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Departments of Anatomy, Physiology, and Kinesiology, Kansas State University, Manhattan, Kansas 66506-5802
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The exercising Thoroughbred
horse (TB) is capable of exceptional cardiopulmonary performance.
However, because the ventilatory equivalent for O2
(
E/O2) does not
increase above the gas exchange threshold (Tge), hypercapnia and
hypoxemia accompany intense exercise in the TB compared with humans, in
whom E/O2 increases
during supra-Tge work, which both removes the CO2 produced
by the HCO
CO2) and
O2 [V-slope lactate threshold
(LT) estimation] during an incremental test to fatigue (7 to ~15
m/s; 1 m · s
1 · min1) in
six TB. Peak blood lactate increased to 29.2 ± 1.9 mM/l. However,
as neither E/O2 nor
E/CO2 increased,
PaCO2 increased to 56.6 ± 2.3 Torr at peak
O2
(O2 max). Despite the presence of a
relative hypoventilation (i.e., no increase in
E/O2 or
E/CO2), a distinct
Tge was evidenced at 62.6 ± 2.7%
O2 max. Tge occurred at a significantly
higher (P < 0.05) percentage of O2 max than the lactate (45.1 ± 5.0%) or pH (47.4 ± 6.6%) but not the bicarbonate (65.3 ± 6.6%) threshold. In addition, PaCO2 was elevated
significantly only at a workload > Tge. Thus, in marked contrast to
healthy humans, pronounced V-slope
(
CO2/O2) behavior occurs in TB concomitant with elevated PaCO2
and without evidence of a ventilatory threshold.
equine; lactate threshold; ventilatory threshold; exercise-induced pulmonary hemorrhage; hypoxemia
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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IN CONTRAST TO
HUMANS, THE VENTILATORY RESPONSE to incremental exercise is a
close to linear function of speed and O2 consumption (O2) in the Thoroughbred horse (TB) such
that the ventilatory equivalent for O2 does not rise across
the spectrum of achievable metabolic rates (1, 33). This
is thought to be primarily because of a compulsory coupling of
ventilatory and stride frequencies (6) combined with the
relative insensitivity of the TB respiratory control system to
increased arterial partial pressure of CO2
(PaCO2) (26). In humans, an
increase in the ventilatory equivalent for O2
(E/O2) is necessary
to prevent a rise in PaCO2 during supralactate threshold and subrespiratory compensation threshold work
(37), whereas an increase in the ventilatory equivalent
for CO2
(E/CO2) drives
PaCO2 below resting levels during suprarespiratory
compensation threshold work (34). Therefore, an increase
in PaCO2 to the level predicted for a linear
ventilatory response to incremental exercise (i.e., 50-55
Torr; Ref. 36) is expected and found in TB during
incremental exercise (3, 4, 33). In addition, experimental
perturbations, such as He/O2 (79:21%; Ref.
13) and hypoxic (16%; Ref. 25) gas
breathing, which are designed to induce a greater ventilatory response,
do not prevent hypercapnia during heavy exercise in TB.
Despite the absence of an elevated
E/O2, TB exhibit an
increase in
CO2/O2
and arterial lactate [i.e., LT] during incremental exercise
(20, 22). In human subjects, the increase in
CO2/O2 [i.e., gas exchange threshold (Tge)] is thought to be a direct consequence of HCOE/O2. This elevated
ventilatory response clears additional CO2 (produced by
HCOE/O2 in
TB, Tge is linked causally to an elevated blood lactate and
PaCO2. However, the proximity of these events has not
been determined to date. In this regard, it is pertinent that
breath-by-breath technology, essential to resolving the temporal
profiles of these events with high fidelity, has not, to date, been
used for this purpose in exercising TB.
Currently, humans are the sole species in which the breath-by-breath
gas exchange response to exercise has been related mechanistically to
metabolic and humoral events. It is likely that analysis of such
relationships in another species will provide a novel and insightful
perspective on respiratory control during exercise. The purpose of this
investigation was to analyze the relationship between
O2,
CO2, and E
on a breath-by-breath basis during incremental treadmill exercise in
TB. We tested the hypothesis that for Tge to occur during treadmill
exercise in the absence of a ventilatory threshold (VT; defined as the
O2 at which
E/O2 begins to rise
systematically), an elevated PaCO2 must precede Tge.
In addition, it was hypothesized that LT and Tge would not occur at
similar time points because PaCO2 will only start to rise progressively after LT.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Animals. Six healthy geldings (all TB; age = 4-10 yr; weight = 470-600 kg) were used in this study. Animals were housed in enclosed dry lots, with a shed and free access to water and salt, and were fed alfalfa, grass hay, and concentrate twice daily. They were dewormed and vaccinated at regular intervals and exercised on a high-speed treadmill (SATO, Uppsala, Sweden) at least twice weekly. All procedures herein were approved by the Kansas State University Institutional Animal Care and Use Committee.
