INFLUENCE OF POSTURE ON PULMONARY O2 UPTAKE KINETICS, MUSCLE DEOXYGENATION
AND MYOLECTRICAL ACTIVITY DURING HEAVY-INTENSITY EXERCISE
Motor Efficiency and Deficiency EA 2991, Faculty of Sport Sciences, University
of Montpellier I, 34090 Montpellier, France
08 February 2006
Journal of Sports Science and Medicine (2006) 5, 254
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|The aim of the present study was to test the hypothesis that compared
to upright posture, slower oxygen uptake (VO2) kinetics
resulting from exercise at the same relative metabolic load in the
supine posture will be associated with increased muscle de-oxygenation
and greater myoelectrical activity. Nine subjects completed one 12-min
heavy-intensity constant-load exercises in each of the supine and
upright postures on an electronically braked cycle ergometer at a
same gain in metabolism per unit increase in work intensity (10.8
± 1.3 vs. 11.8 ± 1.1 mlO2·min-1·W-1
in upright and supine, respectively) on separate days. Breath-by-breath
VO2 kinetics were analyzed with a double exponential model
to characterize the primary and slow component phases. Myoelectrical
activity (RMS) of the vastus lateralis (VL), rectus femoris, and biceps
femoris muscles was recorded at different epochs of the exercise.
Oxygenation of the VL muscle was recorded continuously by near-infrared
spectroscopy. In supine compared with upright cycling, the primary
time constant of VO2 kinetics was significantly increased
(32.7 ± 10.7 s vs. 23.5 ± 6.7 s, respectively) while
the absolute magnitude of VO2 slow component was decreased
(p < 0.05) but not the relative amplitude. VL de-oxygenation was
higher (p < 0.05) in supine cycling throughout the exercising period
whereas RMS values for all muscles did not change appreciably over
time. Our findings suggest that lowered oxygen supply induced by supine
heavy exercise, alters oxidative metabolism dynamics and increases
muscle de-oxygenation. However, cycling supine did not increase markedly
the rate of muscle fatigue.
WORDS: muscle perfusion, heavy cycling exercises, NIRS, VO2
Changes in muscle oxygen delivery and muscle perfusion are known
to affect force or power output of the muscle (Hepple, 2002;
Wright et al., 1999).
When blood flow is diminished both muscle endurance and oxygenation
decrease, leading to muscle fatigue (Tachi et al., 2004).
Motor unit firing and recruitment patterns have been showed to be
altered during ischemia (Moritani et al., 1992),
suggesting that the lack of oxygen availability increases motor
unit discharge rate of high- threshold units (i.e. which are more
likely to lead to a fatigue state). Limb elevation or muscle heart
configuration-related changes are known to engender circulatory
changes leading to a decrease in perfusion pressure (Wright et al.,
and muscle fatigue (Lind et al., 1978;
Tachi et al., 2004).
The postural effects on the rate of muscle fatigue are thus induced
by changes in the perfusion pressure (Eiken, 1988;
Fitzpatrick et al., 1996).
A recent study of Egana and Green, 2005
demonstrated that the endurance of the calf muscle was improved
when the body was tilted from the horizontal to an incline posture.
This indicated that the fatigue resistance was mediated by an increase
in blood flow when the body was tilted up at least for static exercises.
In a different context, diminished perfusion pressure induced by
position-related changes has been shown to decrease the oxygen supply
and alter the oxidative metabolism dynamics as reflected by a slower
pulmonary oxygen uptake (VO2) kinetics (Convertino et
Hughson et al., 1991)
for moderate-intensity constant-load test in supine compared to
upright postures at the same absolute workload. Gravity adds about
40-50 mmHg perfusion pressure to the arterial supply of the quadriceps
muscles in the upright posture, and therefore could have important
implications in blood flow regulation during exercise. Based on
that, the hypothesis advanced in the literature is that, muscle
blood flow is inadequate at the onset of supine compared to upright
exercise at the same power output (Folkow et al., 1971;
MacDonald et al., 1998).
