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1 Centre for Activity and Ageing, School of Kinesiology, and 2 Department of Physiology, The University of Western Ontario, London, Ontario, Canada N6A 3K7
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The effect of carbonic anhydrase (CA) inhibition with
acetazolamide (Acz, 10 mg/kg body wt iv) on exercise performance and the ventilatory
(
ET) and
lactate (LaT) thresholds was studied in seven men during ramp exercise
(25 W/min) to exhaustion. Breath-by-breath measurements of gas exchange
were obtained. Arterialized venous blood was sampled from a dorsal hand
vein and analyzed for plasma pH,
PCO2, and lactate concentration
([La
]pl).
ET
[expressed as O2 uptake
(O2), ml/min] was
determined using the V-slope method. LaT (expressed as
O2, ml/min) was determined
from the work rate (WR) at which
[La]pl
increased 1.0 mM above rest levels. Peak WR was higher in control (Con)
than in Acz sutdies [339 ± 14 vs. 315 ± 14 (SE) W].
Submaximal exercise O2 was
similar in Acz and Con; the lower O2 at exhaustion in Acz
than in Con (3.824 ± 0.150 vs. 4.283 ± 0.148 l/min) was
appropriate for the lower WR. CO2
output (CO2) was lower in
Acz than in Con at exercise intensities 
125 W and at exhaustion
(4.375 ± 0.158 vs. 5.235 ± 0.148 l/min).
[La]pl
was lower in Acz than in Con during submaximal exercise 150 W and at
exhaustion (7.5 ± 1.1 vs. 11.5 ± 1.1 mmol/l).
ET was similar in Acz and Con (2.483 ± 0.086 and 2.362 ± 0.110 l/min, respectively), whereas the LaT occurred at a higher
O2 in Acz than in Con
(2.738 ± 0.223 vs. 2.190 ± 0.235 l/min). CA inhibition with Acz
is associated with impaired elimination of
CO2 during the non-steady-state
condition of ramp exercise. The similarity in
ET in Con
and Acz suggests that La
production is similar between conditions but
La appearance in plasma is
reduced and/or La uptake by
other tissues is enhanced after the Acz treatment.
ramp exercise; acetazolamide; exercise performance; acid-base status
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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CARBONIC ANHYDRASE (CA), the enzyme that catalyzes the
reversible reaction involving the hydration-dehydration of
CO2 and HCO3, facilitates the transport of
CO2 from the tissues to the lungs.
Although previous reports indicate an acetazolamide (Acz)-induced
reduction in exercise tolerance (18, 20), maximal aerobic capacity,
determined from peak O2 uptake (O2 peak) was reduced
(18) or unaffected by Acz administration (20, 22). In these studies,
Acz was administered chronically and resulted in a metabolic acidosis
before the onset of exercise. Although the reason(s) for the reduced
exercise tolerance could not be confirmed in these studies, it was
suggested that an altered acid-base status may have played a role in
limiting exercise performance (18, 20). Kowalchuk et al. (9) reported a
lower O2 peak but
similar power output after acute infusion of Acz compared with the
uninhibited condition during 30 s of maximal-intensity exercise. This
effect was not associated with any difference in plasma acid-base
status before or immediately after the exercise bout, suggesting that
CA inhibition may directly affect the exercise response (9).
During exercise of progressively increasing intensity, a work
rate (WR) is reached where, relative to
O2 uptake
(O2), there is a
disproportionate increase in CO2
output (CO2) and ventilation [E;
i.e., ventilatory threshold
(ET)],
as well as an increase in muscle and blood lactate
(La) concentration
{[La];
i.e., lactate threshold (LaT)}. The
ET and LaT are
typically observed at the same exercise intensity; however, a
"cause-effect" relationship remains controversial (3). Lactic
acid (HLa) is almost completely dissociated at physiological pH
(pKa = 3.8). The
H+ generated coincident with
La formation is buffered
primarily by HCO3, resulting in the
formation of CO2 and
H2O at the tissues according to
the net reaction
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3, thus ensuring rapid equilibrium
between CO2 species. Consequently,
this increase in muscle CO2 production results in an
increase in venous blood PCO2 and
H+ concentration
([H+]), which
contributes to the disproportionate increases in
E and
CO2 relative to
O2 that are observed
coincident with the ET (4). Acute
CA inhibition with Acz is associated with a lower
CO2 and a reduction in plasma
[La]
([La]pl)
during short-term maximal exercise (9), both of which may be expected
to affect the
ET and/or the
LaT, but the effect of acute Acz administration on the exercise
response to ramp exercise has not been examined.
