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O2
kinetics in heavy submaximal exercise by hyperoxia and prior
high-intensity exercise
1 Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1; and 2 Department of Physical Education, Odense University, Odense DK-5230, Denmark
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
MacDonald, Maureen, Preben K. Pedersen, and Richard L. Hughson. Acceleration of
O2 kinetics in heavy
submaximal exercise by hyperoxia and prior high-intensity exercise.
J. Appl. Physiol. 83(4):
1318-1325, 1997.
We examined the hypothesis that
O2 uptake (O2) would
change more rapidly at the onset of step work rate transitions in
exercise with hyperoxic gas breathing and after prior high-intensity
exercise. The kinetics of
O2 were determined from the
mean response time (MRT; time to 63% of total change in
O2) and
calculations of O2 deficit and
slow component during normoxic and hyperoxic gas breathing in one group
of seven subjects during exercise below and above ventilatory threshold
(VT) and in another group of seven subjects during exercise above VT
with and without prior high-intensity exercise. In exercise transitions below VT, hyperoxic gas breathing did not affect the kinetic response of O2 at the
onset or end of exercise. At work rates above VT, hyperoxic gas
breathing accelerated both the on- and off-transient MRT, reduced the
O2 deficit, and decreased the
O2 slow component from
minute 3 to minute
6 of exercise, compared with normoxia. Prior exercise
above VT accelerated the on-transient MRT and reduced the
O2 slow component from
minute 3 to minute
6 of exercise in a second bout of exercise with both
normoxic and hyperoxic gas breathing. However, the summated
O2 deficit in the second normoxic
and hyperoxic steps was not different from that of the first steps in
the same gas condition. Faster on-transient responses in exercise
above, but not below, VT with hyperoxia and, to a lesser degree, after
prior high-intensity exercise above VT support the theory of an
O2 transport limitation at the
onset of exercise for workloads >VT.
ventilatory threshold; oxygen transport; oxygen utilization; oxygen
deficit; oxygen debt
INTRODUCTION A REDUCTION IN THE MAGNITUDE of the
O2 deficit at the onset of
exercise during hyperoxic, compared with normoxic, breathing (19, 23)
suggested that if one supplied more
O2 to working muscle during this
transient, it could be used. These data were obtained with Douglas bag
collections of mixed expired air during tests requiring ~70-80%
of maximal O2 uptake
( For step increases or decreases in work rates above compared with below
the ventilatory threshold (VT), there might be different rate-limiting
steps that establish the time course of change in For work rates above VT, making more
O2 available might accelerate
The purposes of this study were threefold. First, we wanted to obtain
data from breath-by-breath analysis of
METHODS The present study was conducted in two parts. The first examined the
effect of hyperoxia on Subjects
O2). To date, the only
studies to follow the O2
responses at the onset of exercise during hyperoxia with
breath-by-breath techniques found that there was no difference from
control (11, 18). It is possible that hyperoxia failed to accelerate
O2 kinetics because the
fractional concentration of O2 was
relatively low [inspiratory O2 fraction
(FIO2) = 0.30] (18) or that the work rates studied were of a relatively
lower intensity, at which increasing arterial
PO2 has not been shown to increase
O2 kinetics (11, 18), than in
those studies in which O2
kinetics were accelerated (19, 23). In the face of conflicting evidence for accelerated or unaltered
O2 kinetics with hyperoxic
gas breathing, it is appropriate to set out the potential explanations. It is possible that, at least over a range of work rates, adequate O2 is delivered at the onset of
exercise, and O2 utilization
establishes the rate at which
O2 increases (8).
Alternatively, hyperoxia might not supply more
O2 over this same range of work
rates because of reduced blood flow as noted by some (26), but not all
(16), previous investigators.
O2 (18). In either case, the
mechanisms can be expressed simply as being related to the delivery and
distribution of O2 to the working
muscles (10, 12, 18) or to utilization of
O2 determined by the kinetics of
the intramuscular oxidative processes (8, 24). During leg-cycling
exercise below VT, there have been numerous examples in which
reductions in O2 transport could
slow the increase in
O2 at the onset of
exercise, including a start from a baseline of existing mild exercise
(12), hypoxia (21), 
-adrenergic-receptor blockade (9), and supine
compared with upright exercise (15). These examples hold open the
possibility that O2 transport
might be rate limiting. It has been shown that, when constant-load
exercise has been constrained to be only 60-65% of the work rate
at VT, the O2 kinetics can be
altered by manipulation of arterial perfusion pressure (10). Thus, in
subjects in the upright and supine positions during application of
lower body negative pressure, the
O2 kinetics were faster than
when the sub-VT exercise was conducted in a supine posture (10).
However, in healthy individuals, for upright exercise below VT in
normoxia, it has never been demonstrated that increasing O2 transport can increase
O2 kinetics.
