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1 University of Surrey Roehampton, London SW15 3SN; 2 Exercise Physiology Group, Manchester Metropolitan University, Alsager ST7 2HL, United Kingdom; 3 Department of Kinesiology, Kansas State University, Manhattan, Kansas 66506-0302; and 4 Chelsea School Research Centre, University of Brighton, Eastbourne BN20 7SP, United Kingdom
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The purpose of this study was to examine the effect of
endurance training on oxygen uptake (
O2)
kinetics during moderate [below the lactate threshold (LT)] and heavy
(above LT) treadmill running. Twenty-three healthy physical education
students undertook 6 wk of endurance training that involved continuous
and interval running training 3-5 days per week for 20-30 min
per session. Before and after the training program, the subjects
performed an incremental treadmill test to exhaustion for determination of the LT and the O2 max and a series
of 6-min square-wave transitions from rest to running speeds calculated
to require 80% of the LT and 50% of the difference between LT and
maximal O2. The training program caused
small (3-4%) but significant increases in LT and maximal
O2 (P < 0.05). The
O2 kinetics for moderate exercise were
not significantly affected by training. For heavy exercise, the time
constant and amplitude of the fast component were not significantly
affected by training, but the amplitude of the
O2 slow component was significantly
reduced from 321 ± 32 to 217 ± 23 ml/min (P < 0.05). The reduction in the slow component was not significantly
correlated to the reduction in blood lactate concentration
(r = 0.39). Although the reduction in the slow
component was significantly related to the reduction in minute
ventilation (r = 0.46; P < 0.05), it
was calculated that only 9-14% of the slow component could be
attributed to the change in minute ventilation. We conclude that the
O2 slow component during treadmill
running can be attenuated with a short-term program of endurance
running training.
oxygen uptake slow component; lactate threshold; gas exchange; modeling
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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CARDIORESPIRATORY
ADAPTATIONS to a period of endurance training have been well
documented. Changes in maximal oxygen uptake (O2;
O2 max; Refs. 17, 43), exercise economy
(9, 27), and the blood lactate response to exercise
(16, 47, 51) have all been previously reported. The
response characteristics of pulmonary
O2 to step changes in work rate have
been comprehensively described for cycle exercise (4, 7)
and may be altered by a period of endurance training (3, 13,
57).
For moderate constant-load exercise below the lactate threshold (LT),
after the initial cardiodynamic phase,
O2 rises monoexponentially until a
steady state is reached, usually within 2-3 min in healthy subjects. Heavy constant-load exercise above the LT, however, results
in O2 kinetics that are considerably
more complex. For constant-load exercise above the LT,
O2 may reach a delayed steady state that
is higher than the O2 requirement
estimated by extrapolating the relationship between
O2 and work rate for moderate exercise
(5, 55) or may rise continuously until O2 max is attained and/or exercise is
terminated (39). The physiological mechanism(s)
responsible for this slow-component rise in
O2 with time during supra-LT exercise
remains to be determined but appears to reside in the exercising muscle
(38) and to be related to the temporal profile of changes
in blood lactate (39, 55).
Although few studies have examined the
O2 slow component during treadmill
running, it appears that its magnitude is lower in running than in
cycling (10, 31). However, in the previous studies that
have assessed O2 kinetics in running,
the magnitude of the slow component has been determined rather
simplistically by calculating the increase in
O2 between 3 and 6 min of exercise (28, 31) or between 3 min of exercise and the time at
which exhaustion was reached (8, 10). It has been shown
that the O2 response to a square-wave
heavy exercise challenge is better described by using three exponential
terms, with the three terms describing the cardiodynamic phase (phase
I), the fast component (phase II), and the
O2 slow component (phase III),
respectively (7).
The O2 slow component has been suggested
to be an important determinant of exercise tolerance in both patient
populations (54) and athletic groups (18).
After a period of endurance training, the steady-state
O2 during moderate-intensity,
constant-load cycle ergometry is unchanged (16, 21, 22),
although the phase II kinetics may be speeded (21, 22,
35). In contrast, after training, the
O2 slow component during heavy cycle
exercise is attenuated (3, 13, 40, 57). Recent studies
(10, 31) have suggested that differences in muscle
contraction modes between running and cycling exercise may result in
differences in O2 kinetics. It is not
known whether endurance running training can affect
O2 kinetics in running.
Therefore, the purpose of the present study was to comprehensively
characterize the O2 response to
constant-speed moderate- and heavy-intensity treadmill running and to
test the hypothesis that a period of endurance running training will
alter the O2 kinetics, in particular the
amplitude of the slow component.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects. Twenty-three subjects (14 men; age 22 ± 3 yr, height 1.73 ± 0.06 m, body mass 70.3 ± 9.1 kg; means ± SD) volunteered to take part in this study. The subjects were young, healthy physical education students who were recreationally active in sport but not specifically trained for endurance running. Subjects were fully familiar with the laboratory environment and were habituated to treadmill running before the study commenced. The subjects gave written, informed consent after the experimental procedures and the associated risks and benefits of participation were explained. The procedures used in this study were approved by the Chelsea School Ethics Committee, University of Brighton. The subjects were all fully familiar with laboratory exercise testing procedures, having previously participated in other similar studies.