Therefore, the purpose of this study was to examine the exercise
response to an acute infusion of Acz during progressively increasing
ramp exercise to determine the role of CA on gas exchange at the lungs
and the plasma La response
during submaximal and maximal exercise. We hypothesized that CA
inhibition would result in a rightward shift in the
ET-O2 and LaT-O2 relationship
subsequent to a slowed equilibration between
CO2 species at the muscle and
delayed appearance of plasma La. By administering Acz
acutely, the effects of CA inhibition alone could be examined without
the associated metabolic acidosis that occurs with long-term Acz use.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects. Seven healthy men [25 ± 2 (SE) yr old, 178 ± 2 cm height, 80.5 ± 3.1 kg body wt] participated in the study. Informed consent was obtained from each subject after the experimental protocol and all possible risks associated with participation in the study had been outlined to them. The study was approved by The University of Western Ontario Review Board for Health Sciences Research Involving Human Subjects.
Materials and methods.
The subjects were studied on two occasions separated by ~1-2 wk
during control (Con) and after acute Acz administration. For each
subject, testing was performed at the same time of the day. Subjects
were asked to abstain from beverages containing caffeine and from heavy
exercise for 12 h before testing and to consume only a light meal
before reporting to the laboratory. The subjects rested supine while a
percutaneous Teflon catheter (Angiocath, 21 gauge) was placed into a
dorsal hand vein to facilitate blood sampling and for the
administration of Acz. Arterialization of the blood was achieved by
wrapping the hand and forearm in a heating pad. After 15 min of rest, a
blood sample was drawn, then Acz was infused (10 mg/kg body mass over a
3-min period). The administration of Acz was randomly ordered. A
placebo was not administered. It is our experience that the side
effects of Acz administration, although minor, are noticeable by the
subject. After an additional 30 min of rest (15 min supine and 15 min
seated upright), a blood sample was drawn and the subject moved to the
cycle ergometer. Breath-by-breath measurements of ventilation and gas
exchange were made throughout the exercise protocol. Arterialized
venous blood samples were obtained at 1-min intervals during exercise and at exhaustion.
O2 peak was taken as
the highest O2 averaged over a 20-s interval.
ET was
determined from breath-by-breath plots by three independent
observers. The
ET was
defined as the O2 at which
the ventilatory equivalent for
O2
(E/O2) and end-tidal PO2
(PETO2) systematically
increased with no concomitant increase in the ventilatory equivalent
for CO2
(E/CO2)
and decrease in end-tidal PCO2
(PETCO2). The
ET reported
is the mean determined from the values provided by each observer.
Breath-by-breath plots were used to determine the slope
(S) and intercept of the linear
portions of the
CO2-O2
response below and above the
ET
[<ET
(S1) and
>ET
(S2)].
Data during loadless cycling, the 1st min of the ramp function, and the
nonlinear portion above the
ET (with use
of
E/CO2
and PETCO2 to indicate the
onset of respiratory compensation) were excluded from the analysis.
Inspired and expired airflow and volumes were measured during the
exercise test by a low-resistance, low-dead space (90 ml) bidirectional
turbine and volume transducer (model VMM-110, Alpha Technologies); the
volume signal was calibrated before each test with a syringe of known
volume (990 ml). Respired gases were sampled continuously at the mouth
(1 ml/s) by a mass spectrometer (model MGA-1100, Perkin-Elmer) for
determination of the fractional concentrations of
O2,
CO2, and
N2. The mass spectrometer was
calibrated with precision-analyzed gas mixtures. Analog signals from
the mass spectrometer and turbine transducer were sampled every 20 ms
and stored on disk for later analysis. Breath-by-breath computations for O2,
CO2,
E,
PETO2, and
PETCO2 were performed after
delays in the analysis system and fluctuations in lung gas stores were
taken into account in the computer algorithms (1). Temperature and
water vapor corrections were made for conditions measured near the
mouth. Heart rate was monitored using an electrocardiograph, with the
electrodes placed in a modified V5 configuration.