O2 kinetics. Breathing a 70%
inspired O2-gas mixture could
increase dissolved O2 by up to 10 ml O2/l of blood. The examples of
smaller O2 deficits with hyperoxia
were probably for work rates above VT (19, 23). Two reports (6, 7) have suggested that O2 increased
more rapidly in the second of two step transitions to work rates about
halfway between VT and maximum O2 and no effect of prior
high-intensity exercise for a subsequent subthreshold exercise bout.
They attributed this to the existing changes in local muscle
environment that promoted both more rapid increases in blood flow and a
rightward shift of the
O2-hemoglobin dissociation curve
that facilitated O2 release at the
working muscle.
O2 with hyperoxic gas
breathing during the challenge of exercise to work rates both below and
above VT. Second, we wanted to examine the relationships between the
magnitude of the O2 deficit and
the slow component of the O2
increase in normoxia and hyperoxia. Third, we wanted to determine
whether the second of two step increases in work rate to intensities
above VT might be further accelerated by a subject completing this
exercise while breathing a hyperoxic gas mixture. These experiments
allowed the testing of the hypothesis that, at least for work rates
above VT, O2 transport to the
exercising muscle acts as the rate-limiting step for the increase in
O2 at the onset of exercise.
O2
kinetics in response to step changes in work rate to below and above
VT. The second investigated the effect of hyperoxia and prior
high-intensity exercise on
O2 kinetics after step
changes to above VT.
O2. These values were used in choosing the individual work rates for the step tests. The VT was
determined from the point of increased minute ventilation (E)-to-O2
ratio
(E/O2)
with no change in the
E-to-CO2 output (CO2) ratio, as
previously described (11). The number of tests performed by each
subject varied according to the noise observed in the breath-by-breath
signal (17). Normally, four tests were sufficient because of the large
amplitude of the steps.
Experimental Design
Part 1 involved testing both below and above VT with step changes in work rate. Subjects cycled at 25 W for 4 min to establish a baseline, before the following work rate changes: a step increase in work rate to below VT (80% VT) for 6 min, a step decrease back to 25 W for 6 min, a step increase in work rate to a level halfway between VT and peakO2 for 10 min, and a final
step decrease to 25 W for 6 min. Subjects exercised in both normoxia
(room air; FIO2 = 0.21) and
hyperoxia (FIO2 = 0.70).
In part 2 of the study, the focus was
on the effect of previous high-intensity exercise on a subsequent
identical transition in work rate. After a period of 4 min with
subjects pedaling at a baseline work rate of 25 W, the work rate was
increased to approximately halfway between the work rates at VT and
peak O2 for 10 min. This
was followed by a step decrease in work rate back to the 25-W baseline
for 6 min before a second identical step transition was performed. No
warning was given to the subjects before any of the step transitions,
although they were made aware of the protocol before the test.
Experiments were performed with normoxia (room air,
FIO2 = 0.21) and hyperoxia
(FIO2 = 0.70). The four
possible conditions were normoxic breathing in the first and second
step transitions (NN), normoxic breathing in the first followed by
hyperoxic breathing in the second step transition (NH), hyperoxic
breathing in the first and second step transitions (HH), and hyperoxic
breathing in the first followed by normoxic breathing in the second
step transition (HN).
Breath-by-Breath Data
Breath-by-breath ventilation and gas exchange were measured on a computerized system (First Breath, St. Agatha, ON), which sampled inspired and expired volumes with a volume turbine (VMM-110, Alpha Technologies, Laguna Beach, CA) and fractional concentrations of O2, CO2, and N2 by mass spectrometry (Marquette MGA-1100A, Milwaukee, WI) at a frequency of 200 Hz.O2 and
CO2 were calculated as
alveolar values with compensation for lung-gas stores and with computation of the effective lung volume (15).
For the hyperoxic testing, a large Tissot tank was filled with inspiratory gases from cylinders containing 70% O2-30% N2. The gas was not humidified. The Tissot tank was connected to a Y valve (model 2730, Hans Rudolph, St. Louis, MO) to permit inspiration from the tank. The Y valve was open to room air during the normoxic transitions. The volume turbine was calibrated with a manually pumped syringe and with the equipment configured as it was during testing, including hyperoxic gas, for these tests. The mass spectrometer was calibrated for normoxia and hyperoxia by using two precision gas mixtures that spanned the anticipated fractional gas concentrations in both normoxia and hyperoxia. A calibration procedure was performed to determine the time required for gas transport and mass spectrometric response (lag time) (14). Separate lag times were determined for normoxia and hyperoxia because of the effect of gas density. The lag time for the hyperoxic mixture was ~30 ms slower than for the normoxic mixture (11). Heart rate was measured with an electrocardiograph (7803A, Hewlett-Packard) by using standard bipolar electrode placement. Mean heart rate over each breath was recorded.
Data Analysis
Breath-by-breath data forO2 from at least three
repetitions of an identical test condition for each subject were
linearly interpolated between breaths to give values at 1-s intervals. The identical tests were then time aligned, superimposed, and ensemble
averaged to give a single data set per subject. The average individual
response was fit to a curve by using an exponential model. The
curve-fitting procedure involved the calculation of a modeled
exponential output for test values of the various parameters by using
the least- squares error approach (13). These modeled outputs were
compared with the actual individual averaged data set for that
variable. The curve-fitting procedure was iterated until any further
changes in the parameters for the model did not result in a reduction
in the mean squared error between the curve drawn from the model and
the averaged data set.
