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O2 kinetics in
the horse during moderate and heavy exercise
Departments of Anatomy and Physiology and Kinesiology, Kansas State University, Manhattan, Kansas 66506-5602
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Langsetmo, I., G. E. Weigle, M. R. Fedde, H. H. Erickson, T. J. Barstow, and D. C. Poole.
O2 kinetics in the
horse during moderate and heavy exercise. J. Appl.
Physiol. 83(4): 1235-1241, 1997.
The horse is a
superb athlete, achieving a maximal
O2 uptake (~160
ml · min
1 · kg1)
approaching twice that of the fittest humans. Although equine O2 uptake
(O2) kinetics are
reportedly fast, they have not been precisely characterized, nor has
their exercise intensity dependence been elucidated. To address
these issues, adult male horses underwent incremental treadmill testing
to determine their lactate threshold (Tlac) and peak
O2
(O2 peak),
and kinetic features of their O2 response to
"square-wave" work forcings were resolved using exercise
transitions from 3 m/s to a
below-Tlac speed of 7 m/s or an
above-Tlac speed of 12.3 ± 0.7 m/s (i.e., between Tlac and O2 peak) sustained
for 6 min. O2 and
CO2 output were measured using an
open-flow system: pulmonary artery temperature was monitored, and mixed
venous blood was sampled for plasma lactate.
O2 kinetics at work levels
below Tlac were well fit by a
two-phase exponential model, with a phase
2 time constant
(
1 = 10.0 ± 0.9 s) that
followed a time delay (TD1 = 18.9 ± 1.9 s). TD1 was similar to
that found in humans performing leg cycling exercise, but the time
constant was substantially faster. For speeds above
Tlac,
TD1 was unchanged (20.3 ± 1.2 s); however, the phase 2 time constant
was significantly slower (1 = 20.7 ± 3.4 s, P < 0.05) than for exercise below
Tlac. Furthermore, in four of five
horses, a secondary, delayed increase in
O2 became evident
135.7 ± 28.5 s after the exercise transition. This "slow
component" accounted for ~12% (5.8 ± 2.7 l/min) of the net
increase in exercise O2. We
conclude that, at exercise intensities below and above
Tlac, qualitative features of
O2 kinetics in the horse
are similar to those in humans. However, at speeds below
Tlac the fast component of the
response is more rapid than that reported for humans, likely reflecting
different energetics of O2
utilization within equine muscle fibers.
exercise energetics; lactate threshold; ventilation threshold; slow
component of oxygen uptake
INTRODUCTION IN HUMANS THE KINETIC response of
O2 uptake
( It is not known whether other mammalian species display these
responses. However, it has been suggested that the
In humans the METHODS Animals
O2) associated with the
transition to higher metabolic rates after exercise onset or the
transition to a greater work rate is crucially dependent on the
exercise intensity domain in which the work is performed. Specifically,
for all moderate-intensity work rates (i.e., below the lactate
threshold, Tlac), pulmonary
O2 rises as a two-phase exponential process to achieve its steady state within ~3 min in
healthy subjects (2, 39). In marked contrast, all work rates above
Tlac, i.e., in the heavy or severe
exercise intensity domains, evoke a secondary, slow component of the
O2 kinetics that is
superimposed on the initial fast exponential response; this component
delays or prevents attainment of a steady-state O2 (16, 39). This slow
component elevates O2 above
that predicted from the below-Tlac
response or from considerations of chemical-mechanical coupling
efficiencies (16, 39).
O2 response at exercise onset
in the horse may become slower at higher running speeds (11, 19, 22,
28). It is possible that these slowed kinetics resulted from the
emergence of a O2 slow
component (11). However, the relationship among the exercise intensity performed, Tlac, and these slowed
kinetics was not elucidated in those investigations.
O2 slow
component is localized predominantly within the exercising muscles
(27). Thus, of the numerous mediators of the
O2 slow component that have
been proposed, only those operating at this site may contribute
substantially to this response (reviewed in Ref. 14). In this regard,
there is considerable support for the notion that recruitment of
metabolically less efficient fast-twitch muscle fibers may be of
importance (reviewed in Refs. 6 and 14). Specifically, the ATP cost of
tension generation may be two to three times higher in fast-twitch type IIa and IIb fibers than in slow-twitch type I fibers (10, 38). A
progressive recruitment of a greater population of these lower efficiency type IIa and IIb fibers may help explain the
O2 slow component and its
temporal correspondence with blood lactate and catecholamine levels.
