardiovascular function during recovery normally seen with exercise training.

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., (Copyright 2002 Elsevier Science Ltd.)

Objective: To describe neuroendocrine responses that develop in dogs subjected to prolonged periods of ventricular pacing., Animals: 14 adult male hound-type dogs., Procedure: Samples were obtained and neuroendocrine responses measured before (baseline) and after 3 periods of ventricular pacing. A pacemaker was used to induce heart rates of 180, 200, and 220 beats/min (BPM). Each heart rate was maintained for 3 weeks before increasing to the next rate. Atrial natriuretic peptide, antidiuretic hormone, aldosterone, norepinephrine, epinephrine, and dopamine concentrations and plasma renin activity were measured. Severity of left ventricular compromise was estimated., Results: Shortening fraction decreased significantly with increasing heart rates (mean +/- SE, 35.5 +/- 1.4, 25.0 +/- 1.4, 19.5 +/- 1.9, and 12.2 +/- 2.3 for baseline, 180 BPM, 200 BPM, and 220 BPM, respectively). Atrial natriuretic peptide concentrations increased significantly at 180 BPM (44.1 +/- 3.0 pg/mL) and 200 BPM (54.8 +/- 5.5 pg/mL), compared with baseline concentration (36.8 +/- 2.6 pg/mL). Dopamine concentration increased significantly at 200 BPM (70.4 +/- 10.4 pg/mL), compared with baseline concentration (44.2 73 pg/mL). Norepinephrine concentrations increased significantly from baseline concentration (451 +/- 46.2 pg/mL) to 678 +/- 69.8, 856 +/- 99.6, and 1,003 +/- 2676 pg/mL at 180, 200, and 220 BPM, respectively., Conclusions and Clinical Relevance: Dogs subjected to ventricular pacing for 9 weeks developed neuroendocrine responses similar to those that develop in humans with more chronic heart failure and, except for epinephrine concentrations, similar to those for dogs subjected to ventricular pacing for < 6 weeks.

It has long been known that body mass and, more specifically, lean body mass are strongly correlated with maximal oxygen uptake (VO2max) in man and animals. However, there are no data to date describing this phenomenon in the horse. The purpose of this paper is to examine the relationship between body composition and VO2max in the horse. Twenty-three healthy and unfit Standardbred mares performed an incremental exercise test (GXT) to measure VO2max. Rump fat thickness (RTH), a measure of fat covering, was measured using B-mode ultrasound. Plasma volume, total blood volume and red cell volume were determined, using the Evan's Blue dye dilution technique and packed cell volume. VO2max was correlated with body mass (r = 0.541; P<0.01) and exercise haematocrit (exHCT; r = 0.407; P<0.05) but not RTH or the other haematological variables. To eliminate the influence of body mass on the individual variables, a regression analysis was performed on the mass-residuals of VO2max, RTH, plasma volume and exHCT. The residuals of VO2max were correlated negatively with the residuals of RTH (r = -0.687; P = 0.0003) and positively with the residuals of exHCT (r = 0.422; P = 0.045) but not plasma volume. VO2max could be predicted from a linear combination of the residuals of RTH and exHCT (r = 0.767; P<0.0001). These data indicate that VO2max in the horse is significantly related to fat-free mass (FFM), independent of body mass. Red blood cells from the splenic reserve constitute an important factor in the horse's ability to achieve a high VO2max. Therefore, lean body mass may be a more appropriate basis for assessing metabolic function in the athletic horse.