The low-step tests, to work rates below VT, were fit to a two-component model, whereas the high-step tests, to work rates above VT, were fit to a three-component model. Steps from the baseline work rate to a higher work rate were referred to as "on-transients," whereas steps from a higher work rate to the baseline work rate were referred to as "off-transients." Work rate transitions to and from a work rate below VT were referred to as "low steps," and transitions to and from a work rate above VT were referred to as "high steps."
The two-component model used to fit the responses to the low-step tests
had a baseline (G0) and two
amplitude terms (G1 and G2), two time constants
(
1 and
2), and two time delays
(TD1 and
TD2) as previously described
(13)
![<A><AC>V</AC><AC>˙</AC></A><SC>o</SC><SUB>2</SUB>(<IT>t</IT>) = G<SUB>0</SUB> + G<SUB>1</SUB>[1 − <IT>e</IT><SUP>− (<IT>t</IT> − TD<SUB>1</SUB>)/&tgr;<SUB>1</SUB></SUP>] ⋅ u<SUB>1</SUB> + G<SUB>2</SUB>[1 − <IT>e</IT><SUP>− (<IT>t</IT> − TD<SUB>2</SUB>)/&tgr;<SUB>2</SUB></SUP>] ⋅ u<SUB>2</SUB>](/content/vol83/issue4/fulltext/1318/img001.gif)
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O2(t)
is the time-dependent variation in
O2.
The data from the high-step tests were fitted to a three-component
model. The three-component model contained an extra amplitude term
(G3) and time constant
(3) to fit the slower
adaptive phase in these tests. In the absence of a rationale for
letting the third component begin at some time after the second, we
used a model equivalent to that of Linnarsson (18) and had the second and third components start together. This issue is considered further
in DISCUSSION
![<A><AC>V</AC><AC>˙</AC></A><SC>o</SC><SUB>2</SUB>(<IT>t</IT>) = G<SUB>0</SUB> + G<SUB>1</SUB>[1 − <IT>e</IT><SUP> − (<IT>t</IT> − TD<SUB>1</SUB>/&tgr;<SUB>1</SUB></SUP>] ⋅ u<SUB>1</SUB>](/content/vol83/issue4/fulltext/1318/img004.gif)
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![+ G<SUB>2</SUB>[1 − <IT>e</IT><SUP> − (<IT>t</IT> − TD<SUB>2</SUB>)/&tgr;<SUB>2</SUB></SUP>] ⋅ u<SUB>2</SUB> + G<SUB>3</SUB>[1 − <IT>e</IT><SUP> − (<IT>t</IT> − TD<SUB>3</SUB>)/&tgr;<SUB>3</SUB></SUP>] ⋅ u<SUB>2</SUB>](/content/vol83/issue4/fulltext/1318/img005.gif)
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![MRT = [G<SUB>1</SUB>/(G<SUB>1</SUB> + G<SUB>2</SUB> + G<SUB>3</SUB>)] ⋅ (TD<SUB>1</SUB> + &tgr;<SUB>1</SUB>)](/content/vol83/issue4/fulltext/1318/img009.gif)
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![+[G<SUB>2</SUB>/(G<SUB>1</SUB> + G<SUB>2</SUB> + G<SUB>3</SUB>)] ⋅ (TD<SUB>2</SUB> + &tgr;<SUB>2</SUB>)](/content/vol83/issue4/fulltext/1318/img010.gif)
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![+[G<SUB>3</SUB>/(G<SUB>1</SUB> + G<SUB>2</SUB> + G<SUB>3</SUB>)] ⋅ (TD<SUB>3</SUB> + &tgr;<SUB>3</SUB>)](/content/vol83/issue4/fulltext/1318/img011.gif)
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O2 responses were also
analyzed by calculating the O2
deficit and by determining the slow component response of the
O2 response from 3 to 6 min and from 6 to 10 min after the step change in work rate. The
O2 deficit was taken as the
difference between the measured
O2 at any time after the
start of the higher-work-rate exercise and the average
O2 measured during the last
minute of exercise.
Statistics
Statistical analysis was performed by using two-way repeated measures analysis of variance of the main effects. In part 1 the main effects, i.e., inspired gas concentration and work rate, and in part 2 the main effects, i.e., prior exercise and inspired gas concentration, were examined across various parameter estimates forO2. The parameters examined
were those generated from the curve-fitting procedure when applied to
the average individual data set for each subject. Significant
differences in MRT because of main effects were interpreted as
reflecting differences in kinetics, while differences in other
parameters were also noted. In part 2,
when no significant difference in MRT was observed within
step 2 because of the effect of
previous gas condition, tests with the same gas condition for
step 2 and with different previous gas
conditions in step 1 were treated as
identical and averaged before further statistical analysis. When
significant main effects were observed, post hoc testing included
comparisons by the Student-Newman-Keuls test. A significance level of
P < 0.05 was maintained for all
comparisons.
