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O2
kinetics at the onset of work
1 Applied Physiology Laboratory, Kobe Design University, Kobe 651-2196; 3 Yokohama City University, Yokohama 236-0027; 4 Nagoya City University, Nagoya 467-8501; 5 Hiroshima Women's University, Hiroshima 734-8558; 6 Kobe University, Kobe 657-0011, Japan; and 2 Department of Kinesiology, Kansas State University, Manhattan, Kansas 66506-0302
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The dependence of O2 uptake
(
O2) kinetics on the muscle mass
recruited under conditions when fiber and muscle recruitment patterns
are similar following the onset of exercise has not been determined. We
developed a motorized cycle ergometer that facilitated one-leg (1L)
cycling in which the electromyographic (EMG) profile of the active
muscles was not discernibly altered from that during two-leg (2L)
cycling. Six subjects performed 1L and 2L exercise transitions from
unloaded cycling to moderate [<ventilatory threshold (VT)] and heavy
(>VT) exercise. The 1L condition yielded kinetics that was unchanged
from the 2L condition [the phase 2 time constants (
1,
in s) for <VT were as follows: 1L = 16.8±8.4 (SD), 2L = 18.4 ± 8.1, P > 0.05; for >VT: 1L = 26.8 ± 12.0; 2L = 27.8 ± 16.1, P > 0.05]. The overall O2 kinetics (mean
response time) was not significantly different for the two exercise
conditions. However, the gain of the fast component (the amplitude/work
rate) during the 1L exercise was significantly higher than that for the
2L exercise for both moderate and heavy work rates. The slow-component responses evident for heavy exercise were temporally and quantitatively unaffected by the 1L condition. These data demonstrate that, when leg
muscle recruitment patterns are unchanged as assessed by EMG analysis,
on-transient O2 kinetics for both
moderate and heavy exercise are not dependent on the muscle mass recruited.
exercise energetics; one-leg exercise; pulmonary gas exchange; muscle recruitment; control of muscle oxygen uptake
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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AT THE ONSET OF MUSCULAR
EXERCISE, pulmonary and muscle O2 uptakes
(O2) increase with a finite kinetic
profile. There remains considerable debate as to whether the speed of
these kinetics reflects sluggishness of O2 delivery to the
muscle or, alternatively, some intramuscular limitation such as
microvascular O2 delivery-to-O2 requirement
mismatch or oxidative enzyme inertia (2, 8, 18, 26, 31, 38,
39). Experimental paradigms that are expected to impair muscle
O2 delivery, such as reduced arterial O2
content (CaO2), invariably slow pulmonary
O2 kinetics for both moderate and heavy
work rates (WRs) [below ventilatory threshold (<VT) and above VT
(>VT), respectively] (9, 12, 19, 24, 26, 38). In
contrast, attempts to speed O2 kinetics
by augmenting CaO2 and/or O2 delivery in
healthy subjects performing upright cycle ergometry have been
successful only for the >VT domain (15, 27).
In normal healthy subjects, if the speed of the pulmonary
O2 kinetics were indeed limited by the
rapidity of the cardiovascular response and this response remained
independent of muscle mass recruited, it would be expected that
exercise with a smaller muscle mass [i.e., one-leg (1L) exercise vs.
two-leg (2L) exercise] would result in faster
O2 kinetics. Thus, if this were the
case, it may be hypothesized that decreasing the muscle mass recruited would shift the site of limitation of O2
kinetics more toward the exercising muscle(s). Current thinking would
suggest that the expected faster O2
kinetics with a smaller muscle mass is more likely to be true for >VT
than for <VT exercise.
This investigation tested the hypothesis that the
O2 kinetics would be speeded by reducing
the muscle mass recruited for >VT exercise but not for <VT exercise.