The purpose of this study was to test the hypotheses that ageing would result in a decline in maximal heart rate (HRmax) and maximal aerobic capacity (VO2max) and, secondarily, that those effects would be reversible with training. Eighteen, healthy, unfit Standardbred mares representing 3 age groups: young (Y = mean +/- s.e. 6.8 +/- 0.4 years, n = 6); middle-aged (MA = 15.2 +/- 0.4 years, n = 6); and old (O = 27.0 +/- 0.2 years, n = 6) were used. HRmax, VO2max and oxygen pulse at VO2max (OPmax) and the velocities producing HRmax (VHRmax) and VO2max (VVO2max) were measured during pretraining and post-training incremental exercise tests (GXT). During training, mares exercised 3 days/week (Weeks 1-8) and 4 days/week (Weeks 9-12) at a submaximal intensity (approximately 60% HRmax) for approximately 30 min/day. There were no differences (P>0.05) between Y and MA, before (218 +/- 2 vs. 213 +/- 3 beats/min; 116 +/- 3 vs. 109 +/- 3 ml/kg bwt/min; 0.55 +/- 0.01 vs. 0.52 +/- 0.02 ml/kg/beat; 9.0 +/- 0.3 vs. 9.3 +/- 0.2 ms; 8.8 +/- 0.2 vs. 8.8 +/- 0.2 m/s) or after training (224 +/- 2 vs. 218 +/- 2 beats/min; 131 +/- 3 vs. 120 +/- 2 ml/kg bwt/min; 0.58 +/- 0.01 vs. 0.55 +/- 0.01 ml/kg/beat; 10.5 +/- 0.2 vs. 9.5 +/- 0.1 ms; 10.6 +/- 0.2 vs. 9.5 +/- 0.1 m/s) for HRmax, VO2max, OPmax, VHRmax or VVO2max, respectively. Old horses had lower HRmax, VO2max and OPmax and reached them at lower velocities compared to Y and MA (P<0.05), both before (193 +/- 3 beats/min; 83.2 +/- 2.0 ml/kg bwt/min; 0.43 +/- 0.01 ml/kg/beat; 7.8 +/- 0.1 m/s; 7.2 +/- 0.1 m/s) and after training (198 +/- 2 beats/min; 95 +/- 2 ml/kg bwt/min; 0.48 +/- 0.01 ml/kg/beat; 8.2 +/- 0.2 m/s; 8.0 +/-0.2 m/s). Training did not alter HRmax in any age group (P>0.05) but did cause increases in VO2max, OPmax and VVO2max for all groups (P<0.05). Interestingly, training increased VHRmax only in Y (P<0.05). These data demonstrate that there is a reduction in HRmax, VO2max, OPmax, VHRmax and VVO2max in old horses, and that training can partially reverse some effects of ageing.

The purpose of the study was to determine whether 12 weeks of exercise training would affect plasma glucose and plasma insulin concentrations in young and older Standardbred mares. Eighteen healthy, unfit mares representing 3 age groups were used: young (Y = 6.8 +/- 0.4 years; n = 6), middle-aged (MA = 15.2 +/- 0.4; n = 6), and old (O = 27.0 +/- 0.2; n = 6). Pre- and post-training incremental exercise tests (GXT) were performed to measure plasma glucose and insulin concentration from immediately after, until 120 min postexercise. Training consisted of exercise 3 days/week (weeks 1-8) and 4 days/week (weeks 9-12) at a submaximal intensity (approximately 60% of pretraining HRmax) for approximately 30 min/day. Old mares had lower levels of glucose after the GXT when compared to Y and MA mares (P<0.05). There was also a time-by-age interaction (P = 0.003) in that, at 120 min post-GXT, glucose levels had not returned to pre-exercise values. Plasma glucose concentrations, in response to acute exercise, were not altered by training for any age group (P>0.05). Prior to exercise training, O mares had higher plasma insulin compared to Y and MA mares at 120 min postexercise (P<0.05), and insulin was also elevated in O mares compared to all other time points at 120 min post-GXT (P<0.05). Training resulted in increased plasma insulin concentrations at 120 min post-GXT in all age groups (P<0.05). In conclusion, age affected glucose and insulin responses to acute exercise prior to and after 12 weeks of exercise training. With regards to insulin, 12 weeks of exercise training resulted in a postexercise rebound hyperinsulinaemia, which may be related to an increased need for glycogen repletion in the muscle. These factors are important in considering the ability of an older horse to tolerate exercise.

The purpose of the present study was to determine whether the training-induced hypervolaemic response seen in the horse is associated with aldosterone-mediated renal mechanisms affecting sodium conservation during the first days of training. Five healthy, Standardbred mares (weight 450-500 kg, age 4-8 years) that were unfit, but accustomed to running on the treadmill, were used to test the hypothesis that repeated submaximal exercise would alter plasma aldosterone (ALDO) concentration and renal excretion of electrolytes in horses within the first 3 days of training. The experiment consisted of a 2 week housing equilibration period followed by a 1 week control period and a 3 day exercise training period (30 min/day at 60% VO2max). During control, ALDO and renal fluid and electrolyte losses were measured for 24 h on 3 separate days. Renal function (urine volume [UV], 24 h excretion of Na+, K+ and Cl- [UNA+ V, UK+ V, UCl- V], clearance of Na+ [CNa+], K+ [CK+] and Cl- [CCl-], creatinine [CCr], osmotic substances [Cosm], and solute-free water [FWC], and the fractional excretion of Na+, K+ and Cl-) and ALDO were measured for an additional 3 consecutive days during the training period. There were no differences (P>0.05) in any variable during the control period. Plasma volume increased (+18.7%, P<0.05) after 3 days of training. During training, there were no significant changes in plasma osmolality, electrolyte concentrations or CCr. Training caused decreases (P<0.05) in UV (-30%), UNA+ V (-73%), UK+ V, (-55%) and UCl- V (-70%). Training also caused decreases (P<0.05) in Cosm (-30%), through decreases in CNa+ (-60%), CK+ (-60%), and CCl- (-66%). Interestingly, FWC increased (+30%, P<0.05), whereas, there were significant decreases in the fractional excretion of Na+ (-59%), K+ (-48%) and Cl- (-60%). Training caused substantial elevations in both pre-exercise (967%, P<0.05) and postexercise (+3013%, P<0.05) plasma ALDO concentrations suggesting an increase in both basal levels and the responsiveness to acute exercise. Together, these observations suggest that mechanisms affecting tubular conservation of electrolytes contribute to the early response to training. However, it is also concluded that renal mechanisms appear to be only part of the mechanism for conserving sodium and water intake as well as training-induced changes in gastrointestinal mechanisms affecting electrolyte and water balance.