Arterialized venous blood was drawn into syringes containing lithium
heparin, mixed, placed in a slurry of ice and water, and analyzed after
a short delay. Whole blood samples (200 µl) were analyzed at 37°C
for plasma pH, PCO2, and
[La]pl
with selective electrodes (StatProfile 9 Plus blood gas-electrolyte analyzer, Nova Biomedical Canada); the electrodes were calibrated before each test and at regular intervals during analysis. Plasma [H+] was calculated
from measured pH; plasma HCO3 concentration ([HCO3]) was
calculated from measured pH and PCO2.
LaT was taken as the O2
corresponding to the WR at which
[La]pl
increased 1 mmol/l above resting levels.
Statistics. Ventilation, gas exchange, and plasma acid-base responses were analyzed using a two-way repeated-measures ANOVA with Con vs. Acz and time as the main effects. A significant F ratio was further analyzed using Student-Newman-Keuls post hoc analysis. Least-squares linear regression analysis was performed to determine the slopes (S1 and S2) and intercepts for each subject and averaged to provide a group mean response, which was tested for differences with a Student's paired t-test. Statistical significance was accepted at P < 0.05. Values are means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Exercise performance,
E,
O2, and
CO2.
The exercise response of a single subject during Con and Acz-induced CA
inhibition is presented in Fig. 1. CA
inhibition did not alter the ventilatory response, gas exchange, or
plasma acid-base status at rest or during loadless cycling (Table
1). Peak WR achieved during the ramp
exercise test was lower (P < 0.05)
in Acz than in Con (315 ± 14 vs. 339 ± 14 W; Table
2). Submaximal O2 was similar between
conditions, but O2 peak
was lower (P < 0.05) in Acz than in
Con (3.824 ± 0.150 vs. 4.283 ± 0.115 l/min; Fig.
2A, Table
2). When O2 peak was
expressed relative to peak WR
(O2/WR), there was no
difference between Acz and Con (12.2 ± 0.7 and 12.8 ± 0.6 ml · min1 · W1,
respectively).
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CO2 was similar between
conditions during submaximal exercise 
100 W but was lower
(P < 0.05) in Acz than in Con at
exercise intensities 125 W and at exhaustion (4.375 ± 0.158 and
5.235 ± 0.148 l/min in Acz and Con, respectively; Fig.
2B); the lower (P < 0.05) peak
CO2 remained after
normalization for WR
(CO2/WR: 14.0 ± 0.7 and 15.6 ± 0.7 ml · min1 · W1
for Acz and Con, respectively). The slope of the
CO2-O2
relationship was lower (P < 0.05) in
Acz than in Con during exercise below (S1: 0.91 ± 0.03 and 1.01 ± 0.02 for Acz and Con, respectively) and above the
ET
(S2: 1.13 ± 0.02 and 1.35 ± 0.05 for Acz and Con, respectively; Fig.
3).
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E was similar
between conditions at exercise intensities 200 W (Fig.
2C). A higher
E
(P < 0.05) was observed in Acz than in Con at exercise intensities 225 W, although
E was similar at exhaustion (165 ± 11 and 170 ± 10 l/min for Acz and Con,
respectively; Fig. 2C). The
ventilatory equivalents for
O2
(E/O2)
and CO2
(E/CO2)
were higher (P < 0.05) in Acz than
in Con at exercise intensities 250 W (Fig.
4).
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150 W; at exhaustion,
PETCO2 was reduced
(P < 0.05) below loadless cycling
values in both conditions and was lower
(P < 0.05) in Acz than in Con (31 ± 1 vs. 35 ± 1 Torr; Fig.
5B).
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Plasma acid-base status.
To examine the effect of CA inhibition on submaximal and maximal
exercise responses, independent of plasma acid-base changes, Acz was
infused 30 min before the onset of exercise. These data represent the
values measured in equilibrated plasma. Plasma
[H+] was similar in
Acz and Con at rest and during loadless cycling (Fig.
6A, Table
1) but was higher (P < 0.05) in Acz
at all submaximal exercise intensities (Fig.
6A). Plasma
[H+] increased
(P < 0.05) above resting values
during exercise and reached similar values at exhaustion. Plasma
[HCO3] was similar between
conditions at rest or during loadless cycling (Fig.
