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Laboratoire de Physiologie, Faculté de Médecine de
Nancy, 54505 Vand
uvre lès Nancy, France
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The aim of this study was to identify
some of the mechanisms that could be involved in blunted ventilatory
response (
E) to exercise in the supine (S) position.
The contribution of the recruitment of different muscle groups, the
activity of the cardiac mechanoreceptors, the level of arterial
baroreceptor stimulation, and the hemodynamic effects of gravity on the
exercising muscles was analyzed during upright (U) and S exercise.
Delayed rise in E and pulmonary gas exchange
following an impulselike change in work rate (supramaximal leg cycling
at 240 W for 12 s) was measured in seven healthy subjects and six
heart transplant patients both in U and S positions. This approach
allows study of the relationship between the rise in
E and O2 uptake
(O2) without the confounding effects of
contractions of different muscle groups. These responses were compared
with those triggered by an impulselike change in work rate produced by
the arms, which were positioned at the same level as the heart in S and
U positions to separate effects of gravity on postexercising muscles
from those on the rest of the body. Despite superimposable
O2 and CO2 output responses,
the delayed E response after leg exercise was
significantly lower in the S posture than in the U position for each
control subject and cardiac-transplant patient (
2.58 ± 0.44 l
and 3.52 ± 1.11 l/min, respectively). In contrast, when
impulse exercise was performed with the arms, reduction of ventilatory
response in the S posture reached, at best, one-third of the deficit
after leg exercise and was always associated with a reduction in
O2 of a similar magnitude. We
concluded that reduction in E response to exercise in the S position is independent of the types (groups) of muscles recruited and is not critically dependent on afferent signals originating from the heart but seems to rely on some of the effects of
gravity on postexercising muscles.
minute ventilation; supine; baroreflex; muscle afferent fibers; peripheral vascular distension
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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IT HAS ALREADY BEEN
RECOGNIZED that the ventilatory response to a constant work rate
(WR) exercise is affected by the position of the body in humans. For
instance, Weiler-Ravel et al. (38) have shown that the
minute ventilation (E) phase I and phase II
responses to a constant WR exercise are reduced in the supine (S)
position compared with an upright (U) exercise of similar intensity. On
the basis of the observation that the cardiovascular (cardiac output)
changes are also blunted in S position exercise (3, 27,
36), it was proposed (38) that a circulatory mechanism related to the magnitude of the cardiovascular response to
exercise could account for the reduced exercise hyperpnea in the S
position (or exaggerated response in the U position). It remains
unclear, however, through which receptors such a mechanism of
circulatory origin can affect the control of breathing in exercise.
This study was therefore intended to determine the possible mechanisms
that alter the ventilatory response to exercise according to body
position. More specifically, two questions were addressed. Because
different groups (types) of muscles are recruited in the U and S
positions, it was first necessary to determine whether the reduced
E response in the S position does not simply reflect a different muscular efficiency, and thus muscle afferent recruitment or central command involvement (see Refs. 8 and 11
for discussion and review), as a slower and lower O2 uptake
(O2) response in the S position
(38) suggests. This was achieved by analyzing the
relationship between the delayed rise in E,
O2, and CO2 output
(CO2) triggered by an "impulse"
change in WR both in the S and U positions. The rationale for using
such an approach was if a short burst (10-15 s) of a supramaximal
exercise is imposed on a subject, the rise in
O2, CO2,
and E triggered by this "impulse forcing" occurs
well after cessation of the contractions (12, 13, 40). On
the basis of the principle of linearity, an impulse forcing, which can
be regarded as the first derivative of a constant WR exercise, is
expected to trigger delayed ventilatory and metabolic responses that
follow the temporal profile of the first derivative of the response to
a step exercise (12). Indeed, the traditional
E phases I and II (6) are replaced by a
sudden and transient increase in E for a few breaths
followed by a clearly delayed rise in pulmonary gas exchange and
E, which subside exponentially (12-14,
40). The second phase of the E response,
therefore, occurs at a time (>20 s into recovery) when neither the
cortical and subcortical drive to the spinal motoneurons nor muscular
contraction-related information of a mechanical nature is operating
(see Ref. 11 for discussion). Yet the E
response is that expected of a step exercise and follows the change in pulmonary gas exchange (39). Figure
1 gives an example of the responses of
one subject. In other words, an impulselike change in WR offers the
opportunity to study the ventilatory response to exercise while the
body is in the peculiar situation of being at rest but behaving as if
exercising from a metabolic and circulatory point of view. If changing
the body position affects the ventilatory control system during
exercise independently of the type of muscle recruited, the
delayed rise in E, which follows the rise in O2 and
CO2 after the cessation of the muscular
contractions, is still expected to be reduced in the S position at
any given level of pulmonary gas exchange compared with an U exercise.
