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1 University of Surrey Roehampton, West Hill, 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 the present study was to
comprehensively examine oxygen consumption
(
O2) kinetics during running and cycling through mathematical modeling of the breath-by-breath gas exchange responses to moderate and heavy exercise. After determination of the
lactate threshold (LT) and maximal oxygen consumption
(O2 max) in both cycling and running
exercise, seven subjects (age 26.6 ± 5.1 yr) completed a series
of "square-wave" rest-to-exercise transitions at running speeds and
cycling power outputs that corresponded to 80% LT and 25, 50, and
75%
( being the difference between LT and
O2 max).
O2 responses were fit with either a two-
(<LT) or three-phase ( >LT) exponential model. The parameters of the
O2 kinetic response were similar between
exercise modes, except for the O2 slow
component, which was significantly (P < 0.05) greater
for cycling than for running at 50 and 75% (334 ± 183 and
430 ± 159 ml/min vs. 205 ± 84 and 302 ± 154 ml/min, respectively). We speculate that the differences between the modes are
related to the higher intramuscular tension development in heavy cycle
exercise and the higher eccentric exercise component in running. This
may cause a relatively greater recruitment of the less efficient type
II muscle fibers in cycling.
oxygen consumption; O2 slow
component; mathematical modeling; recovery
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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THE RESPONSE
CHARACTERISTICS of oxygen uptake
(O2) to step changes in power output
have been well documented (3). During the transition from
rest or unloaded cycling to constant-load exercise of moderate
intensity [i.e., below the lactate threshold (LT)], after the
cardiodynamic phase (phase I), O2 rises
in an approximately monoexponential fashion (phase II) to attain a new
steady state (phase III) within 2-3 min. However, the
O2 response to constant-load exercise of
heavy intensity (i.e., >LT) is complicated by the development of an
additional component of O2 that causes
O2 to rise above the predicted value
(39).
The cause of this slow rise in O2 over
time during heavy exercise, i.e., the O2
slow component, is an issue of great experimental interest. Putative
mechanisms for the phenomenon include elevation of plasma
catecholamines, increased rates of pulmonary ventilation, and increases
in whole body and muscle temperature (6, 34). However, simultaneous measurement of pulmonary and leg
O2 demonstrated that ~86% of the
excess O2 seen with high-intensity
exercise originates from within the exercising limb (33).
The close correlation between the rate of blood lactate accumulation
and the development of the O2 slow
component has led to the suggestion that the catabolism of lactate as
an exercise substrate, or its use in gluconeogenesis, might increase
exercise O2. However, infusion of
adrenaline and consequent elevation of blood lactate concentration was
not found to affect O2 in exercising
humans (16, 43).
The recruitment of type II muscle fibers during heavy exercise is,
perhaps, the most plausible explanation for the slow component phenomenon (2, 39). Barstow et al.
(2) demonstrated that the contribution made by the slow
component to the total O2 response to 8 min of heavy, constant-load cycling was greater in subjects with a high
proportion of type II fibers. This is in keeping with the observation
that the contraction of type II muscle fibers is less efficient than
that of type I fibers [i.e., the high-energy phosphate produced per
O2 molecule consumed (P:O) is lower in type II
fibers] (12). Furthermore, glycogen depletion (38) and electromyographic (28,
36) studies have demonstrated that type II motor units are
recruited at the exercise intensities at which the slow component is observed.
Relatively few studies have examined O2
kinetics in modes of exercise other than cycling. However, two recent
studies have attempted to characterize the
O2 slow component during treadmill running (4, 23). In both studies, the
magnitude of the slow component was notably smaller than has been
described for cycle exercise at the same relative intensity. Only two
studies have directly compared the O2
slow component response in running and cycling in the same subjects.
Billat et al. (5) reported that the slow component,
defined as the increase in O2 between 3 min and the end of exercise, was significantly greater during cycling
than during treadmill running (~270 vs. 20 ml/min, respectively) when
a group of elite triathletes exercised to exhaustion at 90% of their
mode-specific O2 max. Similarly, Jones
and McConnell (22) reported that the increase in
O2 between 3 and 6 min of heavy exercise
at 50% (i.e., the running speed or power output calculated to
require 50% of the difference between the
O2 at LT and
O2 max) was significantly greater in
cycling than in running (~290 vs. 200 ml/min). However, it should be
noted that the slow component for running in the study of Jones and McConnell (22) was 10-fold higher than that reported by
Billat et al. (5).