RESULTS
The mean peak O2 values of
the subjects during testing in normoxia were 45.3 ± 1.6 (SE)
ml · kg
1 · min1
in part 1 and 44.4 ± 2.4 ml · kg1 · min1
in part 2. The mean
O2 values achieved during the
below-VT (low-step) and above-VT (high-step) tests in
part 1 were 50.4 ± 0.9 and 78.6 ± 1.0% of peak
O2 at average work rates of
125 and 215 W, respectively. In part
2, the mean
O2 achieved during the
high-step tests was 82.0 ± 0.8% of peak
O2 at an average work rate of
195 W.
O2 Response Fitting
O2 kinetics was examined for
work rate transitions to and from below and above VT (Fig.
1, Table 1).
The on-transient kinetics of
O2 represented by the MRT
were not accelerated for low steps with exercise in hyperoxia compared
with exercise in normoxia. In contrast, hyperoxic gas breathing
resulted in a faster adjustment to steady-state O2 for high steps. No effect
of hyperoxic gas breathing on the kinetics of the off-transient
responses was observed for either low- or high-step transitions. For
both on- and off-transients, the MRT was significantly less for low
steps compared with high steps regardless of gas-breathing condition.
The high-step off-transient responses were faster than the
corresponding on-transient responses, for both normoxic and hyperoxic
gas-breathing conditions. The low-step off-transient responses were
slower than the on-transient responses for hyperoxic gas breathing, and
there was no difference between the on- and off-transients during
normoxic gas-breathing tests.
O2) at
baseline and during transitions in exercise to low and high work rates
for 1 subject breathing normoxic gas (dotted line) and hyperoxic gas
(solid line). Lines represent average response for 4 identical
transitions.
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O2 on-response was faster in
hyperoxia than in normoxia, and this was true for both
steps 1 and
2 (Table 2). Similarly, there were no
effects of hyperoxia on off-transient
O2 kinetics after the
step 1 or step
2 test. The
O2 on-transient kinetics were
significantly accelerated as a result of prior exercise in both the
normoxic and hyperoxic gas-breathing tests. Prior high-intensity exercise had no effect on any of the off-transient MRT. In
step 1, during normoxic gas breathing
the off-transient responses were faster than the corresponding
on-transient responses, and no difference was observed between the on-
and off-transients during hyperoxic gas breathing. During the
step 2 transition, slower
O2 kinetics were observed
during the off-transient in hyperoxia than during the corresponding
on-transient, whereas there were no differences between the on- and
off-transient responses in normoxic gas breathing.
O2 at baseline and during
transitions in exercise to high work rates for 1 subject breathing
normoxic gas (dotted line) and hyperoxic gas (solid line). Lines
represent average response for 4 identical transitions.
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O2 Deficit and
O2 Slow Component
O2 in either hyperoxic or
normoxic low-step transitions (Table 3).
These results were consistent with those obtained by curve fitting
(Table 1).
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O2
kinetics, from the O2 slow
component between minutes 3 and
6 of the high-step tests, was
consistent with the curve-fitting results (Tables 1 and 2). There was
significantly less slow component in hyperoxia compared with normoxia,
and the step 1 transition
had a greater O2 slow component
than that in step 2 (Table 3). Only for step
2 in normoxia was there a significant further slow component in O2
between minutes 6 and
10 of the step tests. These results
indicate that most effects of the experimental manipulations were
complete within the first 6 min of exercise.
DISCUSSION
Previous evidence that O2
transport might limit the rate of increase in
O2 at the onset of exercise
came from experiments in which the magnitude of the
O2 deficit was reduced at the
onset of moderately heavy exercise while a subject breathed a hyperoxic gas mixture (19, 23) and in which incomplete recovery after prior
exercise at a similar high intensity might have facilitated blood flow
and O2 release from hemoglobin in
a second bout of exercise (6, 7). This study has combined these
methodologies in an attempt to examine the hypothesis that
O2 transport acts as the
rate-limiting step for the increase in
O2 at the onset of exercise
above VT. Both hyperoxia and prior exercise caused an acceleration of
O2 kinetics (i.e., faster
MRT, smaller O2 deficit, and
reduced O2 slow component
from 3 to 6 min of exercise) for work rates above VT. When the two
manipulations were combined, there was further speeding of the
O2 response, indicating that the two stimuli may work independently to increase
O2 transport at the onset of
exercise. For work rates below VT, there was no significant effect of
hyperoxia on the time course of increase in
O2 at the onset of exercise.
The postexercise rate of decrease in
O2 was faster after the
below-VT exercise than after the above-VT exercise, yet there was no
difference between normoxia and hyperoxia.