Animal preparation. Before the experimental protocol, each horse had one 7-Fr introducer catheter placed in the right jugular vein and one 18-gauge, 2.0-in. catheter placed either in a previously elevated left carotid artery or the transverse facial artery (20 gauge, 1.5 in., two TB) by using aseptic techniques. A thermistor catheter (Columbus Instruments, Columbus, OH) was advanced through the 7-Fr introducer catheter into the right pulmonary artery, 8 cm past the pulmonary valve, for measurement of core body temperature. The thermister was calibrated by using a Physitemp themocouple thermometer (BAT-10, Physitemp, Clifton, NJ). A cannula (1.6 mm ID, 3.2 mm OD) was connected to the arterial catheter to facilitate withdrawal of arterial blood.
Experimental protocol.
Each TB completed one maximal run on the level treadmill. After
collection of resting cardiorespiratory measurements and blood samples,
TB were warmed up at a trot (3 m/s for 800 m). After this warm-up,
the speed was rapidly increased to 7 m/s for 1 min, after which the
speed was increased 1 m · s1 · min1 to maximal
effort. TB were then cooled down (3 m/s) for at least 4 min.
Cardiorespiratory measurements were collected continuously throughout
exercise and cool-down, whereas blood samples were collected during the
last 10 s of each stage and during minutes 2 and
4 of recovery.
Ventilation.
Ventilation was measured by using an ultrasonic phase-shift flowmeter
(model FR-41eq, Flowmetrics-BRDL, Birmingham, UK) that has been
discussed in detail elsewhere (38). Briefly, a light fiberglass mask (<1 kg) is placed on the muzzle of TB. This mask is
fitted internally with silicone rubber and foam gaskets to provide an
airtight seal. Flow tubes are then placed in the front of the mask,
approximately opposite each nostril, so that airflow for each nostril
is measured. Flow tubes are fitted with two ultrasonic transducers,
which quantify the velocity of airflow at a resonant frequency of 40 kHz. In addition, the effects of temperature and gas composition on
zero stability are negated by the dual transducer design
(38). Each transducer pair was calibrated before each experiment as per manufacturer's standards (38).
E was converted to STPD by using
standard equations for determination of
O2 and
CO2. Alveolar ventilation
(A) was calculated by using the A
equation: A = (CO2/PaCO2)k,
where k is 0.863 when converting from BTPS
(A) to STPD
(CO2).
O2 and
CO2.
O2 and
CO2 were calculated as the product of
E (STPD) and
FO2 
(fiO2 
feO2) and fCO2 (feCO2 fiCO2), respectively. FO2 and FCO2 were
determined from the difference between inspired and expired gas
measured via mass spectrometry (Perkin-Elmer, model 1100, Pomona,
CA) by sampling from a port located on the Fiberglas mask midway
between the nares.
Blood analysis. After anaerobic withdrawal (~5 ml into plastic, heparinized syringes), blood samples were placed immediately on ice. After completion of the experimental protocol (within 1-2 h), arterial blood gases, pH, and plasma lactate were quantified with a blood-gas analyzer (Nova Stat Profile, Waltham, MA). Blood gases and pH were corrected to the TB pulmonary arterial blood temperature (14). The above measurements were performed on each occasion by a single technician to maintain internal consistency. Equipment was calibrated before and after each exercise test according to manufacturer's standards.
Threshold analyses.
Tge was determined by using a simplified version (30) of
the V-slope method of Beaver et al. (5). The method
identifies the point (i.e., O2) where
the slope of the CO2 identity line departs from linearity with the slope of the
O2 identity line.
-work rate relationship occurred. This was then
verified by plotting the linear segments of BLa against
O2 and using least-squares regression
analysis to choose the point of intersection, which was then recorded
as LT. The pH (pHT) and HCOO2 where each variable departed from
linearity, and this point was then confirmed by least-squares regression analysis.
Statistical analysis.
A one-way analysis of variance was used to determine whether
differences existed between selected experimental variables. When
significance was revealed, the point of significance was identified by
using a Student-Newman-Keuls post hoc test. Multiple linear regression
was used for threshold analysis (LT, pHT,
HCO
0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Breath-by-breath values for O2,
E, frequency of breathing, and tidal volume
(VT) are shown graphically for a representative TB in
Figs. 1 and
2. All TB attained
O2 max as identified and defined
by a distinct plateau in the O2-speed
relationship (Fig. 1). In addition, no TB exhibited a VT, as
E and A (Fig. 3B) responses did not
demonstrate an upward inflection (compared with humans; Ref.