However, to our knowledge, no study has examined the relationships
between pulmonary VO2 and local muscle de-oxygenation
kinetics during supine and upright heavy exercise and their influences
on the rate of quadriceps muscle fatigue for a same relative metabolic
load. The question about how fast the ATP demand can be covered
under different body posture changes for the same relative metabolic
demand and its effects on muscle function remains unclear. We hypothesized
that supine cycling exercise will slow the VO2 kinetics
and will increase muscle de-oxygenation and myoelectrical activity,
leading to a possible earlier fatigue occurrence.
During heavy-intensity exercise, an additional slow component of
VO2 kinetics is superimposed on the primary VO2
response (Barstow et al., 1996;
Cleuziou et al., 2005;
Koga et al., 1999).
It is well admitted in the literature that the exercising limbs
are considered as the major determinants of the VO2 slow
component (Poole et al., 1991).
The observed increase in muscle deoxygenation signal over the slow
component period suggests that the local balance between muscle
delivery and utilization was altered during the slow component,
and is consistent with the origin of the VO2 slow component
being predominately in the exercising muscle (DeLorey et al., 2005,
Bringard et Perrey, 2004).
However, to our knowledge, the balance between local muscle O2
delivery and utilization during the slow component of VO2
with different muscle perfusion (e.g. supine vs. upright postures)
have not been studied, except in part by Koga et al., 1999.
However as ventilatory threshold (VT) and maximal VO2
are significantly higher in upright compared to supine cycling exercise
(Koga et al., 1999)
and because VO2 slow component occurs for exercise intensities
above VT (Gaesser and Poole, 1996),
a given absolute workload performed in supine cycling will be relatively
lower when performed in upright cycling. As a result, a higher slow
component will occur in supine heavy exercise. Relative metabolic
load is more important in determining the VO2 kinetics
features (e.g. magnitude of the slow component, Gaesser and Poole,
rather than the workload per se (Perrey et al., 2001b).
If supine exercise is really associated with a relative perfusion
inadequacy to the working muscles (Hughson et al., 1993;
Leyk et al., 1994),
this should be exacerbated during supine heavy exercise even at
a high metabolic load. Therefore, the second aim of this study was
to test the hypothesis that the supine exercise would be associated
with a larger slow component (and a higher rate of muscle fatigue
shown by EMG signal changes) compared with the upright exercise
at a same relative metabolic load.
Nine trained male subjects volunteered to take part in this study.
Their mean (SD) values for age, height, and body mass were 25.8
(3.3) years, 1.76 (0.06) m, and 67.2 (8.1) kg, respectively. The
study protocol complied with the Helsinki declaration for human
experimentation. All the experimental procedures used in this study
were in accordance with the standards of the Local Ethical Committee
on Human Experimentation. Possible risks and benefits were explained
and written informed consent was obtained from all subjects after
a full explanation of the protocol. None of them suffered from muscle
soreness, knee injury, or peripheral vascular disorder. Subjects
were asked to avoid caffeine intake within the 8 hours preceding
the tests. The subjects were all fully familiar with laboratory
exercise testing procedures.
In order to standardize the exercising posture, supine and upright
cycling exercises were performed with the same distance separating
the hip of each subject to the crank shaft axis of the cycle ergometer.
Feet position on the pedals was also maintained identical in both
exercises. For supine and upright tests, subjects were asked to
not grip their hands and not use their arms to avoid any upper body
contribution during the exercise.
The tests were performed on an electromagnetically braked cycle
ergometer (Ergoline, Ergoselect 100 P, Germany). In supine cycling,
the crank shaft was positioned 33 cm above the level of the heart.
A home made apparatus was used to lock subjects' shoulders and prevent
from possible rear movements inherent to the forces applied on the
pedals (see Figure 1).
came to the laboratory on four occasions. Two preliminary tests
were realized in order to determine the first ventilatory threshold
(VT1) specific to each cycling posture. Then, subjects
were asked to perform randomly two constant workload tests, one
in each of the upright and supine postures. During these tests,
VO2 was collected breath-by-breath. Electromyographic
activity (EMG) of vastus lateralis (VL), rectus femoris (RF) and
biceps femoris (BF) muscles was recorded at different epochs of
the exercise. We also monitored VL muscle de-oxygenation at rest,
during warm-up and exercising periods.
