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Departments of Veterinary Biosciences and Clinical Medicine, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Strenuously exercising horses exhibit arterial hypoxemia and exercise-induced pulmonary hemorrhage (EIPH), the latter resulting from stress failure of pulmonary capillaries. The present study was carried out to examine whether the structural changes in the blood-gas barrier caused by a prior bout of high-intensity short-term exercise capable of inducing EIPH would affect the arterial hypoxemia induced during a successive bout of exercise performed at the same workload. Two sets of experiments, double- and single-exercise-bout experiments, were carried out on seven healthy, sound Thoroughbred horses. Experiments were carried out in random order, 7 days apart. In the double-exercise experiments, horses performed two successive bouts (each lasting 120 s) of galloping at 14 m/s on a 3.5% uphill grade, separated by an interval of 6 min. Exertion at this workload induced arterial hypoxemia within 30 s of the onset of galloping as well as desaturation of Hb, a progressive rise in arterial PCO2, and acidosis as exercise duration increased from 30 to 120 s. In the single-exercise-bout experiments, blood-gas/pH data resembled those from the first run of the double-exercise experiments, and all horses experienced EIPH. Thus, in the double-exercise experiments, before the horses performed the second bout of galloping at 14 m/s on a 3.5% uphill grade, stress failure of pulmonary capillaries had occurred. Although arterial hypoxemia developed during the second run, arterial PO2 values were significantly (P < 0.01) higher than in the first run. Thus prior exercise not only failed to accentuate the severity of arterial hypoxemia, it actually diminished the magnitude of exercise-induced arterial hypoxemia. The decreased severity of exercise-induced arterial hypoxemia in the second run was due to an associated increase in alveolar PO2, as arterial PCO2 was significantly lower than in the first run. Thus our data do not support a role for structural changes in the blood-gas barrier related to the stress failure of pulmonary capillaries in causing the exercise-induced arterial hypoxemia in horses.
blood-gas tensions in exercise; repeat exercise effects; exertion
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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ARTERIAL HYPOXEMIA IS ROUTINELY observed in horses performing strenuous exercise (1, 2, 4, 17, 18). Among various possibilities for the occurrence of exercise-induced arterial hypoxemia in horses are the significantly shortened transit time for blood in the pulmonary capillaries as a result of the dramatic increase in cardiac output, the so-called "relative" hypoventilation as evidenced by the increased arterial PCO2 (PaCO2) during exertion, despite significantly increased alveolar ventilation [note: exercise-induced arterial hypoxemia in horses is usually attended by hypercapnia as well (2, 4)], and ventilation-perfusion inequality. Recently, histological evidence has been presented to indicate that perivascular edema and, possibly, interstitial pulmonary edema occur during short-term heavy exercise in some animals, and thus it is possible that increased thickness of the blood-gas barrier may also contribute to the diffusion limitation for O2 (13). Despite these observations, however, it was recently reported that prior exercise failed to exaggerate the exercise-induced arterial hypoxemia in healthy human subjects (3, 5, 14), thereby suggesting that the structural alterations at the blood-gas barrier may not be responsible for the exercise-induced arterial hypoxemia (14).
It is noteworthy that the pulmonary capillary blood pressure increases to a much greater extent in strenuously exercising Thoroughbred horses than in other species, and values approaching 85-90 mmHg during high-intensity short-term exercise are not uncommon (8-10). Also, histological evidence has been presented indicating that the very high transmural [intracapillary minus perivascular (alveolar)] pulmonary capillary pressures in exercising Thoroughbreds cause interstitial edema and disruption of the blood-gas barrier, a phenomenon often referred to as "stress failure of pulmonary capillaries" (19). The latter is believed to be responsible for the extremely high incidence (>75%) of exercise-induced pulmonary hemorrhage (EIPH) in racehorses (7, 16). There is evidence that some elite human athletes may also experience stress failure of pulmonary capillaries during high-intensity exertion, leading to EIPH (6). Despite these observations, it is not known whether these structural changes in the blood-gas barrier (19), related to the greater severity of pulmonary capillary hypertension in exercising horses (8-10), play a role in bringing about the exercise-induced arterial hypoxemia (1, 2, 4, 17, 18). Thus the primary objective of the present study was to examine the effects of structural changes in the blood-gas barrier of Thoroughbred horses caused by a prior bout of high-intensity short-term exercise (19) on the arterial and mixed venous blood-gas tensions during a successive bout of exercise performed at the same workload.