Adult horse muscle has a far higher proportion (80-90%) of
fast-twitch fibers than the muscle of most humans (50%) (reviewed in
Ref. 34), of which about one-half are the least efficient type IIb
fibers (31, 36). If fast-twitch fibers are of fundamental importance in
the etiology of the O2
kinetics during heavy and severe exercise intensities, we would expect to find a large slow component in the horse exercising above
Tlac, where these fibers would be
recruited. The present investigation was designed to determine the
dependence of equine O2
kinetics on exercise intensity relative to
Tlac. Specifically, we tested the
hypotheses that 1) the initial rapid
rise of O2 (i.e.,
phases 1 and
2) after the transition to faster
running speeds would be slowed above
Tlac (11, 19, 22, 26,
28, 39), 2) exercise intensities above Tlac would
engender a O2 slow
component that would be initiated 1-2 min after the
transition to an increased running speed, and
3) because of the large type II
fiber population in equine skeletal muscle the proportional
contribution of the slow component would be large.
Animal Preparation
For all portions of the study, each animal was instrumented in a similar manner. Two 7-F introducer catheters were inserted into the right jugular vein after local anesthesia (2% lidocaine) using aseptic technique. A thermistor catheter (Columbus Instruments, Columbus, OH) and a 7-F microtipped pressure transducer (SPC-471A, Millar Instruments, Houston, TX) with a lumen were advanced through the introducers and into the pulmonary artery for measurement of blood temperature and for sampling of mixed venous blood. Location of the pressure transducer was verified by the characteristic pressure wave.Respiratory Gas Measurements
O2 and
CO2 output
(CO2) were measured using
an open-flow system similar to that described previously (18). However, the system was modified by the replacement of the pneumotachograph with
a 2-in. ASME standard flow nozzle. Calculation of bias flow was done
using standard equations (model MFC-3M-1989, ASME, New York, NY).
Ambient air was drawn through a loosely fitting face mask past the
horse's nose and mouth at a rate sufficient to prevent escape of
expired gas. Industrial fans (models 5K901C and C2548C2, Dayton,
Chicago, IL) were used to provide airflow, which was adjusted between
2,000 and 7,500 l/min, depending on the exercise level. Expired
O2 and
CO2 concentrations were measured
using a gas analyzer (model 1100, Perkin-Elmer, Pomona, CA) and
recorded at a sample rate of 100 Hz by a computer-based data
acquisition system (DATAQ, Akron, OH). The pressure differential across
the flow nozzle was determined by means of a differential pressure
transducer (model MC1-3-871, Validyne, Northridge, CA) for
determination of flow. Calculation of flow was verified by use of a
modified N2-dilution technique
(12). The gas analysis system was calibrated before each measurement
using gas mixtures with O2 and
CO2 concentrations that spanned
the measured range. The calibrating mixtures were prepared with mixing
pumps (model 301a-F, H. Wösthoff Instruments, Bochum, Germany).
Transit delay was measured by infusing known flows of
N2 gas into the system and
measuring the response time (<2 s). These delays were taken into
consideration when kinetic responses were calculated. Relative humidity
and temperature in the open-flow system were also measured continuously
(model HS-ZCHDT-2R, Thunder Scientific, Albuquerque, NM). Ambient
temperature and barometric pressure were measured before each run was
started. These variables were used to correct
O2 and
CO2 to
STPD conditions.
Incremental Exercise Protocol
An incremental exercise test was used to determine 1) Tlac measured directly from mixed venous blood samples, 2) Tlac estimated from gas exchange [i.e., Tlac(est)], and 3)O2 peak. All exercise tests were performed on a level treadmill. The increments were selected so that each horse attained its maximum speed in 8-10 min. After a warm-up of 800 m at 3 m/s, the treadmill speed was increased at 1-min intervals in even increments of 1-1.5 m/s. Maximum speed was 13-15 m/s, depending on the capability of each horse. Blood samples for measurement of plasma lactate were taken during the last 5 s of each increment. The samples were placed on ice
and centrifuged immediately after the experiment for separation of
plasma and red blood cells. Plasma lactate was measured with a lactate
analyzer calibrated according to the manufacturer's specifications
(model 23L, Yellow Springs Instruments, Yellow Springs, OH).