Subjects were instructed to arrive at the laboratory in a rested and fully hydrated state, at least 3 h postprandial, and to avoid strenuous exercise in the 48 h preceding a test session. For each subject, tests took place at the same time of day (±2 h) to minimize the effects of diurnal biological variation on the results.Procedures.
All exercise tests were performed on a motorized treadmill (Woodway,
Cardiokinetics, Salford, UK), with the grade set at 1% (29). During the exercise tests, pulmonary gas exchange
was determined breath by breath. Subjects breathed through a low-dead space (90 ml), low-resistance (0.65 cmH2O · l
1 · s1
at 8 l/s) mouthpiece and turbine assembly. Gases were continuously drawn from the mouthpiece through a 2-m capillary line of small bore
(0.5 mm) at a rate of 60 ml/min and were analyzed for O2, CO2, and N2 concentrations by a quadrupole mass
spectrometer (CaSE QP9000, Gillingham, Kent, UK), which was calibrated
before each test by use of gases of known concentration. Expiratory
volumes were determined by using a turbine volume transducer (Interface Associates). The volume and concentration signals were integrated by
computer, after analog-to-digital conversion, with account taken of the
gas transit delay through the capillary line. Respiratory gas exchange
variables [O2, carbon dioxide
production, and minute ventilation (E)] were
calculated and displayed for every breath. The
O2 values were not treated with an
alveolar correction algorithm and therefore represent values measured
at the mouth. Heart rate was recorded telemetrically throughout the
exercise tests (Polar Electro Oy, Kempele, Finland).
O2 max. The
initial treadmill speed was between 6.0 and 7.0 km/h for the women and
between 8.0 and 9.0 km/h for the men. The subjects completed 6-8
submaximal stages of 4-min duration, with running speed increased by
1.0 km/h between stages (30). At the end of each stage,
the subjects grasped the handrails and moved their feet astride the
treadmill belt. A fingertip capillary blood sample (~25 µl) was
collected into a capillary tube for subsequent analysis of blood
lactate concentration ([lactate]) using an automated lactate analyzer (YSI 2300, Yellow Springs, OH). The subjects recommenced running within
10-15 s. When heart rate exceeded 90% of the known or
age-predicted maximum heart rate, the running speed was increased by
1.0 km/h per minute until the subject reached volitional exhaustion.
Plots of blood lactate against running speed and
O2 were provided to two independent
reviewers, who determined the LT as the first sustained increase in
blood lactate above baseline levels. The breath-by-breath gas exchange
data collected during these tests were averaged over consecutive 30-s
periods. The O2 max was defined as the
average O2 attained in the last 30 s of the tests. Attainment of O2 max
was confirmed by a high incidence of a plateau phenomenon in
O2 (96%), respiratory exchange ratio values above 1.10 (78%), and heart rates within 5 beats/min of age-predicted maximum (92%). In all subjects, at least two of the
three criteria were met. The running speed at
O2 max was estimated by extrapolation
of the sub-LT relationship between O2
and running speed. Individual regression equations were calculated using the O2-running speed relationship
for all exercise stages below the LT. The
O2 max was then entered into the
equation given, providing an estimate of the running speed at
O2 max (v-O2 max, where v is
velocity). The individual regression equations were then used
to calculate the running speeds corresponding to 80% of the
O2 at LT and 50% of the difference
between the O2 at LT and
O2 max (50% 
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Subsequently, subjects performed a series of square-wave transitions at
the two exercise intensities on separate days. The subjects completed
three transitions to the moderate-intensity running speed or two
transitions to the heavy-intensity running speed. The days on which the
moderate- and heavy-intensity exercise bouts were performed were
presented to the subjects in random order. The exercise protocol
started with 2 min of standing rest, with the subject's feet astride
the moving treadmill belt and hands holding the guard rails. Subjects
commenced running by supporting their body mass with their hands on the
guard rails until leg speed matched treadmill belt speed, after which
they let go of the handrails and commenced running. This transition
from rest to exercise took 3-5 s. The exercise continued for 6 min. At the end of the 6-min period, the subjects grasped the guard
rails and moved their feet astride the treadmill belt. Fingertip
capillary blood samples were taken immediately before and immediately
after exercise. The difference between the end-exercise lactate and the
resting lactate was expressed as a delta value ([lactate]). For
the moderate-intensity running speed condition, the subjects completed
three identical transitions on the same day, with at least 30 min of
rest between the trials. For the heavy-intensity running speed
condition, the subjects completed two identical transitions on the same
day, with at least 60 min of rest between the trials. Before the second
transition, a capillary blood sample was taken to ensure that lactate
concentration had returned to resting levels. These procedures were
replicated at the end of the training period. In addition, a randomly
chosen subgroup of 10 subjects (5 men) also performed transitions to
the recalculated 50% running speeds derived from the posttraining
incremental test.
Training.