33) even at the highest treadmill speeds and O2. Furthermore,
E/O2 fell (Fig.
3C; comparing equine with human; Ref. 33)
progressively throughout exercise concomitant with a widening of the
alveolar-arterial PO2 difference
(A-aDO2; Fig. 3C). All TB exhibited
distinct metabolic LT and Tge behavior during incremental exercise
(Figs. 4A and
5B), with Tge occurring at
62.6 ± 2.7% of O2 max, which was
significantly greater than both LT (45.1 ± 5.0%) and
pHT (47.4 ± 6.6%; Figs. 4A and 6A) but not
HCO
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Analysis of breath-by-breath gas exchange, ventilation, and the
associated metabolic and blood-gas profiles during maximal incremental
exercise in TB produced several novel findings. Specifically, in TB,
Tge can occur without a discernible VT. In addition, Tge occurred at a
O2 substantially above LT but not
significantly different from HCOO2 at which PaCO2 began
a progressive and sustained increase above baseline values. Thus it
appears that Tge in TB occurs via mechanisms that are qualitatively
different from those described for healthy humans.
Ventilatory responses during incremental exercise: human and TB.
In the human athlete, ventilation increases linearly with respect to
O2 to ~45 to 55% of
O2 max (i.e., LT), after which the
E/O2 ratio increases
systematically (8, 36), which serves to prevent a rise in
PaCO2 (37). At higher work rates (~75%
O2 max), the
E/CO2 ratio rises,
driving PaCO2 downward in an attempt to constrain the
incipient acidemia (35). Therefore, in humans, the
ventilatory system plays an important role in arterial pH homeostasis
during incremental exercise.
E (i.e., E/body weight) at
maximal exercise is elevated in the equine (~40%; 3-4 vs.
2-3 l · kg1 · min1 for
TB and human, respectively) compared with human athlete, relative
O2 max is much greater (~135%;
150-180 vs. 60-80 ml · kg1 · min1 for TB
and human, respectively). Therefore,
E/O2
(33) does not increase (and in fact falls systematically)
during incremental exercise in TB. As TB must couple stride and
breathing frequency (6), relative VT is small
(~40% less than in human athletes per kilogram), which, when coupled
with voluminously large airways, mandates that the dead space fraction
[dead space volume (VD)/VT] is much greater
in TB compared with humans (Fig. 3A) (7, 33). Because VD/VT is so high, A
is relatively low at maximal effort (Fig. 3B). Therefore,
because of this relative hypoventilation in TB (33),
E/O2 falls and
E/CO2 fails to
increase above LT, such that PaCO2 rises in the TB to
55-60 Torr (1, 4, 7, 13, 23, 33). This
PaCO2 level is consistent with that predicted for
humans should an elevated
E/O2 not occur above LT (37).
Gas-exchange responses during incremental exercise: human and TB.
In humans, during incremental exercise there is a distinct threshold of
CO2/O2
(i.e., Tge) occurring at ~45 to 55% of O2 max (36). Tge has been
closely associated with LT (8, 36) and is thought to be
the result of CO2 evolved through HCOE/O2
systematically upward.
CO2/O2
has been noted (22) during incremental work; however, Tge
has never before been described with the same breath-by-breath
techniques as those used in human subjects. Because ventilatory
equivalents for O2 and CO2
(E/O2,
E/CO2, A/O2, and
A/CO2) do not
increase during progressive work in TB (33),
CO2/O2
must increase via a different mechanism than that described above for
humans. According to the relation CO2 = A × FACO2, where
FACO2 is the alveolar
CO2 fraction, CO2 can
increase out of proportion to O2 in the
face of a linear rise in E (and
A; Fig. 3) because of an alinear increase in
FACO2. As an increase in
FACO2 surely accompanies an
increase in PaCO2, it is logical that the substantial
arterial hypercapnia occurring above LT in TB (Figs. 7 and 8) causes Tge.
Blood-gas responses during incremental exercise: human and TB.
During incremental exercise in healthy humans, PaCO2
does not rise (due to the increased
E/O2) and
PaO2 stays constant or falls slightly
(11). In trained human athletes (Fig. 7), PaO2 often falls significantly and the hypoxemia that
develops appears to be directly related to the degree of alveolar
hyperventilation, O2 max, and the
A-aDO2 (11). The reduced
hyperventilatory response is thought to be because of a combination of
the increased work of breathing as
O2 max increases (10),
mechanical constraints to flow (18), and a reduced
sensitivity of the peripheral chemoreceptors to CO2
(15). Increased A-aDO2 has been
attributed to an increased A-cardiac output
(
) mismatch, an alveolar end capillary diffusion limitation, or
a combination of both (11).