The existence of the O2 slow component
during treadmill running appears to be controversial, with three
studies clearly demonstrating the phenomenon during high-intensity
running (22, 23) and two studies suggesting
that it is effectively nonexistent (4, 5).
The demonstration of differences in the
O2 slow component response between
exercise modes might shed light on the physiological mechanisms
underpinning the phenomenon. A limitation to the studies mentioned
above (4, 5, 22,
23) was the characterization of the slow component, which
involved the simple calculation of the difference between
O2 at 3 min and
O2 at the end of exercise. In addition,
no previous study has examined possible differences in the
characteristics of the primary (fast) component between exercise modalities.
Therefore, the purpose of the present study was to compare the fast and
slow component responses of O2 during
cycling and running exercise using the mathematical modeling procedures
validated by Barstow and colleagues (2, 3).
To further our understanding of any differences between the exercise
modes, we studied the responses across a wide range of exercise
intensities, including exercise of moderate intensity (<LT) and
several exercise intensities above LT.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects. Seven recreationally active subjects [three men, four women; age 27 ± 5 (SD) yr; height 1.74 ± 0.08 m; body mass 69.3 ± 9.3 kg] volunteered to take part in this study. The subjects gave written, informed consent after the experimental procedures, the associated risks, and the 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.
The 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.Experimental design.
The subjects were required to visit the laboratory on 10 occasions. The first two visits were used to determine LT and
O2 max for both running and cycling
exercise. During the remaining eight sessions, the subjects performed
2-3 repetitions of square-wave transitions from rest to one of
four exercise intensities: 80% LT and 25, 50, and 75% for both
treadmill and cycle exercise. On a given day, a subject would complete
two or three transitions of the same exercise intensity using the same
mode of exercise. The transitions were separated by 1 h of
recovery. The transitions performed on a given day were determined at
random, and the study was completed within 3 wk for all subjects.
Procedures.
All running tests were performed on a motorized treadmill (Woodway,
Cardiokinetics, Salford, UK) with the grade set at 1% (19). Cycle tests were conducted on an electrically braked
cycle ergometer (Jaeger ER800), with seat and handlebar height kept constant over the sessions for each subject. Pedal frequency was maintained at 80 ± 5 rpm for all cycle tests. During the exercise tests, pulmonary gas exchange was determined breath by breath. We chose
not to apply an alveolar algorithm to correct for possible changes in
pulmonary O2 stores between consecutive
breaths. Subjects breathed through a low-dead space (90 ml),
low-resistance (0.65 mmH2O · l
1 · s 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 analyzed for O2, CO2, and N2 concentrations by a quadripole mass spectrometer
(CaSE QP9000, Gillingham, Kent, UK) that was calibrated before each test using gases of known concentration. Expiratory volumes were determined using a turbine volume transducer (Interface Associates). The volume and concentration signals were integrated by computer after
analog-to-digital conversion, taking the gas transit delay through the
capillary into account. Respiratory gas exchange variables [O2, CO2 uptake
(CO2), and minute ventilation]
were calculated and displayed for every breath. Heart rate was recorded
telemetrically throughout the exercise tests (Polar Electro Oy,
Kempele, Finland).
O2 max during both
treadmill and cycle ergometry. For the treadmill test, the initial
running speed was 6.0-7.0 km/h for the women and 8.0-9.0
km/h for the men. Subjects completed 6-8 submaximal stages of
4-min duration, with running speed increased by 1.0 km/h between stages
(20). At the end of each stage, subjects supported
their weight with their hands and moved their feet to the sides of the
treadmill belt. Fingertip capillary blood samples (~25 µl) were
collected in capillary tubes and subsequently analyzed for lactate
concentration using an automated analyzer (YSI 2300, Yellow Springs).
Subjects recommenced running within 10-15 s. When blood lactate
concentration exceeded 4 mM or heart rate exceeded 90% of the known or
age-predicted maximum heart rate, the running speed was increased by
1.0 km/h every minute until the subject reached volitional exhaustion. We chose to measure LT directly rather than estimate it from gas exchange responses because we wished to equate exercise intensity as
accurately as possible in our comparisons of the
O2 responses in the two exercise modes.
