Search Results

You are looking at 1 - 10 of 12 items for

  • Author or Editor: Warwick M. Bayly x
  • Refine by Access: All Content x
Clear All Modify Search

Abstract

Objective—To determine the relationship between plasma β-endorphin (EN) concentrations and exercise intensity and duration in horses.

Animals—8 mares with a mean age of 6 years (range, 3 to 13 years) and mean body weight of 450 kg.

Procedure—Horses were exercised for 20 minutes at 60% of maximal oxygen consumption (O2max) and to fatigue at 95% O2max. Plasma EN concentrations were determined before exercise, after a 10- minute warmup period, after 5, 10, 15, and 20 minutes at 60% O2max or at the point of fatigue (95% O2max), and at regular intervals after exercise. Glucose concentrations were determined at the same times EN concentrations were measured. Plasma lactate concentration was measured 5 minutes after exercise.

Results—Maximum EN values were recorded 0 to 45 minutes after horses completed each test. Significant time and intensity effects on EN concentrations were detected. Concentrations were significantly higher following exercise at 95% O2max, compared with those after 20 minutes of exercise at 60% O2max (605.2 ± 140.6 vs 312.3 ± 53.1 pg/ml). Plasma EN concentration was not related to lactate concentration and was significantly but weakly correlated with glucose concentration for exercise at both intensities (r = 0.21 and 0.30 for 60 and 95% O2max, respectively).

Conclusions and Clinical Relevance—A critical exercise threshold exists for EN concentration in horses, which is 60% O2max or less and is related to exercise intensity and duration. Even under conditions of controlled exercise there may be considerable differences in EN concentrations between horses. This makes the value of comparing horses on the basis of their EN concentration questionable. (Am J Vet Res 2000;61:969–973)

Full access
in American Journal of Veterinary Research

Summary

Ten healthy sedentary male Thoroughbreds with previous race training experience were studied for 14 weeks. Horses were trained for 9 weeks, using a program designed after those used commonly in the United States. Horses were trained conventionally by slow trotting (250 m/min) for 2 weeks and galloping (390 to 450 m/min) for 4 weeks, followed by 3 weeks of galloping (440 to 480 m/min) and intermittent sprinting exercises (breezes) at distances between 600 and 1,000 m (900 to 950 m/min). The horses were then pasture rested for 5 weeks.

A standardized exercise test (set) involving an 800-m gallop at 800 m/min was administered before and after the 9-week training period and after the 5-week detraining period. Heart rate (hr) was monitored during exercise and at standardized intervals after exercise for 60 minutes. Venous blood for determination of plasma lactate concentration was obtained at 5 minutes after exercise.

Heart rate was monitored daily at rest, during exercise, and through the first 60 minutes of recovery. Venous plasma samples (for lactate determination) were obtained 5 minutes after the sprinting exercises. Horses were observed daily before exercise for signs of lameness and were not allowed to train if lame.

Differences after 9 weeks’ training were seen in the set recovery hr at 0.5 through 5 minutes after exercise (P < 0.05 to P < 0.01). Differences after detraining were seen in the set recovery hr at 40 and 60 minutes after exercise (P < 0.05 to P < 0.01). Neither training nor detraining resulted in differences in plasma lactate concentration after the set gallop.

A training-induced resting bradycardia was not observed. The mean maximal hr (hr max) during workouts was 238 ± 3.4 beats/min (n = 9). When exercise hr was expressed as a function of hr max, 22% of trotting, 89% of galloping, and 100% of sprinting workouts were performed at the ≥ 60% hr max. value characterized by the onset of blood lactate accumulation. Plasma lactate concentration further documented that all the sprinting exercises were performed with concentration above the point of onset of blood lactate accumulation. Mean postsprinting lactate concentration was not different over time and ranged from 13.4 ± 0.9 to 15.6 ± 0.6 mmol/L

As training progressed, some of the horses had days on which they were lame after exercise. Some lameness was judged sufficient to warrant phenylbutazone (pbz) administration. Retrospective analysis of the daily hr data indicated that there were no differences in hr during workouts for lame horses given pbz, compared with those not given pbz. Using analysis of variance, hr for horses that were lame during workouts was significantly higher than that for horses that were sound during workouts, during and 0.5 minutes after trotting; 0.5, 1, 2, 20, 40, and 60 minutes after galloping; and 0.5 and 20 minutes after sprinting (P < 0.05 to P < 0.01).