Fine-tuning of the response to exercise that lasts longer than a few seconds is reliant on the regulation of several key variables governing the cardiopulmonary, vascular, and metabolic response to exercise. This type of integrative response requires communication between organ systems that relies on the secretion of endocrine and paracrine substances by one tissue or organ that are transported remotely to other tissues or organs to evoke a response to adjust to the disturbance.

The objective of the present study was to measure plasma endothelin-1 (ET-1) at rest and during exercise in the horse. Six healthy, Standardbred and Thoroughbred mares (5.3+/-0.8 years; 445.2+/-13.1 kg) which were unfit, but otherwise accustomed to running on the treadmill, were used in the study. Plasma ET-1 concentrations were measured using a commercially available radioimmunoassay kit. Horses performed three trials: a standing control (CON) trial where blood was collected from the jugular vein every minute for 5 min; a graded exercise test (GXT) where blood samples were collected at the end of each 1 min step of an incremental exercise test; and a 15 min submaximal (60% VO(2max)) steady-state exercise test (SST) where blood samples were collected 1 min before, immediately after, and at 2 min, 10 min and 20 min post-exercise. Plasma ET-1 concentration did not change (P>0.05) during the CON trial where it averaged 0.18+/- 0.03 pg/mL (mean+/-SE). Surprisingly, plasma ET-1 concentration did not change during the GXT trial where it averaged 0.20+/-0.03 pg/mL. There were no differences between the mean concentrations obtained in either trial (P>0.05). Plasma ET-1 concentrations were, however, significantly elevated (P<0.05) immediately following exercise and at 2 min post-exercise in the SST. Post-exercise plasma ET-1 concentrations returned to baseline (P>0.05) by 10 min of recovery. Together, these data may suggest that ET-1 concentrations are altered in response to an exercise challenge.

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., (Copyright 2002 Published by Elsevier Science Ltd.)

Purpose: Chronic administration of pharmacological levels of beta2-agonists have been shown to have toxic effects on the heart; however, no data exist on cardiac function after chronic clenbuterol administration. The purpose of this study was to examine the effect of therapeutic levels of clenbuterol on cardiac performance., Methods: Twenty unfit Standardbred mares were divided into four experimental groups: clenbuterol (2.4 microg.kg(-1) twice daily 5 d.wk(-1)) plus exercise (20 min at 50% .VO(2max)) (CLENEX; N = 6), clenbuterol (CLEN; N = 6), exercise (EX; N = 4), and control (CON; N = 4). M-mode and two-dimensional echocardiography (2.5-MHz sector scanner transducer) were used to measure cardiac size and function before and immediately after an incremental exercise test, before and after 8 wk of drug and/or exercise treatments., Results: After treatment, CLENEX and CLEN demonstrated significantly higher left ventricular internal dimension (LVD) at end diastole (+23.7 +/- 4.8%; +25.6 +/- 4.1%), LVD at end systole (+29.2 +/- 8.7%; +40.1 +/- 7.9%), interventricular septal wall thickness (IVS) at end diastole (+28.9 +/- 11.0%; +30.7 +/- 7.0%), IVS at end systole (+29.2 +/- 8.7%; +40.1 +/- 7.9%), and left ventricular posterior wall systolic thickness (+43.1 +/- 14.%; +45.8 +/- 14.1%). CLENEX and CLEN had significantly increased aortic root dimensions (+29.9 +/- 6.1%; +24.0 +/- 1.7%), suggesting increased risk of aortic rupture., Conclusion: Taken together, these data indicate that chronic clenbuterol administration may negatively alter cardiac function.

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.

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.

