Four hours prior to exercise on a high-speed treadmill, 4 dosages of furosemide (0.25, 0.50, 1.0, and 2.0 mg/kg of body weight) and a control treatment (10 ml of 0.9% NaCl) were administered IV to 6 horses. Carotid arterial pressure (CAP), pulmonary arterial pressure (PAP), and heart rate were not different in resting horses before and 4 hours after furosemide administration. Furosemide at dosage of 2 mg/kg reduced resting right atrial pressure (RAP) 4 hours after furosemide injection. During exercise, increases in treadmill speed were associated with increases in RAP, CAP, PAP, and heart rate. Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduced RAP and PAP during exercise in dose-dependent manner, but did not influence heart rate. Mean CAP was reduced by the 2-mg/kg furosemide dosage during exercise at 9 and 11 m/s, but not at 13 m/s. During recovery, only PAP was decreased by furosemide administration. Plasma lactate concentration was not significantly influenced by furosemide administration. Furosemide did not influence PCV or hemoglobin concentration at rest prior to exercise, but did increase both variables in dose-dependent manner during exercise and recovery. However, the magnitude of the changes in PCV and hemoglobin concentration were small in comparison with changes in RAP and PAP, and indicate that furosemide has other properties in addition to its diuretic activities. Furosemide may mediate some of its cardiopulmonary effects by vasodilatory activities that directly lower pulmonary arterial pressure, but also increase venous capacitance, thereby reducing venous return to the atria and cardiac filling.

Hematologic and rheologic changes were examined in 49 Thoroughbreds before and after competitive racing. Mean postrace values for RBC count, hemoglobin concentration, and PCV increased by 58 to 61%, whereas blood viscosity increased 2 to 3 times. Postrace echinocyte numbers were 162% greater than prerace values. Smaller, but statistically significant, changes were found for mean corpuscular hemoglobin concentration, red cell distribution width, plasma total protein concentration, total WBC count, neutrophil count, and lymphocyte count. Variables measured did not predict whether a horse was a bleeder not treated with furosemide, a bleeder treated with furosemide, or a nonbleeder.

Chemotactic locomotion and luminol-dependent chemiluminescence of neutrophils, mitogen-induced lymphocyte blastogenesis, serum cortisol concentration, immunoglobulin quantification, and leukocyte counts were determined to evaluate the effect of a single strenuous exercise in horses. Increased serum cortisol concentration (P < 0.01) and an increased neutrophil-to-lymphocyte ratio P < 0.05) indicated that horses had been stressed. The chemotactic index and peak chemiluminescence production decreased significantly (P < 0.05 and P < 0.01, respectively) 1 day after exercise. Mitogen-induced blastogenesis of lymphocytes and serum immunoglobulin values remained unchanged in response to exercise. Results of this study indicated that a single bout of exercise may transiently impair neutrophil antimicrobial functions and nonspecific defense mechanisms, but not specific immunity in horses.