The subjects were instructed to arrive at the laboratory in a rested
and fully hydrated state, and to avoid strenuous exercise in the
48 hours preceding a test session. For each subject, tests took
place at the same time of day (± 2 hours) to minimize the
effects of diurnal biological variation (Carter et al., 2002).
As it is typically done in VO2 kinetics studies with
heavy exercise, subjects exercise at a relative percentage of workload
between that at VT and maximal VO2 for each position
investigated. Because of the institution's restrictions on maximal
testing of subjects without a physician present, incremental testing
to voluntary exhaustion was not performed. Rather, subjects exercised
at an absolute power (25 W) above their VT, which, from an extensive
review of the literature on VO2 kinetics, was a typical
workload that was ~30% between that at VT and maximal VO2
for the subjects tested in the present study (heavy domain). Some
pilot studies in our laboratory allowed us to check that the same
relative metabolic load was achieved between supine and upright
cycling exercise by using this procedure. Further it has been recently
showed that the steady-state VO2 in supine and upright
postures represented the same percentage of maximal workload (80%)
achieved during the graded test in the same posture (Egana et al.,
On separate days (at least two days apart), a ramp test protocol
(25W·min-1) was thus conducted for each posture
until at least one workload above the VT1 intensity level
was clearly discernable. VT1 was determined by two experienced
investigators from the point of increased minute ventilation (VE)-to-VO2
ratio without a concomitant increase in VE-to- VCO2 output
ratio (Tordi et al., 2003);
there was no case in which the two determinations of VT1 differed.
Then, on two separate days, subjects were asked to perform a 12-min
constant workload cycling exercise test at a constant and similar
pedal frequency comprised between 60-80 rpm. The workload was set
to correspond to posture specific VT1 plus 25 W. As said
before, this level of intensity is known to elicit the slow component
phenomenon during heavy cycling and appears to be sufficient enough
to induce muscle fatigue-related changes (Xu and Rhodes, 1999).
Each constant exercise was preceded by 3-min of rest, followed by
a 3-min warm-up period at 20 W.
Before each constant workload test in supine and upright postures,
mean arterial pressure (MAP) was taken with a standard sphygmomanometer
and a stethoscope during quiet resting from the right brachial artery.
MAP was the sum of diastolic blood pressure added to one third the
pulse pressure; pulse pressure was the difference between systolic
and diastolic pressures. We elected the supine and upright postures
with the arm extended at heart level. Heart rate (HR) was continuously
recorded telemetrically at rest and during the exercising period
using a heart rate monitor (Polar Electro Oy, Kempele, Finland).
Breath-by- breath gas exchange data were carried out throughout
the tests (i.e. during the rest, warm-up and exercising periods)
with the help of a metabolic cart (ZAN 680, Oberthulba, Germany)
using standard algorithms, allowing for the time delay between gas
concentration and volume signals. Subjects breathed through a low
dead space (40 ml), low resistance (<0.05 kPa·L-1·s-1
constant up to 14 L·s-1) mouthpiece and turbine
assembly. Gases were continuously drawn from the mouthpiece through
a 2 m capillary line of small bore, and analyzed for O2
and CO2 concentrations by optical spectrometer and infrared
absorption analyzers, respectively. Expiratory volume was determined
by a flow sensor calibrated before each test using a known volume
syringe (1 l, ZAN 680, Oberthulba, Germany,). Gas analyzers were
calibrated before each test from both the room air and gas of known
concentration. Respiratory gas exchange variables (VO2,
production of carbon dioxide, VCO2 and VE) were calculated
and displayed for every breath.
Local muscle oxygenation profiles were assessed using the NIRS technique.
The NIRS signal provides continuous, non-invasive monitoring of
the relative concentration changes in oxygenation ([HbO2]),
deoxy- hemoglobin ([HHb]) and total hemoglobin ([Hbtot]) concentrations
(Sako et al., 2001).
Because of the overlap of the spectrum it is not possible to distinguish
between changes in hemoglobin (Hb) and myoglobin (Mb). However,
in human skeletal muscle, the ratio of Hb to Mb concentration is
>5 (Mancini, 1997)
so the signal is usually considered as deriving mainly from Hb.