Erythropoietin (EPO) is the primary hormone of erythropoiesis. Administration of recombinant human erythropoietin (rhuEPO) to improve racing performance in the horse represents a new form of blood doping, which has been associated with increased mortality. While immunoassay kits have become plentiful, very few commercial hormone assays are made specifically for equine research. There is a strong degree of sequence homology reported for EPO among species, which has allowed antibodies designed for human EPO research to be used to determine EPO concentration in other species. The objective of the present study was to use Western blot analysis to determine whether the antibody to rhuEPO, provided in a commercial radioimmunoassay (RIA) kit, recognizes horse EPO. Western blot analysis of purified rhuEPO and horse plasma was conducted, using the polyclonal goat-antihuman EPO antibody supplied in the Incstar EPO Trac RIA as the primary antibody. Immunoblot analysis revealed a major band at approximately 52 kDa for both rhuEPO and the horse plasma. Our results demonstrate that a human EPO antibody recognizes equine EPO. These findings show that the Incstar EPO Trac RIA hormone assay system can be used to measure equine EPO.

Six young (mean + s.e., 5.3 +/- 0.8 years, 445 +/- 13 kg bwt) and 6 old (22.0 +/- 0.4 years, 473 +/- 18 kg bwt) Standardbred and Thoroughbred mares were used to test the hypothesis that age would alter the endocrine response to exercise. All of the mares were unconditioned but accustomed to the laboratory, to standing quietly and running on a treadmill, and to the standardised incremental exercise test (SET) used in the experiment. Two weeks prior to the experiment, each horse underwent a SET to determine maximal oxygen uptake (VO2max) and the speeds to be used in the actual experiment. A second graded exercise test (GXT) was performed without instrumentation for the measurement of plasma renin activity (PRA) and the plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP), aldosterone (ALDO), and endothelin-1 (ET-1). Blood samples (30 ml) were collected at rest and at the end of each one minute step of the exercise test. Plasma concentrations of hormones were measured using radioimmunoassay kits. There were no differences (P > 0.05) between old vs. young mares for resting PRA (2.2 +/- 0.3 vs. 1.5 +/- 0.3 ng/ml/h), or the plasma concentrations of ANP (10.0 +/- 0.9 vs. 10.7 +/- 0.6 pg/ml); AVP (0.7 + 0.7 vs. 1.4 +/- 0.4 pg/ml); ALDO (39.2 +/- 10.3 vs. 22.7 +/- 4.6 pg/ml); or ET-1 (0.23 +/- 0.04 vs. 0.18 +/- 0.03 pg/ml). Exercise significantly increased PRA and the concentrations of ANP, AVP, and ALDO in both groups of horses; however, ET-1 was not altered (P > 0.05) by exercise in either group. There were differences (P < 0.05) between means obtained from the old and young groups for PRA (5.4 +/- 0.6 vs. 3.9 +/- 0.8 ng/ml/h and the concentrations of ANP (14.5 +/- 2.3 vs. 26.5 +/- 9.0 pg/ml), AVP (13.6 +/- 0.3 vs. 26.1 +/- 13.9 pg/ml, and ALDO (76.8 +/- 22.0 vs. 41.5 +/- 4.9 pg/ml) measured in samples obtained at the speed eliciting VO2max. These data suggest that older horses have an age-altered endocrine response to exercise.

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.

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.

Objective: To compare exercise-induced immune modulation in young and older horses., Animals: 6 young and 6 aged horses that were vaccinated against equine influenza virus., Procedure: Venous blood samples were collected for immunologic assessment before and immediately after exercise at targeted heart rates and after exercise for determination of plasma lactate and cortisol concentrations. Mononuclear cells were assayed for lymphoproliferative responses and incubated with interleukin-2 (IL-2) to induce lymphokine-activated killer (LAK) cells. Antibodies to equine influenza virus were measured., Results: Older horses had significantly lower proliferative responses to mitogens than younger horses prior to exercise. Exercise caused a significant decrease in lymphoproliferative response of younger horses, but not of older horses. Activity of LAK cells increased slightly with exercise intensity in younger horses. Cortisol concentrations increased in both groups after exercise; younger horses had higher concentrations after exercise at heart rates of 180 and 200 beats/min than those of older horses. Plasma lactate concentrations increased with exercise intensity but there were no differences between older and younger horses. Older horses had lower antibody titers to equine influenza virus than younger horses. Exercise did not affect antibody titers., Conclusion: Although lymphoproliferative responses and antibody titers of older horses were less than those of younger horses, older horses were more resistant to exercise-induced changes in immune function, possibly because of lower cortisol concentrations., Clinical Relevance: Stress and aging are known to affect immune function. Older horses had reduced immune function, but were more resistant to exercise-induced immune suppression than younger horses.

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.

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.

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.