O2 peak was
determined as the point at which no further increase in
O2 occurred, despite an
increase in speed, or as the point at which the animal could no longer
keep up with the treadmill. Tlac
was determined as the
O2 at which blood lactate began increasing systematically.
Tlac(est) was derived by the
V-slope method using plots of
O2 and
CO2 (16).
Constant-Speed Exercise Protocol
For the constant-speed protocols, the moderate-intensity exercise speed was at least 1-2 m/s below the speed at which Tlac occurred. This speed approximated 50%O2 peak. The speed
for the heavy-intensity exercise was chosen to be ~85% of the speed at which O2 peak was
achieved. Thus, at this level, a substantial rise occurred in plasma
lactate; however, the horse could maintain the required speed on the
treadmill for the entire exercise period of 6 min. As with the
incremental test, the horses were warmed up for 800 m at a trot (3 m/s,
~4.5 min), then the speed was rapidly increased (<10 s) to the
target level, where it was maintained for 6 min. The treadmill was then
decelerated to 3 m/s for an 800-m cool-down period. Blood samples were
taken at the end of each minute throughout the exercise bout for
determination of plasma lactate levels. Thermistor readings were taken
every 30 s for determination of pulmonary artery blood temperature.
O2 and
CO2 were measured
continuously by the open-flow method described above.
Data Analysis
Values forO2 and
CO2 were smoothed using a
10-s moving average to reduce noise from the respiratory cycle,
breathto-breath tidal volume variation, and breath holding by the
horse to give values for each second. The time course from 30 s before
exercise to the end of exercise was analyzed. The kinetics of the
moderate and heavy work were then compared.
Modeling Procedure
The time courses forO2
were described in terms of exponential functions that were fit to the
data using nonlinear regression techniques. The computation of best-fit
parameters was chosen by the program to minimize the sum of squared
differences between the fitted function and the observed values (3).
Kinetics for all work rates were fit using a three-term exponential
model, with the first exponential term (phase 1)
beginning at the onset of exercise and the second and third terms
beginning after independent time delays (Fig. 1 in Ref. 3). The
equations are as follows
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![<A><AC>V</AC><AC>˙</AC></A><SC>o</SC><SUB>2</SUB>(<IT>t</IT>) = <A><AC>V</AC><AC>˙</AC></A><SC>o</SC><SUB>2</SUB>(b) + <IT>A</IT>′<SUB>0</SUB> + <IT>A</IT><SUB>1</SUB>[1 − <IT>e</IT><SUP>−(<IT>t</IT> − TD<SUB>1</SUB>)/&tgr;<SUB>1</SUB></SUP>] <IT>phase 2</IT>](/content/vol83/issue4/fulltext/1235/img003.gif)
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![<A><AC>V</AC><AC>˙</AC></A><SC>o</SC><SUB>2</SUB>(<IT>t</IT>) = <IT>phase 2</IT> + <IT>A</IT><SUB>2</SUB>[1 − <IT>e</IT><SUP>−(<IT>t</IT> − TD<SUB>2</SUB>)/&tgr;<SUB>2</SUB></SUP>] slow component](/content/vol83/issue4/fulltext/1235/img005.gif)
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O2(b) is the baseline value
(trotting at 3 m/s);
A0,
A1, and
A2 are the
asymptotic values for the exponential terms; 0,
1, and
2 are the time constants of the
A0,
A1, and
A2 responses, respectively, and TD1 and
TD2 are the independent time
delays. Phase 1 was terminated at the
start of phase 2 (TD1) and assigned the value of
the exponential function at that time:
A
0 = A0(1 
eTD1/
0).
The physiologically relevant amplitude of the primary exponential
component during phase 2 (A1) was then set
equal to the sum of A0 + A1.