The 1L vs. 2L cycling exercise paradigm utilized for this study permits
evaluation of the effect of recruited muscle mass on
O2 kinetics in the absence of
differences in fiber type and muscle recruitment profiles. In previous
studies that used a conventional cycle ergometer for 1L exercise
(11, 21, 35), the contracting muscles were required to
sustain muscular tension throughout the entire cycle of the single limb movement, thereby creating different muscle recruitment strategies and
likely altered physiological conditions within the muscle compared with
that for 2L exercise. We developed a motorized 1L cycle ergometer that
minimized the muscular contractions during the knee-hip flexion
(pedal-up) phase, which allowed the subjects to match more closely the
muscle contraction pattern for 2L exercise. As confirmation, the
present study found that the electromyographic (EMG) profile for
motorized 1L cycle ergometry differed markedly from that with
conventional 1L ergometry but not from conventional 2L ergometry.
Subsequently, the kinetic response of O2
at the onset of moderate (<VT) and heavy (>VT) exercise was compared for motorized 1L and conventional 2L ergometry.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
Six male subjects participated in the study. After a detailed explanation of the study, informed consent was obtained. The study was approved by the Human Subjects Committee of Kobe Design University.Description of the Cycle Ergometry
For the 1L experiments, an electric motor was connected to the left side of the crankshaft of the cycle ergometer. A reduction gear assembly was utilized to match motor speed (1,800 rpm) to that of the subject (60 rpm). A special cam was designed for the motor shaft, which activated a switch to turn on the motor when the right pedal was at bottom dead center and turn it off when the pedal reached top dead center. During the exercise, the subject performed the down stroke on the right pedal with his right leg; at bottom dead center, the motor would be switched on by the cam and return the pedal to the top of the stroke. Throughout the entire exercise bout, the left leg rested on a footrest next to the ergometer. The positions of the ergometer handlebar and the saddle were standardized between the two exercise modes to minimize any difference in O2 cost for body stabilization.Protocol
Incremental exercise tests.
Ramp exercise protocols, preceded by 2-min unloaded cycling on a cycle
ergometer, were utilized to estimate VT and peak
O2 for each exercise mode for each
individual. The ramp exercise protocols were designed to produce
fatigue within 10-15 min, with WR increases of 25 W/min for 2L and
6 W/min for 1L cycling exercise; pedal frequency was held constant at
60 rpm. Responses to 1L and 2L conditions were tested on separate days.
The O2 at the VT was estimated as the
break point in the plot of CO2 output against O2 (V-slope method).
Constant WR exercise tests.
Exercise transition tests were conducted under each exercise
condition (1L vs. 2L exercise) on separate days. Each constant WR
exercise test was performed for 6 min. The moderate WR used for both
exercise conditions corresponded to a O2
of ~90% of the VT estimated for each exercise condition, whereas the
heavy exercise WR was estimated to require a
O2 equal to ~50% of the difference
(
) between the subject's VT and peak
O2, i.e., a value of VT + 0.50,
based on the initial O2-WR observed
during the ramp exercise in each exercise condition. The exercise was preceded by 3 min of unloaded cycling at a pedal frequency of 60 rpm.
To minimize random noise and to enhance the underlying response
patterns for the moderate WR tests, subjects performed a total of four
to seven repetitions of the exercise transition under each exercise
condition. A greater number of transitions were performed in the 1L
exercise than during the 2L exercise tests to improve the
signal-to-noise ratio, in light of the smaller amplitude
O2 response with the small muscle mass
exercise. The number of repetitions was determined according to the
ratio of standard deviation (SD) of breath-by-breath fluctuation to the amplitude of the O2 response
(25). In the present study, the signal-to-noise ratio was
within 5%, which resulted in a SD of ±2 s of the time constant. Each
subject was given 15 min of rest before starting the next exercise
transition. For the heavy WR tests, subjects normally performed three
to five exercise transitions under the 1L condition and two to three
exercise transitions under the 2L condition. Only one heavy exercise
transition was performed on any single day.
