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O2 and leg blood flow
during submaximal exercise
John Rankin Laboratory of Pulmonary Medicine, Department of Preventive 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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The work of
breathing (Wb) normally incurred
during maximal exercise not only requires substantial cardiac output
and O2 consumption (
O2) but also causes
vasoconstriction in locomotor muscles and compromises leg blood flow
(
leg).
We wondered whether the Wb normally incurred during submaximal exercise would also reduce leg.
Therefore, we investigated the effects of changing the Wb on
leg via
thermodilution in 10 healthy trained male cyclists [maximal
O2
(O2 max) = 59 ± 9 ml · kg
1 · min1]
during repeated bouts of cycle exercise at work rates corresponding to
50 and 75% of
O2 max.
Inspiratory muscle work was 1)
reduced 40 ± 6% via a proportional-assist ventilator,
2) not manipulated (control), or
3) increased 61 ± 8% by
addition of inspiratory resistive loads. Increasing the
Wb during submaximal exercise caused O2 to
increase; decreasing the Wb was
associated with lower
O2
(
O2 = 0.12 and 0.21 l/min at 50 and 75% of
O2 max, respectively,
for ~100% change in Wb).
There were no significant changes in leg vascular resistance (LVR),
norepinephrine spillover, arterial pressure, or
leg when
Wb was reduced or increased. Why
are LVR, norepinephrine spillover, and
leg influenced
by the Wb at maximal but not
submaximal exercise? We postulate that at submaximal work rates and
ventilation rates the normal Wb
required makes insufficient demands for
O2 and cardiac output to
require any cardiovascular adjustment and is too small to activate
sympathetic vasoconstrictor efferent output. Furthermore, even a
50-70% increase in Wb during
submaximal exercise, as might be encountered in conditions where
ventilation rates and/or inspiratory flow resistive forces are higher
than normal, also does not elicit changes in LVR or leg.
blood flow distribution; sympathetic vasoconstriction; thermodilution; work of breathing
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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REDUCING THE WORK of breathing
(Wb) at maximal exercise by
unloading the respiratory muscles via proportional-assist ventilation (PAV) is associated with decreased leg vascular resistance (LVR) and
increased leg blood flow
(leg) and leg
O2 consumption
(O2); loading respiratory
muscles by adding inspiratory resistance has the opposite effect (7).
This vasodilation of working limb vasculature when the respiratory
muscles are unloaded at maximal exercise occurs despite a fall in
cardiac output (CO), whereas respiratory muscle loading does not alter
CO (8). Presumably, at maximal exercise, where further increases in CO
are limited, a competition for blood flow among different skeletal
muscle groups exists, such that respiratory muscle blood flow may
increase at the expense of blood flow to working limb muscles. The
important physiological message from these unloading experiments is
that the Wb normally incurred
during maximal exercise causes vasoconstriction in working leg muscles
and decreases
leg.
Our present study asked whether the
Wb normally incurred during
submaximal exercise would elicit significant changes in
O2, leg, and LVR. To
this end, we used the thermodilution technique at two submaximal
exercise intensities during control ventilation and unloading of the
respiratory muscles to repeatedly measure leg.
There are many conditions where the Wb is increased during submaximal exercise in the healthy subject, such as with aging, prolonged exercise, or environmental hypoxia, and also in patients with lung or cardiovascular disease (4, 6, 11, 24). Therefore, we also increased Wb by adding inspiratory resistances during submaximal exercise to determine whether increased work of the respiratory muscles would elicit a vasoconstrictor influence on limb muscle vasculature under conditions where CO was not limited. These effects of unloading and loading the respiratory muscles during submaximal exercise are contrasted with the effects determined during maximal exercise.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects.
Ten male cyclists (nonsmoking, competitive) with resting pulmonary
function within normal limits were recruited to participate in the
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 29.7 ± 1.3 (SE) yr, height 182.7 ± 0.9 cm, weight 76.7 ± 2.5 kg, and maximal O2
(O2 max) 59.0 ± 8.8 ml · kg1 · min1.
Pressure and gas measurements.
During all tests the raw data were recorded on an eight-channel
Hewlett-Packard tape recorder, Gould chart recorder, and computer for
subsequent analysis. Flow rates, esophageal pressure,
O2, and
CO2 production were measured using
equipment and techniques previously reported (2, 12).
