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Department of Preventive Medicine, John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin, Madison, Wisconsin 53705
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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We have recently demonstrated that changes in
the work of breathing during maximal exercise affect leg blood flow and
leg vascular conductance (C. A. Harms, M. A. Babcock, S. R. McClaran, D. F. Pegelow, G. A. Nickele, W. B. Nelson, and J. A. Dempsey. J. Appl. Physiol. 82: 1573-1583,
1997). Our present study examined the effects of changes
in the work of breathing on cardiac output (CO) during maximal
exercise. Eight male cyclists [maximal
O2 consumption
(
O2 max):
62 ± 5 ml · kg
1 · min1]
performed repeated 2.5-min bouts of cycle exercise at
O2 max. Inspiratory
muscle work was either 1) at control
levels [inspiratory esophageal pressure (Pes): 
27.8 ± 0.6 cmH2O],
2) reduced via a proportional-assist
ventilator (Pes: 16.3 ± 0.5 cmH2O), or 3) increased via resistive loads
(Pes: 35.6 ± 0.8 cmH2O).
O2 contents measured in arterial
and mixed venous blood were used to calculate CO via the direct Fick
method. Stroke volume, CO, and pulmonary
O2 consumption
(O2) were not different
(P > 0.05) between control and
loaded trials at
O2 max but were lower
(8, 9, and 7%, respectively) than control with
inspiratory muscle unloading at
O2 max. The
arterial-mixed venous O2
difference was unchanged with unloading or loading. We combined these
findings with our recent study to show that the respiratory muscle work normally expended during maximal exercise has two significant effects
on the cardiovascular system: 1) up
to 14-16% of the CO is directed to the respiratory muscles; and
2) local reflex vasoconstriction significantly compromises blood flow to leg locomotor muscles.
blood flow distribution; intrathoracic pressure
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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THERE ARE SEVERAL TYPES of evidence that point to a
significant role for the work of breathing (Wb) on the cardiovascular response to strenuous exercise. First, the Wb achieved at maximal O2 consumption
(O2 max) in fit
subjects was shown to require an
O2 consumption
(O2) that equaled
10-15% of the
O2 max, or 300-600
ml/min absolute O2 (1).
Presumably, this metabolic demand by the respiratory musculature would
also require a significant share of the total cardiac output (CO). This
presumption was confirmed by the high blood flows to respiratory
muscles found during maximal exercise in animals (10, 11) but has not
been tested directly in humans. Furthermore, 10- to 15-fold changes in
intrathoracic pressure occur from rest to maximal exercise during
inspiration and expiration; theoretically, these swings might be
expected to influence the stroke output of the right and left heart
(17, 19, 23, 24). Whether these changes in pressure
actually cause a net change in stroke volume during exercise has also
not been tested directly.
Second, we recently found that vascular resistance in leg locomotor
muscles during maximal exercise responded reflexly to imposed changes
in the Wb, so that leg blood flow (
legs)
increased with respiratory muscle unloading and decreased with
respiratory muscle loading (8). We do not know how much, if any, of
this change in local blood flow was attributable to coincident changes in CO; similarly, we do not know whether these changes in
legs induced by a changing Wb altered the proportion
of total CO distributed to working locomotor muscles.
Our present study was aimed at determining the effects of changes in
the Wb on CO during maximal exercise. We employed a proportional-assist ventilator (PAV) to unload, and fixed inspiratory resistances to load,
the respiratory muscles during several bouts of maximal exercise in fit
healthy subjects and used the direct Fick technique to measure any
resultant changes in CO. We then combined these findings with our
previous data on legs under similar conditions (8) to quantify the partitioning of the CO normally
achieved at O2 max to
leg locomotor muscle and to respiratory muscles.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Subjects. Eight male cyclists with resting pulmonary function within normal limits were recruited to participate in this study. Informed consent was obtained in writing from each subject, and all procedures were approved by the Institutional Review Board of the University of Wisconsin-Madison. The physical characteristics of the subjects were as follows: age, 29.5 ± 4.6 (SD) yr; height, 184.5 ± 3.1 cm; and weight, 71.1 ± 6.1 kg.