Exercise places large demands on the equine cardiovascular system which are further complicated by environmental factors. In many respects, performance is limited by fluid and electrolyte stores and the ability to maintain cardiovascular and thermoregulatory stability in the face of severe sweat losses. Studies in the exercising horse have been primarily descriptive or associative, with only a limited number seeking to identify physiologic mechanisms associated with the control of fluid and electrolyte balance. More mechanistic studies are needed to fully understand the integration of the cardiovascular, endocrine, and renal systems in the defense of plasma osmolality, blood volume, and blood pressure.

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.

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.

We compared the effects of caffeinated vs non-caffeinated carbohydrate electrolyte (CE) drinks on urine volume (UV), free water clearance (CH2O), fractional excretion of water (FEH2O), and osmolar excretion during 4 h of rest or 1 h rest followed by 3 h of cycling at 60% VO2max in six subjects. We also tested maximal performance at 85% VO2max following the 3-h exercise trials. Throughout the two resting trials and the two rest + exercise trials, subjects ingested CE (total volume = 35 ml/kg) without (PLAC) or with (CAFF) caffeine (25 mg/dl). Blood samples were collected, and body weight and UV were recorded every hour. Urine and blood were analyzed for osmolality and creatinine, and plasma catecholamine concentrations were determined. At rest, mean (+/-SE) UV between 60 min and 240 min was greater for CAFF (1843 +/- 166 ml) vs PLAC (1411 +/- 181 ml) (p < 0.01); during exercise the difference in UV between CAFF (398 +/- 32 ml) and PLAC (490 +/- 57 ml) was not significant. Cycling performance was unaffected by caffeine. Plasma catecholamine concentrations were not different between PLAC and CAFF but were greater during exercise than rest (p < 0.01) and may have counteracted the diuretic effect of caffeine observed at rest. Thus, CAFF consumed in CE during moderate endurance exercise apparently does not compromise bodily hydration status.

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.

The effect of premedication with phenylbutazone on systemic hemodynamic and diuretic effects of furosemide was examined in 6 healthy, conscious, mares. Mares were instrumented for measurement of systemic hemodynamics, including cardiac output and pulmonary arterial, systemic arterial, and intracardiac pressures, and urine flow. Each of 3 treatments was administered in a randomized, blinded study; furosemide (1 mg/kg of body weight, IV) only, phenylbutazone (8.8 mg/kg, PO, at 24 hours and 4.4 mg/kg, IV, 30 minutes before furosemide) and furosemide, or 0.9% NaCl. Phenylbutazone administration significantly attenuated, but did not abolish, the diuretic effect of furosemide. Phenylbutazone completely inhibited the immediate effect of furosemide on cardiac output, stroke volume, total peripheral resistance, and right ventricular peak pressure. Premedication with phenylbutazone did not inhibit equally the diuretic and hemodynamic effects of furosemide, indicating that some of furosemide's hemodynamic effects are mediated by an extrarenal activity of furosemide.

Eleven anesthetized rhesus monkeys were used to study cardiovascular, renal, and endocrine alterations associated with 120 min of head-out water immersion. Five animals underwent complete intrapericardial denervation using the Randall technique, while the remaining six monkeys served as intact controls. Each animal was chronically instrumented with an electromagnetic flow probe on the ascending aorta, a strain gauge pressure transducer implanted in the apex of the left ventricle (LV), and electrocardiogram leads anchored to the chest wall and LV. During immersion, LV end-diastolic pressure, urine flow, glomerular filtration rate, sodium excretion, and circulating atrial natriuretic peptide (ANP) each increased (P < 0.05) for intact and denervated monkeys. There were no alterations in free water clearance in either group during immersion, yet fractional excretion of free water increased (P < 0.05) in the intact monkeys. Plasma renin activity (PRA) decreased (P < 0.05) during immersion in intact monkeys but not the denervated animals. Plasma vasopressin (PVP) concentration decreased (P < 0.05) during the first 30 min of immersion in both groups but was not distinguishable from control by 60 min of immersion in denervated monkeys. These data demonstrate that complete cardiac denervation does not block the rise in plasma ANP or prevent the natriuresis associated with head-out water immersion. The suppression of PVP during the first minutes of immersion after complete cardiac denervation suggests that extracardiac sensing mechanisms associated with the induced fluid shifts may be responsible for the findings.

Exertion has an effect on plasma, serum, and/or urine prostanoid concentrations in many species. We investigated the effect of exercise intensity on plasma prostaglandin concentrations during and after exercise in horses. Six Thoroughbreds completed 4 trials: 3 exercise trials (low-, medium-, and high-speed) and 1 nonexercise (control) trial on a high-speed treadmill. Blood samples were collected from a jugular catheter before, during, and after exercise. The PCV and blood lactate, plasma protein, plasma prostacyclin (6-keto-PGF1 alpha), thromboxane B2 (TXB2), and prostaglandin E2 (PGE2) concentrations were measured before, during, and after exercise. Exercise significantly (P = 0.001) increased plasma TXB2 concentration during and after exercise in the low-, medium-, and high-speed trials, although effect of exercise intensity was not detected. Exercise was associated with an increase in PCV and blood lactate and plasma protein concentrations. There was no effect of exercise on plasma 6-keto-PGF1 alpha concentrations; PGE2 was not detected in plasma from any horse in any trial.