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Horses
Experiments were carried out on seven healthy, sound Thoroughbred horses (2 fillies, 5 geldings), 2.5-5 yr old and weighing 457 ± 18 kg. They were exercise trained for 7 wk before they were subjected to the blood-gas studies. The horses were housed in an air-conditioned building and were accustomed to being handled by people. They were fed a diet of alfalfa hay and oats, and free access to water was provided. The horses were dewormed periodically and were inoculated with tetanus toxoid and strangles vaccine. Our protocols and procedures were approved by the Institutional Laboratory Animal Care and Use Committees.Exercise Training
After the horses were familiarized with walking, trotting, cantering, and galloping on the high-speed treadmill for 1 wk, they were exercised 3 days/wk in the following manner with the treadmill set on the flat, i.e., 0% grade: Beginning with a walk at 2 m/s for 120 s, belt speed was increased at 1 m/s every 60 s until the horse had trotted at 6 m/s for 60 s. Treadmill speed was then raised to 8 m/s, and the horses were cantered for 60 s. Cantering was followed by galloping at 10 m/s for 60 s and at 14 m/s for 120 s. Belt speed was decreased, first to 5 m/s for 60 s and then to 2 m/s for 5 min, before the treadmill was stopped. After initial exercise training for 4 wk in this manner, for the next 3 wk this incremental exercise regimen was performed 3 days/wk with the treadmill set at a 3.5% uphill grade.Work Intensity Eliciting EIPH
Because EIPH documents the occurrence of stress failure of pulmonary capillaries with its attendant consequences on the integrity/thickness of the blood-gas barrier (19), for the present study we intended to use a workload capable of eliciting EIPH consistently. Trials to ascertain work intensity needed to elicit maximal heart rate and EIPH were undertaken on completion of the above-described exercise training. In agreement with our previous work, it was observed that galloping at 14 m/s on a 3.5% uphill grade not only elicited maximal heart rate (217 ± 2 beats/min) but also induced EIPH in all horses, as demonstrated by the presence of fresh blood in the trachea on postexercise airway endoscopic examination (7, 16). It was also observed in these trials that these horses could not sustain galloping at 14 m/s on a 3.5% uphill grade for >120 s, despite vigorous humane encouragement. Thus this workload, i.e., 14 m/s on a 3.5% uphill grade, was selected for further experimentation, inasmuch as it represented a strenuous effort eliciting maximal heart rate and EIPH in the experimental horses.Experimental Procedures
On the day of the study, after local infiltration of 2% lidocaine hydrochloride in the 17th intercostal space, the abdominal aorta was percutaneously catheterized as described previously (11, 12). Then, with the use of local infiltration of 2% lidocaine hydrochloride, cardiac catheters (8-F) equipped with a tip manometer (Millar Instruments, Houston, TX), fluid-filled lumen, and thermistor (Edward Laboratories, Santa Clara, CA) were advanced into the pulmonary artery via introducers inserted into the left jugular vein. The locations of various catheters were confirmed by monitoring the characteristic phasic blood pressure waveforms on an oscillographic recorder (E for M, Lanexa, KS). These catheters permitted simultaneous sampling of the aortic and mixed venous blood as well as continuous monitoring of the pulmonary arterial blood (core) temperature during the experiments. After catheter placement, horses stood quietly on the treadmill for ~45 min before blood-gas tension/pH and lactate studies were undertaken.Blood-gas tensions, pH, Hb concentration, Hb O2 saturation, and O2 content were determined using a carefully calibrated blood-gas analyzer/CO-oximeter (ABL520 system, Radiometer, Copenhagen, Denmark), and all blood-gas tension/pH data were corrected to the simultaneously measured pulmonary artery blood temperature. The calibration of our blood-gas/pH analyzer/CO-oximeter was checked frequently (at 30-min intervals) and was verified using tonometered solutions of known blood-gas tensions, pH, Hb concentration, and O2 saturation. For lactate determinations in these experiments, mixed venous blood samples obtained at various intervals (see Experimental Design and Protocol) were immediately deproteinized with chilled perchloric acid (8% wt/vol), and the supernatant was harvested for lactate analysis (Sigma Diagnostics, Sigma Chemical, St. Louis, MO). All lactate assays were carried out in duplicate.