Measurements
Subjects breathed through a low-resistance valve (Hans-Rudolph, dead space = 90 ml) connected to two pneumotachographs for measurement of inspiratory and expiratory flows, as previously described (22-24). Each system was calibrated repeatedly by inputting known volumes of room air at various mean flows and flow profiles. Respired gases were analyzed by mass spectrometry (model MGA-1100, Perkin Elmer) from a sample drawn continuously from the mouthpiece. Precision-analyzed gas mixtures were used for calibration. Alveolar gas-exchange variables were calculated breath by breath according to the algorithms of Beaver et al. (6). Heart rate (HR) was monitored continuously via a three-lead electrocardiogram.In separate experiments in four of the original subjects, the EMG during constant WR exercise was recorded from bipolar surface electrodes from the rectus femoris, vastus lateralis, biceps femoris, tibialis anterior, and gastrocnemius muscles of the right leg of the subjects. EMG signals were amplified and digitized at a sampling rate of 1 kHz. The raw EMG activity patterns were rectified and triggered at the top dead center of each pedal cycle and averaged over 1-s intervals. In addition, the integrated EMG (iEMG) was calculated over 1-s periods.
Analysis
Individual responses during the baseline-to-exercise transitions were time interpolated to 1-s intervals and averaged across each transition for each subject and condition. To further reduce the breath-to-breath noise so as to enhance the underlying characteristics, each average response was smoothed with a five-point moving-average filter. For the on transients, the response curve ofO2 was fit by a three-term exponential
function that included amplitudes, time constants, and time delays,
using nonlinear least-squares regression techniques (4, 5, 12,
13, 20, 24). The computation of best-fit parameters was chosen
by a computer program (KaleidaGraph, version 3) so as to minimize the
sum of the squared differences between the fitted function and the
observed response. The first exponential term started with the onset of
exercise, and the second and third terms began after independent time
delays
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O2(b) is the unloaded
cycling baseline value; A0,
A1, and A2 are the
asymptotic values for the exponential terms; 0,
1, and 2 are the time constants; and
TD1, and TD2 are the time delays. The phase 1 O2 at the start of phase 2 (i.e., at TD1) was assigned the value for that time
(A'0)
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O2 response during
moderate-intensity exercise (<VT) reaches a new steady state within 3 min after the onset of exercise in normal subjects, the slow
exponential term invariably dropped out during the iterative-fitting
procedure. In addition, to facilitate comparison across the subjects
and different absolute WRs, the gain of the fast primary response
(G1 = A'1/WR) and
relative contribution of slow component to the overall increase in
O2 at end-exercise [A'2/(A'1+
A'2)] were calculated. Furthermore, the
increment in O2 between the 3rd and
6th min of the transition
(O26-3) was calculated as an index of the slow component of the
O2 kinetics.
The overall kinetics of the O2 and HR
responses were determined from mean response time (MRT). They were
calculated by fitting the response data to a monoexponential function
that included a single amplitude, time constant, and time delay,
starting from the onset of the transition. From this, a summary
statistic for the kinetics (MRT = time constant + time delay)
was calculated.
Statistics
Data are presented as means ± SD. The data were analyzed using repeated-measures analysis of variance design. Significant results were further analyzed by Scheffé's post hoc test. Significance was set at P < 0.05. The slope of theO2-WR relationship during ramp exercise
was determined by least-squares regression.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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EMG Profile
Typical EMG activity patterns at a WR of 100 W are shown in a representative subject in Fig. 1. With increasing WR, the iEMG increased for 1L and 2L cycle exercise, as expected (Fig. 2). However, there was a greater activation of the rectus femoris and tibialis anterior during conventional 1L exercise compared with that in 2L exercise. In contrast, the iEMG profile of the active muscles during motorized 1L exercise was not discernibly altered from that during 2L exercise. This is particularly evident within some of the major muscles (rectus femoris, vastus lateralis, biceps femoris, tibialis anterior) for the WR up to 100 W (Fig. 2). This indicates that we were successful in minimizing muscular contractions during the knee flexion (pedal-up) phase for the motorized 1L exercise and matching closely the muscle contraction pattern for 2L exercise.
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Incremental Exercise
The response ofO2 as a function of
WR during the ramp exercise tests is shown in Fig.