A2 represents the
magnitude of the slow component at end exercise. During
moderate-intensity exercise the slow-component term dropped out during
the fitting procedure (Fig. 1).
O2) kinetics.
O2(b), baseline value
(trotting at 3 m/s); TD1 and
TD2, independent time delays;
A0, value of
A0 (amplitude of
phase 1 response) at
TD1.
A1 = A0 + A1 (amplitude of
phase 2 response) and represents
physiologically relevant amplitude.
A2, magnitude of
O2 slow component at end
exercise; EEO2, net increase
in O2 at end of exercise.
Potential relationships between the
O2 slow component and
temperature or blood lactate were determined from the temporal profiles
of the increases in temperature and lactate and the magnitude of the
slow component at the end of exercise. Differences for all parameters
between moderate and heavy exercise intensities were determined by
paired t-tests. Values are means ± SE. Significance was accepted at P 
0.05.
RESULTS
Incremental Work Test
O2 peak averaged 71.1 ± 5.2 l/min (133 ± 10 ml · kg1 · min1) for the group of
seven horses at 13.8 ± 0.4 m/s. As illustrated for one animal in
Fig. 2A,
O2 increased as a
linear function of treadmill speed for all the horses up to
O2 peak.
Tlac occurred at a mean
O2 of 36.0 ± 2.7 l/min,
which corresponded to 50.7 ± 2.4%
O2 peak,
whereas Tlac(est) occurred at a
significantly higher O2 (41.6 ± 2.9 l/min, P < 0.05), which
was 59.6 ± 3.3% O2 peak. The
O2 at
Tlac and
Tlac(est) were significantly
correlated (r = 0.80, y = 4.7 + 0.75x,
P < 0.05), as were
O2 at
Tlac and O2 peak
(r = 0.75, y = 26.4 + 1.24x,
P < 0.05).
O2 vs. treadmill speed.
B: determination of lactate threshold
in 1 horse. +, CO2 output
(CO2); 
, plasma lactate
concentration. Solid line was fit by visual inspection to initial
portion of
O2-CO2
relationship.
O2 Kinetics for
Moderate-Intensity Exercise (Below Tlac )
O2. Of the five remaining
horses, each demonstrated a biphasic response after the transition from
3 to 7 m/s, i.e., a delaylike phase (phase 1)
followed by a monoexponential increase (phase 2)
to the steady-state value (Fig.
3A). The
parameters for this response are given in Table
1. The mean baseline value for
O2 at 3 m/s was 13.2 ± 0.9 l/min. The amplitude of phase 1 (A0) was 4.5 ± 0.2 l/min. The amplitude of phase 2 (A1) was 12.9 ± 1.7 l/min and was well fit by a single-exponential model with a
time constant of 10.0 ± 0.9 s and a time delay of 18.9 ± 1.9 s.
The mean total increase in O2
(A1) for the
moderate work rate was 17.3 ± 1.7 l/min.
O2 response (thick
line) and model (thin line) for 1 horse during moderate-
(A) and heavy-intensity exercise (B). Parameters as defined in Fig. 1
legend.
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O2 Kinetics for
Heavy-Intensity Exercise (Above Tlac )
O2 kinetics after the onset
of heavy (above-Tlac) exercise
(12.3 ± 0.7 m/s) were markedly altered from those for moderate exercise (Fig. 3B, Table 1).
Specifically, in all horses the time constant of the rapid
phase 2 exponential increase
(1) was significantly slower
during heavy-intensity exercise (20.7 ± 3.4 s,
P < 0.05). In addition, a slow
component of the kinetics that began after a time delay of 135.7 ± 28.5 s was seen in four of the five horses. An increase in
O2 of an additional 5.8 ± 2.7 l/min (10.4 ± 4.9 ml · kg1 · min1)
occurred by the end of exercise (11.9% of total increase in O2) as a result of this slow
component. For two of the horses the slow component was well described
by an exponential function (2 = 74.4 s, A2 = 8.2 l/min), whereas for the other two horses, the process was more
accurately described by a linear function
(A2 = 3.45 l/min).