Pressure and gas measurements.
During all tests, the raw data were recorded for subsequent analysis on
an eight-channel Hewlett-Packard tape recorder, Gould chart recorder,
and computer. Flow rates, flow-volume and esophageal pressure
(Pes)-volume relationships, end-expiratory lung volume, and total body
O2 and
CO2 production were measured by
using equipment and techniques previously reported (1, 9).
The Wb was defined as the integrated area of the pressure-tidal volume loop (16). Wb multiplied by the breathing frequency represents the
amount of work done per minute on the lungs. We note that our use of
the area of the Pes-volume loop underestimates the actual Wb by
variable amounts (1, 7); thus our measurements report only a
conservative estimate of the total amount of work done by the
respiratory muscles during exercise and their changes with unloading
and loading.
Inspiratory unloading and loading. A feedback-controlled PAV was used to reduce the work of the inspiratory muscles during exercise (29). Briefly, subjects breathed through a Hans Rudolph valve that was connected (on the inspiratory side) to the PAV. The PAV contains a linear motor that drives a piston (5-liter volume capacity) which develops pressure in proportion to inspiratory airflow and volume. The level of assist is controlled by potentiometers on the control panel of the ventilator, and there are separate controls for volume assist and flow assist. During inspiration, the PAV makes mouth pressure positive in proportion to flow such that the proportional assist (unloading) of the respiratory muscles occurs throughout the inspiratory cycle. In practice, the amount of assist is set at the maximal level that each subject can tolerate, as determined from practice sessions before testing. During practice and testing sessions, subjects were verbally coached to relax and permit the PAV to assist each inspiration as much as possible.
To increase inspiratory work during exercise, we added ventilatory loads that consisted of mesh screens in the inspiratory line with resistances of 3-7 cmH2O · l1 · s.
These resistances were sufficient at the high flow rates achieved in
maximal exercise to increase the Wb by 20-80% above control
levels. Subjects participated in practice sessions to familiarize
themselves with the inspiratory loads.
CO and blood-gas measurements.
A Swann-Ganz catheter was inserted under sterile conditions in the left
brachial vein and advanced caudally to the pulmonary artery for
sampling of mixed venous blood. The position of the catheter tip was
verified via fluoroscopy. A 20-gauge arterial catheter (Arrow) was
inserted percutaneously in the right brachial artery under local 1%
lidocaine anesthesia. CO was calculated via the direct Fick method: CO = O2/arterial-mixed venous
O2 difference
(a-
DO2).
The
a-DO2
was divided by arterial O2 content to give O2 extraction. Vascular
resistance was calculated as the ratio of mean arterial blood pressure
to CO.
Experimental protocols.
Subjects initially completed a progressive incremental
O2 max exercise test
on an electromagnetically braked cycle ergometer (Elema) beginning at
150 W (~30-40%
O2 max) followed by
an increase in work rate of 50 W every 2.5 min until exhaustion.
Subjects selected their preferred pedaling frequency during the test,
and this cadence was maintained constant throughout all subsequent testing through visual inspection of a digital cadence output. After a
20-min recovery, subjects cycled to exhaustion at 5-10% above
their peak workload (WL) (as determined by the previous progressive
test) to verify
O2 max. A plateau
(<150 ml) or decrease in
O2 was observed for each
subject between the final two WL of the incremental
O2 max test
and/or between the final WL of the incremental test and the WL
of the repeat test. The mean
O2 max was 62 ± 5 ml · kg1 · min1
(range 55-74
ml · kg1 · min1).
O2 max WL (383 ± 33 W) and that could be maintained for 2.5-3.0 min (as determined
from a separate practice session). These tests consisted of one trial
with no ventilatory intervention (control), one trial of inspiratory
muscle unloading, and one trial of inspiratory muscle loading. The
first maximal trial of each day was a control trial, and the order of
the remaining two trials was randomized. Control submaximal exercise
bouts set at 50 and 75% of
O2 max WL were also
performed to establish a relationship between CO and
O2. During all exercise
bouts, subjects first increased work rate progressively to the required
WL over 30 s, and then three simultaneous collections of
O2 and blood sampling were taken at 45 s to 1 min, 1 min 30 s to 1 min 45 s, and 2 min 15 s to 2 min 30 s.