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.

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.

Effects of furosemide administration on exertion-induced changes in plasma renin activity and plasma concentrations of atrial natriuretic peptide and aldosterone in horses during sustained submaximal exertion were examined. Furosemide (1 mg/kg of body weight) or heparinized saline solution was administered IV to each of 6 mares not conditioned to exercise, either 4 hours or 2 minutes before 60 minutes of sustained submaximal running on a treadmill. Horses ran at a speed that induced heart rate approximately 65% of maximal after saline treatment. After 15 minutes of running, furosemide suppressed the exertion-induced increase in plasma concentrations of atrial natriuretic peptide (mean [95% confidence interval] values of 63.9 [9.9 to 421] pg/ml vs 100 [15.4 to 652] pg/ml after furosemide or saline treatment, respectively), and enhanced the response of plasma renin activity to exertion (18.6 [5.7 to 60.4] ng/ml/h vs 6.0 [1.8 to 19.4] ng/ml/h, respectively). An effect of furosemide on the exertion-induced increase in plasma aldosterone concentration was not detected.

This article has presented information on the importance of the sympathetic nervous system in the response to exercise. The authors have reviewed the very limited information on the effects of sympathomimetic and sympatholytic drugs on exercise performance in the horse. Most of these drugs are specifically prohibited under the rules of racing, and they have significant side effects that either decrease performance or make their use dangerous to both the horse and horse-man. Additionally, all of these drugs or their metabolites are readily detected by current drug testing protocols. Further information is needed to expand our knowledge of how each of these substances affects the health of the equine athlete.

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)

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)

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)

Six intact (IN) and five splenectomized (SP) mares were subjected to an incremental exercise test to examine the effects of splenectomy on blood pressure responses during exercise. During the test the horses ran up a 6 degree grade on a treadmill set at an initial speed of 4 m/s. Speed was increased 1 m/s every 1 min until heart rate (HR) reached a plateau. Hemodynamic data were collected continuously and analyzed for the last 18 s of the 4, 5, 6, and 7 m/s steps of the exercise test. There were no differences (P > 0.05) between the groups for resting means for any parameter measured in the study. HR increased (P < 0.05) in both groups of horses during exercise with significantly greater HR in the SP horses during the first two steps of the test. There were no differences (P > 0.05) in maximal HR between the groups. Right atrial pressure (RAP) did not change during exercise in the SP horses; however, it did increase 20 mmHg (493%, P < 0.05) in the IN horses. Right ventricular pressure (RVP) increased (P < 0.05) during exercise with no differences (P > 0.05) between the groups. Right ventricular maximum change in pressure over time increased (P < 0.05) in a similar fashion in both groups of animals. Mean arterial pressure (MAP) increased 29 mmHg (30%, P < 0.05) in SP horses, reaching a plateau by the 5 m/s step of the test.(ABSTRACT TRUNCATED AT 250 WORDS)