In the present study, only changes in VL muscle de-oxygenation were
continuously monitored at 6 Hz using a near-infrared spatially resolved
spectroscopy oximeter (NIRO-300, Hamamatsu Photonics, Japan). VL
muscle was chosen due to its great involvement in cycling exercise
(Ericson et al., 1985).
NIRO-300 optodes were housed in an optically dense plastic holder,
ensuring that their position relative to each other was fixed and
invariant. The probe (i.e. the optodes support) was secured on the
cleaned skin surface with tape and then covered with a black home-made
cotton tissue, thus minimizing the intrusion of extraneous light
and loss of infrared light from the field of interrogation. The
probe was placed over the VL muscle belly, ~12 cm above the right
external part of the patella. Skinfold thickness was measured on
the area we investigated using a skinflod caliper (Holtain Ltd.,
Crymmych, UK), and was divided by 2 to determine the adipose tissue
thickness (i.e. fat + skin layer) covering the muscle. The obtained
values were 3.8 ± 1.3 mm, and were well below the minimum
required, allowing the NIRS proton to penetrate through the muscle
(Ferrari et al., 1997;
van Beekvelt et al., 2001).
The absorption of light at different wavelengths (775, 810, 850
and 910 nm) was analyzed according to the modified Beer- Lambert's
law. A 3.8 differential pathlength factor (DPF) was used for the
VL muscle (DeLorey et al., 2005),
thus changes in HHb concentrations are reported as a change from
baseline in micromolar units (µM). It has been proposed that
HHb was less sensitive to blood volume changes than its counterpart
HbO2 (Delpy and Cope, 1997).
Thus we used HHb as an estimator of changes in intramuscular oxygenation
and O2 extraction. After each test, probe emplacement
was carefully marked.
Surface EMG from the muscle belly of VL, RF and BF were recorded
during the 12-min constant workload exercise. We used bipolar Ag/AgCl
electrodes (Contrôle Graphique Medical, Brie-Comte-Robert,
France) with a diameter of 9 mm and an inter-electrode distance
of 25 mm maintained constant. The ground electrode was placed on
the wrist. Low impedance at the skin-electrode surface (< 5 kΩ)
was each time obtained by abrading the skin with emery cloth and
cleaning with alcohol. EMG signals were band-pass filtered at 30-500
Hz and sampled at 2000 Hz, with the Biopac A/D device (MP30, Biopac,
Inc., Santa Barbara, USA). After each test, care was taken to mark
the electrodes emplacement.
Occasional errant data points (e.g. consequent to a cough, sneeze
or sigh) were at first visually deleted from the respiratory data
set to enhance the underlying characteristics. Then, non-linear
regression techniques were used to fit the VO2 kinetics
data during the warm-up (20W) to exercise transitions in both positions
with a bi-exponential model commonly used in the literature for
heavy cycling (Barstow et al., 1996;
Cleuziou et al., 2005;
Koga et al., 1999).
The mathematical model consisted of two exponential terms, each
representing one phase of the response (primary and slow components).
Based on previous literature (Barstow et al., 1996),
the model was constrained to aid in identification of the key parameters.
As suggested by Whipp et al., 1982,
VO2 values recorded at the early beginning of the transition
(< 20 s) were visually excluded from the analysis since they
do not contribute to the muscle metabolism. The computation of best-fit
parameters was chosen by the program to minimize the sum of the
squared differences between the fitted function and the observed
response. Data fitting were analyzed with successive iteration,
using the squared differences method. The equation was:
= VO2 (b) + AP x (1 - e -
(t - TDp) /τp) + AS x (1 - e
- (t - TDs /τs)
where VO2 (b) is the average value of VO2
during the 3-min warm-up, AP and AS are the asymptotic amplitudes
of the exponentials; TDp and TDs are the time delays, and p and
s are the time constants of the primary and slow component phases,
increase in VO2 above baseline level as a function of
the net increase in power output was also calculated. Then, following
the procedure outlined previously (Lamarra et al., 1987)
the 95% confidence intervals for estimation of the primary component
(as determined by p) were calculated. We found a single transient
to be sufficient in our subjects as the large amplitude of response
was associated with a good signal-to-noise ratio. Moreover, we cannot
exclude the fact that the breath-to-breath variability may possess
biological significance, although Lamarra et al., 1987
suggested stochastic properties of the breath-to-breath noise. In
the present study, the lack of relationship between the residuals
and the time (p > 0.1) and the sum of the residuals lower than
10-6 support the view of these authors. Even if a single
transition may be spoiled by inherent noise, the use of a higher-order
model (two exponential terms) during heavy exercise is justifiable
because the parameters estimated from the data produced a statistically
significant reduction in the error between the modeled and measured
responses compared to a first-order model (monoexponential fit).