Statistical analysis.
Relationships between Wb and the dependent variables under the three
conditions, control, inspiratory muscle load, and inspiratory muscle
unload at
O2 max WL,
were determined from simple regression. ANOVA was used to determine
treatment differences between group mean values under each of the three
conditions. Tukey's post hoc analysis was used to determine where the
differences between pairs of mean values were present. Significance was
set at P 
0.05.
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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We present our findings concerning the effects of changing the Wb on
several variables of O2 transport
by showing 1) absolute values for
each subject and 2) values as a
percentage of control across all subjects. The group mean changes for
each variable measured during inspiratory unloading, control, and
inspiratory loading obtained during the final 2.5-min measurement
period at O2 max are
summarized in Tables 1 and
2.
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Wb.
Table 1 shows the average change in Wb, peak inspiratory and expiratory
Pes, and ventilatory output achieved with inspiratory unloading and
loading. Inspiratory muscle unloading during maximal exercise reduced
Wb by variable amounts to average 54.9 ± 6.2% of control, whereas
with resistive loads Wb was increased to 156.7 ± 8.6% of control.
Peak inspiratory Pes was increased 41 ± 3% with inspiratory unload
(less negative) and was reduced 22 ± 4% with inspiratory loading
(more negative). Peak expiratory Pes was reduced by 24 ± 3% with
inspiratory unload (less positive) but was not different from control
with inspiratory loading. The difference between peak inspiratory and
peak expiratory Pes was 50 cmH2O
during control, 34 cmH2O during
unloaded trials, and 59 cmH2O
during loaded trials. Tidal volume, breathing frequency, minute
ventilation (E), arterial and mixed
venous PCO2, pH,
PO2,
O2 saturation, lactate, and
hemoglobin did not change systematically
(P > 0.05) across the range of Wb
values within each subject (see Table 1). The ratio of inspiratory time to total time was 0.48 ± 0.09 during unloading, 0.49 ± 0.12 during control, and 0.56 ± 0.13 during loading.
Effects of changing Wb on O2 transport.
Figure
1A shows
individual absolute values for
O2, CO,
and a-DO2
vs. Wb obtained during the final 2.5-min measurement period at
O2 max. Without
exception, O2 and CO fell
with inspiratory unloading but did not change systematically with
loading. The fall in O2 and
CO with unloading averaged 0.29 ± 0.07 l/min (P < 0.04) and 2.4 ± 0.4 l/min
(P < 0.03), respectively (see also Table 2).
a-DO2
averaged 16.7 ± 0.3 ml/dl and did not vary across the range of Wb
values.
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O2 for all subjects combined,
expressed as a percentage of control and described by a best fit
curvilinear regression. Note that, with unloading, CO averaged 91.9 ± 0.6% of control and O2
averaged 93.5 ± 0.5% of control (see Table 2).
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O2, and
a-DO2
during maximal exercise at each of the three measurement periods
throughout the 2.5-min trials. The increase in CO was almost complete
by the first minute of maximal exercise and rose only an additional
2.5% over the final 1 min 45 s of exercise. O2 increased steeply at the
first and second time period and then tended to plateau over the final
45 s. Almost all increases in
O2 beyond the first minute of
exercise were due to a widening of
a-DO2.
The finding that CO and O2
were lower with inspiratory muscle unloading and that they remained
unchanged with loading was consistent and significant at all three time
points of maximal exercise.
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Association of changes in
O2 and pleural pressure with
changes in CO during maximal exercise.
