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Carroll, G. L., Matthews, N. S., Hartsfield, S. M., Slater, M. R., Champney, T. H., & Erickson, S. W. (1997). The effect of detomidine and its antagonism with tolazoline on stress-related hormones, metabolites, physiologic responses, and behavior in awake ponies. Vet Surg, 26(1), 69–77.
Abstract: Six ponies were used to investigate the effect of tolazoline antagonism of detomidine on physiological responses, behavior, epinephrine, norepinephrine, cortisol, glucose, and free fatty acids in awake ponies. Each pony had a catheter inserted into a jugular vein 1 hour before beginning the study. Awake ponies were administered detomidine (0.04 mg/kg intravenously [i.v.]) followed 20 minutes later by either tolazoline (4.0 mg/kg i.v.) or saline. Blood samples were drawn from the catheter 5 minutes before detomidine administration (baseline), 5 minutes after detomidine administration, 20 minutes before detomidine administration which was immediately before the administration of tolazoline or saline (time [T] = 0), and at 5, 30, and 60 minutes after injections of tolazoline or saline (T = 5, 30, and 60 minutes, respectively). Compared with heart rate at T = 0, tolazoline antagonism increased heart rate 45% at 5 minutes. There was no difference in heart rate between treatments at 30 minutes. Blood pressure remained stable after tolazoline, while it decreased over time after saline. Compared with concentrations at T = 0, tolazoline antagonism of detomidine in awake ponies resulted in a 55% increase in cortisol at 30 minutes and a 52% increase in glucose at 5 minutes. The change in free fatty acids was different for tolazoline and saline over time. Free fatty acids decreased after detomidine administration. Free fatty acids did not change after saline administration. After tolazoline administration, free fatty acids increased transiently. Tolazoline tended to decrease sedation and analgesia at 15 and 60 minutes postantagonism. Antagonism of detomidine-induced physiological and behavioral effects with tolazoline in awake ponies that were not experiencing pain appears to precipitate a stress response as measured by cortisol, glucose, and free fatty acids. If antagonism of an alpha-agonist is contemplated, the potential effect on hormones and metabolites should be considered.
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Sloet van Oldruitenborgh-Oosterbaan, M. M., Spierenburg, A. J., & van den Broek, E. T. W. (2006). The workload of riding-school horses during jumping.
Abstract: REASONS FOR PERFORMING THE STUDY: As there are no reports on the real workload of horses that jump fences, this study was undertaken in riding-school horses. OBJECTIVE: To compare the workload of horses jumping a course of fences with that of horses cantering over the same course at the same average speed without jumping fences. The workload variables included heart rate (HR), packed cell volume (PCV), acid-base balance (venous pH, pCO2, HCO3-) and blood lactate (LA), glucose, total protein and electrolyte concentrations. METHODS: Eight healthy riding-school horses performed test A (a course of approximately 700 m with 12 jumps from 0.8-1.0 m high at an average speed of approximately 350 m/min) and test B (same course at the same speed, but without the rails) in a crossover study with at least 4 h between the 2 tests. Before each test the horses were fitted with a heart rate meter (Polar Electro). Blood samples were taken from the jugular vein at rest prior to the test, after warm-up before starting the course, immediately after the course and after recovery. All samples were analysed immediately. RESULTS: The mean +/- s.d maximal HR (beats/min) during the course (184 +/- 17 and 156 +/- 21, respectively) and the mean HR after recovery (75 +/- 6 and 63 +/- 7, respectively) were significantly higher in test A compared to test B (P = 0.001 and P = 0.007 respectively). The mean LA concentrations after the course and after recovery (mmol/l) were significantly higher in test A (3.6 +/- 2.7 and 1.0 +/- 0.9, respectively) compared to test B (0.9 +/- 0.5 and 0.3 +/- 0.1, respectively), (P = 0.016 and P = 0.048 respectively). The mean PCV (I/l) after the course and after recovery was also significantly different between tests A (0.48 +/- 0.04 and 0.39 +/- 0.03, respectively) and B (0.42 +/- 0.04 and 0.36 +/- 0.03, respectively) (P<0.01). The mean pH and the mean HCO3- (mmol/l) after the course were significantly lower in test A (7.40 +/- 0.04 and 28.9 +/- 1.4, respectively) compared to test B (7.45 +/- 0.03 and 30.4 +/- 2.3, respectively) (P<0.05). CONCLUSIONS: This study indicates that in riding-school horses jumping fences, even at a low level competition, provokes a significant workload compared to cantering the same distance and speed without fences. POTENTIAL RELEVANCE: This study makes it clear that the extra workload of jumping fences should be taken into account in the training programmes of jumping horses. Further research with more experienced horses jumping higher fences will reveal the workload for top-level jumping horses.
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