Six intact (IN) and six splenectomized (SP) mares were subjected to an incremental exercise test to examine the role of decreases in plasma volume (PV) in the changes in hematocrit (Hct) normally seen with exercise. Each horse underwent an incremental exercise test in which it ran on a treadmill up a fixed incline of 6 degrees. The test started at a speed of 4 m/s, and speed was increased 1 m/s each min until heart rate reached a plateau. Blood samples were obtained at rest and at the end of the 4, 5, 6, and 7 m/s steps of the exercise test. Resting PV was greater (P < 0.05) in the IN group (28.6 +/- 0.5 liters) compared with SP horses (22.7 +/- 2.2 liters). Exercise produced a significant increase in Hct in both groups of horses; however, the increases were greater (P < 0.05) at all exercise intensities in IN compared with SP horses. Hct increased rapidly during the first step (4 m/s) in the exercise test in the IN animals. After this, Hct increased slowly in IN horses, and values for the 5, 6, and 7 m/s steps paralleled the changes observed in the SP horses. Corrected Hct values were then used to calculate the relative change in PV. Exercise produced a significant decrease in PV in both groups of horses; however, there were no differences (P > 0.05) between the groups when IN horses (-13 +/- 3 and -18 +/- 2%) were compared with SP horses (-14 +/- 4 and -17 +/- 4%) at the 6 and 7 m/s steps of the exercise test.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Six nontrained mares were subjected to steady-state, submaximal treadmill exercise to examine the effect of exercise on the plasma concentration of atrial natriuretic peptide (ANP) in arterial, compared with mixed venous, blood. Horses ran on a treadmill up a 6 degree grade for 20 minutes at a speed calculated to require a power equivalent to 80% of maximal oxygen uptake (VO2MAX). Arterial and mixed venous blood samples were collected simultaneously from the carotid and pulmonary arteries of horses at rest and at 10 and 20 minutes of exercise. Plasma was stored at -80 C and was later thawed; ANP was extracted, and its concentration was determined by radioimmunoassay. Exercise caused significant (P < 0.05) increases in arterial and venous plasma ANP concentrations. Mean +/- SEM arterial ANP concentration increased from 25.2 +/- 4.4 pg/ml at rest to 52.7 +/- 5.2 pg/ml at 10 minutes of exercise and 62.5 +/- 5.2 pg/ml at 20 minutes of exercise. Mean venous ANP concentration increased from 24.8 +/- 4.3 pg/ml at rest to 67.2 +/- 14.5 pg/ml at 10 minutes of exercise and 65.3 +/- 13.5 pg/ml at 20 minutes of exercise. Significant differences were not evident between arterial or mixed venous ANP concentration at rest or during exercise, indicating that ANP either is not metabolized in the lungs or is released from the left atrium at a rate matching that of pulmonary metabolism.

Six untrained mares were subjected to incremental treadmill exercise to examine exercise-induced changes in plasma renin activity (PRA) and plasma aldosterone (ALDO) and plasma arginine vasopressin (AVP) concentrations. Plasma renin activity, ALDO and AVP concentrations, and heart rate (HR) were measured at each step of an incremental maximal exercise test. Mares ran up a 6 degree slope on a treadmill set at an initial speed of 4 m/s. Speed was increased 1 m/s each minute until HR reached a plateau. Plasma obtained was stored at -80 C and later was thawed, extracted, and assayed for PRA and ALDO and AVP values by use of radioimmunoassay. Exercise caused significant increase in HR from 40 +/- 2 beats/min (mean +/- SEM) at rest to 206 +/- 4 beats/min (HRmax) at speed of 9 m/s. Plasma renin activity increased from 1.9 +/- 1.0 ng/ml/h at rest to a peak of 5.2 +/- 1.0 ng/ml/h at 9 m/s, paralleling changes in HR. Up to treadmill speed of 9 m/s, strong linear correlations were obtained between exercise intensity (and duration) and HR (r = 0.87, P less than 0.05) and PRA (r = 0.93, P less than 0.05). Heart rate and PRA reached a plateau and did not increase when speed was increased from 9 to 10 m/s. Plasma ALDO concentration increased from 48 +/- 16 pg/ml at rest to 191 +/- 72 pg/ml at speed of 10 m/s. Linear relation was found between exercise intensity (and duration) and ALDO concentration (r = 0.97, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

A headward fluid shift occurs in humans exposed to space-flight. This shift is thought to be the stimulus for the observed reduction in plasma volume, and may produce a sustained rise in intracranial pressure (ICP). In order to determine the effect of head-down tilt (HDT) and water immersion on intracranial pressure (ICP), five anesthetized rhesus monkeys were fitted with intracranial pressure-monitoring transducers and subjected to -6 degrees HDT followed by head-out thermoneutral (34.7 degrees) water immersion. ICP was elevated from 3.8 +/- 1.1 mm Hg in the horizontal control period to 5.3 +/- 1.3 mm Hg (p less than 0.05) during the 15 min pre-immersion HDT. When seated in the empty immersion tank, ICP stabilized at -6.3 +/- 1.3 mm Hg for the control period and increased to -2.2 +/- 1.9 mm Hg (p less than 0.05) when the water level was maintained for 30 min at the sternal notch. The ICP returned toward pre-immersion levels (-5.5 +/- 1.4 mm Hg) as the tank was drained. Mean blood pressure (MBP) remained constant during the pre-immersion tilt test. In the pre-immersion control period, MBP was 91 +/- 3 mm Hg compared to 90 +/- 4 mm Hg (p greater than 0.05) during immersion and 82 +/- 1 mm Hg (p less than 0.05) in the post-immersion recovery period. In summary, exposure of rhesus monkeys to either head-down tilt or water immersion produced a prompt rise in ICP during the stimulus period.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of furosemide administration (1 mg/kg body weight, i.v.) on plasma and blood volumes in 6 intact and 4 splenectomized horses was measured using Evans blue dye dilution, hematocrit, and hemoglobin and plasma total solids concentrations. Body weight decreased by 33.6 +/- 3.3 and 33.7 +/- 0.8 g/kg 4 h after furosemide administration to intact and splenectomized mares, respectively. Plasma volume, estimated by Evans blue dye dilution, was reduced by 8.3 +/- 3.3% (mean +/- SE) 4 h after furosemide administration. The reduction in plasma volume was first detectable 5-10 min after furosemide administration and was greatest 15-30 min (13.0 +/- 0.8%) after dosing. This study demonstrates that furosemide produces significant and rapid reductions in plasma volume in horses. These decreases in plasma volume only partially resolve 4 h after furosemide administration.