Experimental Design and Protocol
All horses were studied in two sets of experiments: the double-exercise experiments and the single-exercise-bout experiments. Sequence of these treatments was randomized for all horses, and 7 days were allowed between the experiments. All experimentation was carried out in an air-conditioned laboratory, where the ambient temperature was maintained at 20°C. In both sets of experiments, first, measurements were made in duplicate (5 min apart) on quietly standing horses when heart rate and pulmonary vascular pressures had been stable for 10-15 min. Then exercise was performed on the high-speed treadmill set at a 3.5% uphill grade in the following manner.Double-exercise experiments. Beginning with a walk at 2 m/s for 120 s, the belt speed was raised in increments of 1 m/s every 60 s until the speed was 6 m/s. After the horses had trotted for 60 s at 6 m/s, belt speed was raised to 8 m/s for 60 s and then to 14 m/s. On completion of 120 s of galloping at 14 m/s on a 3.5% uphill grade (hereafter, this part of the double-exercise protocol is referred to as the first run), the belt speed was decreased to 5 m/s (trot) for 60 s and then to 2 m/s. On completion of 5 min of walk at 2 m/s, the treadmill speed was rapidly increased to 14 m/s. Horses galloped at 14 m/s on a 3.5% uphill grade for 120 s (hereafter, this part of the double-exercise protocol is referred to as the second run). Then treadmill speed was lowered to 5 m/s for 60 s and, subsequently, to 2 m/s for 5 min before the treadmill was stopped.
In this exercise protocol, along with continuous core temperature measurement, simultaneous aortic and pulmonary arterial blood samples were obtained for determining blood-gas tensions, pH, Hb concentration, Hb O2 saturation, and O2 content at 55 s of trotting at 6 m/s, 55 s of exercise at 8 m/s, 30, 60, 90, and 120 s of galloping at 14 m/s on a 3.5% uphill grade in the first run, 5 min of walk at 2 m/s, 30, 60, 90, and 120 s of galloping at 14 m/s on a 3.5% uphill grade in the second run, and 5 min of walk at 2 m/s. For lactate determination in the present study, pulmonary arterial blood samples were also obtained before exercise (at rest) and at 5 min of walk after the horses galloped at 14 m/s on a 3.5% uphill grade in both runs.Single-exercise-bout experiments. Horses were exercised exactly in the same manner as described above for the first run of the double-exercise experiments, and after the horses completed 5 min of walk at 2 m/s, the treadmill was stopped. Along with continuous core temperature measurement, arterial and mixed venous blood-gas tensions, pH, Hb concentration, Hb O2 saturation, O2 content, and mixed venous blood lactate concentration were also determined at the same intervals described above for the first run of the double-exercise experiments.
Postexercise Airway Endoscopic Examination
In all experiments, a flexible fiber-optic endoscope (Pentax Fiberscopes, Orangeburg, NY) was used for careful endoscopic examination of the nasopharynx, larynx, and trachea (up to the carina) at 45-50 min after exercise (7, 16). The presence of fresh blood in the airway(s) was regarded as indicative of EIPH (7, 16).Data Analysis
In the present study, all data were subjected to repeated-measures, split-plot design ANOVA using the SAS statistical software package (SAS version 6.12, SAS Institute, Cary, NC), and the treatment comparisons were made using the least-squares significant difference method (15). Data for the double-exercise as well as single-exercise-bout experiments were also individually subjected to ANOVA followed by Newman-Keuls multiple-range test (15) (SAS version 6.12) to determine the significant effects of work intensity/duration within each treatment. For all statistical analyses, the level of significance was set at P < 0.05, and the data are presented as means ± SE.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Double-Exercise Experiments
Core temperature. The core temperature of horses increased significantly from 37.5 ± 0.1°C at rest to 40.6 ± 0.2°C at 120 s of galloping at 14 m/s on a 3.5% uphill grade in the first run. The core temperature had decreased significantly at 5 min of walk after the first run of high-intensity exercise, reaching 40.0 ± 0.2°C. Galloping at 14 m/s on a 3.5% uphill grade during the second run caused the core temperature to further increase significantly, and at 120 s of galloping it had reached 42.2 ± 0.2°C.
Changes in arterial PO2 and arterial
O2 saturation.