6B, Table 1) and decreased
(P < 0.05) below rest values at
exercise intensities 250 W in Acz and 225 W in Con (Fig. 6B). Plasma
[HCO3] was lower
(P < 0.05) in Con than in Acz at WRs
225 W (Fig. 6B).
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]pl
was not affected by CA inhibition at rest or during loadless cycling
(Fig. 6C). With exercise,
[La]pl
increased (P < 0.05) above rest
values at exercise intensities corresponding to 175 W in Con and
225 W in Acz (Fig. 6C). At exercise intensities 150 W,
[La]pl
was lower (P < 0.05) in Acz than in
Con and was lower (P < 0.05) at
exhaustion (7.5 ± 1.1 and 11.5 ± 1.1 mmol/l in Acz and Con,
respectively);
[La]pl
remained lower (P < 0.05) in Acz
after normalization for differences in peak WR
([La]pl/WR:
23.7 ± 3.1 and 33.9 ± 2.7 µmol · l1 · W1
in Acz and Con, respectively; Fig.
6C).
Plasma arterial PCO2
(PaCO2) was similar in Acz and Con at
rest and during loadless cycling (Fig.
6D). After Acz treatment, plasma
PaCO2 increased
(P < 0.05) above resting values during light-intensity exercise (50 W) and remained elevated throughout exercise to exhaustion (Fig.
6D). During Con, plasma PaCO2 remained at resting values
throughout light- to moderate-intensity exercise and decreased
(P < 0.05) below resting values
during heavier-intensity exercise (275 W; Fig.
6D). Plasma
PaCO2 was higher
(P < 0.05) in Acz during submaximal
exercise (150 W) and at exhaustion (42 ± 1 and 34 ± 2 Torr in
Acz and Con, respectively; Fig. 6D).
The
PETCO2-PaCO2
difference decreased (P < 0.05),
i.e., became more negative, in Acz during submaximal exercise and
at exhaustion (
11 ± 1 Torr; Fig.
5C). In Con, the
PETCO2-PaCO2 difference increased (P < 0.05)
transiently during submaximal exercise (7 ± 1 Torr at 250 W) but
returned to near-zero values at exhaustion (1 ± 2 Torr; Fig.
5C).
ET and LaT.
The ET,
determined by ventilatory and gas exchange responses, occurred at a
similar O2 during Acz and Con
(2.483 ± 0.086 and 2.362 ± 0.110 mmol/l, respectively; Fig.
7). The
O2 corresponding to the LaT
was higher (P < 0.05) in Acz than in
Con (2.738 ± 0.223 vs. 2.190 ± 0.235 l/min). During
Acz, the O2 corresponding to LaT was higher (P < 0.05) than that
corresponding to the
ET (for either
Acz or Con); during Con a similar
O2 was observed for the LaT
and the ET
(for both Con and Acz) (Fig. 7).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Acz-induced CA inhibition was associated with a lower
[La]pl
during moderate-to-heavy submaximal and maximal exercise, a similar ET, and a
higher LaT than in Con. In addition, peak
CO2 and the slope of the
CO2-O2
relationship below and above the
ET were
reduced in Acz. There was also a reduction in peak exercise performance (i.e., reduction in peak WR) and a lower
O2 peak, which was appropriate for the lower peak WR.
Effect of CA inhibition on CO2 equilibrium. A limitation of the present study is the inability to determine with certainty the location (i.e., extracellular and intracellular CA in the lungs, muscle, and erythrocytes) and/or the specific isozyme(s) of CA that may have been inhibited by the dose of Acz administered. However, at the dose given in this study (10 mg/kg), we estimate that, for an 80-kg human (~16 liters of extracellular fluid), the extracellular fluid Acz concentration would be ~225 µmol/l, which would result in a plasma Acz concentration severalfold higher than required to inhibit >99.95% of the total erythrocyte CA activity (23).