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Our second objective was to determine whether receptors located in the
circulatory system could, due to certain effects of gravity, depress
the E response to exercise in the S position, as
suggested by Weiler-Ravell et al. (38).
Hydrostatic effects of gravity can affect many compartments of the
circulatory system, which might in turn modify the ventilatory response
to exercise. For instance, the blunted rise in cardiac output at
the onset of exercise in the S position has been suggested to account
for the accompanying relative hypopnea (38). A
higher pressure at the level of the arterial baroreceptors in the S
than in the U position may also reduce the E
response (4, 18, 32). On the other hand, the mechanical
load applied by the venous return from the exercising limbs in the U
position, together with a higher perfusion pressure, might represent an
additional stimulus to breath compared with the S position through the
stimulation of muscle slow-conducting afferent fibers (15, 18,
24). To clarify the putative role of 1) the cardiac
mechanoreceptors, 2) the arterial baroreceptors, and
3) the muscle circulation, the delayed ventilatory responses
to an impulse change in WR in the S and U positions were also studied
in heart transplant patients and in a condition where the effects of
gravity on the postexercising muscles could be dissociated from those
on the rest of the body by using a group of muscles positioned at the
same distance of the heart in both positions.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
Seven healthy male subjects and six patients with heart transplant were studied. They were informed about the general purpose of the study, and an informed consent was obtained after the agreement of our local ethical committee. Mean age, height, and weight were 36 yr (range of 30-48 yr), 1.75 m (range of 1.65-1.90 m), and 72 kg (range of 69-92 kg), respectively, for control subjects, and 45 yr (range of 27-51 yr), 1.74 m (range of 1.70 -1.85 m), and 71 kg (range of 62-86 kg) for heart transplant patients. Patients were studied 30 ± 16 mo (range of 2-108 mo) after the transplantation when in a stable condition, and none of them had symptoms of cardiac or respiratory insufficiency. One patient had had a heart and lung transplantation.Equipment
Subjects exercised on a table-mounted electromagnetically braked ergometer and breathed room air through a low- dead-space face mask (small or medium size, Hans Rudolph mask, Hans Rudolph, Kansas City, KS) connected to a pneumotachograph (MediGraphics Prevent pneumotachograph, Medical Graphics, St. Paul, MN). The ergometer could be tilted from the vertical to horizontal position and was modified to allow the subjects to pedal with their arms, which could be positioned at any desired level from the heart in either posture. Inspiratory and expiratory flows were measured, and the respiratory gas was continuously sampled from the pneumotachograph. O2 and CO2 concentrations were determined by rapidly responding O2 and CO2 analyzers (Datex analyzers, Medical Graphics). Respiratory flow, PO2, and PCO2 were digitized at 100 Hz for breath-by-breath calculation ofE and pulmonary gas
exchange. All data were processed on-line and stored on disk for
further analysis. Systemic arterial blood pressure (BP) was estimated
noninvasively from the measurement of finger arterial pressure
(Finapres system, Ohmeda, Louisville, LA). A Finapres cuff was placed
around the index finger and connected to a Finapres monitor (model
Ohmeda 2300, Ohmeda). This approach allows uninterrupted recording of
the BP signal, which, at least for the mean BP, is a very reliable
estimate of intra-arterial BP (see Ref. 19 for review).
The finger with the cuff was positioned at a level corresponding to
that of the carotid bifurcation (upper part of the neck). The
electrocardiogram was monitored from a three-lead configuration. Output
signals from the Finapres were fed to an analog-to-digital converter
(Mac Lab system) and displayed on-line on a microcomputer screen. The
frequency of numerization was set at 200 Hz.
Protocol
Control measurements. The impulse load consisted of a 240-W exercise for the legs and a 175-W exercise for the arms applied for 12 s. This WR level was selected so that each subject could pedal in both positions without too much unnecessary movement of the trunk.