Methodological Considerations
There are two components of the design of this study that merit further consideration before physiological interpretation of the data can be discussed. The first is the selection of the work rates for the study, and the second is the model used to fit the experimental data. We selected work rates that were constant across the normoxia or hyperoxia treatments even though the peak work rate andO2 are often found to be
increased by up to 10% by hyperoxia (25). It was felt that this would
not affect the kinetics responses because in each of the below- and
above-VT cases, the work rates were clearly within the domains
required. Furthermore, it has been observed that kinetics of
O2 are altered across a range
of work rates, being slower for above-VT work rates, as we found;
except for minor differences in percentage of peak work rate, there is
little effect on the time course of
O2 at the onset of exercise
(4, 28). In this study, our focus was on the effects of hyperoxia
and/or prior exercise on the
O2 response to a fixed work
rate.
Fitting of the O2 response at
the onset and end of exercise has been done by a variety of methods,
primarily on the basis of the observation of an exponential, or
near-exponential, change (18). At the below-VT work rate, we used a
two-component exponential, in which the first component accounted for
the rapid increase in
O2 at the onset or
decrease in O2 at the end of
exercise, because the return of venous blood is altered with the change in work rate. The second component represents the major change to the
new steady-state value and is described by a single time constant with
time delay (15). The major difference between studies has been in the
description of the O2
response to work rates above VT. We used a three-component exponential
model.
The first component of the above-VT model was identical to that in the
below-VT exercise. The second and third components represent a
relatively rapid and a more slowly developing component, respectively.
This interpretation is consistent with other research (28) and with our
observations from the O2
slow-component analysis (Table 3). In accord with Linnarsson (18), we
had both phases 2 and
3 start at the same time point. In
contrast, some researchers have allowed the time delay of the third
phase to vary, demonstrating that this component of the response
started 90-120 s after the onset of the exercise (2, 22). Curve
fitting of physiological responses can incorporate physiological
correlates, or it can simply attempt to minimize the error of the
distribution of the data points about the line of best fit. In this
case, it is not possible to identify specifically the physiological
mechanism responsible for the slow component of the
O2 response (28). Therefore,
we justify our selection of the model with a common time delay for
phases 2 and
3 by the absence of a statistically significant improvement in fit between our model and that with an extra
parameter for a third time delay. Whichever model is selected, the
physiological interpretation as presented below is not altered.
Effect of Hyperoxia
In the steady-state phases of the present experiments, there were only minor differences in measuredO2 between normoxia and hyperoxia. In the baseline period before step
1 of part 2 of the
study (Table 2), there was a small but significantly greater O2 with hyperoxia compared
with normoxia. Later within this same protocol, during the baseline
period before step 2,
O2 was also higher
with hyperoxia. Some previous research (25) has found an increase in
fat utilization with hyperoxic breathing, although this was not
suggested in the present study because the respiratory exchange ratio
was unaltered. The elevated
O2 could have also been a
consequence of inadequate time for equilibration to hyperoxia. Careful
calibration of the equipment in this study was performed. We cannot,
however, totally disregard the possibility that small errors in our
measurements might have caused this statistical finding.
The faster O2 on-transient
MRT and the smaller O2 deficit and
O2 slow component observed
for the above-VT steps in hyperoxia, compared with normoxia, are in
agreement with previous studies using Douglas bags and measurements of
O2 deficit to estimate O2 kinetics (19, 23). The
faster O2 responses at the
same absolute work rate are consistent with the pattern to be expected when the relative work rate is reduced by hyperoxia. Closer examination of the parameter estimates for the exponential curve fitting (Tables 1
and 2) shows that the increase during phase
3 was less in the hyperoxia tests than in normoxia.
Therefore, to attain similar O2 values at the end of
exercise, a greater slow increase (see G3 and
3 in Tables 1 and 2) occurred
in normoxia. This observation is also supported by a greater slow
component between minutes 3 and
6 during normoxia compared with
hyperoxia (Table 3). This observation supports the findings of Paterson
and Whipp (22).
Hyperoxic gas breathing was used in this study in an attempt to
increase the transport of O2 to
working muscle and therefore to determine whether
O2 transport is a limiting factor
in the transient O2 response
after a step increase in work rate above and below VT. Others have
shown that hyperoxia does not accelerate the kinetics of
O2 for step transients below
VT (11, 18). The mechanism responsible for this could be that adequate
O2 is already being delivered at
the onset of this light exercise, and hence
O2 delivery would not be limiting,
or that hyperoxia does not, in fact, provide more
O2 at the onset of exercise.
During steady-state exercise, blood flow to working muscles is reduced (26) or unaltered (16) with hyperoxic gas breathing. It is not known
whether hyperoxic breathing resulted in decreased blood flow to the
exercising muscle in this study. A reduction in blood flow, to counter
the increase in blood O2 content,
would serve to maintain the O2
delivery to the working muscle at approximately the same level as in
normoxia. Another unknown is the mean capillary PO2. Knight et al. (16) identified an
apparent nonlinear relationship between their estimated value for mean
capillary PO2 and peak leg muscle
O2 with hyperoxia. Among
other mechanisms that might account for this, Knight et al. included heterogeneity of flow distribution to the exercising muscle because of
hyperoxia-induced vasoconstriction. The observation that on-transient O2 kinetics were accelerated
with hyperoxic gas breathing for step transitions to levels above VT
indicates that the rate of O2
transport was probably accelerated by hyperoxia during these step
transitions.