Submaximal exercise at 6 and 8 m/s did not cause statistically
significant changes in arterial PO2
(PaO2) and/or arterial O2 saturation
(SaO2; Fig. 1).
Galloping at 14 m/s on a 3.5% uphill grade in both runs was attended
by a significant reduction in PaO2 at 30 s, but
further statistically significant changes did not occur as exercise
duration progressed to 120 s. However, during galloping at 14 m/s
on a 3.5% uphill grade in the second run, PaO2 was
significantly (P < 0.01) higher (mean increment being 5.3 Torr; see Fig. 4) than corresponding values in the first run.
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Changes in mixed venous PO2 and mixed venous O2 saturation. Work-intensity-related significant reductions in mixed venous PO2 as well as mixed venous O2 saturation were observed in all horses, and statistically significant differences between the two runs at 14 m/s on a 3.5% uphill grade were not found.
Changes in PaCO2 and arterial
HCO
PaCO2 see Fig. 4). Also, interestingly, whereas in the first run a significant hypercapnia was evident, PaCO2 values in the second run did not
exceed the resting values.
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Changes in arterial pH. A significant metabolic acidosis developed in exercising horses (Fig. 3). Galloping at 14 m/s on a 3.5% uphill grade in the first run caused arterial pH to decrease significantly, approaching 7.124 ± 0.026 at 120 s. Galloping in the second run intensified the metabolic acidosis, and arterial pH further decreased significantly, reaching 7.027 ± 0.060 at 120 s of galloping at 14 m/s on a 3.5% uphill grade.
Changes in arterial and mixed venous O2 content. A significant rise in arterial O2 content was observed in exercising horses (principally due to a 50% rise in Hb concentration resulting from release of the splenic erythrocyte reservoir into the circulation), whereas mixed venous O2 content decreased. Statistically significant differences in mixed venous O2 content were not found between the first and second runs at 14 m/s on a 3.5% uphill grade. However, because of the significantly lower SaO2 in the second run (Fig. 1), arterial O2 content during galloping at 14 m/s on a 3.5% uphill grade in the second run was significantly less than corresponding values in the first run.
Lactate production. Galloping at 14 m/s on a 3.5% uphill grade in the first run was attended by a large significant increase in the mixed venous blood lactate concentration (15.9 ± 2.5 mM), which further increased significantly to 20.9 ± 3.8 mM in response to galloping at 14 m/s on a 3.5% uphill grade in the second run.
EIPH status. Airway endoscopic examination revealed that all horses had experienced EIPH in the double-exercise experiments.
Single-Exercise-Bout Experiments
The arterial and mixed venous blood-gas/pH data (Table 1) as well as the mixed venous blood lactate concentration (17.4 ± 2.4 mM) in these experiments resembled values recorded during the first run of the double-exercise experiments (Figs. 1-3), and statistically significant differences were not found. However, all horses had experienced EIPH in these experiments as well.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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In terms of assessing the reasons for the development of arterial hypoxemia in exercising horses, there were several interesting observations in the present study. 1) The arterial hypoxemia developed very quickly, being evident at 30 s of the high-intensity exercise in the double- as well as single-exercise-bout experiments (Fig. 1, Table 1). 2) Despite the significant rise in PaCO2 [and, therefore, alveolar PCO2 (PACO2)] as exercise duration progressed from 30 to 120 s (Fig. 2, Table 1), the magnitude of arterial hypoxemia in each high-intensity exercise bout remained unaffected (Fig. 1, Table 1). Because this significant increment in PACO2 from 30 to 120 s of galloping at 14 m/s on a 3.5% uphill grade (Fig. 2, Table 1) would have caused alveolar PO2 (PAO2) to decrease (the correct term for determining PAO2 using alveolar gas equation is PACO2/R, where R is respiratory exchange ratio; however, in the present study O2 consumption and CO2 production were not measured and, therefore, R could not be calculated), it follows that the arterial hypoxemia in strenuously exercising horses was unaffected by the changing PAO2. These observations, namely, the extremely rapid development of arterial hypoxemia with onset of high-intensity exercise and the fact that its magnitude was unaffected by the intensifying hypercapnia (and the associated reduction in PAO2), suggest that the exercise-induced arterial hypoxemia in horses may not have a structural basis related to the changes in the integrity of the blood-gas barrier brought about by stress failure of pulmonary capillaries (19) resulting from the high transmural pulmonary capillary pressures (8-10). This is because whereas the structural changes in the blood-gas barrier would be expected to intensify with increasing exercise duration and should, therefore, cause an intensification of the arterial hypoxemia in exercising horses, this was not the case in the present study (Fig. 1, Table 1). Thus our data are more consistent with the thesis that the exercise-induced arterial hypoxemia in strenuously exercising horses has a functional basis, probably related to the significant shortening of the transit time for blood in the pulmonary capillaries, as cardiac output increases dramatically. A similar conclusion was reached by St. Croix et al. (14) in exercising human subjects.