Following a visual signal, subjects were asked to pedal at a frequency between 85 and 95 rpm. At this frequency, the torque applied to the pedals was reduced and the test could be performed by each subject with no difficulties. Subjects were familiar with this protocol because they had all carried out the various tests of the protocol on at least three occasions in the days preceding experimentation. Sixteen tests were performed by each subject in a random order. On eight occasions, subjects exercised with their legs. The exercise was performed either in the S position (4 tests) or in the U position (4 tests). Responses to the impulse change in WR performed with the legs were compared with the responses triggered by an exercise performed with the arms, which were placed in the same position and at a similar level from the heart in both S and U positions. (Pedal axis was placed at ~40 to 45 cm from heart level in both positions, depending on the height of the subject.) After the period of contractions, the arms of the subjects could rest passively at the same level as during the contractions. During and after the arm exercise, arterial baroreceptors were exposed to the effect of gravity as they were during leg exercise, but the degree of distension of the venous and venular systems and the perfusion pressure in postexercising muscles were no longer dependent on the direct effects of gravity. Also worthy of note is that this approach can dissociate the possible contribution of receptors located in the postexercise limbs from that of all the receptors of the rest of the body (see DISCUSSION). On eight occasions, each subject performed an exercise with the arms either in the S or U positions.Heart transplant patients. Patients performed the initial part of the protocol, i.e., the leg exercise, both in the S and U positions.
Data Analysis
All data were processed on-line and stored on disk for further analysis. Breath-by-breath data were transformed into second-by-second files that could be temporally aligned and then averaged for each condition. Mean BP was computed from the raw data (Mac Lab), converted into a second-by-second file, and temporally aligned to the ventilatory data.The second phase of E,
O2, and
CO2 responses was compared between the S
and U positions and between arm and leg exercises by comparing the peak
response of E, O2,
CO2, end-tidal partial pressure of
CO2 (PETCO2),
E/O2, heart rate
(HR), and BP (computed over 15 s, paired t-test). The
E vs. O2 relationship was established by regression analysis for the 90-s period following the peak of the delayed response.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Control Tests With the Leg Exercise
Figure 2 illustrates the averaged temporal profile ofE,
O2, and BP responses to the 12-s bout of
leg exercise for all subjects in U and S positions.
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Exercise in the U position.
Responses consisted of two different phases for both the
ventilatory and gas exchange responses. An initial
increase in E occurred as soon as the contractions
started. E increased from the resting values of
9.47 ± 0.39 to 21.6 ± 3.1 l/min. This initial rise in
E was associated with an increase in
O2 and
CO2, both of which subsided and reached
their nadir within 15-25 s after the end of the contraction.
E started to increase again 17-27 s into
recovery and reached its maximum value (17.59 ± 1.08 l/min)
30 s later. The second rise in E followed that
in O2 (752 ± 55 ml/min),
CO2 (602 ± 42 ml/min), and
PETCO2 (46 ± 0.9 Torr). Mean BP
changes had a very similar pattern of response. After an initial
increase in BP (from 95 ± 10 to 108 ± 6 mmHg), mean BP
decreased then increased again to 106 ± 4 mmHg (Fig. 2). Finally,
HR increased abruptly during the contracting phase and then subsided
toward resting values (Fig. 3).
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Exercise in the S position.
Resting ventilation was lower in the S than in the U position
(8.73 ± 0.22 l/min) but did not reach significance. Impulse exercise triggered a delayed increase in
O2 and
CO2, which was similar to that in the U
position (Fig. 2), but the peak of the second component of the
ventilatory response was significantly lower in every subject by an
average of 2.58 ± 0.44 l/min (change = 17.2 ± 9%,
P < 0.001). The level of
PETCO2 associated with the second rise in
ventilation was significantly higher in the S position than in the U
position (48.3 ± 0.8 Torr, P < 0.01; Fig. 2).
Because the O2 peak response was similar
in both positions, the
E-to-O2
ratio was significantly lower in the S position than in the U position
(20.3 ± 0.7 vs. 23.6 ± 1.0, P < 0.001). Finally, mean BP (at neck level) was significantly higher in the S than
in the U position at rest (by 7 ± 3 mmHg) and remained higher
during and after the impulse exercise by ~7 mmHg (Fig. 2), whereas HR
was significantly reduced in the S position by 13-15 beats/min
(P < 0.001; Fig. 3 ) both at rest and during impulse exercise.