Effect of Prior Exercise
Prior high-intensity exercise was also used in this study as a means of attempting to increase the O2 transport to the working muscle. A prior bout of high-intensity exercise (>VT) accelerated theO2 on-transient kinetics in
normoxia and in hyperoxia, as evidenced by a smaller MRT. These
findings are in agreement with previous research using a similar work
rate protocol (6, 7), which found that, for exercise in normoxia at
work rates above VT, prior exercise accelerated the
O2 kinetics of a subsequent exercise bout.
Metabolic acidosis as a result of the prior exercise bout has been
suggested as a possible explanation for the faster
O2 kinetics of the second
exercise bout (6, 7). These previous reports postulated that the prior
exercise elevated the concentration of blood lactate and decreased the
pH in the working muscle, thereby promoting changes in osmolality and
acidity that result in vasodilation in the working muscles. Other
vasoactive substances might also still be elevated after 6 min of
recovery. An additional factor that could promote
O2 delivery to the working muscle
would be a rightward shift of the
O2-hemoglobin dissociation curve
resulting from the accumulation of
H+ and increased
CO2 (5). These results support the
theory that O2 transport is
a limiting factor to high-intensity-exercise
O2 on-transient kinetics,
although changes in the intracellular metabolic environment that might
promote a more rapid increase in oxidative metabolism have not been
investigated.
The time course of increase in oxidative phosphorylation at the onset
of exercise has been estimated by a range of techniques, yet it is
uncertain over what range of work rates the time course of the adaptive
process remains constant (14, 20, 28). With cycling exercise, there are
definitely slower kinetics for
O2 measured at the
mouth at high work rates (28). Results from recent studies with nuclear
magnetic resonance spectroscopy indicate both slower changes (20) and
no differences in the rates of change in phosphocreatine (30) at higher
work rates. Measurement of muscle
O2 as the product of blood
flow and arteriovenous O2 content
difference also showed a slower response at higher work rates (14).
None of the experimental conditions resulted in high-step kinetics that
were as fast as the low-step kinetics (Tables 1 and 2). This indicates
either that O2 transport was not
the only limiting factor for the high steps or that the experimental conditions did not completely alleviate the
O2 transport deficit.
O2 Deficit and O2 Debt
The literature contains reports of the magnitude of O2 debt exceeding, equaling, or being less than the magnitude of the O2 deficit. Part of this discrepancy arises from the differences in exercise work rates studied, and part arises from differences in baseline state after the exercise. In an earlier study (1) in which debt exceeded deficit, the intensity of exercise studied was high, and the baseline after exercise was considered to be basal rest. In many studies in which lighter intensities of exercise (<VT) were studied with either rest or light exercise baselines, O2 deficit and O2 debt were normally about equal (9, 27, 31). The present results for below VT in both normoxia and hyperoxia, in which the time course of recovery (MRT) and the magnitude of change are almost the same as those at the onset of exercise, are in agreement with this. When the O2 deficit is increased, by-adrenergic-receptor blockade (9) or by
higher intensity exercise, as shown in the present study by the slower
MRT, the O2 debt can be found to
be smaller than O2 deficit when
the recovery baseline is mild exercise. The most probable explanation
for this is that lactate produced during the on-transition to
compensate for the inadequate O2
delivery is metabolized as a substrate during exercise and in the mild
exercise recovery (3). That is, it is not necessary to repay this
component of the debt (11).
Wilson et al. (29) have shown that the ATP-to-ADP ratio can be altered
at a given steady-state O2 as
a function of intracellular PO2. This
could account for the different concentrations of lactate observed in
hypoxia vs. normoxia or hyperoxia (19). Recently, Hughson et al. (14)
speculated that altered intracellular PO2 at the onset of exercise might
modify the O2 response during
the non-steady-state transition. The intracellular
PO2 at this time would be a function
of O2 delivery (arterial
PO2 and blood flow) and
O2 utilization. The present
results are consistent with this hypothesis for work rates >VT.
The O2 deficit and
O2 slow-component values were
smaller than the corresponding measurements of Gerbino et al. (7).
These differences are likely to be because of the higher work rates used in the high-step transitions of the previous study. Although in
both studies subjects were assigned a high work rate that was approximately halfway between VT and peak
O2, the measured values in
the previous study (92% peak
O2) were considerably higher than in the present study (79 and 82% of peak
O2). These differences in
protocol may also explain the observation that prior high-intensity exercise did not influence the magnitude of the
O2 deficit in the present study,
in contrast to the findings of Gerbino et al. (7). The major
contribution to O2 deficit occurs
before 3min. However, we measured
O2 deficit over the full 10 min of
exercise. The lack of effect of prior exercise could have resulted from small differences in the early response or in the apparent plateau value with the longer exercise duration in this
study.