The mean area and minimal diameter of 3 histochemically determined myofiber types (1, 2A, and 2B; myosin ATPase in acid buffer) were calculated in middle gluteal muscle biopsy specimens from 62 stallions, 47 Andalusians and 15 Arabians, ranging in age from 6 to 12 years. Fourteen Andalusians and 7 Arabians were untrained, and the remainder were actively endurance-trained. The 6-month training schedules involved walking, slow trotting, and cantering. Fourteen Andalusians were moderately endurance-trained, whereas the other 19 Andalusians and 8 Arabians were strongly endurance-trained. Significant differences were not recorded between untrained and endurance-trained Arabians with respect to the area (type 1, 3,194 +/- 869 micrometers(2) and 3,150 +/- 370 micrometers(2); type 2A, 3,819 +/- 890 micrometers(2) and 3,380 +/- 356 micrometers(2); and type 2B, 4,872 +/- 962 micrometers(2) and 4,417 +/- 646 micrometers(2) or minimal diameter (type 1, 52.2 +/- 7.4 micrometers and 52.8 +/- 3.1 micrometers; type 2A, 58.1 +/- 6.7 micrometers and 55.0 +/- 2.8 micrometers; and type 2B, 65.3 +/- 6.4 micrometers and 63.4 +/- 4.3 micrometers) of the 3 fiber types, nor between untrained and endurance-trained Andalusians with respect to the area (untrained, 3,990 +/- 690 micrometers(2) moderately endurance-trained, 3,882 +/- 347 micrometers(2); and strongly endurance-trained, 3,758 +/- 510 micrometers(2)) and minimal diameter (untrained, 58.1 +/- 4.7 micrometers; moderately endurance-trained, 59.7 +/- 2.7 micrometers; and strongly endurance-trained, 58.7 +/- 4.5 micrometers) of 2A fibers. Moderately endurance-trained Andalusians had larger 2B fibers (area 18.6%; minimal diameter 14.3%) than untrained Andalusians, and the minimal diameter of type-1 and type-2B fibers was greater in strongly endurance-trained Andalusians than in untrained Andalusians (9.5% for type 1; 10.0% for type 2B). These results suggest minimal effects of endurance training on the myofiber size of adult Andalusians and Arabians, but a tendency toward increased type-1 and -2B fiber size was found for Andalusians.

On the basis of results in dogs, conditioning exercise may increase sensitivity to nondepolarizing muscle relaxants. Five Thoroughbreds were exercised/conditioned 3 times weekly on a treadmill for 8 months. Increasing maximal rate of O2 consumption verified that the horses were responding to exercise conditioning. Six nonexercised Thoroughbreds served as the control group. Studies were done with horses under general anesthesia by use of halothane during partial paralysis by a brief constant-rate infusion with the muscle relaxant, metocurine iodide. Quantification of degree of paralysis of the hoof twitch (eg, digital extensor) occurred with simultaneous quantification of blood values of metocurine. Pharmacokinetic and pharmacodynamic analyses of the data were done by a nonlinear regression program, using the Hill equation. There were no differences in findings between exercised and nonexercised horses. The mean blood concentration for the 50% paralyzing dose of metocurine was 0.44 +/- 0.11 (SD) micrograms/ml in exercised horses, and 0.58 +/- 0.22 micrograms/ml in nonexercised horses. Despite evidence for a response to conditioning, a significant change in the sensitivity of the neuromuscular junction to metocurine was not found.

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. 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 degrees 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.

The lungs of sensitized horses were exposed to aerosolized ovalbumin. Some horses (n = 4) were given ovalbumin in 1 lung only, whereas in others (n = 7), ovalbumin or vehicle were inoculated in the cranial, ventral, and caudal regions of the caudal lung lobe. Horses were exercised 5 hours after ovalbumin exposure. Immediately before exercise, endoscopy failed to reveal any abnormality. After exercise, endoscopic examination of horses subjected to unilateral ovalbumin exposure revealed extensive blood in airways leading to the exposed lung in all horses. Blood was not observed in the airways leading to the control lung. Mean (+/- SEM) minimum volume of the exposed and control lungs was 9.5 +/- 1.5 and 5.5 +/- 1.6 L, respectively; this difference was statistically significant (P < 0.05). Bronchoscopy of horses subjected to regional ovalbumin or vehicle exposure and exercise revealed a small amount of blood-tinged fluid in the bronchi serving the regions of the lung inoculated with ovalbumin. Minimum volumes of such regions were not significantly different from one another. However, their minimum volume was significantly (P < 0.05) larger than that of vehicle-inoculated regions. Gross and histologic examination confirmed inflammation and hemorrhage in the ovalbumin-exposed, but not the control lungs or lung regions. Thus, exercise can cause blood from an injured region of lung to appear in the larger airways. Regional differences in lung structure and function do not influence the appearance of blood in the airways.

