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Exercise Physiology Laboratory, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio 43210-1089
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Hinchcliff, K. W., K. H. McKeever, W. W. Muir, and R. A. Sams. Furosemide reduces accumulated oxygen deficit in
horses during brief intense exertion. J. Appl.
Physiol. 81(4): 1550-1554, 1996.
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 ~120% maximal
O2 consumption. Furosemide (FU)
increased O2 consumption (ml · 2 min
1 · kg1)
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 min1 · kg1)
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.
weight carriage; locomotion; energy expenditure
INTRODUCTION PERFORMANCE OF MUSCULAR work, such as running, requires
the expenditure of energy. The amount of energy required to support running is related to the body mass of the animal and the speed of
running (27). The effect of weight carriage on energy expenditure can
be determined at submaximal work intensities by measurement of the rate
of O2 consumption
( Furosemide administration to horses denied access to feed and water
results in reductions in body weight of ~3-4% over a 4-h period
(9, 14, 22). We theorized that furosemide-induced weight reduction
would reduce the contribution of anaerobic metabolism to energy
expenditure of horses during intense exertion. Specifically, our
hypothesis was that furosemide administration would reduce the
accumulated O2 deficit and rate of
increase in blood lactate concentration of horses during an intense
exercise test of defined duration. Furthermore, we hypothesized that
the addition of weight equal to that lost in response to furosemide
administration would prevent the effect of furosemide on accumulated
O2 deficit.
MATERIALS AND METHODS
O2) (15, 18, 24, 27). Determining the energetic cost of locomotion for work intensities above
that inducing maximal
O2
(O2 max) is
problematic, because energy used above that produced by the maximal
rate of aerobic metabolism is generated by anaerobic metabolism.
Anaerobic capacity may limit exercise at intensities above
O2 max (8). The rate of
anaerobic energy production during supramaximal exertion can be
estimated from the accumulated O2
deficit, and relative rates of anaerobic energy production can be
compared by the rate of appearance of lactate in the blood (13). The
effect of increasing or decreasing body weight on the energetic cost of
locomotion at exercise intensities above that inducing
O2 max has not been investigated to our knowledge. If acute weight reduction is
accomplished without a reduction in aerobic capacity, the accumulated
O2 deficit and rate of increase in
blood lactate concentration would be less after weight reduction for
individuals performing a given supramaximal exercise test.
O2 and plasma lactate
concentration during high-intensity exercise were examined in a
three-way balance randomized crossover study. Nine horses participated
in each of three trials: 1) a
control (C) trial in which the horse was given 10 ml of isotonic saline solution intravenously 4 h before running,
2) a furosemide-unloaded (FU) trial
in which the horse received furosemide (50 mg/ml, 1 mg/kg
body wt iv; Lasix, Hoeschst-Roussel, Somerville, NJ) 4 h before running, and 3) a furosemide
weight-loaded (FL) trial during which the horse received furosemide 4 h
before running and while running carried a saddle pad containing weight
equal to the urinary and insensible weight losses that occurred over
the 3.75 h after furosemide administration. The study could not be
blinded because of the need to add weights to FL horses. Trials in
individual horses were performed 
7 days apart.
O2 max.
O2 max and the
relationship between O2 and
speed were determined for each horse during an incremental exercise
test within 7 days of the experiment. The incremental exercise test
consisted of the horse running on a treadmill inclined at 4° for 90 s at 4 m/s, after which treadmill speed was increased by 1 m/s every 90 s until the horse was unable to maintain its position on the treadmill.
O2 was measured
every 10 s during the exercise test. O2 max was defined as
the value at which O2
reached a plateau, despite further increases in speed. A plateau was
defined as a change in O2
of <4
ml · min1 · kg1
with an increase in speed.
Experimental protocol.
On the day of each trial, between 0800 and 0930, the horse was weighed,
saline or furosemide was administered, and the horse was placed in a
clean stall. Access to food and water was denied until completion of
the trial. A pulmonary artery catheter (PE-240, Becton Dickinson,
Parsippany, NJ) for collection of mixed venous blood was aseptically
placed through a catheter introducer placed in the right jugular vein.
The position of the catheter was confirmed before and after exertion by
examination of the pressure waveforms displayed on a physiograph (VR12
Physiologic Monitoring System, PPG Biomedical Systems, Pleasantville,
NY). The horse was weighed 3.75 h after furosemide or saline
administration, and all feces produced during that time were collected
and weighed. Lead weights equal to the body weight lost over the 3.75 h
after furosemide administration were added to a saddle pad of mares in
the FL trial. The amount of weight added to horses in the FL trials was
calculated as the difference between the initial body weight, recorded
immediately before furosemide administration, and the body weight
recorded 3.75 h later, less the weight of feces produced during the
3.75-h period.