Free access
in American Journal of Veterinary Research

Abstract

Objective

To determine whether plasma von Willebrand factor (vWf) concentration changes in horses during and after treadmill exercise.

Animals

5 mature, fit Thoroughbreds.

Procedure

A blood sampling catheter was placed in the right jugular vein. A warm-up period was followed by a 3-minute rest period. Horses were galloped at racing pace until fatigued (about 2 minutes). Blood samples were collected prior to warm-up, during the postwarm-up rest period, 1 minute into the run, at cessation of the run, and 5 to 120 minutes after cessation of the run. vWF activity was measured by ELISA and corrected for plasma volume changes (measured by changes in plasma albumin concentration). Platelet-poor plasma from 10 clinically normal, resting horses was pooled, assigned a value of 100 U/dl, and served as a control for all assays.

Results

vWf activity began increasing 1 minute after horses reached full speed. At 5 minutes after cessation of exercise, vWf values had increased by mean of 92% (P < 0.05) from baseline. vWf activity returned to baseline by 15 minutes after exercise, and remained there until 90 minutes after exercise, when it began to increase.

Conclusion and Clinical Relevance

The spontaneous decrease in vWf values after completion of exercise was unexpected because vWf has a long half-life in circulation. This unexpected finding is compatible with increased vWf consumption and suggests that microvascular trauma may occur in horses during strenuous exercise. (Am J Vet Res 1997;58:71–76)

Free access
in American Journal of Veterinary Research

Abstract

Objective—To investigate the effects of formaldehyde fixation on equine platelets using flow cytometric methods to evaluate markers of platelet activation.

Sample Population—Blood samples from 6 Thoroughbreds.

Procedure—The degree of fluorescence associated with binding of fluorescein isothiocyanate (FITC)-conjugated anti-human fibrinogen antibody and FITCannexin V in unactivated and adenosine diphosphate (ADP)-, platelet activating factor (PAF)-, and A23187- activated platelet samples in unfixed and 0.5, 1.0, and 2.0% formaldehyde-fixed samples was assessed by use of flow cytometry.

Results—In samples incubated with FITC-anti-human fibrinogen antibody prior to fixation, addition of 2.0% formaldehyde resulted in a 30% increase in total fluorescence in ADP- and PAF-activated samples and a 60% increase in A23187-activated samples. Fixation for 24 hours prior to addition of antibody resulted in reduced fluorescence of samples containing antihuman fibrinogen antibody for all 3 concentrations of formaldehyde in PAF-activated samples. The addition of all 3 concentrations of formaldehyde after incubation with FITC-annexin V resulted in significant increases in fluorescence in unactivated and activated platelet samples. As length of fixation time increased, there was a gradual increase in fluorescence that was significant at 24 hours.

Conclusion and Clinical Relevance—Because fixation with 2.0% formaldehyde results in significant changes in fluorescence in activated platelet samples containing anti-fibrinogen antibody, lower concentrations of formaldehyde should be used to fix equine platelet samples. Formaldehyde-fixed platelet samples should be analyzed within 12 hours of fixation to avoid artifactual increases in fluorescence. Fixation of samples containing FITC-annexin V should be avoided because of significant increases in fluorescence that may interfere with interpretation of results. (Am J Vet Res 2002;63:840–844)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To investigate the potential use of fluorescent- labeled annexin V, anti-human fibrinogen antibody, and anti-human thrombospondin antibody for detection of the activation of equine platelets by use of flow cytometry.