A higher order model was not accepted as a superior representation
of the response if the decrease in summed-square error was sufficient
to offset the loss in degrees of freedom associated with the increased
number of model parameters as determined by an F-test (F=model variance
· residual variance-1) (Motulsky and Ransnas, 1987).
Plots of residuals were also examined to help determine the appropriate
At rest, mean [HHb] values were averaged on a 30 s interval at the
2nd minute for the two postures. During the exercise,
[HHb] values were averaged on a 30 s interval basis at the 3rd
minute of the warm-up, and at the 2nd and 11th
minutes of the exercise. These times were chosen since they allowed
us to investigate a large range of the exercising period and corresponded
to the different phases of the VO2 kinetics-related adaptations.
In this study, we also analyzed [HHb] kinetics with a mono-exponential
model (DeLorey et al., 2003).
Kinetics of [HHb] during the rest-to-exercise transition were fitted
from the time of initial increase in HHb to 90 s with a mono-exponential
model of the form in equation for O2 uptake kinetics
without the slow component (DeLorey et al., 2003).
Analysis of the EMG amplitude for the three muscles investigated
have been performed with the Biopac software (Acqknoweldge, BSL
Pro 3.6.7, Inc., USA). Root Mean Square (RMS in mV) EMG values were
calculated for the three muscles on a burst by burst basis around
the 2nd, 6th and 11th minutes of
the constant workload cycling exercise for 6 consecutive contractions
before being averaged together. Then for each minute investigated
(i.e. 2, 6 and 11), average RMS values were divided by the corresponding
values of VO2, in order to estimate the adjustment of
RMS to the muscle metabolism (RMS/VO2 ratio, Jammes et
Data are presented as mean values (± SD). At rest, the results
regarding the differences between upright and supine postures for
HR, MAP, [HHb] and VO2 values were analyzed using the
Student's t-test for paired data. During the constant workload tests,
similar analyses were carried out to compare the mean power output
and the parameters of VO2 and [HHb] kinetics. Two-way
repeated measures ANOVA with post hoc Student-Newman-Keuls
tests were used to test for difference in average [HHb] and EMG
values among specific time of exercise and between postures. Significance
was set at p < 0.05.
nine subjects cycled at 197.2 (42.3 W) in upright position and at
149.9 (30.0 W) in supine position (p < 0.05). All the subjects
were able to cycle for 12 minutes in both postures.
rate, mean arterial pressure and VO2 kinetics
At rest, HR and MAP values were significantly higher in upright
compared to supine postures (+ 12.4 ± 7.7 beats·min-1,
+ 9.2 ± 0.7 mmHg, p < 0.05, respectively). During the
exercise steady-state HR values averaged between the 10th
and 11th minutes were significantly higher in upright
cycling (+18.0 ± 8.4 beats·min-1).
Figure 2 represents the VO2
kinetics for a representative subject for the two postures at a
similar relative metabolic load. The increase in VO2
from baseline level per unit increase of work intensity before the
appearance of the slow component of the VO2 kinetics
was not significantly different between upright and supine cycling
(10.8 ± 1.3 vs 11.8 ± 1.1 mlO2·min-1·W-1,
respectively). The main differences among VO2 kinetics
parameters between the two postures are reported in Table 1. The VO2 primary component
amplitude (Ap) was greater
in upright cycling compared to supine cycling; similar findings
were found regarding the slow component. However the relative magnitude
of the slow component represented a similar percentage of the total
increase in VO2 during upright and supine cycling exercise
but with large standard deviations. The time constant of the primary
component was significantly higher in supine compared with upright
cycling. The mean 95% confidence intervals for the estimation of
τp were ± 3.9 s and ± 5.9 s during upright and
Values of [HHb] were significantly higher in supine cycling than
in upright during the warm-up period and at the 2nd and
11th minutes of exercise (Figure
3). For both postures, post- hoc tests revealed that [HHb] was
significantly higher at the 2nd and 11th minutes
compared with the warm-up period. For each time analyzed, [HbO2]
and [Hbtot] values were significantly lower in supine compared with
(p < 0.05).