Was the reduction in CO with respiratory muscle unloading at
O2 max
associated with the concomitant increases in intrathoracic pressure or
with reductions in O2? To
address this question, we first determined the relationship between CO
and O2 in our subjects
exercising under control conditions at 50, 75, 90, and 100% of
O2 max (see
Fig. 4). The resulting regression equation (Fig. 4, top) agrees closely with published linear
correlations in normal subjects (21). We superimposed data obtained
during respiratory muscle unloading at
O2 max on
this regression line, as shown in Fig. 4, bottom, for each
of the eight subjects and for the mean values. Note that the reduction
in CO with respiratory muscle unloading was slightly but consistently
in excess of that predicted by the relationship of
O2 to CO
(O2-CO) obtained under control conditions. Thus, on the basis of the average regression equation, the 0.29 l/min reduction in
O2 with unloading at
O2 max would be
associated with a 1.1 l/min reduction in CO. This predicted reduction
in CO amounted to 46% of the total reduction in CO actually observed
with respiratory muscle unloading at
O2 max.
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O2 that might have caused the
reduction in CO with unloading, we compared two WLs of
1) near-equal
O2 (maximal work rate with unloading vs. 93% of
O2 max control), but
2) with average intrathoracic pressures, which were different by 9 ± 1 and 7 ± 1 cmH2O at peak inspiration and
expiration, respectively (see Fig.
5A).
Note in Fig. 5A that stroke volume was
higher in all subjects by 7 ± 1 ml
(P < 0.05) when intrathoracic
pressure was less negative (by 9 ± 1 cmH2O), i.e., at 93% of
O2 max
(P < 0.001), even though O2 was the same. Because
heart rate fell an average of 5 ± 1 beats/min
(P < 0.05) at the lower work rate,
CO was not affected by the increased stroke volume. Note also that this
increase in stroke volume between these two WLs was slightly less than
one-half of the reduction in stroke volume achieved when respiratory
muscles were unloaded at
O2 max.
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O2 max. Despite
an almost 8 cmH2O more negative
peak inspiratory Pes with loading at
O2 max, stroke volume
and CO remained unchanged.
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Summary of findings.
Our findings demonstrate a significant effect of respiratory muscle
unloading on stroke volume and CO during maximal exercise in the
healthy, trained human. We found that reducing the Wb via proportional-assist ventilation during maximal exercise caused significant decreases in O2
and in CO, due primarily to reduced stroke volume, whereas increasing
the Wb during maximal exercise had no effect on CO or
O2. Correlational analysis
implied that the effect of respiratory muscle unloading on CO was
attributable to reductions in metabolic demand (i.e.,
O2) by the respiratory muscles and/or to the effects of an increased (i.e., less
negative) intrathoracic pressure on venous return. These findings, in
combination with those we recently reported (8),
demonstrate that the respiratory muscle work experienced under normal
physiological conditions at maximal exercise exerts two types of
effects on the cardiovascular response:
1) a substantial portion of the CO
(up to 14-16%) is directed to the respiratory muscles to support
their metabolic requirements; and 2)
blood flow is reduced to (or "stolen from") working locomotor
muscles because of sympathetically mediated vasoconstriction induced
reflexly and possibly originating in contracting respiratory
musculature.
Speculation as to the cause of the unloading effect on CO.
Why did CO decrease with respiratory muscle unloading at
O2 max? First, and most
straightforward, the decreased respiratory muscle work and
O2 mean less demand for blood
flow, and the reduced CO may merely have followed the well-established
relationship of CO to whole body
O2 as determined over a wide
range of increasing exercise intensities and with a variety of exercise
modalities that involved predominantly the arms or leg cycling (see
Fig. 4; Ref. 21). We used this regression equation obtained under control conditions to estimate that, when respiratory muscles were
unloaded at O2 max,
about one-half of the reduction in CO was associated with (and
predictable from) the reduction in O2. This apparent dependency
of reductions in blood flow on reductions in
O2 is consistent with the
findings of Coast et al. (5) and Anholm et al. (3), who increased the
Wb by using resistive loading or hyperpnea in subjects at rest and
reported significant increases in heart rate, CO, and
O2. Because these increases
in CO developed slowly (i.e., they required >20 s of hyperpnea), they
were attributed to the associated changes in O2. Therefore, we think it
reasonable to suggest that at least a significant portion of the
reduction in CO with respiratory muscle unloading during maximal
exercise was attributable to a corresponding reduction in
O2.