In a previous study, Jones and Doust (18) demonstrated
that the O2 max measured after a 25-min
LT determination was not significantly different from the O2 max measured with a conventional
10-min incremental protocol.
A similar procedure was used in the incremental cycle test. All
subjects began the test at 50 W, with increases in power output of 25 W
every 4 min, and brief (10-15 s) pauses in exercise to facilitate
fingertip capillary blood sampling between stages. As in the treadmill
test, when blood lactate concentration exceeded 4 mM or heart rate
exceeded 90% of the known or age-predicted maximum, the incremental
rate was increased 25 W per minute until the subject reached volitional exhaustion.
Plots of blood [lactate] against running speed or power output and
O2 were provided to two independent
reviewers, who determined LT was the first sudden and sustained
increase in blood lactate above resting concentrations. The
breath-by-breath gas exchange data collected during the incremental
tests were averaged over consecutive 30-s periods.
O2 max was defined as the average O2 attained in the last 30 s of the
tests. The running speed and power output at
O2 max were estimated by extrapolation of the sub-LT relationship between O2
and running speed/power output. The running speeds and power outputs
calculated to require 80% of O2 at LT
(moderate-intensity exercise), and 25, 50, and 75% (heavy-intensity
exercise) were determined [e.g., 50% = LT + 0.5 × (O2 max 
LT)].
Subsequently, subjects performed a series of square-wave
transitions of 6-min duration at the four exercise intensities for both
cycling and running on separate days. The exercise protocol began with
2 min of seated rest (cycle ergometer) or standing rest with feet
astride the moving treadmill belt and hands holding the guard rails
(treadmill). At the start of cycling exercise, the experimenters
accelerated the flywheel, while the subjects' legs moved passively,
until a pedal cadence of 80 rpm was reached, and the resistance was
applied. We chose this approach because it most closely reflects the
situation for the running trials, in which the subjects supported
their body mass with their hands on the guard rails until leg
speed matched treadmill belt speed, after which, they let go of the
guard rails and began running. For both exercise modes, the transition
from rest to exercise took <5 s. Fingertip capillary blood samples
were taken immediately before and after the 6-min exercise period.
The difference between the end-exercise lactate and the resting lactate
concentration was expressed as a delta value (lactate
concentration). For the running trials, stride frequency was calculated
by timing the completion of 10 strides at 2 min and again at 5 min of
exercise. After a 1-h recovery period, another blood sample was taken
to ensure that blood lactate had returned to resting levels. The subjects then performed an identical square-wave transition using the
same mode of exercise as for the first test. For the moderate exercise trial (80% LT), the subjects performed a total of three transitions for each exercise mode, whereas for the heavy exercise trials (25, 50, and 75%), the subjects performed two transitions for each exercise mode.
Data analysis. For each exercise transition, the breath-by-breath data were interpolated to give second-by-second values. The transitions for each intensity were then time aligned to the start of exercise and averaged to enhance the underlying response characteristics.
Nonlinear regression techniques were used to fitO2 data after the onset of exercise with
an exponential function. An iterative process ensured the sum of
squared error was minimized. The mathematical model consisted of two
(moderate exercise) or three (heavy exercise) exponential terms, each
representing one phase of the response (2,
3). On the basis of previous literature (2),
the model was constrained to aid in identification of the key
parameters. The first exponential term started with the onset of
exercise (time zero), whereas the other terms began after independent
time delays
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(1) |
O2(b) is the
average value over 2 min of resting baseline;
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 was assigned the
value for that time (A'0)
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(2) |
O2 at the end of phase 1 (A'0) and the amplitude of
phase 2 (A1) were summed to calculate
the amplitude of the fast primary component
(A'1). The slow component at the end of
exercise (A'2) was calculated and is used
in preference to A2 (2).
The O2 kinetics in recovery were
analyzed in a similar way to those in exercise, with one exception.
After phase 1, both the primary and slow component
shared TD1 (2). With the use of the procedures
outlined by Motulsky and Ransnas (29), fitting the
recovery data with a more complex model (separate TD1 and TD2) did not lead to a significantly better fit
(t51 = 0.46, P = 0.65);
therefore, the simpler model was adopted.
Statistical analysis.