Regarding [HHb] kinetics, no differences were found between the
two exercising postures. However, whatever the posture [HHb] time
constant and time delay of the primary component (i.e. p [HHb] and
TDp [HHb], respectively) were significantly lower than those of
the corresponding values of VO2 (Table 2).
There was a significant increase in the VL RMS amplitude during
upright cycling from the 2nd minute of exercise to the
6th and 11th minutes (+20% and +25%, respectively,
Figure 4). In supine cycling, no differences in RMS were found
RMS/VO2 ratio was significantly higher in supine compared
to upright postures only at the 2nd minute (0.0065 vs.
0.0052 mV mlO2·kg-1, Figure 4).
Then this ratio significantly decreased over time in supine posture.
No significant differences were
found for upright exercise over time. Whatever the cycling position,
RMS and RMS/VO2 values for the RF and BF muscles did
not show any significant changes throughout the exercise period.
this work, we aimed to study the effects of circulatory difference
induced by body posture on the oxidative metabolism dynamic adaptations
related to muscle de-oxygenation and myoelectrical activity during
cycling exercises for a same relative metabolic load. The main findings
of this study are i) an increase of the primary component time constant
during supine cycling; ii) a higher muscle de-oxygenation in supine
cycling whereas no differences were found among [HHb] kinetics between
the two postures; iii) and an increase in the VL RMS amplitude over
time during upright cycling.
rate, mean arterial pressure
In the present study, we did not measure muscle blood flow. However,
it has been showed that despite a greater cardiac output (Hughson
et al., 1991;
Leyk et al., 1994)
the effective blood flow to the working muscles decreases in supine
posture (Eiken, 1988;
Egana and Green, 2005;
Folkow et al., 1971;
MacDonald et al., 1998)
as a consequence of a lower arterial pressure in the legs when the
hydrostatic gradient effect is removed. Furthermore, body posture
changes are known to determine a gravitational gradient that acts
on both the cardiovascular and cardiopulmonary systems and consequently
affect optimal blood flow and oxygen delivery (Jones and Dean, 2004).
With regards to the amplitude of the primary component (i.e. Ap
in Table 1), differences between
supine and upright heavy exercises can be logically attributed to
differences in absolute power output (mean difference of 47.3 W).
However as expected with the experimental approach used, our data
indicate that the subjects performed similar relative work intensities
in both upright and supine postures. The equal gain in metabolism
per unit increase in work intensity in upright and supine postures
does support the premise that subjects were performing equal relative
work rates (10.8 ±1.3 vs. 11.8 ± 1.1 mlO2·min-1·W-1,
respectively) before the appearance of the slow component in the
"heavy" domain. There appears
to be a reasonable assumption that the VT1 determined for each subject
in each exercise posture represents the same %VO2max.
A recent study showed that VO2 end- exercise values for
constant-load cycling tests (upright and supine) expressed as a
percentage of those measured during the graded test (~80% of maximal
power output) in the same posture were not different between both
postures (Egana et al., 2006).
Consequently, our results suggest that the fiber pool recruitment
was likely similar during the first 2-3 min of exercise (confirmed
in part by identical VL RMS values at min 2 of the constant- load
exercise in both postures, Figure
Our results show that VO2 kinetics primary component
was significantly slower in supine cycling compared to upright cycling
(τp decreased by ~39%). Even if a single transition was performed
(first limitation), 95% confidence intervals for τp as 4 s
and 6 s for upright and supine exercises were judged acceptable
when comparing τp values that are substantially different between
supine and upright exercise transients (Table
1). Our findings confirm past studies when moderate-intensity
exercises were used but at the same absolute workload (Convertino
et al., 1984;
Hughson et al., 1991).