Conclusions
The fasterO2 kinetics
observed for the on-transient during step changes above VT with
hyperoxia, and to a lesser degree with prior exercise, provide evidence
that the supply of O2 contributes to the control of tissue O2
for this relatively high exercise intensity. The observation of no
change in O2 kinetics for
steps below VT may indicate that
O2 transport is not a limiting
factor in this light-exercise-intensity condition. However, in the
absence of definitive data concerning
O2 transport in the critical
adaptive phase, it is not possible to rule out the alternative
hypothesis. Off-transient kinetics above VT did not change
significantly because of prior exercise or hyperoxic gas breathing,
indicating that regulatory mechanisms for
O2 supply and utilization may be
different in on- and off-transients above VT.
ACKNOWLEDGEMENTS
This research was supported by the Natural Sciences and Engineering Research Council (NSERC) of Canada. M. MacDonald is an NSERC Graduate Scholarship recipient.
FOOTNOTES
Address for reprint requests: R. L. Hughson, Dept. of Kinesiology, Univ. of Waterloo, Waterloo, Ontario, Canada N2L 3G1 (E-mail: hughson{at}cgsa.uwaterloo.ca).
Received 24 September 1996; accepted in final form 11 June 1997.
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H B Rossiter, S A Ward, J M Kowalchuk, F A Howe, J R Griffiths, and B J Whipp Dynamic asymmetry of phosphocreatine concentration and O2 uptake between the on- and off-transients of moderate- and high-intensity exercise in humans J. Physiol., June 15, 2002; 541(3): 991 - 1002. [Abstract] [Full Text] [PDF]
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Y. Fukuba, N. Hayashi, S. Koga, and T. Yoshida VO2 kinetics in heavy exercise is not altered by prior exercise with a different muscle group J Appl Physiol, June 1, 2002; 92(6): 2467 - 2474. [Abstract] [Full Text] [PDF]
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B. J Behnke, C. A Kindig, T. I Musch, W. L Sexton, and D. C Poole Effects of prior contractions on muscle microvascular oxygen pressure at onset of subsequent contractions J. Physiol., March 15, 2002; 539(3): 927 - 934. [Abstract] [Full Text] [PDF]
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B. W. Scheuermann, C. Bell, D. H. Paterson, T. J. Barstow, and J. M. Kowalchuk Oxygen uptake kinetics for moderate exercise are speeded in older humans by prior heavy exercise J Appl Physiol, February 1, 2002; 92(2): 609 - 616. [Abstract] [Full Text] [PDF]
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S. P Campbell-O'Sullivan, D. Constantin-Teodosiu, N. Peirce, and P. L Greenhaff Low intensity exercise in humans accelerates mitochondrial ATP production and pulmonary oxygen kinetics during subsequent more intense exercise J. Physiol., February 1, 2002; 538(3): 931 - 939. [Abstract] [Full Text] [PDF]
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M. K. Evans, I. Savasi, G. J. F. Heigenhauser, and L. L. Spriet Effects of acetate infusion and hyperoxia on muscle substrate phosphorylation after onset of moderate exercise Am J Physiol Endocrinol Metab, December 1, 2001; 281(6): E1144 - E1150. [Abstract] [Full Text] [PDF]
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H B Rossiter, S A Ward, J M Kowalchuk, F A Howe, J R Griffiths, and B J Whipp Effects of prior exercise on oxygen uptake and phosphocreatine kinetics during high-intensity knee-extension exercise in humans J. Physiol., November 15, 2001; 537(1): 291 - 303. [Abstract] [Full Text] [PDF]
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S. Perrey, A. Betik, R. Candau, J. D. Rouillon, and R. L. Hughson Comparison of oxygen uptake kinetics during concentric and eccentric cycle exercise J Appl Physiol, November 1, 2001; 91(5): 2135 - 2142. [Abstract] [Full Text] [PDF]
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P. Krustrup, J. Gonzalez-Alonso, B. Quistorff, and J. Bangsbo Muscle heat production and anaerobic energy turnover during repeated intense dynamic exercise in humans J. Physiol., November 1, 2001; 536(3): 947 - 956. [Abstract] [Full Text] [PDF]
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C. A. Kindig, P. McDonough, H. H. Erickson, and D. C. Poole Effect of L-NAME on oxygen uptake kinetics during heavy-intensity exercise in the horse J Appl Physiol, August 1, 2001; 91(2): 891 - 896. [Abstract] [Full Text] [PDF]
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R. L. Hughson, M. J. MacDonald, M. E. Tschakovsky, A. M. Jones, M. Burnley, H. Carter, and J. H. Doust Interpreting {V}O2 Kinetics in Heavy Exercise J Appl Physiol, July 1, 2001; 91(1): 530 - 532. [Full Text] [PDF]
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F Ozyener, H B Rossiter, S A Ward, and B J Whipp Influence of exercise intensity on the on- and off-transient kinetics of pulmonary oxygen uptake in humans J. Physiol., June 15, 2001; 533(3): 891 - 902. [Abstract] [Full Text] [PDF]