Paired t-tests were used to determine the significance of
differences between running and cycling trials. The effects of
exercise intensity on O2, blood lactate
concentration, and stride frequency responses were tested using one-way
ANOVA with Tukey's post hoc tests where appropriate. Pearson product
moment coefficients (r) were used to assess the significance
of relationships between the slow component and the increase in blood
lactate. Statistical significance was accepted at 5%. Results are
presented as means ± SD.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Incremental tests.
Both O2 max and LT were significantly
higher for treadmill than for cycle ergometry. The
O2 max for running was 50.7 ± 13 ml · kg1 · min1 vs.
43.1 ± 11 ml · kg1 · min1 for cycling (t6 = 6.5, P = 0.001). O2 at LT
was 36.8 ± 7 and 23.8 ± 8 ml · kg1 · min1 for running and cycling,
respectively (t6 = 12.8, P
<0.001). Consequently, the LT occurred at a significantly
higher percentage of O2 max in running
(73.4 ± 5.8%) than in cycling (54.7 ± 6.7%;
t6 = 6.4, P = 0.001).
Square-wave transitions.
Despite the significant differences between the exercise modes in terms
of O2 max and the absolute and relative
O2 at LT attained by the subjects, there
were no significant differences in exercise stress between modalities,
as evidenced by the blood lactate concentration and percentage of
maximum heart rate achieved (Table 1).
The relative exercise intensities of the square-wave transitions
(calculated as %) were not significantly different between exercise
modes.
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O2 max and
O2 at LT during running, the
end-exercise O2 and
A'1 were significantly higher in running
than in cycling during both moderate and heavy exercise (Table
2). Other parameters of the
O2 response were similar across
modalities, with the exception of the O2
slow component (A'2). The absolute
magnitude of A'2 was significantly higher
for cycling than for running at both 50% (334 ± 183 vs. 205 ± 84.3 ml/min, respectively; t6 = 2.65, P = 0.038) and 75% (430 ± 159 vs. 302 ± 154 ml/min, respectively; t6 = 3.47,
P = 0.001). Likewise, the proportion of the total
O2 response attributable to the slow
component (relative A'2) was
significantly greater in cycling than in running at both 50 and 75%
(15.3 ± 3.6 vs. 7.3 ± 1.4%, t6 = 6.01, P = 0.001; and 16.9 ± 2 vs. 9.6 ± 3.1%, t6 = 6.46, P
< 0.001). The O2 response of a
typical subject to the four different intensities across exercise modes
is shown in Fig. 1.
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O2 slow
component and the degree of blood lactate accumulation during the
exercise transition increased with exercise intensity in both running
(F2,20 = 10.1, P = 0.001 and F2,20 = 8.1, P = 0.003, respectively) and cycling (F2,20 = 10.3, P = 0.001 and F2,20 = 63.4, P < 0.001, respectively). The
O2 slow component was significantly
correlated with lactate concentration for both cycling
(r = 0.56) and running (r = 0.81).
The parameters for the response of O2
during recovery are given in Table 3. As
with the on-transient responses, only A'1 and A'2 varied significantly with
exercise mode. For cycling, a comparison of the off-transient with the
on-transient revealed parameters to be generally similar in recovery,
suggesting symmetry between the exercise and recovery
O2 kinetics. However, for running,
there was a significant trend for 1 to be greater during recovery than during exercise at moderate intensity (11.6 ± 7.9 vs. 39.3 ± 15.9 s, t6 = 5.9,
P = 0.001), at 25% (19.4 ± 8.0 vs. 34.7 ± 8 s, t6 = 4.3, P =
0.005), at 50% (20.1 ± 5.2 vs. 31.5 ± 5.9 s,
t6 = 3.6, P = 0.012) and at
75% (15.9 ± 5.8 vs. 27.6 ± 8.9 s,
t6 = 2.9, P = 0.027).
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(81.6 ± 4.2 strides/min), to 50% (83.7 ± 4.1 strides/min), and to 75% (86.1 ± 4.8 strides/min), with only
the increase from moderate to 75% exercise being significant
(F3,27 = 3.6, P = 0.03).
There were no significant changes in stride frequency between minutes 3 and 6 of exercise.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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To our knowledge, this study is the first to describe and compare
O2 kinetics for treadmill and cycle
exercise and recovery in the same subjects using a comprehensive
mathematical modeling procedure.