Six untrained mares were subjected to incremental treadmill exercise to examine exercise-induced 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 degrees 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 < 0.05) and PRA (r = 0.93, P < 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 < 0.05). Plasma AVP concentration increased from 4.0 +/- 3.0 pg/ml at rest to 95 +/- 5.0 pg/ml at speed of 10 m/s. The relation between AVP concentration and exercise intensity (and duration) appeared to be curvilinear, and was described by an exponential function (r = 0.92, P < 0.05). These data indicate that PRA and ALDO and AVP concentrations increase in horses during progressive treadmill exercise.

Distribution of blood flow among various respiratory muscles was examined in 8 healthy ponies during submaximal exercise lasting 30 minutes, using radionuclide labeled 15-micrometers diameter microspheres injected into the left ventricle. From the resting values (40 +/- 2 beats/min; 37.3 +/- 0.2 C), heart rate and pulmonary arterial blood temperature increased significantly at 5 (152 +/- 8 beats/min; 38.6 +/- 0.2 C), 15 (169 +/- 6 beats/min; 39.8 +/- 0.2 C), and 26 (186 +/- 8 beats/min; 40.8 +/- 0.2 C) minutes of exertion, and the ponies sweated profusely. Mean aortic pressure also increased progressively as exercise duration increased. Blood flow increased significantly with exercise in all respiratory muscles. Among inspiratory muscles, perfusion was greatest in the diaphragm and ventral serratus, compared with external intercostal, dorsal serratus, and scalenus muscles. Among expiratory muscles, blood flow in the internal abdominal oblique muscle was greatest, followed by that in internal intercostal and transverse throacic muscles, in which the flow values remained similar. The remaining 3 abdominal muscles had similar blood flow, but these values were less than that in the internal intercostal, transverse thoracic, and internal abdominal oblique muscles. Blood How values for all inspiratory and expiratory muscles remained similar for the 5 and 15 minutes of exertion. However, at 26 minutes, blood flow had increased further in the diaphragm, external intercostal, internal intercostal, transverse thoracic, and the external abdominal oblique muscle as vascular resistance decreased. On the basis of our findings, all respiratory muscles were activated during submaximal exercise and their perfusion had marked heterogeneity. Also, blood flow in respiratory muscles was well maintained as exercise duration progressed; in fact, several muscles had a further increase in perfusion late during exercise.

Experiments were carried out on 8 healthy ponies to examine the effects of prolonged submaximal exercise on regional distribution of brain blood flow. Brain blood flow was ascertained by use of 15-microm-diameter radionuclidelabeled microspheres injected into the left ventricle. The reference blood was withdrawn from the thoracic aorta at a constant rate of 21.0 ml/min. Hemodynamic data were obtained with the ponies at rest (control), and at 5, 15, and 26 minutes of exercise performed at a speed setting of 13 mph on a treadmill with a fixed incline of 7%. Exercise lasted for 30 minutes and was carried out at an ambient temperature of 20 degrees C. Heart rate, mean arterial pressure, and core temperature increased significantly with exercise. With the ponies at rest, a marked heterogeneity of perfusion was observed within the brain; the cerebral, as well as cerebellar gray matter, had greater blood flow than in the respective white matter, and a gradually decreasing gradient of blood flow existed from thalamushypothalamus to medulla. This pattern of perfusion heterogeneity was preserved during exercise. Regional brain blood flow at 5 and 15 minutes of exercise remained similar to resting values. However, at 26 minutes of exercise, vasoconstriction resulted in a significant reduction in blood flow to all cerebral and brain-stem regions. In the cerebellum, the gray matter blood flow and vascular resistance remained near control values even at 26 minutes of exercise. Vasoconstriction in various regions of the cerebrum and brainstem at 26 minutes of exertion may have occurred in response to exercise-induced hypocapnia, arterial hypertension, and/or sympathetic neural activation.