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S. E. Bearden and R. J. Moffatt {V}O2 and heart rate kinetics in cycling: transitions from an elevated baseline J Appl Physiol, June 1, 2001; 90(6): 2081 - 2087. [Abstract] [Full Text] [PDF]
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M. C. Hogan Fall in intracellular PO2 at the onset of contractions in Xenopus single skeletal muscle fibers J Appl Physiol, May 1, 2001; 90(5): 1871 - 1876. [Abstract] [Full Text] [PDF]
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 P. Cerretelli and B. Grassi Gas Exchange, MRS and NIRS Assessment of Metabolic Transients in Skeletal Muscle Integr. Comp. Biol., April 1, 2001; 41(2): 229 - 246. [Abstract] [Full Text] [PDF]
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B. W Scheuermann, B. D Hoelting, M L. Noble, and T. J Barstow The slow component of O2 uptake is not accompanied by changes in muscle EMG during repeated bouts of heavy exercise in humans J. Physiol., February 15, 2001; 531(1): 245 - 256. [Abstract] [Full Text] [PDF]
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S. Koga, T. J. Barstow, T. Shiojiri, T. Takaishi, Y. Fukuba, N. Kondo, M. Shibasaki, and D. C. Poole Effect of muscle mass on {V}O2 kinetics at the onset of work J Appl Physiol, February 1, 2001; 90(2): 461 - 468. [Abstract] [Full Text] [PDF]
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M. J. MacDonald, H. L. Naylor, M. E. Tschakovsky, and R. L. Hughson Peripheral circulatory factors limit rate of increase in muscle O2 uptake at onset of heavy exercise J Appl Physiol, January 1, 2001; 90(1): 83 - 89. [Abstract] [Full Text] [PDF]
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B. Grassi, M. C. Hogan, K. M. Kelley, W. G. Aschenbach, J. J. Hamann, R. K. Evans, R. E. Patillo, and L. B. Gladden Role of convective O2 delivery in determining VO2 on-kinetics in canine muscle contracting at peak VO2 J Appl Physiol, October 1, 2000; 89(4): 1293 - 1301. [Abstract] [Full Text] [PDF]
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M. Burnley, A. M. Jones, H. Carter, and J. H. Doust Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise J Appl Physiol, October 1, 2000; 89(4): 1387 - 1396. [Abstract] [Full Text] [PDF]
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R. L. Hughson, D. D. O'Leary, A. C. Betik, and H. Hebestreit Kinetics of oxygen uptake at the onset of exercise near or above peak oxygen uptake J Appl Physiol, May 1, 2000; 88(5): 1812 - 1819. [Abstract] [Full Text] [PDF]
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S. E. Bearden and R. J. Moffatt VO2 kinetics and the O2 deficit in heavy exercise J Appl Physiol, April 1, 2000; 88(4): 1407 - 1412. [Abstract] [Full Text] [PDF]
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R. A. Howlett, G. J. F. Heigenhauser, and L. L. Spriet Skeletal muscle metabolism during high-intensity sprint exercise is unaffected by dichloroacetate or acetate infusion J Appl Physiol, November 1, 1999; 87(5): 1747 - 1751. [Abstract] [Full Text] [PDF]
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M. L. Parolin, A. Chesley, M. P. Matsos, L. L. Spriet, N. L. Jones, and G. J. F. Heigenhauser Regulation of skeletal muscle glycogen phosphorylase and PDH during maximal intermittent exercise Am J Physiol Endocrinol Metab, November 1, 1999; 277(5): E890 - E900. [Abstract] [Full Text] [PDF]
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S. Koga, T. Shiojiri, M. Shibasaki, N. Kondo, Y. Fukuba, and T. J. Barstow Kinetics of oxygen uptake during supine and upright heavy exercise J Appl Physiol, July 1, 1999; 87(1): 253 - 260. [Abstract] [Full Text] [PDF]
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M. E. Tschakovsky and R. L. Hughson Interaction of factors determining oxygen uptake at the onset of exercise J Appl Physiol, April 1, 1999; 86(4): 1101 - 1113. [Abstract] [Full Text] [PDF]
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B. Grassi, L. B. Gladden, C. M. Stary, P. D. Wagner, and M. C. Hogan Peripheral O2 diffusion does not affect VO2 on-kinetics in isolated in situ canine muscle J Appl Physiol, October 1, 1998; 85(4): 1404 - 1412. [Abstract] [Full Text] [PDF]
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L. J. Haseler, R. S. Richardson, J. S. Videen, and M. C. Hogan Phosphocreatine hydrolysis during submaximal exercise: the effect of FIO2 J Appl Physiol, October 1, 1998; 85(4): 1457 - 1463. [Abstract] [Full Text] [PDF]
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B. J. Behnke, C. A. Kindig, T. I. Musch, W. L. Sexton, and D. C. Poole Effects of prior contractions on muscle microvascular oxygen pressure at onset of subsequent contractions J. Physiol., January 25, 2002; (2002) 200101316. [Abstract] [PDF]
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