Wb was defined as the product of
peak inspiratory esophageal pressure and breathing frequency. This
measurement yielded results, when expressed as percentage of control
values, similar to those from the integrated area of the pressure-tidal
volume (VT) loop (7). This
index of Wb was chosen over the
previously used pressure-volume loop estimation, because hysteresis in
some of the unloaded loops at these submaximal workloads made
calculations of area difficult to interpret.
Inspiratory unloading and loading. A feedback-controlled PAV (Winnipeg) was used to reduce the work of the inspiratory muscles during exercise (26). Briefly, subjects breathed through a two-way low-resistance nonrebreathing valve (7200 series, Hans Rudolph) that was connected on the inspiratory side to the PAV. The PAV develops pressure in proportion to inspiratory airflow and volume, and the level of assist can be adjusted separately 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. The amount of assist was set at a level at which each subject felt comfortable for each workload, 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, resistive loads consisting of mesh screens and rubber stoppers with various-sized orifices were added to the inspiratory side; these resulted in resistances of 3-10 cmH2 · l1 · s
at the flow rates generated during the cycle exercise. Resistances were
selected for each individual and at each work rate and increased the
Wb above control levels by 79 ± 9 and 58 ± 6% at 50 and 75% of
O2 max, respectively.
In 7 of 10 subjects, slightly smaller resistive loads were applied
during additional trials; these increased the
Wb by 58 ± 16 and 37 ± 10% at 50 and 75% of
O2 max, respectively. Subjects participated in practice sessions to familiarize
themselves with the inspiratory loads.
leg measurements.
leg and leg
O2 were measured using the
techniques previously reported (7). A 4.0-Fr catheter, 40 cm long, with
10 side ports, for cold saline infusion (Royal Flush II Nylon, Cook,
Bloomington, IN) was introduced percutaneously into the right femoral
vein 2 cm below the inguinal ligament and advanced ~7 cm toward the knee. A second identical catheter was advanced from near the same location proximally toward the heart ~8 cm into the same femoral vein. A thin (0.64-mm-diameter) Teflon-coated thermocouple (model IT-18, Physiotemp Instruments, Clifton, NJ) was inserted through this
catheter, with the tip extending ~1 cm beyond the catheter. The
placement of the catheter and thermocouple was checked at rest by
infusion of 20 ml of saline to produce a 0.5°C deflection in blood
temperature and was not changed between trials of exercise. Assumptions
regarding this method have been discussed previously (7, 16).
leg was
calculated on the basis of thermal-balance principles described by
Andersen and Saltin (3).
O2 was
calculated as the product of radial arterial-femoral venous
O2 content and
leg (Fick
equation). leg
data and leg O2 are
presented as twice the calculated value to represent both exercising
legs. The arterial-femoral venous
O2 content was divided by arterial
O2 content to give
O2 extraction. LVR was calculated
as the ratio of mean arterial pressure (MAP) to
leg (1 leg).
Blood-gas measurements, blood pressure, and blood lactate. Samples (3-10 ml) of arterial and venous blood were drawn anaerobically over 10-20 s during each trial for measurement of PO2, PCO2, and pH with a blood-gas analyzer calibrated with tonometered blood (model ABL300, Radiometer) and measurement of O2 saturation and Hb with a CO-oximeter (model OSM 3, Radiometer). Blood gases were corrected for temperature changes during exercise by measurement with a thermocouple placed intranasally into the lower third of the esophageal lumen (model 6500, Mon-a-Therm) for arterial blood temperature and from the femoral thermocouple for venous temperature. Arterial and femoral venous blood pressures were measured with pressure transducers (model P10EZ, Ohmeda) attached to the respective arterial and venous lines. Blood lactate concentration was analyzed by means of a lactate analyzer (model 1500 Sport, Yellow Springs Instrument). Hematocrit was determined by microcentrifuge.
Norepinephrine spillover technique. Plasma epinephrine, norepinephrine (NE), and dopamine were determined by a high-pressure liquid chromatography method with electrochemical detection. The rate of spillover of NE into plasma was determined as previously reported using blood flow rates, hematocrit, the difference in NE concentration between femoral venous and arterial plasma, and the fractional extraction of epinephrine (22).
Experimental protocol.
Each subject completed a progressive incremental
O2 max exercise test
on a cycle ergometer, as previously described (7). The mean
O2 max was 59.0 ± 8.8 ml · kg1 · min1
(range 48-73
ml · kg1 · min1).