Temperature
Mixed venous blood temperature rose 1.3 ± 0.3°C during moderate-intensity exercise and 3.5 ± 0.1°C during heavy-intensity exercise. The change in temperature and the magnitude of theO2 slow component were
not significantly correlated (r = 0.44, P > 0.05).
Lactate Accumulation
As expected, there was no appreciable plasma lactate accumulation in the moderate-intensity exercise bout: lactate concentration was 1.0 ± 0.2 mmol/l at 3 m/s, and end-exercise lactate concentration was 1.2 ± 0.3 mmol/l. In marked contrast, the mean lactate concentration at the end of heavy-intensity exercise was 8.1 ± 1.4 mmol/l. The lactate concentration was not significantly correlated with the magnitude of theO2 slow
component (r = 0.49, P > 0.05).
DISCUSSION
The principal original finding of the present investigation was that
O2 kinetics across the
transient to higher running speeds in the horse are exercise intensity
dependent. 1) Transients below
Tlac are well fit by a two-phase
exponential model, with the time constant of the dominant response
being markedly shorter (1 = 10.0 ± 1.8 s) in the horse than in humans
(1 > 20 s) (2). Thus the
steady state at these exercise intensities is achieved within
50-60 s for the horse, rather than 2-3 min, as observed in
humans. 2) The
1 is significantly slower
(i.e., approximately doubled) for transients above
Tlac.
3) Exercise above
Tlac results in a slow component
of the O2 response. This slow
component is initiated ~136 s, on average, after the exercise
transition and elevates end-exercise
O2 5.8 l/min (10.4 ± 4.9 ml · kg1 · min1)
above that found after the rapid kinetic phases (i.e.,
phases 1 and
2) were completed.
Physiological Interpretation
Moderate-intensity exercise (below Tlac ). Increases in pulmonary gas exchange during phase 1 are considered primarily to represent alterations in cardiac output and pulmonary blood flow and a secondary fall in venous O2 content (8), which occur before the arrival of venous blood emanating from the exercising muscles (reviewed in Refs. 5, 14, 39). The duration of phase 1 depends on the ratio of the interposed venous blood volume to blood flow. Both of these variables are likely to change rapidly during phase 1 (and phase 2). Unfortunately, the technology necessary to follow such changes in the horse is not available. However, it is interesting to note that the transit delay (TD1) from the exercise-exercise transition to the start of phase 2 was very similar to that reported for humans performing cycle ergometer exercise (i.e., 19 s for horses and 15-25 s for humans) (2, 15). Whereas the phase 1 response is attributable largely to increased pulmonary blood flow, the exponential phase 2 that elevatesO2 to the steady state is
thought to reflect muscle metabolism (4, 15, 39). Rapid measurements of
leg O2 across the transition
to higher metabolic rates have confirmed that phase 2 pulmonary
O2 kinetics are a close
representation of muscle O2
kinetics (15).
As mentioned above, 1 in the
horse exercising below Tlac is
about twice as fast as that found in humans (2, 15). In humans,
O2 kinetics at the onset of
below-Tlac exercise are related to
fitness and thus are faster in individuals with a higher maximum
O2
(O2 max) (29; reviewed
in Ref. 39). Moreover, these kinetics can be accelerated with exercise
training (17). O2 peak
of the horses in this investigation averaged 133 ± 10 ml · kg1 · min1, which is two- to
threefold higher than in healthy humans. Thus, by this criterion, fast
O2 kinetics are expected in
the horse. There is strong support for the notion that
O2 kinetics during moderate-intensity exercise are limited by some intramuscular process,
either inertia of the oxidative enzyme machinery or possibly blood flow
distribution (or maldistribution), rather than bulk muscle
O2 delivery (reviewed in Ref. 15).
Whereas this has not been addressed systematically in the horse, it is
evident that cardiac output increases more rapidly than
O2 at exercise onset in the
Shetland pony (13, 25), suggesting that, as in humans, bulk
O2 transport is not limiting
equine O2 kinetics, at least for moderate-intensity exercise.