; Ref.
28), where DO2 is the lung
diffusing capacity for O2 and is the mean slope of the
linear portion of the O2-dissociation curve. Variables on
both sides of this equation increase with exercise. However,
increases to a greater degree than does DO2
because of the massive of TB (11), and thus
hypoxemia results from the lowered DO2/ ratio. In addition, at
least part of the hypoxemia must also be because of the hypercapnia
according to the alveolar gas equation approximated as
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E/O2 (and
E/CO2) is falling
(Fig. 3C). However, during the last few stages of exercise,
the degree of hypoxemia and hypercapnia did not worsen (Figs.
4B and 7). Although this may seem strange, E is increasing (Fig. 1A; due to
increases in both frequency of breathing and VT; Fig. 2),
whereas O2 is beginning to plateau (Fig.
1B) at these time points. Thus an attenuation of the
hypercapnia would be expected. In addition, the plateau in
PaCO2 should cause a similar plateau in
PaO2 (see alveolar gas equation). This same phenomenon
has been noted in trained human subjects as well (18) but
is more likely due to respiratory compensation for metabolic acidosis
(i.e., rise in E/CO2)
and its effect on PaO2 in these subjects.
Metabolic responses during incremental exercise: human and TB.
The inflection points of plasma lactate, pH, and HCOO2 max in human subjects
(35).
O2 max and
PaCO2 began to rise after LT, HCOO2 max in the TB. Because
PaCO2 rose systematically above LT (Fig. 8), it
appears that the TB does not have an isocapnic buffering period but
what might instead be called "isocarbic buffering" (i.e., no change in HCOMechanistic explanation for exercise responses in TB.
One potential explanation for the arterial hypoxemia and hypercapnia in
TB is that the coupling of stride and breathing frequency results in
relatively small VT and thereby limits
A. However, the elite Standardbred (a breed
genetically related to TB) can uncouple stride and breathing frequency
when trotting at very high speeds. This uncoupling results in a
substantially greater VT (and reduced
VD/VT) compared with TB (2) but
does not constrain the magnitude of the blood-gas perturbations common
to both of these equid breeds. These data suggest that
locomotory-respiratory coupling cannot singularly be responsible for
the hypoxemia and hypercapnia that attend heavy exercise in TB.
O2 max (both ~24% lower), found that
this procedure completely abolished both arterial hypoxemia and
hypercapnia at maximal exercise. In addition, peak pulmonary arterial
pressure (~45%; Ref. 31) and right ventricular
(~20%) and atrial (~85%) pressures (25) were substantially reduced, whereas
E/O2 was ~65%
higher in splenectomized horses (31). These findings
suggest that sequelae to pulmonary hypertension (i.e., perivascular
cuffing, pulmonary edema, and exercise-induced pulmonary hemorrhage),
very short pulmonary capillary red blood cell transit time (Ref.
9; due in part to the near doubling of systemic hematocrit;
Fig. 4B), and relative hypoventilation (i.e.,
E/CO2 falls at
increased O2, in marked contrast to the
rise seen in humans) may each contribute importantly to the arterial
blood-gas derangement found in intact TB at maximal exercise.
In conclusion, TB exhibit a clearly discernible Tge in the absence of a
VT. However, the insensitivity of TB to elevated PaCO2 (26) combined with high cellular (very high carnosine
levels; Ref. 12) and intravascular (elevated exercise
arterial hemoglobin concentration; Ref. 27) buffering
capacities allows a breathing strategy that minimizes respiratory
muscle work, while providing acid-base balance matching that of humans.
Although this may cause profound arterial hypoxemia and likely reduce
O2 max, it may be construed as
beneficial, as an increase in E to maintain blood-gas homeostasis would likely divert a substantial portion of
from the locomotory to the ventilatory musculature (1, 4,
16), thereby causing early fatigue and reduced performance.
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ACKNOWLEDGEMENTS |
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The authors thank Casey Ramsel, Angie Dick, Ann Otto, Leslie Mikos, Joanna Thomas, and Dani Goodband.
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FOOTNOTES |
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This work was supported, in part, by National Heart, Lung, and Blood Institute Grant HL-50306, National Institutes of Health short-term training grant, and the American Quarterhorse Association.
Present address for C. A. Kindig: VCSD, Dept. of Medicine, Physiology Div., La Jolla, CA 92093-0623.
Address for reprint requests and other correspondence: P. McDonough, Dept. of Anatomy and Physiology, 133 Coles Hall, Kansas State Univ., Manhattan, KS 66506-5802 (E-mail: pjmcdono{at}vet.ksu.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.
10.1152/japplphysiol.00909.2001
Received 4 September 2001; accepted in final form 5 December 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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