After completion of the initial testing battery, the subjects began a
6-wk program of endurance training. Table
1 describes the training undertaken and
shows the increases in training duration and frequency over the 6-wk
period. For the continuous sessions, the LT was used to regulate the
training intensity because this should provide a high-quality aerobic
training stimulus without the accumulation of lactate that might
compromise training duration. It has been shown that this type of
training significantly improves the LT (33). Although the
average intensity of the continuous and interval training sessions was
similar, the interval efforts were designed to be appreciably above the
LT to invoke lactate accumulation. In a previous study, this training
program significantly increased the running speed at LT, the running
speed at the maximal lactate steady state, and the
O2 max in 16 subjects of similar
initial fitness status to the subjects of the present study
(11).
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O2 max or ~67%
v-O2 max) for the continuous session
and 11.9 ± 2.2 km/h (76.9 ± 4.3%
O2 max, or ~77%
v-O2 max) for the interval session.
Heart rate data from individual training sessions were checked on a
weekly basis to ensure that subjects exercised at the prescribed heart
rates. All subjects completed training diaries listing all physical
activity performed over the 6-wk study period so that training
compliance could be ascertained. In addition, subjects recorded their
diet before the pretraining laboratory visits and replicated this diet
for their return visits to the laboratory at the end of the training period.
Data analysis. For each exercise transition, the breath-by-breath data were interpolated to give second-by-second values and were time aligned to the start of exercise. The transitions for each intensity were then averaged to enhance the underlying response characteristics.
Nonlinear regression techniques were used to fit the time course of theO2 response after the onset of exercise
with an exponential function. An iterative process was used to minimize the sum of squared error. The empirical model consisted of two (moderate exercise) or three (heavy exercise) exponential terms, each
representing one phase of the response (see Ref. 6). The first
exponential term started with the onset of exercise (time = 0),
whereas the other terms began after independent time
delays
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(1) |
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O2 (t) is the
O2 at a given time;
O2 (b) is the resting baseline
value; A0, A1, and
A2 are the asymptotic amplitudes for the
exponential terms; 
0, 1, and
2 are the time constants; and TD1 and
TD2 are the time delays. The phase 1 term was terminated at the start of phase 2 (i.e., at
TD1) and assigned the value for that time
(A0')
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O2 at the end of phase
1 (A0') and the amplitude of
phase 2 (A1) were summed to calculate
the amplitude of phase 2 (A1').
The amplitude of the slow component was determined as the increase in
O2 from TD2 to the end of
exercise (defined A2'), rather than from the
asymptotic value (A2), which lies beyond physiological limits (6). The slow component was also
described by using the difference in O2
between 3 and 6 min of exercise (using the average
O2 values between 2.75 and 3.00 and
between 5.75 and 6.00 min). The gain of the phase II exponential
response (A1'/running speed expressed
relative to body mass) for the two exercise intensities was also calculated.
Statistical analysis.
Paired t-tests were used to determine the significance of
any differences in the measured variables before vs. after training. Statistical significance was set at the 5% level. A repeated-measures ANOVA (Wilks lambda) was used to identify differences in the subgroup of subjects. Pearson product-moment correlation coefficients were used
to examine the significance of relationships between the slow component
and changes in blood lactate and E. The results are
presented as means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Table 2 shows the effect of training
on the physiological variables that were measured during the
incremental treadmill test. There were significant increases in
O2 max (t22 = 
4.22, P <0.001), the O2
at the LT (t22 = 3.78, P
<0.001), and a significant reduction in maximal heart rate
(t22 = 3.36, P = 0.03).
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For moderate exercise, which caused no increase in blood
lactate above baseline, the kinetics of the
O2 response were fit with two
exponential terms. The O2 kinetics for
moderate exercise, including the amplitudes, time constants, and
time delays, were unchanged with training (Table
3). For heavy exercise, which caused a
significant increase in blood lactate above baseline, the kinetics of
the O2 response were fit with three
exponential terms. Endurance training caused a significant reduction in
the blood lactate accumulation (t22 = 3.11, P = 0.005) but did not affect the time delays or the
time constants of the exponential model or the amplitude of phase II
(Table 3). It was of interest that the time constant for phase II was
unchanged with training (t22 = 0.49, P = 0.63). However, it should be noted that our
subjects were relatively fit at the time of recruitment to the study.
When the data of six subjects (2 men, 4 women) who had the lowest
fitness on recruitment to the study were examined
(O2 max of 40.2 ± 1.2 ml · kg1 · min1),
1 for heavy exercise was reduced from 31.5 ± 1.0 to 19.5 ± 1.5 s by the training period
(t5 = 2.92, P = 0.033).
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The amplitude of the O2 slow component
was significantly reduced with training both in absolute terms (Fig.
1, t22 = 3.53, P = 0.002) and when expressed as a proportion of
the total O2 response to the exercise
(Table 3, t22 = 3.57, P = 0.002). All subjects demonstrated an attenuated slow component with
training, although the magnitude of the reduction varied between
individuals (range 8-308 ml/min). This reduction in the slow
component resulted in a significantly reduced end-exercise
O2 (t22 = 4.90, P = 0.004). Neither the increase in
O2 max nor the increase in LT was
correlated with the decrease in the amplitude of
O2 slow component (r = 0.03 and r = 0.04, respectively).
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There was no significant improvement in running economy with training
in the subjects. The average steady-state
O2 at 80% LT (calculated from the three
transitions of 6-min duration that our subjects performed at this
exercise intensity) was not significantly different before and after
training. Furthermore, there was no consistent or significant reduction
in O2 during the submaximal stages of
the incremental test.