Cardiac-Transplant Patients
The second phase of theE response was
significantly higher in the U position than in the S position
(22.52 ± 1.21 vs. 18.83 ± 0.421 l/min, respectively,
P < 0.01) with a rise in
O2 of a similar magnitude (Fig.
4). In addition, although a relative hyperventilation was consistently observed in patients, the effects of
body position were, if anything, larger than in the control group,
despite lower PETCO2 in the transplant
patients (Figs. 2 and 4). The reduced ventilatory response in the S
position was, however, always associated with a significantly higher
PETCO2 (39 ± 2 vs. 36 ± 2 Torr). It is worth noting that the blunted ventilatory response in the
S position was observed in the patient who had had a heart-lung
transplantation, as illustrated in Fig. 5.
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Except for the mean BP levels, which were higher and more variable than in the control group, BP responses were similar to those observed in control subjects. Pressure at the carotid level was higher by ~4.8 ± 3 mmHg in the S posture than in the U posture. At rest, all subjects displayed a tachycardia, with a slight difference between S and U positions (97 ± 4 vs. 102 ± 5 beats/min). HR response to exercise was virtually abolished in both positions (Fig. 3).
Arm Exercise
Effects of body position on the response to arm exercise were both qualitatively and quantitatively different than during leg exercise (Fig. 6). First,O2 response to arm exercise was significantly higher in the U than in the S position (650 ± 32 vs. 700 ± 31 ml/min, P < 0.01, 7.6 ± 1.6%). On average, ventilation was higher in the U position
(17.79 ± 0.84 vs. 16.90 ± 0.94 l/min, P < 0.05) but in the same proportion as O2
(5.9 ± 2.2%). This ventilatory reduction represented less than
one-third of the difference observed after leg exercise (Fig.
7). Subject-by-subject analysis revealed
that, in contrast to leg exercise, three subjects had a virtually
identical level of ventilation with arm exercise whether in the S or U
positions. Because E was depressed when
O2 was low in the S position,
E-to-O2 ratio was
similar in both positions (25.6 ± 0.7 vs. 25.9 ± 0.6, not
significant). Finally, during the 90 s following the peak response
of the second phase, the slope and intercept of the
E vs. O2 regression
were similar in either position (Fig. 8).
In contrast, after leg exercise, the slopes of the E
vs. O2 regression lines were
significantly lower in the S than in the U posture (10.4 ± 1.3 vs. 16.1 ± 2.5, P < 0.01) but with no difference
in the intercepts (Fig. 8).
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The difference in the PETCO2 peak response
between S and U positions (1.3 ± 1 Torr) did not reach
significance (Fig. 6). Finally, mean BP could not be accurately
measured during and after arm exercise, but mean BP before the boot of
exercise was 6.9 ± 4 mmHg higher in the S position.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We used an impulselike change in WR to study the control of
breathing in a situation where the rise in pulmonary gas exchange and
ventilation can be dissociated from muscle contractions. As in previous
reports (12-14, 40), we found that 20 s after
the end of the exercise bout a second rise in E
occurs, which closely follows the increase in
O2 and
CO2 by a few seconds. This second phase
of the ventilatory response has already been shown to have the
characteristics expected from the response to a constant WR exercise,
despite no contractions being performed (see Refs. 39 and
40 for discussion).
The major finding of the present study was that the delayed
E response to an impulse change in WR was
significantly reduced in the S position, despite a similar magnitude of
pulmonary gas exchange. Furthermore, this effect was still observable
in patients who lack afferent information from the heart but was
virtually abolished when the impulse exercise was performed with the
arms positioned at a similar level from the heart in both the S and U
positions. Indeed, the difference between the two postures in response
to arm exercise was 1) dramatically less than after leg exercise and 2) proportional to the change in pulmonary gas
exchange (Fig. 7), leading, unlike after leg exercise, to a
similar E-to-O2 ratio
in both positions.
The effect of posture on the level of ventilation has already been
investigated both at rest (1) and during a constant WR
exercise (38). Alveolar ventilation has been found to be lower at rest in the S position than in the U position (1) but with no clear explanation for this finding. During exercise (38), ventilatory phases I and II have also been reported
to be reduced and slowed. In addition, Weiler-Ravell et al.