3 for a representative subject, and mean
summary responses are presented in Table
1. The inflection point in the plot of
O2 against WR seen for 1L but not for 2L exercise was determined by computer analysis. The slope of the O2-WR below the inflection point for 1L
was significantly higher than for 2L exercise (1L = 21.2 ± 2.8 ml · min
1 · W1;
2L = 10.1 ± 1.3 ml · min1 · W1). Beyond the
inflection point, O2 gain
(ml · min1 · W1) was
increased significantly from 21.2 to 33.1 for 1L, whereas the slope
remained constant for 2L exercise.
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Constant WR Exercise
The response forO2 from baseline
to exercise is shown in a representative subject for the two conditions
in Fig. 4. To facilitate comparison of
relative increase in O2 between the two
exercise conditions, O2 responses were
normalized to the difference between baseline
O2 and end-exercise
O2. The
O2 kinetics were the same for the two
exercise conditions and elicited similar time constants (as
1) and MRT but higher gains (G1) for the
fast component of O2 for 1L compared
with 2L exercise (Tables 2 and
3). The absolute amplitude of the slow
component per single leg
(A'2/leg, i.e.,
A'2 for 1L and
A'2/2 for 2L) was not different for the 1L vs. 2L exercise. The O2
6-3 tended to be smaller for the 1L than for the 2L
exercise (P = 0.06). However, the
O26-3 per
single leg was not different for the two exercise modes.
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HR Responses
The response for HR from baseline to exercise for each of the exercise conditions is shown in Table 4. The end-exercise values of HR were significantly lower for 1L than for 2L during moderate and heavy exercise. There was no significant difference in MRT of HR kinetics between the 1L and 2L exercise during moderate exercise. However, the MRT of HR was faster for 1L than for 2L during heavy exercise.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We had hypothesized that O2
kinetics would be faster during the 1L exercise if the speed of the
O2 kinetics were limited by the rapidity
of the cardiovascular response during the 2L exercise. However,
O2 kinetics after the onset of exercise
were not speeded by recruitment of a smaller muscle mass for either
moderate or heavy WR. Furthermore, the relative contribution of the
slow component of O2 to the overall
O2 increment was also not significantly different for the two modes of exercise. These results represent the
first quantitative comparison of O2
kinetics between 1L and 2L cycle exercise. In addition, the present
study furthers our understanding of O2
kinetics during 2L cycle exercise, which has been utilized as a
standard exercise mode for recruitment of a large muscle mass. In
particular, for the upright 2L cycle exercise condition in healthy
humans, the present finding supports the notion that those factors that
determine the primary component of pulmonary and muscle
O2 kinetics for both <VT and >VT WRs are limited by the rapidity of factors intrinsic to the skeletal muscles, such as microvascular O2
delivery-to-O2 requirement mismatch or oxidative enzyme
inertia, rather than the cardiovascular response.
Incremental Exercise
PeakO2 of 1L exercise averaged
70% of 2L exercise. Previous studies reported that the peak
O2 ratio between conventional (i.e.,
nonmotorized) 1L and 2L exercise ranged between 70 and 85% (11,
16, 21). The slopes of the O2-WR
relationship for 2L exercise agree closely with literature values
(30, 31). However, the slope of the
O2-WR below the inflection point for 1L
exercise was significantly higher than for 2L exercise. Specifically, the slopes were 21.2 and 10.1 ml · min1 · W1 for 1L and
2L exercise, respectively. Our results are similar to those found for
1L knee extension exercise (i.e., 15-17
ml · min1 · W1) (1,
31, 33). Moreover, as WR approached the maximum, O2 per watt began to rise even further
for 1L exercise. This profile was markedly different from the linear
increase in O2 seen for 2L exercise. The
greater O2 per watt seen for 1L exercise above the inflection point might reflect an increased
O2 cost of metabolic processes of exercising leg muscles
(see greater iEMG for 1L exercise than for 2L at WR = 150 W in
Fig. 2) and muscles for postural support (including contralateral leg
muscle O2 for body stabilization work)
during exercise with a small muscle mass (1, 30, 31, 33).