The primary objective of the present study, however, was to examine whether the structural changes in the blood-gas barrier caused by a prior bout of high-intensity short-term exercise (capable of inducing stress failure of pulmonary capillaries leading to EIPH) in Thoroughbred horses would affect the severity of arterial hypoxemia induced during a successive bout of exercise performed at the same workload. In this context, our results demonstrated that PaO2 during the second run at 14 m/s on a 3.5% uphill grade was, in fact, maintained at a significantly (P < 0.01) higher level (mean increment being 5.3 Torr) than that during the first run at 14 m/s on a 3.5% uphill grade (Figs. 1 and 4). The fact that PaO2 of our horses did not decrease during the second run (as would have been expected with an intensification of the structural changes in the blood-gas barrier) also supports the argument that the arterial hypoxemia in exercising horses has a functional, rather than a structural, basis, as suggested previously (14). The findings of the present study in regard to changes in PaO2 during the second run (vs. the first run; Fig. 1) are also in agreement with previous data in human subjects where a repeat bout of maximal exertion failed to exaggerate the severity of arterial hypoxemia and a similar conclusion was reached (3, 5, 14).
Despite the above-mentioned agreement with human data (14)
in regard to changes in PaO2, there were a few
differences between the studies as well. 1) Despite the fact
that PaO2 of our horses performing a repeat bout of
high-intensity exercise exceeded that during the first run, the
SaO2 during the second run was significantly less
(Fig. 1). This is in contrast to the human data where
PaO2 as well as SaO2 increased during
the second exercise bout (14). The divergent findings
probably are related to the fact that, in the present study,
hyperthermia and acidosis (Fig. 3) were significantly more pronounced
during the second run, resulting in a greater rightward shift of the
Hb-O2 dissociation curve. By contrast, in human subjects,
the second exercise bout was not reported to have accentuated the
hyperthermia and/or the acidosis, and, consequently, the increased
PaO2 in the second exercise bout was attended by an
increment in SaO2 as well (14).
2) In the present study, although PaCO2 did
increase significantly from 30 to 120 s of galloping at 14 m/s on
a 3.5% uphill grade in both runs (Fig. 2), the PaCO2
values were significantly less in the second run than in the first run
(where significant hypercapnia had occurred; for
PaCO2 see Fig. 4) and, in fact, did not exceed the
resting values (Fig. 2). This is also in contrast to data from human
subjects (14), where significant differences in
PaCO2 were not observed between the two exercise
bouts (14). The reduction in PaCO2
during the second exercise bout is indicative of a significantly increased alveolar ventilation. It is well known that the respiratory frequency of galloping horses is tightly coupled with the stride frequency. Thus it is unlikely that, during galloping at the same workload (14 m/s on 3.5% grade) in the second exercise bout, an increased frequency of breathing could have contributed to the increased ventilation. The reduction in PaCO2 observed
during the second exercise bout in the present study is similar to that reported by Bayly et al. (2) when exercise duration was
increased from 2 to 4 min, and it was suggested that alveolar
ventilation in galloping horses is not entirely mechanically limited
during heavy exercise. In the context of the lower values of
PaCO2 during the second run, it should also be noted
that, during the 6-min interval (1 min of trot + 5 min of walk)
between the high-intensity exercise bouts, a dramatic hyperventilation
had occurred, presumably in response to the severe metabolic acidosis
(Fig. 3), and as the second run was initiated, the
PaCO2 (23.6 ± 1.8 Torr) and [HCO
The above-mentioned differences between the human (14) and the equine experimental data regarding the PaCO2 values in the first vs. the second run (Fig. 2) suggest that the mechanism(s) responsible for the observed higher values of PaO2 during the successive bout of high-intensity exercise in horses (Fig. 1) was probably different from that in the human studies (14). In exercising humans, PaCO2 and PAO2 had remained unchanged during the second exercise bout, and thus the observed increase in PaO2 resulted from a narrowing of the PAO2-PaO2 difference (14). However, our data suggest that the higher PaO2 in the second high-intensity exercise bout (Figs. 1 and 4) resulted from an increased PAO2, as PaCO2 (and, therefore, PACO2) was significantly lower than in the first high-intensity exercise bout (Fig. 2).