Exercise test.
During each experimental trial (C, FL, and FU), horses ran at 3 m/s for
3 min, at a predetermined high speed for 2 min, and at 3 m/s for 5 min
(recovery) on a treadmill inclined at 4°. The transition from 3 m/s
to the high speed was accomplished in ~10 s. The speed at which each
horse performed the high-speed test was determined during pilot trials
and was the speed at which the horse could just complete the 2-min
high-speed test. The average high speed was 10.8 ± 0.2 (SE) m/s,
representing an average intensity of 121 ± 2.9%
O2 max.
O2 was measured every 10 s
during the exercise test (see below).
O2.
O2 was measured with an
open-circuit calorimeter (Oxymax-XL, Columbus Instruments, Columbus,
OH), as previously described (15). Flow through the system was ~1,500
l/min STP with the horse
stationary and 10,000 l/min during running. Gas collection systems of
this design have been demonstrated not to impair the respiratory
function of running horses compared with closed systems, and the
overall accuracy of the system was verified repeatedly by nitrogen
dilution (7, 10). The O2 sensor
(Electrochemical cell, Columbus Instruments) was calibrated against
gases of known composition immediately before the start of each
exercise test. Discrepancy between simulated
O2 produced by nitrogen
dilution and the value measured by the system was ±3% at nitrogen
flow rates equivalent to a
O2 of 54 l/min (~140
ml · min1 · kg1
for a 385-kg horse).
Calculation of O2 deficit.
Accumulated O2 deficit was
calculated as the difference between the expected
O2 and the actual
O2 during the 2-min
high-speed run with use of previously described assumptions (19).
Actual O2 was calculated
using the trapezoidal rule (11). Expected O2 was calculated from the
speed-O2 relationship
determined during the incremental exercise test and the speed of the
horse during the experimental trials. The
speed-O2
relationship was determined using
O2 rates below
O2 max.
Blood collection.
Mixed venous blood samples for measurement of hematocrit, plasma total
protein, and lactate concentration were collected with the horse
standing on the treadmill, after the warm-up period, at the end of the
high-speed run, and at the end of the 5-min recovery period. Plasma for
measurement of lactate concentration was collected after centrifugation
(1,500 g for 20 min) of mixed venous
blood collected into evacuated glass tubes containing sodium fluoride
and potassium oxalate (Vacutainer, Becton Dickinson). Lactate
concentration was measured electrochemically (model 23L, Yellow Springs
Instruments, Yellow Springs, OH). Hematocrit of blood collected into
evacuated glass tubes containing EDTA (Vacutainer) was measured in
triplicate by the microhematocrit technique. Plasma total protein was
measured by refractometry.
Interpretation of plasma lactate concentration is confounded by changes
in blood volume (13). Therefore, plasma lactate concentrations after
furosemide treatment were adjusted for the effect of the
furosemide-induced reduction in plasma volume (14) by the formula
![[Lac]<SUB>adj</SUB> = (TP<SUB>c</SUB> / TP<SUB>f</SUB>) · [Lac]](/content/vol81/issue4/fulltext/1550/img001.gif)
|
![R<SUB>Lac</SUB> = [Lac]<SUB>adj</SUB>/2 min/BW](/content/vol81/issue4/fulltext/1550/img002.gif)
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Statistical analysis. Data from this study were analyzed as a three-way crossover design by use of a two-way repeated-measures analysis of variance [repeated measures on treatment (i.e., C, FL, or FU) and time factors] or as a one-way repeated-measures analysis (repeated measures on the treatment factor) depending on the data being analyzed (12, 20). Significance was defined as P < 0.05 for each of the main effects (treatment or time) and as P < 0.1 for the interaction. Results are expressed as the means of each group at specified times and the standard error of the mean or of the mean differences (20). All mass proportional variables (
O2, O2 deficit) for the C and FU
treatments are expressed relative to the body weight of the horse 3.75 h after furosemide or saline administration. Mass proportional
variables for the FL treatment are expressed relative to the sum of the
3.75-h weight and the weight added to the horse.
RESULTS
O2 max and
speed-O2 relationship.