Several observations from this study suggest that, at least, the erythrocyte CA isozymes, CA I and CA II, were effectively inhibited by the dose of Acz administered. In addition to a lower peakCO2, CA inhibition resulted
in a lower CO2 during
submaximal exercise at intensities >100 W. Furthermore, the slope of
the CO2-O2
relationship for exercise below and above the
ET was lower
in Acz, indicating that CO2
was impaired by CA inhibition during the non-steady-state condition. CA
inhibition results in a disequilibrium between
CO2 species, such that the rate of
CO2 formation from plasma and
erythrocyte HCO3 is slowed and does
not reach equilibrium during the relatively short transit time through
the pulmonary capillaries. The incomplete equilibration of
CO2 species in the pulmonary
capillaries results in a progressive increase in
PaCO2 as equilibrium is approached. The
negative
PETCO2-PaCO2
difference in Acz demonstrates the dissociation between the
instantaneous measure of PaCO2 in the
pulmonary capillaries (i.e.,
PETCO2) and the
PCO2 of equilibrated plasma. These
findings are consistent with the physiological responses reported in a
previous study in which Swenson and Maren (22) calculated, using a dose
similar to that used in the present study, that CA I and CA II were
~93.3 and 99.3% inhibited, respectively.
Effect of CA inhibition on
ET and LaT.
The excess CO2 produced by the
buffering of HLa and the subsequent increase in arterial
[H+] are generally
held as the underlying stimuli invoking the nonlinear increases in
E
and CO2 relative to
O2 that typically occur during incremental exercise. We hypothesized that since CA is involved
in the removal of CO2 produced by
aerobic metabolism and from the buffering of HLa, the
ET and LaT
would occur at a higher O2
during Acz-induced CA inhibition than in the uninhibited condition. In
contrast to our hypothesis, the
ET occurred at a similar O2 in Acz
and Con, but the LaT occurred at a higher O2 in Acz than in
Con. These results are supported by studies that have utilized various
experimental interventions, including caffeine ingestion (2),
-blockade (6), glycogen depletion (7), and exercise training (5,
14), which have demonstrated a dissociation between the temporal
occurrence of the
ET and LaT. In
these studies the mechanism underlying the
ET response when the LaT was shifted to a higher
O2 has not been reconciled.
]pl
during moderate-to-heavy submaximal exercise and at exhaustion.
Consequently, the LaT-O2
relationship was shifted to the right in Acz compared with Con studies.
This finding is in partial agreement with a previous study that
reported a delayed plasma
La appearance during ramp
exercise at the heavier exercise intensities but did not demonstrate a
difference in the LaT-O2
relationship with Acz administration (8). The reason(s) for the
discrepancy is not readily apparent. However, the different results may
be associated with the lower dose of Acz administered (3.5 mg/kg) or
the method of determining the LaT (8). The lower
[La]pl
observed at exhaustion in Acz was related to the lower peak WR and to a
process related to La
appearance in and/or disappearance from the plasma, since the [La]pl
normalized for WR
([La]pl/WR)
was still lower in Acz than in Con. The effect of acute CA inhibition
on muscle La production is
not known. During chronic Acz administration, however, muscle
[La] was
unaffected (12) or reduced (15) compared with control conditions. In
the present study the appearance of nonmetabolically produced
CO2, indicated by the break point
between S1 and
S2, occurred at
the same O2 in both
conditions and is consistent with a similar production of
La in the muscle. The lower
[La]pl
suggests that La appearance
in plasma is delayed or La
uptake into other tissues is enhanced during Acz.
In a previous study, Kowalchuk et al. (9) demonstrated that a lower
arterial [La]
in Acz during recovery from 30 s of high-intensity exercise was
associated with a lower arterial-venous
[La] difference
across the inactive forearm muscle, suggesting that La uptake was reduced, not
enhanced, after the Acz treatment. However, an enhanced uptake of
La by other tissues, such
as inactive and active muscle groups, the heart, brain, liver, and
erythrocytes (for review see Ref. 21), after Acz administration cannot
be ruled out; such an enhanced uptake of
La would also contribute to
a lower
[La]pl.
Effect of CA inhibition on
CO2.