Sample Population—Platelets obtained from 6 Thoroughbreds.

Procedure—Flow cytometry was used to assess platelet activation as indicated by detection of binding of fluorescent-labeled annexin V, anti-human fibrinogen antibody, and anti-thrombospondin antibody to unactivated and ADP-, collagen-, platelet activating factor (PAF)-, and A23187-activated equine platelets. Human platelets were used as control samples. Determination of 14C-serotonin uptake and release was used to assess the extent of platelet secretion.

Results—Anti-human thrombospondin antibody failed to bind to equine platelets. Annexin V bound to platelets activated with PAF or A23187 when platelets had undergone secretion. Anti-human fibrinogen antibody bound to ADP-, PAF-, and A23817- activated platelets, but binding was not dependent on platelet secretion. The extent of binding of anti-fibrinogen antibody was less in equine platelets, compared with that for human platelets, despite maximal stimulation.

Conclusions and Clinical Relevance—Activation of equine platelets can be detected by use of fluorescent- labeled annexin V and anti-human fibrinogen antibody but not by use of anti-human thrombospondin antibody. These flow cytometric techniques have the potential for detection of in vivo platelet activation in horses at risk of developing thrombotic disorders. (Am J Vet Res 2002;63:513–519)

Full access
in American Journal of Veterinary Research

Abstract

Objectives—To establish maximum oxygen consumption (O2max) in ponies of different body weights, characterize the effects of training of short duration on O2max, and compare these effects to those of similarly trained Thoroughbreds.

Animals—5 small ponies, 4 mid-sized ponies, and 6 Thoroughbreds.

Procedure—All horses were trained for 4 weeks. Horses were trained every other day for 10 minutes on a 10% incline at a combination of speeds equated with 40, 60, 80, and 100% of O2max. At the beginning and end of the training program, each horse performed a standard incremental exercise test in which O2max was determined. Cardiac output (), stroke volume (SV), and arteriovenous oxygen content difference (C [a-v] O2) were measured in the 2 groups of ponies but not in the Thoroughbreds.

Results—Prior to training, mean O2max for each group was 82.6 ± 2.9, 97.4 ± 13.2, and 130.6 ± 10.4 ml/kg/min, respectively. Following training, mean O2max increased to 92.3 ± 6.0, 107.8 ± 12.8, and 142.9 ± 10.7 ml/kg/min. Improvement in O2max was significant in all 3 groups. For the 2 groups of ponies, this improvement was mediated by an increase in ; this variable was not measured in the Thoroughbreds. Body weight decreased significantly in the Thoroughbreds but not in the ponies.

Conclusions and Clinical Relevance—Ponies have a lower O2max than Thoroughbreds, and larger ponies have a greater O2max than smaller ponies. Although mass-specific O2max changed similarly in all groups, response to training may have differed between Thoroughbreds and ponies, because there were different effects on body weight. (Am J Vet Res 2000; 61:986–991)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To investigate the effects of sodium citrate, low molecular weight heparin (LMWH), and prostaglandin E1 (PGE1) on aggregation, fibrinogen binding, and enumeration of equine platelets. Sample Population—Blood samples obtained from 4 Thoroughbreds.

Sample Population—Blood samples obtained from 4 Thoroughbreds.

Procedure—Blood was collected into syringes in the ratio of 9 parts blood:1 part anticoagulant. Anticoagulants used were sodium citrate, LMWH, sodium citrate and LMWH, or 300 nM PGE1/ml of anticoagulant. Platelet aggregation in response to ADP, collagen, and PGE1 was assessed, using optical aggregometry. Platelet activation was evaluated, using flow cytometry, to detect binding of fluorescein- conjugated anti-human fibrinogen antibody. Plasma concentration of ionized calcium was measured, using an ion-selective electrode.