O2 max of the nine
horses was 137.7 ± 4.3 ml · min1 · kg1
at a treadmill speed of 9.1 ± 0.2 m/s. The correlation coefficient for the speed-O2 regression
averaged 0.998 ± 0.0001 (P < 0.01), the slope of the regression line was 0.258 ± 0.01 ml
O2 · m1 · kg1,
and the ordinate intercept was 5.1 ± 0.7 ml
O2 · min1 · kg1.
Accumulated O2 deficit.
Work intensity during the high-speed run was 121 ± 2.9%
O2 max. Calculated
O2 demand during the 2-min
high-speed run was 348.7 ± 18.3 ml/kg. FL-treated horses carried
16.1 ± 1.6 kg of weight during the exercise test. Body weight of
horses 3.75 h after furosemide or saline administration was 401 ± 7, 391 ± 8, and 393 ± 8 kg for C, FU, and FL, respectively.
O2 (ml · 2 min1 · kg1)
during the high-speed run was significantly affected by furosemide administration and weight carriage (P < 0.02; Fig. 1). Furosemide administration (FU) increased (P < 0.05) the mass-specific O2 rate, whereas the combination of furosemide treatment and weight carriage (FL) did not affect the mass-specific rate of
O2 compared with saline
treatment. Accumulated O2 deficit
was significantly (P < 0.05) lower
after furosemide administration (FU) than after saline treatment (Fig.
2). There was no effect
(P > 0.05) of the combination of
furosemide treatment and weight carriage (FL) on accumulated
O2 deficit compared with saline
treatment.
Absolute
O2 (liters of
O2 per horse) during the
high-speed test for FU and FL did not differ significantly
(P > 0.05) from C: 103 ± 4, 104 ± 4, and 99 ± 4 l O2/2 min
for C, FU, and FL treatments, respectively.
The proportion of energy derived from anaerobic sources, calculated as
the difference between estimated and actual
O2 during the high-speed run,
differed significantly (P < 0.03)
among treatments. Anaerobic energy sources supplied 25.6 ± 2.0, 22.6 ± 2.3, and 27.0 ± 2.1% of energy during the
high-speed run after C, FU, and FL treatments, respectively. Anaerobic
energy sources supplied significantly less energy during the FU trial
than during the C or FL trials.
Plasma lactate, hematocrit, and total protein.
Hematocrit and plasma total protein concentration were
significantly (P < 0.01) greater
after furosemide treatment (FU and FL) than after the control treatment
(Figs. 3 and
4). Plasma lactate concentration, after
correction for furosemide-induced hemoconcentration, was significantly
(P < 0.05) lower during recovery
after FU treatment than after C or FL treatments (Fig.
5). The rates of increase in blood lactate
concentration of C and FU, but not of FL, were significantly different
(P < 0.05) during the high-speed
test: 0.061 ± 0.001, 0.058 ± 0.001, and 0.061 ± 0.001 mmol/kg for C, FU, and FL, respectively.
DISCUSSION
This study demonstrated that administration of furosemide decreased the
accumulated O2 deficit and rate of
increase of blood lactate concentration of horses during brief
high-intensity exertion. The reduction in accumulated
O2 deficit in furosemide-treated horses that did not carry added weight was attributable to an increase
in the mass-specific rate of
O2 during the high-intensity exercise test. Therefore, acute weight reduction, with preservation of
the maximal rate of aerobic metabolism (expressed as liters of
O2 per individual) resulted in a
reduction in energy supplied by anaerobic metabolism during brief
intense exertion of defined duration. Addition of weight increased the
accumulated O2 deficit and rate of
increase in blood lactate concentration, suggesting that the effect of
furosemide was mediated by weight reduction. If the duration of intense
exertion is limited by anaerobic capacity, then acute weight reduction
may exert an ergogenic effect by decreasing the anaerobic cost of
exertion at a given speed, provided that the absolute aerobic capacity
of the individual is maintained.
Addition of weight to various quadripedal species, including horses,
increases the energy cost of locomotion at speeds below that eliciting
O2 max (26, 28).