As would be expected for subjects who are not specifically cycle
trained, both O2 max and LT (in l/min
and as a percentage of O2 max) were
higher for running than for cycling. The difference in the percentage
of O2 max utilized at LT in running and
cycling exercise is intriguing, but it appears to be inevitable unless
elite athletes, equally well-trained in cycling and running exercise,
are studied (5). The mechanisms underpinning this
difference are not clear but may be similar to those responsible for
the difference in the magnitude of the slow component between exercise
modes (14).
To make a valid comparison of O2
kinetics across exercise modes, we chose to normalize the exercise
intensity with reference to both the LT and
O2 max determined for the two exercise modes (i.e., we used the "%" concept). This approach is
preferable to normalizing the exercise intensity by
O2 max alone (i.e., by testing subjects
at fixed percentages of the mode-specific O2 max), because the latter can lead to
differences in metabolic and perceptual stress, depending on the
proximity of the exercise intensity to the LT (24). In the
present study, despite differences in the absolute
O2, the relative intensity of each
square-wave transition was successfully matched across exercise modes
because the %O2 achieved, the
increase in blood lactate above baseline, and the percent of maximum
heart rate achieved were not significantly different (Table 1).
Therefore, our study allows a comparison of
O2 kinetics between running and cycling
when the degree of metabolic stress, reflected as blood lactate
concentration, is the same.
A comparison of the O2 response to
moderate exercise (80% LT) revealed very similar patterns in treadmill
and cycle ergometry (Table 2). As can be seen in Fig. 1 A,
the only differences are in the amplitudes of the
O2 response (A0
and A1). Steady state was attained within ~2
min and was maintained for the entire exercise period. Blood lactate
concentration did not change from resting concentrations during running
or cycling (mean change: 0.0 ± 0.3 and 0.0 ± 0.4 mM,
respectively). These results confirm earlier descriptions of
O2 kinetics in cycle exercise
(3, 40).
For the three heavy exercise conditions, the overall dynamics of the
O2 response were generally similar
between running and cycling (Table 2). Interestingly, there were no
differences in any of the time-based parameters (i.e., TD1,
TD2, 1, 2) between the two
exercise modes. Our values for the time constant of the primary
component (1) are somewhat faster than have been
reported previously (2, 15). This is likely
to be related to the fact that our subjects were young, healthy,
physical education students who were active in competitive sports and
who had a high level of aerobic fitness. Recent work in our laboratory
has shown that endurance training results in faster phase II
O2 kinetics (Carter, Jones, Barstow,
Burnley, Williams, and Doust, unpublished observations). It
should also be noted that 1 was not significantly
different over the range of exercise intensities studied for either
cycling or running (Fig. 2). Controversy
surrounds the issue of whether phase II
O2 kinetics are slowed for exercise
above compared with below the LT. Our data support the position that
phase II O2 kinetics are not slowed for
exercise above the LT (3), but this issue requires further
investigation with a larger number of subjects to increase statistical
power.
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The increase in the amplitude of the primary
O2 component was linearly related to the
increase in exercise intensity for both running and cycling (i.e., the
"gain" of the primary response calculated as
A'1 divided by the exercise intensity)
was not significantly different between 80% LT and 75% for either
running (192 ± 24.5, 199 ± 23.3, 195 ± 15.6 and
192 ± 35 ml/min per km/h for 80% LT, and 25, 50, and 75%,
respectively) or cycling (12.1 ± 3.6, 11.4 ± 1.3, 10.4 ± 0.6, and 10.2 ± 0.6 ml/W for 80% LT, and 25, 50, and 75%,
respectively). These results confirm previous reports (3)
that the primary O2 response to
square-wave exercise approximates that of a linear, first-order,
time-invariant system, and imply that the
O2 slow component is a phenomenon of
delayed onset that causes O2 to rise
above the expected O2 for that exercise intensity.
The differences between the exercise modes were primarily related to
the amplitude of response. The A'1 was
significantly higher in running exercise than in cycling exercise at
every intensity (Table 2), as a result of the higher
O2 at LT and
O2 max in running and the
consequently higher absolute O2
requirement at each of the exercise intensities studied. Despite the
significantly higher end-exercise O2 and
A'1 in running compared with cycling for
each exercise intensity, A'2 was
significantly greater for cycling than for running. This was true for
all of the heavy exercise conditions, and the difference was
statistically significant at 50 and 75%. At these two exercise
intensities, the slow component accounted for a significantly higher
proportion of the total increase in O2
above baseline for cycling (~15-17%) compared with running (~7-10%). These results confirm the findings of two previous
studies, which demonstrated that the increase in
O2 between 3 and 6 min of heavy exercise
is greater for cycling than for treadmill running at the same relative
exercise intensity (5, 22).