In the 10 subjects who performed a bout of heavy exercise at 50%
recalculated after training, despite increases in the running speed
utilized and the amplitude of phase II (t9 = 2.7, P = 0.02), the slow component
amplitude was similar compared with the pretraining 50% condition
(Table 4, t9 = 1.37, P = 0.20). Data from a typical subject can be seen in Fig. 2.
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Before training, there was a strong correlation between the
O2 slow component and the increase in
blood lactate above baseline (r = 0.69; P
<0.001). However, after training, the strength of this association
diminished (r = 0.45; P = 0.03). The
relationship between the reduction in blood lactate accumulation and
the reduction in the slow component with training was not significant
(r = 0.39, P = 0.65). Similarly, there
was a strong relationship between the O2
slow component and the increase in E over the same time frame before training (r = 0.70; P < 0.01), which diminished after training (r = 0.20;
P = 0.86). There was a significant relationship between
the reduction in E and the reduction in the slow
component with training (r = 0.46; P = 0.03).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The principal finding of this study was that a 6-wk
period of endurance training caused an attenuation of the slow
component in running of ~35%, i.e., from 321 to 217 ml/min, on
average. This is of interest in that our subjects were young, healthy
subjects who were actively engaged in sports and were of a relatively
high fitness at entry into the study. These results suggest that the O2 slow component can be reduced
by a short period of endurance training despite relatively small
changes in traditional measures of aerobic fitness such as
O2 max and LT.
The endurance training program that our subjects undertook was
successful in causing a significant improvement in the
O2 at LT (~4%) and
O2 max (~3%), although these
improvements were less than those reported in other training studies
(16, 23, 53). Our subjects recorded their training in
diaries over the course of the study and also used heart rate monitors
to guide their training. From the heart rate records, subjects adhered to their prescribed training intensities, and, from diary records, the
training compliance of the subjects was 87 ± 1.7%. The mean pretraining O2 max of ~55
ml · kg1 · min1 (in a
mixed-gender group) highlights the fact that our subjects were already
of good aerobic fitness on recruitment to the study. The rather small
increases in O2 max should therefore not be considered surprising.
In our study, there were no significant relationships between
1 and O2 max for
moderate or heavy exercise either before or after training. Our results
differ from those of Powers et al. (41), who reported
that, in subjects of similar training status to subjects of the present
study, O2 kinetics were faster in
trained subjects with the higher O2 max
values. Our results also contrast with the study of Chilibeck et al.
(14), which showed significantly faster
O2 kinetics in subjects with higher
O2 max values in 16 young subjects.
However, their subjects were of generally lower aerobic fitness and
showed greater heterogeneity in O2 max
(25-59
ml · kg1 · min1) than our subjects.
The training program had no effect on the kinetics of the
O2 response to moderate exercise or on
phase II during heavy exercise. These results are in contrast
to other studies that have shown a speeding of
O2 kinetics with training for exercise
intensities up to ~70% O2 max
(21, 22, 58). The relatively high aerobic fitness of our
subjects at the start of the training study may provide an explanation
for this. Indeed, in the six subjects with the lowest initial
O2 max values (~40
ml · kg1 · min1), we found
that 1 was significantly decreased (i.e., the adjustment of O2 was speeded) by training for heavy
exercise (by 12 s) but not for moderate exercise. The faster
kinetics of phase II in our low-fit subjects may be related to improved
oxygen delivery to muscle or to increases in muscle mitochondrial
density with training, which would improve the sensitivity of
respiratory control (20).
Another explanation for the apparent discrepancy between the present
study and previous literature is that earlier studies (21, 22,
41) did not attempt to partition out any effect of the possible
development of the O2 slow component on
the total O2 response but simply
calculated the half-time of the response to the steady state. It is not
clear in these studies whether the subjects were exercising above or
below their LT. When the mean response time is considered in the
present study, it can be seen that, whereas the overall
O2 kinetic response for moderate
exercise was unchanged at ~22 s, the mean response time was
significantly decreased for heavy exercise (from ~58 to 47 s;
t22 = 4.2, P <0.001; see Table
3). However, the latter results from the reduction of the slow
component and not from any speeding of phase II.
Our results that the time constant of phase II does not differ
significantly above and below the LT (Table 3) supports the findings of
some (5, 7, 12), but not all (34), previous studies using cycle exercise. To consider whether the lack of difference in 1 between moderate and heavy exercise
might be a consequence of the fitness of the subjects, we looked at the unfit subgroup. Interestingly, this subgroup had a considerably slower
1 in heavy exercise (~31 s) than in moderate exercise (~17 s) pretraining. The period of endurance training speeded the
phase II response in heavy exercise (~20 s) but not in moderate exercise (~13 s), bringing 1 near to the values of the
other 17 subjects and to the whole-group mean (~19 s). This would
suggest that a period of endurance training speeds suprathreshold
kinetics in less fit individuals, causing 1 to reduce
toward subthreshold values. Despite the training improvement, the heavy
exercise 1 was still slower than in moderate exercise in
this group. This tends to support the work of Paterson and Whipp
(34), who suggest slower kinetics during suprathreshold
work. However, further specific studies of treadmill running are
clearly required before firm conclusions can be drawn.