(38) found that O2 response
was always blunted. Whereas a reduced O2
phase I reflected the limited increase in cardiac output at the onset
of a constant WR exercise in the S posture (3, 27, 36),
the lower steady-state O2 reported in
that study (38) makes it difficult to interpret the
resulting ventilatory outcome because a low
O2 may simply have reflected a better mechanical muscular efficiency [and, therefore, a reduced ventilatory stimulation from central or muscular origin (see Ref. 8
for discussion)] in the S position. The recruitment of different
groups (types) of muscles during the contractions (e.g., muscles from the back) could thus account for part of the difference in ventilation reported by Weiler-Ravell et al. Nevertheless, the present
finding that an intense leg exercise of short duration in the S
position triggers a lower E response than in the U
position, despite similar O2, still
supports the conclusion of that study: E response to
exercise is reduced in the S position independently of (or in addition
to) the effects of recruitment of different types of muscles. Position,
therefore, affects the control of breathing in exercise by altering the
coupling between ventilation and pulmonary gas exchange, a fundamental
tenet of blood-gas homeostasis. It becomes relevant for our
understanding of the regulation of exercise hyperpnea to determine the
nature of the afferent signal that is depressed in the S position.
Contribution of the Chemical Control of Respiration
Ventilatory response to CO2 has consistently been shown to be similar in S and sitting positions (1, 28, 29), whereas the response to hypoxia has been reported to be either diminished or unchanged in the S position. The levels of hypoxia at which such a difference is observable (28) have no equivalent value with the changes in arterial partial pressure of O2 that may occur after the impulse exercise. One should, therefore, not expect that the largerE response to
exercise in the U position to be accounted for by a change in the
chemical regulation of breathing, at least through a change in
CO2 sensitivity. This is of importance because the delayed
rise in ventilation occurs after a rise in PETCO2 by several Torr, as has already
been reported (12, 14). Such a rise in
PETCO2 (Figs. 1 and 2) could be accounted
for by at least two mechanisms: 1) the phase lag between the
rise in CO2 and in ventilation could
transiently have disrupted the alveolar gas composition and thus
arterial blood-gas homeostasis and 2) perhaps more
importantly, the abrupt increase in CO2 output to the lungs
after the impulse should increase the slope of the expired
PCO2 "plateau" and thus
PETCO2 out of proportion of the changes in
mean arterial partial pressure of CO2
(PaCO2). The exact magnitude of the change in
PaCO2 and its contribution to the ensuing hyperpnea
is, therefore, hard to predict, but, even if the level of
PETCO2 differs from that of
PaCO2, the
E-PETCO2 relationship
obtained in control subjects in both positions clearly shows that
PETCO2 is dictated by the level of
ventilation rather than the opposite, i.e.,
PETCO2 being lower in the U position when
E was higher.
Role of cardiac receptors.
Although distension of the right heart or pulmonary arteries can
experimentally stimulate ventilation (21, 23), their role
in adjusting the level of ventilation to the rate of incoming blood has
never been confirmed (2, 17). The hypothesis that the
blunted increase in cardiac output may contribute to the blunted increase in ventilation in the S posture (38) could offer
a rather unifying explanation for the present observations. However, the blunted increase in the delayed E response in
the S posture in cardiac-transplant patients does show that
information originating from the right or left heart is not a
prerequisite for a reduced E response in the S
posture to occur. Indeed, although a limited functional sympathetic
reinnervation has been demonstrated in humans several years after a
cardiac transplantation (5), no clear anatomic evidence
has been forthcoming to suggest that this was associated with a
reconnection of the cardiac afferent system, which follows both the
sympathetic and parasympathetic pathways. The almost totally abolished
HR response to the short burst of heavy exercise in our patients, even
in those who were studied several years after transplantation, also
supports the contention that these patients do lack significant
afferent innervation from the heart.
Other effects of gravity on respiratory control.
The lack of a specific reduction in the E response
when exercise was performed in the S position with a group of muscles positioned in such a way that the hydrostatic effect of gravity on
their circulation was minimized may help us to distinguish between
several other putative mechanisms.
E when the carotid pressure is high. The gain of the
relationship between carotid pressure and ventilation has been
established in vagotomized dogs and was found to be ~0.5 to 1.0 ml · min
1 · kg1 · Torr1
(see also Refs. 16 and 18 for discussion), but the
magnitude of the ventilatory component of the arterial baroreflex is
unknown in humans. We found that BP was 7 mmHg higher at the carotid
level before arm exercise in the S position than in the U position, just as for leg exercise. Such a difference in baroreceptor stimulation during arm exercise was associated with HR responses, which were to be
expected from the involvement of the arterial baroreflex, i.e., higher
HR level in the U position but with little or no effect on ventilation.