Exercise-induced changes in renal function were examined during steady-state submaximal treadmill exercise in six unfit mares. Horses were randomly assigned to either an exercise or parallel control (no exercise) trial on day 1 and the alternate trial 1 wk later. The mares ran on a treadmill, set at a 6 degrees incline, for 1 h at 55-60% of maximal heart rate. Exercise significantly (P less than 0.05) increased plasma osmolality, plasma [K+], urine flow (+ 45%), Na+ excretion (+ 371%), K+ excretion (+ 57%), osmotic clearance (+ 32%), Na+ clearance (+ 391%), K+ clearance (+ 33%), and fractional Na+ excretion (+ 320%) and significantly decreased plasma [Cl-], Cl- excretion (-46%), Cl- clearance (-41%), and fractional Cl- excretion (-47%). Glomerular filtration rate, fractional K+ excretion, and free water clearance did not change during exercise. Atrial natriuretic peptide increased during exercise from 11 +/- 1 pg/ml at rest to a peak of 40 +/- 9 pg/ml (264%, P less than 0.05) at 40 min. Increases in plasma renin activity (66%, P less than 0.05) were accompanied by increases in plasma aldosterone concentration (760%, P less than 0.05). Vasopressin concentration increased (P less than 0.05) steadily over the 60-min period of exercise. It was concluded that, in horses, submaximal exercise-induced increases in urine flow and sodium excretion are associated with a concurrent increase in the plasma concentration of atrial natriuretic peptide.

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.

Changes in clotting time (CT) and fibrinolytic activity (FA) were evaluated in 6 mature, female horses during exercise. Two trials were performed on consecutive days, using a randomized crossover design. Each mare was assigned to either an exercise trial or a control trial on the first day, and to the alternate trial 24 hours later. Mares exercised for 20 minutes on a treadmill at an elevation of 2 degrees and a velocity of 5 m/s. Venous blood samples were collected immediately before exercise, at 4, 8, 12, 16 and 20 minutes during exercise, and 15 minutes after cessation of exercise. Blood was placed into plain glass tubes for determination of CT, and into chilled, citrated tubes for determination of FA, plasminogen/plasmin complex activity (PLG), one-stage prothrombin time (OSPT), activated partial thromboplastin time (APTT), and antithrombin-III (AT-III) activity. There were significant differences (P less than 0.05) between the control and exercise groups for CT, FA, and PLG. During exercise, clotting time decreased from 21.5 +/- 1.6 minutes to 9.9 +/- 1.6 minutes (mean +/- SD; P less than 0.05), without significant changes in OSPT, APTT, or AT-III. Fibrinolytic activity and PLG increased (P less than 0.05) during exercise. Changes in CT, FA, and PLG were significant at 4 minutes of exercise, remained altered until the end of exercise, and returned to baseline values by 15 minutes of recovery. Clotting time, OSPT, APTT, FA, AT-III, and PLG did not change (P greater than 0.05) during control trials.

We investigated the effects of 1 h of sustained submaximal exertion on the renal and systemic hemodynamics of six horses. The horses ran on a treadmill at a speed that produced heart rates of 55-60% of each horse's maximum heart rate. Exertion produced heart rates of 121 +/- 6.6 and 126 +/- 6.1 (SE) beats/min after 15 and 60 min, respectively. Cardiac output increased significantly (P less than 0.05) from 70.1 +/- 3.1 to 246.2 +/- 4.7 ml.min-1.kg body wt-1 after 15 min of exertion and thereafter did not change. There was no significant change from rest in p-aminohippuric acid and creatinine clearances, filtration fraction, or renal blood flow during exertion. Plasma total solid concentration and hematocrit increased by 3.8 and 8.6%, respectively, between 20 and 60 min of exertion. Pulmonary artery temperature increased significantly from 37.6 degrees C at rest to 38.6 degrees C at 60 min of exertion. This study demonstrates the ability of the horse to maintain renal hemodynamics similar to resting values and systemic hemodynamics at steady-state values despite hemoconcentration and increased body temperature during sustained submaximal exertion.