O2-CO relationship
established across increasing work rates is dependent primarily on
changes in heart rate (see Fig. 5; Ref. 20). This dependency of changes
in CO on heart rate contrasts with the reduction in CO with respiratory
muscle unloading that we observed during maximal exercise, which was
primarily dependent on the reduction in stroke volume (see Fig.
1B). Furthermore, we also compared
stroke volumes between conditions of equal
O2, i.e., the unloaded
condition at maximal exercise vs. the control condition at an average
of 93% of O2 max (see
Fig. 5), and observed that stroke volume was reduced during the
unloaded condition. Therefore, these significant effects on stroke
volume from respiratory muscle unloading (even at comparable
O2) implied that some factor
associated with the unloading, other than the reduced
O2, may also be important in
determining CO. Perhaps increases in (i.e., less negative) intrathoracic pressures may have caused the reduced stroke volume.
Changes in intrathoracic pressure imposed primarily at rest in supine
humans (18) and anesthetized animals (24) have been shown to exert
effects on both the left and right heart. With increasing negativity of
intrathoracic pressure on inspiration, venous return increases, at
least up to the point at which excessive negative pressure causes
collapse of the veins entering the thorax, especially under conditions
in which inspiration is prolonged. On the other hand, increasing
negativity of intrathoracic pressure also means increased transmural
pressure across the left ventricle, and, because of limited space
within the pericardium, increased right atrial and ventricular filling
will compromise left ventricular expansion (19). Both of these latter
influences would impede left ventricular stroke volume and CO. In the
healthy heart, preload effects are usually expected to dominate the
(net) effect of changing intrathoracic pressures on stroke volume, but,
during strenuous exercise, several additional factors arise that may
facilitate or override the effects of a changing intrathoracic pressure
per se. These factors include 1) the
"peripheral pump" provided by contracting skeletal muscles, which
is important, especially in strenuous exercise, in enhancing venous
return from the legs (21); 2) the
large swings in lung volume that will influence the compliance of the
intrathoracic vasculature (24); and
3) reduced systemic venous
compliance because of high levels of sympathetic efferent output during
exercise. Furthermore, very large negative and positive swings in
intrathoracic pressure occur with inspiration and expiration during
strenuous exercise, and it is difficult to predict what the net effect
of the opposing influences would be on stroke volume in the steady
state.
Given our finding of reduced stroke volume with respiratory muscle
unloading during maximal exercise, we would speculate that the less
negative pleural pressure during inspiration reduced venous return
(relative to control), thereby resulting in a net reduction in stroke
volume and CO in the steady state. Additional mechanical influences
that might have affected stroke volume during respiratory muscle
unloading via PAV would include 1)
the less positive pleural pressure during expiration, which may have
aided left ventricular filling; and
2) the relatively small but
consistent increase in pulmonary vascular resistance, which would
increase afterload on the right ventricle. Given the relatively small
change in Ppa values, we think that these possibilities are highly
unlikely (22). There are some limited, indirect data that
support our findings and interpretation with unloading, including the
higher venal caval flow rate observed during inspiration compared with expiration at both rest and mild exercise in supine humans (27), and
the decrease in stroke volume and CO observed in healthy humans at rest
when intrathoracic pressure was increased via continuous positive
airway pressure (4, 15). Conversely, during mild exercise, Giesbricht
et al. (6) found no effect of unloading (with PAV) or elastic loading
on breath-by-breath O2, which probably also reflected an unchanging CO.
Our reduced stroke volume during unloading was also not predictable
from the lack of effect of inspiratory resistive loading on stroke
volume and CO that we observed at
O2 max (see Fig. 5).
This lack of effect of further negativity in pleural pressure during
inspiration may mean that the extreme negative pressure incurred during
loading was beyond the level at which venous return would be enhanced
(24). Alternatively, we may have simply reached the limits of
ventricular expansion during diastole imposed by the pericardium (26).