This suggests that the ventilatory component of the arterial baroreflex
cannot account for the difference between S and U positions during leg exercise.
Similarly, the lack of a specific effect of body position after arm
exercise suggests that afferent information originating "outside"
exercising muscles, including the lungs and respiratory muscles, cannot
fully explain the present observation. Incidentally, the fact that
changing body position during arm exercise has little effect on the
level of ventilation, even though this may have affected the mechanics
of breathing [change in chest wall compliance or respiratory muscle
recruitment (9)], is not unexpected. Indeed, application
of an external elastic load or mechanical "unloading" of the
respiratory system during a constant WR exercise results in an
appropriate compensatory increase (or decrease) in respiratory drive,
meaning that total ventilation remains unchanged (see Ref.
39 for review). It is worth noting that the patient with a
lung and heart transplant that we studied also had a lower E response in the S position than in the U position,
suggesting that the lungs, which must accommodate a large blood volume
in the S position, do not participate in this response either. Finally, the difference in ventilatory behavior between leg and arm exercise according to position also implies that any change in the cerebral or
brain stem perfusion induced by the change in posture cannot explain
the difference between S and U positions.
Because structures outside postexercising muscles seem to contribute
little to the reduced ventilatory response to exercise in the S posture
during arm exercise, the possibility that the effect of gravity on
postexercising muscles could be responsible for part of this effect
should be examined. Obviously, the metabolic or chemical impact of a
lower perfusion pressure in the S position, with the leg above heart
level, was not strong enough to cause the so-called muscle chemoreflex
through stimulation of small myelinated or unmyelinated muscle afferent
fibers (10, 22, 26, 30, 33). This confirms previous
reports on the lack of ventilatory stimulation during vascular
occlusion after dynamic exercise in humans (7, 16, 18, 20,
31). However, the lack of contraction does not necessarily imply
that muscle afferent fibers in postexercising limbs are not involved. A
higher perfusion pressure, together with greater distension of the
venous or venular end of the muscular circulation in the U position
than in the S position, could have affected the afferent traffic from
hyperemic postexercising muscles. Group IV muscle afferent fibers are
located in the adventitia of the vascular structures of the muscle
(mostly the venules) (34, 37) and can respond to
mechanical distension of the peripheral vascular network (14,
15) in hyperemic resting muscle. It has already been suggested
that change in the volume of blood in the venular system could be one
of the physiological stimuli for these fibers (14, 18,
25). Because the load imposed on the venous return was much
higher in the U than in the S position, we could speculate that the
degree of distension of the venular side of muscle circulation could
stimulate thin muscle afferent fibers in metabolically active and
hyperemic muscles in the U position and reduce this activity in the S position.
Although the present results are consistent with such a mechanism being
a contributor to the difference in E responses
between body positions, testing this hypothesis specifically will
require examination of the effects of gravity on the same group of
exercising or postexercising muscles.
It is concluded that the difference in the ventilatory response after
an impulse exercise between the S and U positions persists even after
cessation of the contractions and cannot be accounted for by the
involvement of cardiac mecanoreceptors. The slight difference observed
when the exercise was performed with the arms suggests that factors
other than those related to the ventilatory component of the arterial
baroreflex or to information originating from the respiratory system
are responsible for the reduced ventilatory response in the S position
during leg exercise.
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ACKNOWLEDGEMENTS |
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The authors are grateful to Drs. J. P. Villmenot and M. F. Mattei from the Departement of Cardiac Surgery and to C. Creusat for secretarial assistance.
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FOOTNOTES |
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This work was supported by le Ministère de la Recherche, Equipe d'Accueil Interactions des Régulations Respiratoires Chez l'Adulte et l'Enfant.
Address for reprint requests and other correspondence: P. Haouzi, Laboratoire de Physiologie, Faculté de Médecine de
Nancy, 9 Ave. de la Forêt de Haye, B.P. 184 F-54505, Vanduvre
lès Nancy, France (E-mail: p.haouzi{at}chu-nancy.fr).
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.
10.1152/japplphysiol.00598.2001
Received 11 June 2001; accepted in final form 26 November 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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) and U positions (
).
Left: response to arm exercise. Right: response
to leg exercise. Slope of the