Interestingly, it appears that the increase in power output between
supine and upright postures in Koga et al., 1999
(almost a difference of 100 W) did not influence τp but lowered
significantly the relative metabolic demand (in mlO2·min-1·W-1)
in supine compared to upright heavy cycling exercises. Altogether
even if in our study design only relative and not absolute workloads
were compared (second limitation), we think that all observed differences
among VO2 kinetics (between the two experimental conditions)
were likely due to posture-related changes in local blood flow and
not to concomitant changes in power output. Speeding of VO2
kinetics has already been reported in various experimental contexts:
with endurance training (Philips et al., 1995),
by inducing an important metabolic acidosis (Tordi et al., 2003)
or by eliciting a muscle chemoreflex to increase MAP and blood flow
to an exercising muscle mass (Perrey et al., 2001a).
Based on the literature, we may suggest that O2 transport
appeared to slow the VO2 kinetics in supine compared
to upright cycling at the same relative metabolic demand, and was
likely the limiting factor under the actual experimental conditions
(Convertino et al., 1984;
Hughson et al., 1991;
MacDonald et al., 1998).
Moreover we showed for the first time that the VO2 slow
component amplitude (absolute terms) was significantly lower in
supine than in upright cycling exercise performed at the same relative
metabolic demand; a seemingly large physiological difference was
observed in relative terms for slow component but was not significant
due to large standard deviations. To the best of our knowledge,
the only study investigating the effects of upright and supine cycling
exercises on VO2 slow component was the study of Koga
et al., 1999
who found a higher VO2 slow component (in both absolute
and relative terms) in supine cycling but at the same absolute power
output. It is well known that the magnitude of the slow component
depends on the relative exercise intensity (Gaesser and Poole, 1996)
and may in part explain the differences between the two studies.
By analogy, our result is in full agreement with that of Cleuziou
et al. (2005)
who showed that under hypoxia, subjects exhibited a lower slow component
compared to normoxic condition at identical exercise intensities
(equivalent relative metabolic demand) but an equivalent slow component
amplitude in relative terms. They suggested that the decrease in
inspired gas concentration was the main possible explanation for
the lower slow component amplitude observed in their experimental
design. Decrease in slow component amplitude could arise from differences
in O2 availability per se (probably not in the current
study due to the same relative exercise intensity), or from possible
change in muscle fiber recruitment as a consequence of the differences
in O2 availability (Pringle et al., 2003).
In several experiments (Barstow et al., 1996;
Borrani et al., 2001;
Shinohara and Moritani, 1992),
the slow component phenomenon has been linked to a progressive recruitment
of fast twitch fibers. The RMS increase for VL observed in upright
cycling confirms partly the above studies. However, all remaining
EMG analyses for the two remaining muscles and mainly during supine
condition suggest that it is still difficult to link EMG data to
the slow component phenomenon (Scheuermann et al., 2001).
We proposed that the reduction in the absolute amplitude of slow
component in supine position might be explained by a greater contribution
of the type I fibers to the exercise after 2-3 min. At an intensity
above VT, a large number of type II fibers are recruited during
the first 2-3 min of the heavy exercise before the entire type I
fiber pool is active (Pringle et al., 2003).
The increased local O2 extraction ([HHb]) observed in
the present study in both exercising postures is consistent with
the literature. Chance et al., 1992
and Neary et al., 2001
showed that the de-oxygenation magnitude was proportional to the
exercise intensity level. Our study was the first to investigate
muscle oxygenation changes induced by posture, among large muscle
masses. Tachi et al., 2004
demonstrated that isometric exercise performed in a leg up condition
induced a decrease in muscle oxygenation. Regarding our results,
we observed the same tendency. In supine cycling [HHb] was significantly
higher at all the time periods investigated (i.e. warm-up, 2nd
and 11th minutes) compared to upright cycling. This confirms
our hypothesis concerning an increase in muscle de- oxygenation
related to a decrease in O2 delivery (evidenced by a
diminution of baseline HR and of local oxygenation), due to the
modifications induced by the supine posture (i.e. hydrostatic pressure
gradients in blood vessels oriented longitudinally in the body are
larger in upright than in supine). Overall, significant increase
in [HHb] appeared to reflect a mismatch between the oxygen supply
and the increasing metabolic demand of the active muscle due to
both the exercise intensity and the decrease in O2 delivery.