In either case, stroke volume and CO would be independent of further
reductions in pleural pressure under control conditions at
O2 max. We also note
that respiratory muscle loading reduced inspiratory pleural pressure
but did not change expiratory pressures. If expiratory pressure had
been increased (as sometimes occurs normally with increasing expiratory
flow resistance during strenuous exercise), stroke volume may actually have fallen during maximal exercise.
In summary, our findings show a clear, consistent, and substantial
effect of respiratory muscle unloading on reducing stroke volume and CO
at maximal exercise, which we speculate may be due both to a reduced
metabolic requirement and to the effects of a less negative pleural
pressure on venous return. Certainly, more direct testing is needed to
address these mechanisms. Perhaps the use of direct visualization
techniques to obtain a beat-by-beat time course of change in stroke
volume with unloading during maximal and submaximal exercise would
provide a more definitive test of the effect of changes in pleural
pressure per se.
Respiratory muscle work and CO distribution.
Our present results, when combined with our previous thermodilution
measurements of legs (8), permit us to address for the first time the effects of respiratory muscle work on CO and its
distribution during maximal exercise. We summarize the key findings in
Fig. 6, which shows the average effects on
O2 transport and uptake, of the
increases and reductions in the Wb by ±50% and also shows the
extrapolation of these unloading effects to a zero Wb, based on the
regression lines developed from data over the range of 25-75%
reductions in the Wb (see Fig. 2 and Ref. 8). Note that, under control
conditions with a maximal CO of 26.5 l/min and
O2 of 4.40 l/min, 77% of CO
was distributed to working locomotor muscles, and
a-DO2
across the legs and across the whole body exceeded 85-90% of
O2 extraction. With an increased work of inspiration (greater than control), CO remained unchanged, whereas leg vascular resistance increased and legs
fell (secondary to decreased leg vascular conductance), resulting in a
substantial reduction in the fraction of CO distributed to working
limbs (8). O2 extraction across
the legs was unchanged, and therefore a substantial reduction occurred
in leg O2. However, with
respiratory muscle unloading, CO and total
O2 were reduced, and
legs and O2 were increased, secondary to decreased leg vascular resistance. Thus
unloading of the respiratory muscles resulted in a substantial increase
in the fraction of total CO distributed to leg muscles and in the
fraction of total O2 consumed
by the legs.
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legs with
unloading and loading, respectively, are not attributable to
coincidental changes in total CO (which fell with unloading and was
unchanged with loading). Thus these data support our previous contention that a change in the Wb during exercise caused local reflex
vasodilation or vasoconstriction of working limb vasculature, presumably mediated by a changing sympathetic efferent output (8).
Second, the fall in legs with respiratory muscle
loading was almost double the increase in legs with
unloading (see Fig. 6), and this difference may be attributable to the
fact that CO was maintained with respiratory muscle loading but fell
substantially with respiratory muscle unloading. Thus, with respiratory
muscle unloading, the reflex vasodilation in leg muscle resulted in
relatively small increases in blood flow, in part because the total
"available" blood flow was markedly reduced.
Finally, Fig. 7 shows the estimated
distribution of total CO to respiratory and to leg locomotor muscles
under physiological control conditions at
O2 max. The mean value
shown for legs (20.3 ± 0.5 l/min) is the measured
value with the use of the thermodilution technique obtained under
control conditions at
O2 max (see Fig. 6;
Ref. 8). This value is labeled as "leg" blood flow, but we are
uncertain whether this measurement includes blood flow to all limb
musculature actually involved in the exercise. The value for
respiratory muscle blood flow (4.2 ± 0.1 l/min) is taken from the
reduction in CO observed between control and unloaded conditions and
extrapolated to zero levels of Wb (see Fig. 6). Thus these values would
mean that, of the mean maximal 26.5 l/min CO in our subjects, 77% of
this total was directed to working legs, 16% to the respiratory
muscles, and 7% to other metabolically active tissues. This derived
7% estimate appears to be low, given the mean of 9% of CO estimated
by others as the minimum blood flow required by skin, heart, brain,
kidneys, and liver at
O2 max (21).
Accordingly, we propose in Fig. 7 a range of blood flow distribution
that recognizes both the present findings of respiratory muscle
unloading effects on blood flow and published data on blood flow
requirements of nonskeletal muscle tissue during maximal exercise.