The amplitude of phase II was linearly related to exercise intensity
because the gain (A1'/running speed
expressed relative to body mass) was not significantly different
between the 80% LT and the 50% conditions before
(t22 = 0.65, P =0.67) or after
training (t22 = 0.44, P = 0.20). This is in accordance with previous work (7, 12,
34) and confirms that the slow component is a phenomenon of
delayed onset that causes O2 to rise
above (rather than toward) the predicted steady-state value.
Despite the relatively small increases in LT and
O2 max caused by the training program,
there was a substantial and significant reduction in the slow component
for the same running speed posttraining. This was true even when the
six less fit subjects were removed from the analysis and when men and
women were analyzed separately. The reduction of the
O2 slow component has significant implications for exercise tolerance in athletic, sedentary, and patient
populations. For the competitive athlete, the ability to run at a
faster running speed for a given metabolic stress (i.e., same
O2 slow component) may result in
performance enhancement. This is exemplified by the data from the
subgroup within the present study (Table 4). In addition to a reduced
slow component at the same absolute exercise intensity, these subjects
were able to run at a faster speed while eliciting a slow component of
similar magnitude (~250-300 ml/min) to that of pretraining heavy
exercise. For patients with cardiac and/or pulmonary disorders, even
very low exercise intensities, such as slow walking, represent a severe metabolic stress (50). Endurance training will increase
the range of intensities over which the
O2 slow component would not be expected
to develop. This would improve the functional ability of these
individuals irrespective of any change in LT or
O2 max (36).
This study is the first to investigate the effect of training on
O2 kinetics by using mathematical
modeling. Previous studies (13, 57) have defined the slow
component as the increase in O2 between
3 min and the end of exercise (O2).
The slow component first becomes evident at about 2 min into exercise
(~114 ± 6.0 s; see Table 3 and Ref. 6). Therefore,
defining the slow component as an increase in
O2 above the value at 3 min of exercise
will significantly underestimate the magnitude of the slow component. Indeed, calculating the O2 in the
present study showed a reduction in the slow component of ~60 ml/min
with training (193 ± 22 vs. 130 ± 15 ml/min,
t22 = 3.18, P = 0.004).
This more simplistic characterization of the slow component might also
explain why some studies have reported that the slow component is
trivially small during treadmill running (8, 10).
Our results are similar to those of Casaburi et al. (13)
and Womack et al. (57), who showed that the
O2 slow component could be significantly
reduced after 8 wk and 6 wk, respectively, of cycle ergometer training.
In agreement with Casaburi et al. (13), we found that the
reduction in the slow component was related to the reduction in the
E and the [lactate], although the latter
relationship did not attain significance in our study. We did not
assess the relationship between the reduction in the O2 slow component and changes in other
putative mediators of the slow component such as body temperature and
catecholamine concentrations. However, previous studies have shown that
infusion of epinephrine during exercise has no effect on the exercise
O2 despite causing significant increases
in plasma epinephrine and lactate (19, 37). Furthermore,
Casaburi et al. found no significant relationship between the changes
in catecholamines and the changes in the slow component that occurred
with endurance training. In the same study, there was no significant
relationship between changes in rectal temperature and changes in the
slow component with training (13).
It was of interest that the strong relationship between the
[lactate] and the slow component found before training
(r = 0.69) was reduced considerably after training
(r = 0.45). Furthermore, the changes in lactate and the
slow component with training were not significantly related. Several
previous cross-sectional studies have shown a close relationship
between the magnitude of the blood lactate increase and the slow
component for cycle exercise (39, 42, 55). It has been
suggested that lactic acidosis is important in the maintenance of
muscle PO2 during heavy exercise
(48), and that the metabolic cost of glycogenesis from
lactate during exercise above the LT may contribute to the development
of the slow component (13). The proportion of the lactate
produced during exercise the fate of which is gluconeogenesis as
opposed to oxidation is not certain, but it can be calculated that the additional oxygen cost of lactate catabolism is not sufficient to make
a significant contribution to the slow component (54). In
two recent studies, a weaker relationship between lactate and the slow
component was reported in runners (r = 0.36; Ref. 31) and triathletes (r = 0.12; Ref. 9) during treadmill
exercise. In these studies, the slow component was significantly
greater for cycling than for running for the same elevated blood
lactate concentrations (10, 31). These results support the
suggestion that the relationship between lactate increase and the slow
component is coincidental rather than causal. This interpretation is
supported by studies that show an unchanged
O2 when 1) blood lactate is increased through infusion of epinephrine during exercise (19, 37), 2) exercise blood lactate is lowered by the
inhibition of carbonic anhydrase with acetazolamide (45),
and 3) L-(+)-lactate is infused into the
arterial blood supply of dogs who were exercised using electrical
stimulation (37). In addition, the time at which the
O2 slow component emerges
(~80-140 s) is much later than the time at which lactate appears
in the femoral vein (42).