In considering the possible reasons for the above-mentioned disparities between the human data (14) and the equine data, it should also be noted that the interval between the successive bouts of high-intensity exercise in the present study was much shorter (6 min) than the interval allowed between the repeat exercise bouts in human studies [from 20 min (14) to 2 h (5)]. The shorter interval between the successive exercise bouts in the present study was intended to minimize the time available for recovery of the blood-gas barrier from structural changes induced by stress failure of pulmonary capillaries during the first run. In this context, it has been reported by West and colleagues (19) that the histological changes due to stress failure of pulmonary capillaries in the equine lungs are reversed quickly, although the exact time table for recovery remained uncertain.
In the present study, we intentionally incorporated a separate set of experiments where horses performed only a single bout of high-intensity exercise at the same workload (14 m/s on a 3.5% uphill grade) used in the double-exercise experiments. These single-exercise-bout experiments not only duplicated the blood-gas/pH (Table 1) and lactate data recorded during the first run of our double-exercise experiments but also demonstrated that the workload used for the high-intensity exercise caused EIPH in all horses as demonstrated by airway endoscopic examination (7, 16). Thus there can be no doubt that, before the second bout of galloping at 14 m/s on a 3.5% uphill grade in the present study, the lungs of our horses had indeed been subjected to stress failure of pulmonary capillaries (with its attendant structural changes in the blood-gas barrier) during the first run.
In conclusion, the results of the present study demonstrated that exercise-induced arterial hypoxemia in strenuously exercising horses develops quickly, being evident at 30 s of exertion, and remains unaffected by the hypercapnia that intensified as exercise duration progressed from 30 to 120 s. It was also demonstrated that a prior bout of high-intensity exercise capable of inducing stress failure of pulmonary capillaries leading to EIPH failed to exaggerate the severity of arterial hypoxemia in horses. In fact, the PaO2 values during the successive high-intensity exercise bout significantly exceeded those in the first run as PAO2 increased. These findings are more consistent with the thesis that the exercise-induced arterial hypoxemia in strenuously exercising horses has a functional, rather than a structural, basis, probably related to the significant shortening of the transit time for blood in the pulmonary capillaries as cardiac output increases dramatically (14).
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ACKNOWLEDGEMENTS |
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The authors are grateful to Sarah Humphrey, Kristi Machmer, and Walter C. Crackel for excellent technical assistance.
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FOOTNOTES |
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This work was supported in part by grants-in-aid from the Illinois Department of Agriculture Equine Research Fund, the Illinois Thoroughbred Horsemen's Association, and the US Department of Agriculture-Hatch funds. The high-speed treadmill at the University of Illinois College of Veterinary Medicine was procured in part with financial support provided by the Illinois Thoroughbred and Standardbred Breeders Fund.
Address for reprint requests and other correspondence: M. Manohar, Dept. of Veterinary Biosciences, College of Veterinary Medicine, University of Illinois, 1102 West Hazelwood Dr., Urbana, IL 61802 (E-mail: mmanohar{at}uiuc.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 26 October 2000; accepted in final form 27 December 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Significant
difference from rest. *Significant difference from all data for
galloping at 14 m/s in both runs. 
Significant difference
from data for 30 s of galloping at 14 m/s in the same run.
Significant difference from data for 60 s of
galloping at 14 m/s in the same run. 
Significant
difference from corresponding data in the first run.
Significant
difference from data for 60 s of galloping at 14 m/s in the same
run. *Significant difference from all data for galloping at 14 m/s in
the first run. 
Significant difference from all data for
galloping at 14 m/s in the second run. 
Significant difference from data for 90 s of
galloping at 14 m/s in the same run. *Significant difference from all
data for galloping at 14 m/s in both runs. 