It is generally held that CA inhibition does not affect the elimination
of CO2 at rest or during the
steady state of moderate- or heavy-intensity exercise (13, 22) but that
the evolution of CO2 during
maximal exercise may be impaired (9, 10, 20). In the present study, Acz
administration was associated with a lower
CO2 during moderate-to-heavy
submaximal exercise and at maximal exercise. Although the peak WR was
lower in Acz, the CO2/WR was
also lower at exhaustion in Acz. In addition, the slope of the
CO2-O2
relationship was lower below
(S1) and above
(S2) the
ET in Acz than
in Con. These data demonstrate that
CO2 elimination is not only
impaired during maximal exercise but is also reduced during light- to
moderate-intensity exercise during non-steady-state conditions, in
agreement with slower CO2
kinetics observed at the onset of moderate-intensity constant-load
exercise (17).
CO2 in Acz in the present
study, removal of CO2 from the
active muscle may also be impaired by CA inhibition. A membrane-bound
CA isozyme, CA IV, has been localized on the sarcolemma and on the
endothelial layer of skeletal muscle capillaries of humans, with the
activity directed toward the intravascular space (19). This CA isozyme
facilitates the uptake of CO2 by the blood as it passes through the skeletal muscle capillaries. Inhibition of this CA isozyme may prevent the rapid equilibration of
CO2 between muscle, plasma, and
erythrocytes, resulting in a higher extracellular
PCO2 and a decrease in the
intracellular-extracellular PCO2
gradient. Thus inhibition of CA at the level of the tissue capillaries
and/or at the level of the lungs may contribute to the lower
CO2-O2
relationship found even at the light WRs.
Maximal exercise performance.
Acz administration was associated with a reduction in peak WR and a
decrease in O2 peak,
although the O2 achieved was appropriate for the WR. Kowalchuk et al. (9) reported a reduction in
O2 peak at a similar
peak and average power output during 30 s of maximal-intensity cycling
exercise after acute Acz administration. Previous studies utilizing
long-term Acz administration have shown a lower (18) or an unchanged
(20, 22) peak WR and/or
O2 peak, which was attributed to an Acz-induced metabolic acidosis that accompanies chronic Acz treatment. When CA is completely inhibited, the
generation of H+ from the
hydration of CO2 is slowed,
thereby limiting the rate of O2
off-loading (i.e., Bohr effect) (11). Although we cannot conclude from
the present study whether the reduction in
O2 peak is due to a
limited Bohr effect, results from a previous study (16) suggest that CA
inhibition does not alter O2
during moderate- or heavy (~80%
O2 peak)-intensity exercise.
Summary.
The results of the present study demonstrate that Acz administered
acutely resulted in lower submaximal and peak
CO2 and CO2-O2
slope below and above the
ET, suggesting
that the facilitated removal of
CO2 is impaired, despite the
relatively short duration between Acz administration and the onset of
exercise. Although the
ET was
unchanged with Acz, the
LaT-O2 relationship was
shifted to the right, demonstrating a dissociation between the
ET and the
LaT. The occurrence of the
ET at the same
O2 during Acz and Con may
indicate that muscle La
production was similar between conditions and that
La efflux from the muscle
was impaired and/or La
uptake by other tissues was enhanced with CA inhibition, resulting in a
lower
[La]pl
in Acz. It was unlikely that the reduction in peak exercise performance
was associated with changes in extracellular acid-base status but,
rather, may be related to an intracellular acidosis consequent to
CO2 retention within the muscle
during CA inhibition.
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ACKNOWLEDGEMENTS |
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The authors thank the participants who took part in the study. The technical support of Brad Hansen was greatly appreciated.
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FOOTNOTES |
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Financial support was provided by an operating grant from the Natural Sciences and Engineering Research Council of Canada. B. W. Scheuermann was supported by a National Sciences and Engineering Research Council Graduate Fellowship.
This research was carried out at The Centre for Activity and Ageing (affiliated with the Faculty of Health Sciences, School of Kinesiology and the Faculty of Medicine at The University of Western Ontario and The Lawson Research Institute at St. Joseph's Health Centre).
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. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: J. M. Kowalchuk, School of Kinesiology, 3M Centre, The University of Western Ontario, London, ON, Canada N6A 3K7 (E-mail: jkowalch{at}julian.uwo.ca).
Received 19 June 1998; accepted in final form 14 October 1999.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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) and Acz (
)
during progressive ramp exercise to exhaustion. During submaximal
exercise, only work rates in which all 7 subjects contributed to mean
are plotted. Dashed lines extend to data points corresponding to
exhaustion and reflect difference in peak work rate achieved in Acz and
Con studies.