The O2 slow component was significantly
related to the change in E over the same period of
time before (r = 0.70) but not after (r = 0.20) training. The reduction in E for the same running speed after training was also significantly related to the
reduction in the slow component at that running speed. This, of course,
does not necessarily indicate that the increase in E
over time during heavy exercise is an important mediator of the slow
component, because a reduced O2 with
training is likely to require a reduced E. The
lowering of blood lactate concentrations caused by training would
reduce the ventilatory load consequent to a reduced bicarbonate
buffering of the lactic acidosis (13). Using the estimates
of Aaron et al. (1) that the oxygen cost of
E ranges from 1.79 ml O2 per liter for
ventilatory rates of 63-79 l/min to 2.85 ml O2 per
liter for ventilatory rates of 117-147 l/min, the reduction in the
E we observed with training (Table 3) could account
for only 9-14% of the reduction in the slow component. These
results are consistent both with previous studies showing that
E contributes minimally (
20%) to the slow component (28, 57) and with the study of Poole et al.
(38), which demonstrated that ~86% of the
O2 slow component could be accounted for
by processes inherent to the exercising limbs.
One possibility for the significant reduction in the slow component
posttraining is an alteration in the motor unit recruitment pattern.
Both electromyographic (46) and glycogen depletion studies
(49) indicate that type II muscle fibers are recruited at
exercise intensities associated with the slow component. It is known
that the type II muscle fiber is less efficient than the type I muscle
fiber and that the ratio of phosphate produced to oxygen molecule
consumed (P-O) is ~18% lower in the isolated type II fiber due, in
part, to a greater reliance on the 
-glycerophosphate shuttle over
the malate-aspartate shuttle (15, 44, 52, 56). This would predict a greater O2 for any
given rate of ATP resynthesis. Barstow et al. (6) showed
that the contribution of the slow component to the total
O2 response to 8 min of heavy exercise was significantly positively related to the proportion of type II
fibers in the vastus lateralis. Endurance training is known to result
in a significant enhancement in the mitochondrial density and the
capillarity of type I and type II muscle fibers (2, 24).
Interconversion of fiber types may also be possible (type IIb 
IIa
I) (2, 26), although this has not been demonstrated in
short-term human training studies. Although we cannot be certain of the
extent to which our training program required the recruitment of type
II muscle fibers, changes such as an increased muscle mitochondrial
content and improved perfusion in type I muscle fibers might result in
the recruitment of fewer type II motor units for the same exercise
intensity after training.
In conclusion, we have shown that an endurance training program that
produced small but significant increases in
O2 max and LT did not affect the
O2 response to moderate exercise or the
phase II response during heavy exercise. However, the training led to a
significant reduction in the O2 slow
component at the same absolute running speed. Although we did not
measure performance directly, our results demonstrating a slow
component of similar magnitude when individuals exercised at higher
running speeds after training suggests improved exercise tolerance. We
speculate that the reduced slow component may be linked to the
recruitment of fewer low-efficiency type II muscle fibers for the same
exercise intensity after training.
| |
FOOTNOTES |
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Address for reprint requests and other correspondence: H. Carter, Univ. of Surrey Roehampton, West Hill, London SW15 3SN, UK (E-mail: helen.carter{at}roehampton.ac.uk).
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.
Received 1 September 1999; accepted in final form 8 June 2000.
| |
REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Aaron, EA,
Johnson BD,
Seow CK,
and
Dempsey JA.
Oxygen cost of exercise hyperpnea: measurement.
J Appl Physiol
72:
1810-1817,
1992
2.
Anderson, P,
and
Henriksson J.
Capillary supply of the quadriceps femoris muscle of man: adaptive response to exercise.
J Physiol (Lond)
270:
677-690,
1977
3.
Babcock, MA,
Paterson DH,
and
Cunningham DA.
Effects of aerobic endurance training on gas exchange kinetics of older men.
Med Sci Sports Exerc
26:
447-452,
1994[ISI][Medline].
4.
Barstow, TJ.
Characterization of O2 kinetics during heavy exercise.
Med Sci Sports Exerc
26:
1327-1334,
1994[ISI][Medline].
5.
Barstow, TJ,
Casaburi R,
and
Wasserman K.
O2 uptake kinetics and the O2 deficit as related to exercise intensity and blood lactate.
J Appl Physiol
75:
755-762,
1993
6.
Barstow, TJ,
Jones AM,
Nguyen PH,
and
Casaburi R.
Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise.
J Appl Physiol
81:
1642-1650,
1996
7.
Barstow, TJ,
and
Mole P.
Linear and nonlinear characteristics of oxygen uptake kinetics during heavy exercise.
J Appl Physiol
71:
2099-2106,
1991
8.
Billat, V,
Binsse V,
Petit B,
and
Koralsztein JP.
High level runners are able to maintain a O2 steady-state below O2 max in an all-out run over their critical velocity.
Arch Physiol Biochem
107:
1-8,
1998.
9.
Billat, V,
Flechet B,
Petit B,
Muriaux G,
and
Koralsztein JP.
Interval training at O2 max: effects on aerobic performance and overtraining markers.
Med Sci Sports Exerc
31:
156-163,
1999[ISI][Medline].
10.
Billat, V,
Richard R,
Binsse VM,
Koralsztein JP,
and
Haouzi P.
O2 slow component for severe exercise depends on type of exercise and is not correlated with time to fatigue.