The magnitude of the slow component has been reported to be almost
negligible in elite endurance athletes during treadmill running
(4, 5). The discrepancy between these studies
and the present study may be the result of methodological differences. Billat et al. (4, 5) characterized the slow
component as the difference in O2
between 3 and 6 min of heavy exercise. Because the
O2 slow component begins to develop at
~2 min into heavy exercise, it is possible that a significant portion
of the slow component was not accounted for in this analysis. It is
also known that subjects of higher aerobic fitness and/or a higher proportion of type I fibers in the vastus lateralis have a greater initial gain of the primary component and a proportionately smaller slow component (2). In addition, it is not clear from
these previous studies (4, 5) if the running
speed selected was sufficiently above the critical velocity to elicit a
substantial slow component response.
Several physiological and mechanical differences between treadmill and
cycle ergometry may account for the differences in the amplitude of the
slow component that we observed. During high-intensity exercise,
especially in subjects not experienced in cycle exercise, an increased
handlebar grip and rocking of the torso can be observed as subjects
fatigue. In this situation, the muscular work is increased with no
contribution to the generation of external power output. It is possible
that the increased energetic cost of isometric contraction of these
auxiliary muscles contributes to the development of the slow component.
In support of this suggestion, Ozyener et al. (31)
recently demonstrated that the rate of Hb desaturation in the arm
musculature was significantly correlated with the magnitude of the
O2 slow component observed in cycle
exercise at 80%.
Running and cycling comprise different types of muscle contraction. In running, ~60% of the time taken to complete one stride is spent in the support phase (i.e., foot in contact with the ground) for speeds between 12 and 23 km/h (30). Approximately 34% of this time involves eccentric muscle action (27). This eccentric muscle action may have two important consequences for the oxygen cost of running. Firstly, the metabolic cost of eccentric exercise is substantially lower than that of comparable concentric exercise (37). White (41) explained this difference by contrasting the ATP-driven detachment and resetting of the actin-myosin cross-bridges during concentric work with the forcible detachment and reattachment of the cross-bridge during eccentric exercise. The latter does not require the cleaving of ATP and therefore reduces the oxygen cost of exercise. Secondly, the "preloading" of muscle during the eccentric phase of the muscle action during running may improve the efficiency of the subsequent concentric phase. Cavanagh and Kram (8) have provided evidence that the mechanical efficiency of running exceeds that predicted from simple conversion of chemical energy to kinetic energy by muscles. The stretch-shortening cycle in running allows for storage of elastic energy during the eccentric phase and its subsequent release during the concentric phase of the action, thereby enhancing force production for a given neural input (7, 13). It is possible that the greater eccentric muscle action in running may in some way offset or delay the onset of peripheral fatigue and/or reduce the recruitment of type II motor units during running compared with cycling for the same relative exercise intensity.
It has been proposed that the oxygen consumption occurring in the legs
makes up a smaller proportion of the total
O2 response measured at the mouth during
running than cycling (22). Electromyographic studies have
revealed high bursts of phasic activity in the arm and trunk muscles
that suggest that the upper body musculature is responsible for
significant oxygen consumption during running (17). It is
likely that the metabolic cost of upper body work makes a smaller
contribution to the total exercise O2
during cycling than running, except perhaps when auxiliary muscles are recruited as the subject becomes fatigued. Therefore, for a given whole
body O2, the leg musculature may be
closer to its individual maximal oxygen consumption and its maximal
voluntary contraction during cycling than running. This might require a
progressive recruitment of the less efficient type II muscle fibers as
the initially recruited type I fibers become fatigued.
During heavy exercise, the cycling action is associated with high intramuscular tension development for the majority of the pedal revolution, peaking from 90 to 180° (10). Ahlquist et al. (1) demonstrated that the recruitment of type II motor units is closely related to the requirements for muscle force generation. The high intramuscular pressures may lead to partial occlusion of femoral arterial blood flow (14), which may reduce oxygen delivery and lead to a greater recruitment of type II motor units.