Although the energy cost of locomotion above
O2 max has not been
precisely defined, it is generally assumed that the energy (expressed
as O2 equivalent)-speed relationship developed for submaximal exercise applies during supramaximal exercise (13, 19). We are not aware of studies that have
examined the effect of acute weight reduction on the energy cost of
locomotion at intensities above
O2 max. Our results suggest that the acute weight reduction induced by furosemide is
responsible for the lower O2
deficit of horses during brief intense exercise. Although furosemide
has potent dose-dependent hemodynamic effects in stationary and running
horses (16, 21, 22), furosemide administration did not affect the
maximal aerobic capacity of the horse, as indicated by similar
absolute (liters of O2 per horse)
O2 rates of horses after each
treatment during the high-speed test. Therefore, the reduction in
O2 deficit appears to be due to a
decrease in body weight, and therefore absolute O2 demand, with no reduction in
the absolute maximal aerobic capacity of the horse. The effect of the
decrease in body weight is to reduce the difference between the
absolute O2 demand and the
absolute O2, hence reducing
the absolute O2 deficit.
O2 deficit, in relative and
absolute terms, is reduced by the reduction in body weight.
The effect of furosemide to reduce accumulated O2 deficit is consistent with the reduced rate of increase in blood lactate concentration measured in the furosemide-treated unloaded horses. A lower accumulated O2 deficit implies a lesser requirement for energy production from anaerobic sources, which is consistent with the lower rate of increase in blood lactate concentration.
Furosemide, a potent diuretic, is administered to performance horses as prophylaxis for exercise-induced pulmonary hemorrhage (17). Because of the widespread use of furosemide in racehorses, there is concern that furosemide may alter athletic performance of these animals separate from any effect on the incidence or severity of exercise-induced pulmonary hemorrhage, a putative performance-limiting condition (25). Addition of weight equal to that of the furosemide-induced acute weight loss prevented the effect of furosemide administration on O2 deficit and rate of increase in blood lactate concentration. This suggests that any ergogenic effect of furosemide may be attributable to its reduction of body weight, although other mechanisms, such as altered acid-base status, cannot be ruled out.
Our values for O2 deficit are similar to those previously reported for exhaustive exercise in horses (128 ml O2 equivalents/kg) (23) but are substantially greater than the maximal accumulated O2 deficit of 32 ml O2 equivalents/kg reported by other investigators for Thoroughbred horses (6). The reason for the differences between the values for accumulated O2 deficit reported by us and Rose et al. (23) and those reported by Eaton et al. (6) is not apparent.
A methodological concern with estimation of the
O2 deficit is that the
O2-speed relationship
developed for work intensities below
O2 max may not be valid
for work intensities above
O2 max. This issue is
addressed elsewhere (13) but does not seem to have been problematic in
the estimation of maximal accumulated O2 deficit of horses or humans (6,
19, 23). A related concern in this study is that furosemide may have
altered the O2-speed relationship. We previously demonstrated that furosemide does not alter
the aerobic efficiency (ml
O2 · kg1 · m1)
of running, as demonstrated by the virtually identical
O2 of horses at various
intensities during incremental exertion, including that producing peak
O2 (15). Therefore,
our estimates of the O2-speed
relationship developed in the untreated horses should be valid for use
in furosemide-treated horses.
Another concern is that furosemide may have altered
O2 max and therefore
the intensity at which the high-speed test was performed. Bayly et al.
(3) reported that furosemide increased peak or maximal
O2, whereas others have not
detected an effect of furosemide on mass-specific peak
O2 of horses (15, 18). Furosemide does not affect or decreases
O2 max in humans (1, 2,
4). However, an effect of furosemide on
O2 max does not affect
interpretation of the results of this study. The variable of primary
interest was the O2 deficit
incurred during a high-speed test of defined duration. The choice of
speed was determined to be the speed at which the horses could just
complete the high-speed test, not the speed associated with a specific
relative work intensity. The primary dependent variable was therefore
not dependent on the relative intensity of the exertion, but rather on
the absolute work intensity.
In conclusion, the choice of exercise test was based on our
hypothesis that furosemide would reduce the
O2 deficit during an exercise test
of defined duration. This hypothesis was chosen because athletic
capacity of horses to which furosemide is administered often is judged
by their performance in races of ~2-min duration. The intensity at
which the horses in this study completed their high-speed test (120%
O2 max) is similar to
that at which racehorses compete (5). It should be emphasized that we
did not measure athletic or anaerobic capacity of the horses in this
study and therefore did not demonstrate an ergogenic effect of
furosemide.
ACKNOWLEDGEMENTS
We thank J. Dutson and M. Kipp for technical assistance.
FOOTNOTES
Address for reprint requests: K. W. Hinchcliff, Exercise Physiology Laboratory, Dept. of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, 601 Vernon L. Tharp St., Columbus, OH 43210-1089.
Received 2 January 1996; accepted in final form 7 May 1996.
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