If the limit to O2 kinetics
does indeed reside within the exercising equine musculature, it is
pertinent that, despite the high type IIa and IIb fiber content, equine
muscles have the structural attributes necessary for rapid
O2 exchange. Specifically, equine locomotory muscles have a dense capillary network and a high
mitochondrial volume density (1, 20) compared with human muscle
(reviewed in Refs. 21 and 30). Thus it is not surprising that equine O2 kinetics are extremely
fast in comparison with those found in humans.
The rapid phase 2 kinetics in the
horse are remarkable, especially in light of two factors that could
potentially slow or distort the kinetics of pulmonary
O2. First, although
attainment of the new higher treadmill speed was rapid (within 10 s),
it was not instantaneous. The physiological response to this
not-quite-square-wave transition would be a quasi-exponential rise in
O2 that would be
slightly slower than the exponential response to a pure step increase
in work rate. Second, it is unclear in a quadruped such as the horse
whether the circulation time and, specifically, the transit time from
the muscle to the pulmonary capillaries would be similar for the fore-
and hindquarters. Substantially different transit times from the two
quarters would lead to a smearing of the end of phase
1 and a lengthening of the rise in pulmonary O2 during
phase 2 relative to that in the
muscles, even if the two compartments had similar muscle
O2 kinetics. The observation that the phase 2 O2 response was visually well
described by a monoexponential function
(1) in the present
investigation suggests that any differences in transit times between
the two quarters were not physiologically appreciable.
Heavy-intensity exercise (above
Tlac ).
The phase 1 time delay,
TD1, was not different at
running speeds above
Tlac. However, the
phase 2 time constant,
1, was significantly slowed
from 10.0 s (below Tlac) to 20.7 s (above Tlac). This is in
agreement with the findings of Paterson and Whipp (26) in humans and
was considered by those authors as evidence that, during exercise at
intensities above Tlac, muscle
O2 availability was insufficient
to permit aerobic metabolism to fully meet the ATP resynthesis
requirement.
In marked contrast to below-Tlac
exercise, heavy exercise was attended by a slow component of the
O2 response in four of five
horses. Specifically, at ~136 s, on average, after the transition to
a faster speed, a further increase in
O2 became evident that elevated O2 ~6
l/min above that found at 2 min, i.e., after completion of the fast
exponential phases 1 and
2. Also,
O2 was elevated 5.3 l/min, on average, above that predicted for this speed on the basis of
the O2-speed relationship
from the incremental test. In similar fashion to humans, this response
was described by an exponential (2 horses) or a linear (2 horses) fit
(7, 24, 26; reviewed in Ref. 14).
Mechanistic Basis of O2
Slow Component
O2 slow component arises from
within the exercising muscles in humans (27). Furthermore, there are
examples that show that slow component behavior can be temporally and
quantitatively dissociated from that of three of the primary candidate
mechanisms that might potentially act within the exercising leg muscles
to elevate O2, specifically, catecholamines, blood lactate, and temperature (reviewed in Refs. 7 and
14). In the present investigation the
O2 slow component was not
related to increases in blood lactate concentration or blood
temperature responses. In humans, ~86% of the slow component response arises from within the exercising limb muscle (reviewed in
Ref. 14), and thus the O2
associated with ventilatory, cardiac, and accessory muscle work at
sites remote from the limb muscles contributes proportionally little to
this facet of the O2
response. However, it remains to be determined whether this is also the
case for the horse, and thus the possibility must at this point be
acknowledged that augmented ventilatory, cardiac, and accessory muscle
work contributes to the observed
O2 slow component.
One enduring hypothesis, however, is that recruitment of a less
energetically efficient fast-twitch (type IIa and IIb) fiber population may induce the slowed
O2 kinetics and elevated
end-exercise O2. In the mouse
(10) and rat (38) and in humans (9), there is evidence that the
energetic cost of producing tension or work is higher when type II
fibers are recruited. In addition, the kinetics of this fiber
population are slower than the kinetics for type I fibers (23). The
association between increased integrated electromyogram and the
O2 slow component suggests
that progressively more fibers are being recruited while
O2 is increasing (35). Given
the high type IIa and IIb fiber content of equine locomotory muscle, it
is almost certain that the heavy-intensity exercise will have mandated
recruitment of at least some of these fibers. We hypothesized that this
would be the case and further that this would result in a large
O2 slow component. However,
the slow component educed here was relatively modest in size (~12%
of the O2
associated with exercise) and was similar in relative amplitude to that
in humans exercising at equivalent relative exercise intensities (2).