It is unclear why the 1L exercise did not achieve a maximum WR per leg (i.e., 95 and 146 W per leg for 1L and 2L exercise, respectively) similar to that for the 2L exercise, despite a muscle contraction pattern that closely matched that for 2L exercise. Before the start of the study, during calibration of the 1L ergometer, we had confirmed the ability of the electrical motor to substitute for the contralateral leg motion (the left leg) to rotate the crank axis and the fly wheel against WRs up to 350 W. The lower maximal performance with the 1L exercise may have been the consequence of postural instability (particularly of the hips and thorax) at very high WRs compared with the 2L exercise because the subjects were required to minimize body sway without moving the contralateral leg.
Constant WR Exercise
O2 fast component.
As explained above, we had hypothesized that
O2 kinetics would be faster during the
1L exercise if the O2 kinetics were cardiovascular O2 delivery dependent in the control
condition (i.e., the 2L exercise) and the cardiovascular responses to
exercise were unchanged. However, O2
kinetics after the onset of exercise were not speeded by recruitment of
a smaller muscle mass for either moderate or heavy WR.
O2 can be slowed by
decreasing CaO2 and/or arterial O2
delivery (9, 12, 19, 24, 26, 38). However, to date, there
is no compelling evidence that increased muscle O2 delivery
can speed the kinetics of O2 during
moderate exercise in healthy humans. Recently, Grassi et al.
(17) demonstrated that faster adjustment of O2
delivery did not affect O2 kinetics during submaximal contractions in isolated canine muscle, suggesting that the kinetics were determined principally by some intramuscular process(es) under these conditions. In humans, MacDonald et al. (27) demonstrated acceleration of
O2 kinetics (faster MRT) in heavy
exercise by hyperoxia and a prior bout of heavy exercise. However, this
could be attributed to a reduction of the slow component without a
speeding of the phase 2 time constant. The reduction of the slow
component without speeding of the phase 2 time constant during heavy
exercise that follows prior heavy exercise has been confirmed in recent
studies (13, 36). The present finding of an unaltered
phase 2 time constant in the face of greatly different recruited muscle
mass suggests that those factors that determine the primary component
of pulmonary and muscle O2 kinetics, at least for the upright cycle exercise condition in healthy humans, were
not affected by muscle mass.
For non-cycling-type exercise, pulmonary
O2 kinetics during moderate leg exercise
with a small muscle mass yields response features that are
quantitatively similar to those evidenced by large muscle mass exercise
(3, 10, 28). For example, Barstow et al. (3)
and Chilibeck et al. (10) reported no significant difference of phase 2 time constants of pulmonary
O2 during moderate exercise with
different muscle mass (upright 2L cycling vs. ankle plantar flexion in
young adult subjects). Furthermore, Rossiter et al. (34)
showed close agreement of the time constants for phase 2 O2 and for phosphocreatine determined
simultaneously during prone knee extension exercise. Collectively,
these findings imply that phase 2 O2
during moderate exercise reflects muscle oxidative phosphorylation
kinetics in the face of adequate O2 delivery to the muscle
(2), despite differences in muscle mass. However, caution
should be exercised when interpreting these data, since
O2 kinetics have been shown to vary with
the type of exercise or muscle group and body position, e.g., arm
cranking vs. leg cycling (7, 9, 22), knee extension vs.
cycling (37), and supine vs. upright cycling (9, 19,
24).