J Appl Physiol
85:
2118-2124,
1998
11.
Carter, H,
Jones AM,
and
Doust JH.
Effect of six weeks endurance training on the lactate minimum speed.
J Sports Sci
17:
957-967,
1999[ISI][Medline].
12.
Casaburi, R,
Barstow TJ,
Robinson T,
and
Wasserman K.
Influence of work rate on ventilatory and gas exchange kinetics.
J Appl Physiol
67:
547-555,
1989
13.
Casaburi, R,
Storer TW,
Ben-Dov I,
and
Wasserman K.
Effect of endurance training on possible determinants of O2 during heavy exercise.
J Appl Physiol
62:
199-207,
1987
14.
Chilibeck, PD,
Paterson DH,
Petrella RJ,
and
Cunningham DA.
The influence of age and cardiorespiratory fitness on kinetics of oxygen uptake.
Can J Appl Physiol
21:
185-196,
1996[Medline].
15.
Crow, MT,
and
Kushmerick MJ.
Chemical energetics of slow- and fast-twitch muscles of the mouse.
J Gen Physiol
79:
147-166,
1982
16.
Davis, J,
Frank M,
Whipp BJ,
and
Wasserman K.
Anaerobic threshold alterations caused by endurance training in middle-aged men.
J Appl Physiol
46:
1039-1046,
1979
17.
Ekblom, B.
Effect of physical training on oxygen transport system in man.
Acta Physiol Scand Suppl
328:
5-45,
1969.
18.
Gaesser, GA.
Influence of endurance training and catecholamines on exercise O2 response.
Med Sci Sports Exerc
26:
1341-1346,
1994[ISI][Medline].
19.
Gaesser, GA,
Ward SA,
Baum VC,
and
Whipp BJ.
Effects of infused epinephrine on slow phase of O2 uptake kinetics during heavy exercise in humans.
J Appl Physiol
77:
2413-2419,
1994
20.
Grassi, B,
Poole DC,
Richardson RS,
Knight DR,
Erickson BK,
and
Wagner PD.
Muscle O2 kinetics in humans: implications for metabolic control.
J Appl Physiol
80:
988-998,
1996
21.
Hagberg, JM,
Hickson RC,
Ehsani AA,
and
Holloszy JO.
Faster adjustment to and recovery from submaximal exercise in the trained state.
J Appl Physiol
48:
218-224,
1980
22.
Hickson, RC,
Bomze HA,
and
Holloszy JO.
Faster adjustment of O2 uptake to the energy requirement of exercise in the trained state.
J Appl Physiol
44:
877-881,
1978
23.
Hickson, R,
Hagberg J,
Ehsani A,
and
Holloszy J.
Time course of the adaptive responses of aerobic power and heart rate to training.
Med Sci Sports Exerc
13:
17-20,
1981[ISI][Medline].
24.
Holloszy, JO,
and
Coyle EF.
Adaptations of skeletal muscle to endurance exercise and their metabolic consequences.
J Appl Physiol
56:
831-838,
1984
26.
Jansson, E,
Esbjornsson M,
Holm I,
and
Jacobs I.
Increase in the proportion of fast-twitch muscle fibres by sprint training in males.
Acta Physiol Scand
140:
359-363,
1990[ISI][Medline].
27.
Jones, AM.
A five year physiological case study of an Olympic runner.
Br J Sports Med
32:
39-43,
1998
28.
Jones AM, Carter H, and Doust JH. A disproportionate increase in
O2 coincident with lactate threshold
during treadmill exercise. Med Sci Sports Exerc 31:
1299-1306.
29.
Jones, AM,
and
Doust JH.
A 1% treadmill grade most accurately reflects the energetic cost of outdoor running.
J Sports Sci
14:
321-327,
1996[Medline].
30.
Jones, AM,
and
Doust JH.
Specific considerations for the assessment of middle distance and long distance runners.
In: The British Association of Sport and Exercise Sciences Physiological Testing Guidelines (3rd ed.). Leeds, UK: BASES, 1997, p. 108-111.
31.
Jones, AM,
and
McConnell AM.
Effect of exercise modality on oxygen uptake kinetics during heavy exercise.
Eur J Appl Physiol
80:
213-219,
1999.
33.
Londeree, BR.
Effect of training on lactate/ventilatory thresholds: a meta analysis.
Med Sci Sports Exerc
29:
837-843,
1997[ISI][Medline].
34.
Paterson, DH,
and
Whipp BJ.
Asymmetries of oxygen uptake transients at the on and offset of heavy exercise in humans.
J Physiol (Lond)
443:
575-586,
1991
35.
Phillips, SM,
Green HJ,
MacDonald MJ,
and
Hughson RL.
Progressive effect of endurance training on O2 kinetics at the onset of submaximal exercise.
J Appl Physiol
79:
1914-1920,
1995
36.
Poole, DC,
Barstow TJ,
Gaesser GA,
Willis WT,
and
Whipp BJ.
O2 slow component: physiological and functional significance.
Med Sci Sports Exerc
26:
1354-1358,
1994[ISI][Medline].
37.
Poole, DC,
Gladden LB,
Kurdak S,
and
Hogan MC.
L-(+)-Lactate infusion into working dog gastrocnemius: no evidence lactate per se mediates O2 slow component.