One feature that may help explain this observation is that type IIa and
IIb fibers in the horse have a fairly high oxidative enzyme activity.
In fact, citrate synthase activity in the type IIa and IIb fibers of
the gluteus medius muscle of Thoroughbreds averaged 60-80% of
that in the type I fibers (37). This might be associated with the
ability of these fibers to operate at a lower energetic cost than
similar fiber types in other mammalian systems.
Relationship to Previous Work
There is universal agreement that equineO2 kinetics are extremely
rapid (13, 19, 28, 32). Five features of previous experiments have
precluded retrospective analysis of the equine kinetic response:
1) The sampling interval has been
too long, i.e., 10-60 s. 2)
There has been a long or unspecified time lag between initiating and
finalizing the target treadmill speed. 3) The exercise time has been
insufficient to permit development of a slow component.
4) The running speed has been so
high (
O2 max) that
the O2 projects rapidly to
O2 max (33).
5)
Tlac or Tlac(est) has not been measured,
and so the relative intensity of the exercise is unknown. There is the
suggestion of a O2 slow
component at the "62%
O2 max" treadmill
speed used by Hodgson et al. (19) and the 100%
O2 max treadmill speed
examined by Evans and Rose (11). Also, Powers et al. (28) noted slowed O2 kinetics at the higher of
two running speeds in the Shetland pony. In addition, Jones et al. (22)
found that the slope of O2
vs. speed was approximately doubled for horses running on a 6% incline
at >4.9 m/s compared with that below this speed. None of these
earlier studies, however, focused on the relationship of
O2 kinetics to
exercise intensity per se. Fundamental to this process is the
mathematical procedure by which the
O2 response is analyzed. The
triple-exponential model used here allowed us to partition the
O2 response into discrete
components representing distinct metabolic events such as
1) the
O2 attributable to augmented pulmonary blood (or deoxygenated hemoglobin) flow
(phase 1), 2)
the O2 derived from rising
muscle O2 extraction
(phase 2), and
3) manifestation of the
O2 slow component and its gas exchange consequences.
One interesting feature of the equine
O2 response that has been
noted by some (13) but not other (19, 28, 32) investigators is an early
overshoot of O2. This
O2 overshoot
resulted in the O2 kinetics
for those particular Shetland ponies being nonexponential. We observed
a O2 overshoot in only two of
our horses in this study, and this was attributed to their inexperience
on the treadmill. It was clear that these inexperienced
animals were pulling on their halter ropes at moderate
treadmill speeds in anticipation of going faster. Once they settled
into their pace, O2 fell. This pattern was not seen in any horses used in this investigation at
the faster treadmill speed.
Also, the O2 slow component
was not found above Tlac in one
horse in this investigation. This is similar to the occasional observation in humans where the slow component response is absent (6).
We can discern no obvious mechanistic basis for this phenomenon.
In conclusion, this investigation has demonstrated that the underlying
features of the equine O2
kinetics associated with increased running speeds are exercise
intensity dependent. Thus, for exercise intensities above
Tlac, the rapid initial kinetics are markedly slowed, and a secondary, slow component becomes manifest ~136 s after the transition to the higher speed. Presence of this slow component elevates O2
above that predicted from exercise below
Tlac or from the
O2-speed relationship
determined during incremental exercise. To our knowledge, this
investigation represents the first rigorous kinetic analysis of the
effect of exercise intensity on non- human
O2 kinetics. Given the marked
differences in biomechanics (i.e., quadrupedal vs. bipedal) and
respiratory and hematologic exercise responses between the horse and
humans, the qualitative similarity in the
O2 kinetics of the horse to that reported previously in humans is remarkable.
ACKNOWLEDGEMENTS
We are grateful to R. Petrisko, P. Davis, K. Schweitzer, and L. Rall for technical assistance.
FOOTNOTES
Address for reprint requests: D. C. Poole, Dept. of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506-5602.
Received 6 January 1997; accepted in final form 17 June 1997.
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