Regarding [HHb] kinetics, they were significantly faster than those
of VO2 in both supine and upright postures. These results
are in agreement with those of DeLorey et al., 2003
and Bringard and Perrey, 2004.
For both postures, after a time delay of ~14 s, HHb increased rapidly
toward a "steady- state" level (τp mean value of
10 s), suggesting that muscle perfusion or the local distribution
of blood flow and O2 delivery in the on-transient of
heavy-intensity cycling exercise was not adequate to meet the metabolic
demand of the muscle, thus requiring a rapid increase in O2
extraction. However, by using the mean response time for the on-kinetics
of HHb (TD plus ) and the τp (i.e., the time constant of the
metabolically relevant "primary phase") of the pulmonary
VO2 on-kinetics, the upright comparison is 24 and 26
s for VO2 and HHb, and 33 s versus 24 s for the supine
comparison. The difference in supine (p < 0.05), but not in upright
may suggest that the kinetics of O2 delivery was indeed
limiting the VO2 kinetics in supine. According to the
Fick principle the VO2 / [HHb] ratio can be used to estimate
the muscle capillary blood flow (Ferreira et al., 2005).
In the present study the muscle capillary blood flow kinetics was
thus likely slower in supine position (Eiken, 1988;
Folkow et al., 1971),
suggesting that a delay occurred probably between O2
supply-diffusion mechanisms and muscle demand.
In the present study, our unexpected results about EMG were different
of Tachi et al., 2004.
These last authors found an increase in the integrated EMG when
subjects performed static dorsiflexion with their legs up compared
to the same exercise realized with their legs down. Conversely,
we observed an increase in the VL RMS amplitude only when subjects
were cycling upright in which the slow component was found to be
the highest. In supine cycling, RMS signal was constant throughout
the exercise for all the muscles investigated. Steady RMS signal
found in supine cycling can be explained by the position-related
O2 supply changes leading to a change in neuromuscular
activity. Motor unit recruitment has been shown to be not only dependent
on the level of force developed but also on the oxygen availability
(Moritani et al., 1992).
Regarding the EMG myoelectrical activity of RF and BF muscles, no
differences were found between the two postures, and their respective
RMS values remained steady throughout the exercise. This result
shows that for the same relative exercise metabolic demand, VL muscle
was likely the main muscle to participate to the cycling task in
upright posture (Van Ingen Schenau et al., 1995).
The ratio between total EMG energy (RMS) to the corresponding VO2
was higher in supine posture only for the VL muscle at the second
minute of the exercise. Thereafter, this ratio decreased to the
6th minute of the exercise and remained stable as it
did during upright cycling. A possible explanation of a higher RMS/VO2
ratio at the minute 2 of supine exercise could be the existence
of a longer time delay between the power production and the energy
supply adjustment during the first minutes of exercise (Jammes et
aimed at evaluating the effects of heavy cycling exercise in supine
and upright postures on the oxidative metabolism and muscle oxygenation
kinetics in relation to muscle activity at the same relative metabolic
load. In supine cycling, muscle de-oxygenation was greater, oxidative
metabolism adaptation was slowed significantly, but RMS did not change
for any of the investigated muscles. These results indicate that the
decrease in O2 supply induced by a decrease in hydrostatic
pressure gradient in supine posture impaired oxidative metabolism
adjustment without inducing premature muscle fatigue at the same relative
pressure gradients in blood vessels oriented longitudinally in
the body are lesser in supine than in upright posture.
oxygen supply induced with supine exercise slows oxidative metabolism
dynamics and increases muscle de-oxygenation during heavy exercise.
to upright, supine exercise did not increase markedly the rate
of muscle fatigue at a same relative metabolic load.
Employment: Student, Faculty of Sport Sciences, University
of Montpellier I.
Research interests: Exercise physiology.
Employment: Prof. at the Department of Physical Training
& Sports Engineering, Faculty of Sport Sciences, University
of Montpellier I, France.
Research interests: Exercise physiology, acute and chronic
cardiorespiratory and muscle responses of human to physical
activity, physiological responses of endurance and power athletes,
and neuromuscular fatigue