J Appl Physiol
76:
787-792,
1994
38.
Poole, DC,
Schaffartzik W,
Knight DR,
Derion T,
Kennedy B,
Guy HJ,
Prediletto R,
and
Wagner PD.
Contribution of exercising legs to the slow component of oxygen uptake kinetics in humans.
J Appl Physiol
71:
1245-1253,
1991
39.
Poole, DC,
Ward SA,
Gardner GW,
and
Whipp BJ.
Metabolic and respiratory profile of the upper limit for prolonged exercise in man.
Ergonomics
31:
1265-1279,
1988[Medline].
40.
Poole, DC,
Ward SA,
and
Whipp BJ.
The effects of training on the metabolic and respiratory profile of high-intensity cycle ergometer exercise.
Eur J Appl Physiol
59:
421-429,
1990[ISI].
41.
Powers, SK,
Dodd S,
and
Beadle RE.
Oxygen uptake kinetics in trained athletes differing in O2 max.
Eur J Appl Physiol
54:
306-308,
1985.
42.
Roston, WL,
Whipp BJ,
Davis JA,
Cunningham DA,
Effros RM,
and
Wasserman K.
Oxygen uptake kinetics and lactate concentration during exercise in humans.
Am Rev Respir Dis
135:
1080-1084,
1987[ISI][Medline].
43.
Saltin, B,
Blomqvist G,
Mitchell J,
Johnson RL,
Wildenthal K,
and
Chapman CB.
Response to exercise after bed rest and after training.
Circulation
38, Suppl 7:
1-78,
1968
44.
Schantz, PG,
and
Henriksson J.
Enzyme levels of the NADH shuttle systems: measurements in isolated muscle fibres from humans of differing physical activity.
Acta Physiol Scand
129:
505-515,
1987[ISI][Medline].
45.
Scheuermann, BW,
Kowalchuk JM,
Paterson DH,
and
Cunningham DA.
O2 uptake kinetics after acetazolamide administration during moderate- and heavy-intensity exercise.
J Appl Physiol
85:
1384-1393,
1998
46.
Shinohara, M,
and
Moritani T.
Increase in neuromuscular activity and oxygen uptake during heavy exercise.
Ann Physiol Anthrop
11:
257-262,
1992[Medline].
47.
Sjodin, B,
Jacobs I,
and
Svedenhag J.
Changes in onset of blood lactate accumulation (OBLA) and muscle enzymes after training at OBLA.
Eur J Appl Physiol
49:
45-57,
1982.
48.
Stringer, W,
Wasserman K,
Casaburi R,
Porszasz J,
Maehara K,
and
French W.
Lactic acidosis as a facilitator of oxyhemoglobin dissociation during exercise.
J Appl Physiol
76:
1462-1467,
1994
49.
Vollestad, NK,
Vaage O,
and
Hermansen L.
Muscle glycogen depletion patterns in type I and subgroups of type II fibres during prolonged severe exercise in man.
Acta Physiol Scand
122:
433-441,
1984[ISI][Medline].
50.
Wasserman, K,
Hansen JE,
Sue DY,
Whipp BJ,
and
Casaburi R.
Principles of Exercise Testing and Interpretation (2nd ed.). Philadelphia: Lea & Febiger, 1994.
51.
Weltman, A,
Seip R,
Snead D,
Weltman J,
Haskvitz E,
Evans W,
Veldhuis J,
and
Rogol A.
Exercise training at and above the lactate threshold in previously untrained women.
Int J Sports Med
13:
257-263,
1992[ISI][Medline].
52.
Wendt, IR,
and
Gibbs CL.
Energy production of rat extensor digitorum longus muscle.
Am J Physiol
224:
1081-1086,
1973.
53.
Weston, A,
Myburgh K,
Lindsay F,
Dennis S,
Noakes T,
and
Hawley J.
Skeletal muscle buffering capacity and endurance performance after high intensity interval training by well-trained cyclists.
Eur J Appl Physiol
75:
7-13,
1997[ISI].
54.
Whipp, BJ.
The slow component of O2 uptake kinetics during heavy exercise.
Med Sci Sports Exerc
26:
1319-1326,
1994[ISI][Medline].
55.
Whipp, BJ,
and
Wasserman K.
Oxygen uptake kinetics for various intensities of constant-load work.
J Appl Physiol
33:
351-356,
1972
56.
Willis, WT,
and
Jackman MR.
Mitochondrial function during heavy exercise.
Med Sci Sports Exerc
26:
1347-1354,
1994[ISI][Medline].
57.
Womack, CJ,
Davis SE,
Blumer JL,
Barrett E,
Weltman AL,
and
Gaesser GA.
Slow component of O2 uptake during heavy exercise: adaptation to endurance training.
J Appl Physiol
79:
838-845,
1995
58.
Yoshida, T,
Udo M,
Ohmori T,
Matsumoto Y,
Uramoto T,
and
Yamamoto K.
Day-to-day changes in oxygen uptake kinetics at the onset of exercise during strenuous endurance training.
Eur J Appl Physiol
64:
78-83,
1992[ISI].
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)
and after (
) the training intervention. Note the
reduced A'2 posttraining.