Almost identical average values were obtained for the partitioning of
total O2 max
of 4.40 l/min.
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Applicability of findings.
These cardiovascular effects of respiratory muscle work normally
encountered at O2 max
are indeed substantial, in terms of both the requirement of these
muscles for an average of 14-16% share of total CO and the
apparent reflex vasoconstriction of leg locomotor muscle vasculature
normally elicited by respiratory muscle work. How realistic are these
estimates of blood flow requirements of the respiratory muscles and
their effect on blood flow distribution during maximal exercise? First,
our data are consistent with measurements of the changes in
O2 in respiratory
muscles and CO associated with hyperpnea reported in humans. Anholm et
al. (3) increased E to 127-193 l/min
over a 4-min period in resting humans and observed increases of 4.3 ± 1.0 l/min in CO and 411 ± 92 ml/min in
O2. Also in resting subjects,
Aaron et al. (1) mimicked the Wb and respiratory muscle recruitment
patterns experienced by healthy subjects during maximal
exercise. They reported that the
O2 of respiratory muscles
averaged almost 400 ml/min (or 10% of total
O2 max) at
E values of 113-185 l/min and was 14-15% of
O2 max in several of
the subjects with high levels of E,
significant expiratory flow limitation, and high levels of the Wb at
maximal exercise.
legs associated
with respiratory muscle work at
O2 max are
sufficient to cause changes of up to 20% in the proportion of the
total CO made available to working legs (see Fig. 6).
How generalizable are these findings beyond our specific experimental
design? First, we emphasize that our data were obtained in highly fit
young male subjects at greater than normal
O2 max. Our previous
study of these types of fit subjects showed that they commonly
experienced high ventilatory outputs, significant expiratory flow
limitation with increased end-expiratory lung volume during strenuous
and maximal exercise, use of up to 90-95% of their inspiratory
muscle capacity for pressure generation, and exponential increases in
the O2 cost of breathing as
exercise intensity increased from strenuous through maximal levels (1, 9). Accordingly, we would expect the blood flow requirements of the
respiratory muscles at maximal exercise as presently reported to
represent maximal values in healthy young men. Other subjects or
conditions in which we would also expect a high Wb with similar substantial cardiovascular consequences would include elderly healthy
fit subjects (9) and young fit female subjects (12), both of whom show
excessive flow limitation and/or ventilatory requirements
during moderate-to-strenuous exercise. Similarly, strenuous exercise in
environments with added ventilatory stimuli such as hypoxia or heat
would also be expected to require high levels of ventilatory work and
to impose substantial cardiovascular consequences. On the other hand,
we do not know how the amount of reflex vasoconstriction influenced by
respiratory muscle work during maximal exercise may differ among
subjects and conditions. For example, the amount of sympathetically
induced reflex vasoconstriction in response to isometric exercise has
recently been shown to be reduced by physical training (13, 25).
Whether the ventilatory load in any of these conditions is ever
sufficient to cause measurable effects on CO or limb vascular
resistance during submaximal exercise remains untested.
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ACKNOWLEDGEMENTS |
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We are indebted to Dr. Magdy Younes, who invented the proportional-assist ventilator and loaned us one of his prototypes to conduct these studies. We are also grateful to the very helpful advice and critique supplied by Dr. Loring Rowell and the valuable input on cardiac dynamics provided by Drs. Steven Scharf, James Robotham, and John Newman.
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FOOTNOTES |
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This research was supported by National Heart, Lung, and Blood Institute (NHLBI) Grant RO1 HL-15469. C. A. Harms, T. J. Wetter, and S. R. McClaran were supported by an NHLBI training grant. C. A. Harms was additionally supported by a Parker B. Francis Foundation Fellowship.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests: C. A. Harms, Dept. of Kinesiology, 8 Natatorium, Kansas State Univ., Manhattan, KS 66506 (E-mail: caharms{at}ksu.edu).
Received 22 January 1998; accepted in final form 1 April 1998.
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Abstract
Introduction
Methods
Results
Discussion
References
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