Results—Number of platelets (mean ± SEM) in samples containing LMWH (109.5 ± 11.3 × 103 cells/µl) was significantly less than the number in samples containing sodium citrate (187.3 ± 30.3 × 103 cells/µl). Increasing concentrations of sodium citrate resulted in reductions in platelet aggregation and plasma concentration of ionized calcium. Addition of PGE1 prior to addition of an agonist inhibited platelet aggregation in a concentration-dependent manner, whereas addition of PGE1 4 minutes after addition of ADP resulted in partial reversal of aggregation and fibrinogen binding.

Conclusion and Clinical Relevance—A high concentration of sodium citrate in blood samples decreases plasma concentration of ionized calcium, resulting in reduced platelet aggregation and fibrinogen binding. Platelets tend to clump in samples collected into LMWH, precluding its use as an anticoagulant. Platelet aggregation and fibrinogen binding can be reversed by PGE1, which may result in underestimation of platelet activation. (Am J Vet Res 2001; 62:547–554)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine the cardiovascular and respiratory effects of water immersion in horses recovering from general anesthesia.

Animals—6 healthy adult horses.

Procedure—Horses were anesthetized 3 times with halothane and recovered from anesthesia while positioned in lateral or sternal recumbency in a padded recovery stall or while immersed in a hydropool. Cardiovascular and pulmonary functions were monitored before and during anesthesia and during recovery until horses were standing. Measurements and calculated variables included carotid and pulmonary arterial blood pressures (ABP and PAP, respectively), cardiac output, heart and respiratory rates, arterial and mixed venous blood gases, minute ventilation, end expiratory transpulmonary pressure (PendXes), maximal change in transpulmonary pressure (ΔPtpmax), total pulmonary resistance (RL), dynamic compliance (Cdyn), and work of breathing ().

Results—Immersion in water during recovery from general anesthesia resulted in values of ABP, PAP, PendXes, ΔPtpmax, RL, and that were significantly greater and values of Cdyn that were significantly less, compared with values obtained during recovery in a padded stall. Mode of recovery had no significant effect on any other measured or calculated variable.

Conclusions and Clinical Relevance—Differences in pulmonary and cardiovascular function between horses during recovery from anesthesia while immersed in water and in a padded recovery stall were attributed to the increased effort needed to overcome the extrathoracic hydrostatic effects of immersion. The combined effect of increased extrathoracic pressure and PAP may contribute to an increased incidence of pulmonary edema in horses during anesthetic recovery in a hydropool. (Am J Vet Res 2001;62:1903–1910)

Full access
in American Journal of Veterinary Research

Abstract

Objectives

To determine whether IV administration of furosemide (250 mg) to horses before maximal exercise affected maximal oxygen consumption (V⃙o2max), breathing mechanics, or gas exchange during exercise.

Animals

7 healthy, well-conditioned Thoroughbred horses.

Procedures

5 horses initially performed an incremental treadmill exercise test to determine V⃙o2max 4 hours after IV administration of furosemide (250 mg IV) or placebo (saline [0.9% NaCl] solution). Time to fatigue and distance run were recorded. All 7 horses were then used to determine the effects of furosemide on gas exchange and breathing mechanics at 40, 60, 80, and 100% of V⃙o2max. Horses were weighed immediately before exercise.

Results

Furosemide treatment significantly increased mass-specific V⃙o2max (5.3%), but absolute V⃙o2max was not significantly altered. In the 2 parts of the study, body weights were 2.9 and 2.5% higher when horses were given placebo than when they were given furosemide. Time and distance run at speeds ≥ 11.0 m/s were significantly greater following furosemide administration. Furosemide treatment had no effect on breathing mechanics or gas exchange.

Conclusions and Clinical Relevance

Previous studies have suggested that prerace administration of furosemide may have a positive effect on performance. Results of this study indicate that this may be attributable, in part, to an increase in mass-specific V⃙o2max but not to improvements in breathing mechanics or gas exchange. Most of the increase in mass-specific V⃙o2max appeared to be attributable to weight loss associated with diuresis induced by furosemide. (Am J Vet Res 1999;60:1415–1422)

Free access
in American Journal of Veterinary Research