The mechanisms presented herein implicate the recruitment of type II
motor units in the development of the O2
slow component. Indeed, the recent research literature has focused much
attention on their importance (2, 39,
42). Type II fibers are less efficient than type I fibers,
possessing an 18% lower phosphate produced to oxygen consumed ratio
(12, 25). Subjects with a high proportion of
type I fibers have been reported to sustain a higher power output for
the same O2 than subjects with a lower proportion of type I fibers during prolonged cycle exercise
(11). A higher proportion of type I fibers in the vastus
lateralis was also associated with a larger gain
(O2/ work rate) of the fast component for O2 and a reduced slow
component as a percentage of the total
O2 response during exercise at 50%
(2). Electromyographic and glycogen depletion studies have
demonstrated that type II muscle fibers are active at exercise
intensities associated with the slow component (36,
38).
Previous research in this field has typically used a cadence of 60 rpm
during cycle exercise bouts. In the present study, it was decided to
allow subjects to pedal at 80 ± 5 rpm. We felt it important for
the interpretation of the results that subjects utilize a similar
movement frequency in running and cycling. In a previous study from
this laboratory, it was reported that stride frequency during
high-speed treadmill running was ~85 strides/min (21).
In the present study, freely chosen stride frequencies of ~80
strides/min were observed across the range of exercise intensities. As
expected, stride frequency increased somewhat with running speed, but
it did not change between 3 and 6 min of exercise in any of the
transitions. The procedures used were therefore successful in equating
muscle contraction frequencies across exercise modes, thereby
eliminating this as a possible explanation for the difference in the
magnitude of the O2 slow component we observed.
Several previous studies have noted a strong relationship between the
accumulation of blood lactate during heavy exercise and the magnitude
of the O2 slow component
(6, 35). In contrast, in two recent studies
the increase in blood lactate over 6 min of exercise has been shown to
be poorly correlated with the O2 slow
component for both running and cycling (4, 22). In the present study, both modes of exercise were
associated with moderate to good correlations between the two variables
(r = 0.56 in cycling and r = 0.81 in
running). Interestingly, there was a greater slow component rise in
O2 during cycling compared with running,
despite similar increases in blood lactate above baseline in the two
modes of exercise. These results support the suggestion that the
relationship between the rate of blood lactate accumulation and the
O2 slow component is coincidental rather than causal (16, 43).
The procedures used in this study allowed the on- and off-transient
responses to be compared across exercise modes for the first time.
Analysis of recovery kinetics may provide further insight into the
mechanisms controlling O2 kinetics
during exercise. In moderate exercise, there appeared to be reasonable
symmetry between exercise and recovery kinetics for
O2 in the amplitude of response.
However, in both running and cycling, the time constant for the primary
response (1) was greater during recovery than during
exercise, i.e., the kinetics were slower in recovery (see Table 3). The
slowing of phase II kinetics was also evident when considering the
recovery from heavy running exercise. It is difficult to explain this
asymmetry other than through considering the subjects' position during
the recovery period. In cycling exercise, subjects completed recovery
in a seated position. However, due to the nature of the exercise,
recovery from running was made while standing. The present study
demonstrates the presence of a slow component for recovery of
O2 similar to the magnitude found in
both running and cycling exercise. This supports the suggestion that
the slow component is slow to both develop and recover
(15) and may indicate that similar mechanisms are
responsible for both phenomena.
In conclusion, this study has shown that the oxygen uptake kinetics in running and cycling are generally similar, with the exception of the amplitude of the primary and slow components. Although a slow component does indeed develop during treadmill running, its magnitude is considerably lower than in cycling of a similar relative intensity. This difference may be related to differences in muscle contraction regimens between the exercise modes that may include: an increased isometric contraction of the upper body musculature during cycling; a higher muscle tension development during the concentric phase of the cycle action leading to rhythmic ischemia; and a greater storage and return of elastic energy during the stretch-shortening activity of running. We suggest that the latter points implicate a greater recruitment of type II muscle fibers in cycling compared with running at the same relative intensity. This may support the postulate that type II fiber recruitment is the primary mechanism responsible for the development of the slow component.
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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. §1734 solely to indicate this fact.
Received 19 August 1999; accepted in final form 14 April 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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) and cycling (
). Despite differing absolute