We found the gain of the fast O2
component during the 1L exercise (~20
ml · min1 · W1) to be
higher than that observed for the 2L exercise (~10
ml · min1 · W1) for both
moderate and heavy WRs. These results are in contrast to the findings
of Gleser (16), who found similar
O2 per watt for 1L cycling as for 2L,
when the former was performed by two subjects, each cycling with one
leg. However, our results are compatible with the O2 cost
reported for 1L knee extension exercise (15-17
ml · min1 · W1) (1,
31, 33). The reasons for these discrepancies in findings for 1L
exercise are currently unclear and require further investigation. Recognizing that, to a certain extent, the slope of the
O2-WR relationship can be a function of
the rate of WR increase (39), the
O2-WR slope was determined for ramp
increases of 6 and 12 W/min for 1L exercise. We found that the
O2-WR slope was not different between
the two protocols (Koga S, Barstow TJ, Shiojiri T, Takaishi T, Fukuba
Y, Kondo N, Shibasaki M, and Poole DC, unpublished observations). It is entirely feasible that proportionally
higher O2 costs of metabolic "support" processes
outside the exercising muscles contribute to the greater
O2 per watt gain for 1L exercise, particularly at very high WRs beyond the inflection point in the O2-WR relationship (Fig. 3) (1,
30, 31, 33). However, it is also possible that the specific
neuromuscular recruitment patterns necessary to yield a cycling
efficiency commensurate with a O2 of
~10 ml · min1 · W1 are
peculiar to 2L cycling exercise. If this is the case, EMG analysis as
used herein may not be sufficiently sensitive to detect such differences.
O2 slow component.
It has been proposed that the slower O2
kinetics and the presence of a slow component during 2L heavy exercise
are likely to be associated with an inadequate O2 delivery
to the working muscles (15, 20, 24, 26, 27, 39).
Consistent with this, previous studies demonstrated the reduction of
the slow component of O2, under
conditions in which muscle O2 delivery may have been
increased (and mean capillary O2 pressure certainly was
increased) (13, 15, 23, 27, 36). Therefore, if 1L exercise
created a condition in which perfusion and O2 delivery to
the working muscles at the onset of heavy exercise with a small muscle
mass were facilitated compared with that for large muscle mass
exercise, this should have resulted in a smaller slow component of
O2 during 1L heavy exercise. Because the
primary origin of the O2 slow component
appears to be the working muscles (2, 4, 14, 29, 32) and
thus the size of the slow component depends on the size of the
exercising musculature, we normalized the amplitude of the slow
component to recruited muscle mass performing the exercise (i.e.,
A'2 and
O26-3 for
1L; A'2/2 and
O26-3/2 for
2L). No difference was observed between the 1L and the 2L exercise in
this respect.
O2 for the 1L compared
with 2L exercise might be that any improved perfusion-related decrease
in the slow component may have been offset by an augmented
O2, due to factors such as the
O2 cost for energetic processes within the exercising muscles and for body stabilization (11, 16, 35), such that the net result was no measurable change in the slow component. Alternatively, the mechanisms responsible for the slow component may
not have been sensitive to any improvement in flow-dependent O2 delivery during the 1L exercise, in contrast to previous
manipulations that had resulted in reduction of the slow component,
i.e., prior heavy exercise, increased muscle temperature, and hyperoxia
(13, 15, 23, 27, 36). Similar to a previous study
conducted for the 2L cycle exercise (32), direct
measurement of the leg muscle O2 is
required to isolate unequivocally leg muscle responses from those
occurring within the rest of the body.
In conclusion, when iEMG profiles are unaltered, sentinel features of
the O2 kinetics response to moderate
(TD1, 1) and heavy (TD1,
1, TD2, 2) exercise are
independent of the size of the muscle mass recruited. The lower maximal
performance with the 1L exercise may have been the unavoidable
consequence of postural instability at very high WRs compared with the
2L exercise. Alternatively, altered neuromuscular recruitment patterns
that were not detected from the EMG analysis may have compromised the
1L work output.
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FOOTNOTES |
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Address for reprint requests and other correspondence: S. Koga, Applied Physiology Laboratory, Kobe Design Univ., 8-1-1 Gakuennishi-machi, Nishi-ku, Kobe 651-2196, Japan (E-mail: s-koga{at}kobe-du.ac.jp).
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 6 January 2000; accepted in final form 5 September 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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)
substantially increased the iEMG compared with 2L exercise
(
). In contrast, the iEMG profile of the active muscles
during motorized 1L cycle exercise (
) was not
discernibly altered from that during 2L exercise. This is particularly
evident within the major muscles for work rates up to 100 W.