From the
O2 max
data, workloads for each subject were selected to elicit 50 and 75% of
O2 max.
O2 max followed by
two 15-min bouts at 75% of
O2 max. Each bout was
separated by a rest period of ~10-15 min. During each fixed work
rate (50 and 75% of
O2 max) three or four
continuous 5-min periods of control (no ventilatory intervention),
inspiratory resistive loading, or unloading were applied, with periods
of control and loaded breathing combined in one bout and control and
unloaded breathing combined in the other (the ventilatory interventions
were randomized). Thereafter, in 7 of the 10 subjects, two additional
exercise bouts at 50% of
O2 max were followed
by two bouts at 75% of
O2 max. These trials
were similar to those described above, except the inspiratory resistive
load was decreased slightly during the period of loaded breathing in
these later bouts. Within each 5-min period the sequence of
measurements was as follows:
leg at 2 min
45 s; blood sampling, esophageal, and femoral venous temperatures at 3 min 55 s; femoral venous pressure at 4 min 15 s; and a second
leg at 4 min
35 s. All other measurements were recorded continuously; values
reported and used for calculations (including arterial and esophageal
pressures and O2) were
taken at the same time as the
leg measurements.
Changes in VT were minimized
during unloaded breathing trials via visual feedback from an
oscilloscope marked at control
VT levels, and changes in
breathing frequency were minimized during loaded breathing trials via
auditory feedback from a metronome set at control breathing frequency.
This was done for all exercise bouts at 75% of
O2 max. During some
of the bouts of unloaded and loaded breathing at 50% of
O2 max,
subjects were allowed to self-select
VT and breathing frequency to
whatever felt comfortable. Aside from slight changes in breathing
frequency and VT, this had no
effect on the Wb,
O2,
leg, or LVR;
thus these trials were combined with the other unloaded and loaded
breathing trials and analyzed together.
Statistical analysis.
Relationships between Wb and the
dependent variables under the three conditions, i.e., control,
inspiratory muscle load, and inspiratory muscle unload at each of the
two work rates (50 and 75% of
O2 max), were
determined from simple linear regression. Separate one-way ANOVAs with
repeated measures were used to determine treatment differences among
group mean values across the three conditions within each exercise
level. Tukey's post hoc analysis was used to determine where the
differences existed. 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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Figure 1 is a typical example of the
multiple measurements made for
leg, MAP, and
LVR plotted vs. Wb in one subject
at both submaximal work rates. Regression lines through the individual trials are also displayed. The total number of trials (trial = 2.5 min
of leg cycling during which 1 leg measurement
was made) for each subject was 25 ± 2 at 50% of
O2 max (range
16-28) and 20 ± 2 at 75% of
O2 max (range
12-24), and these were roughly divided as 1:4 unloaded, 1:2
control, and 1:4 loaded inspiration.
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Using the approach displayed in Fig. 1, we present our findings
concerning the effects of changing the
Wb on several variables of
O2 transport by showing regression
lines through the absolute values for each subject and indicating
whether the slopes of these lines are significantly different from
zero. In addition, the mean values of each variable for each of the
three specific conditions (inspiratory unloading, control, or
inspiratory loading) and for each work rate are presented in Tables
1 and 2.
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Wb and minute ventilation.
Estimates of Wb using
pressure-volume loops resulted in values of 98 and 219 J/min for the
control trials at 50 and 75% of O2 max, respectively
(not shown). At both work rates, peak inspiratory esophageal pressures
were significantly increased (less negative) with unloading and
significantly decreased (more negative) with loading compared with
control values. Inspiratory muscle unloading reduced
Wb to 62 ± 8 and 58 ± 4%
of control at 50 and 75% of
O2 max, respectively,
whereas with the inspiratory resistive loads
Wb was increased to 171 ± 10%
of control at 50% of
O2 max and 151 ± 5% at 75% of
O2 max
(Tables 1 and 2).
O2 max.
Blood gases.
During control conditions, arterial and femoral venous
O2 saturations were 96.0 ± 0.1 and 25.1 ± 5.3% at 50% of
O2 max and 95.2 ± 0.3 and 17.9 ± 3.7% at 75% of
O2 max; arterial
PO2 and
PCO2 were 92.3 ± 2.0 and 39.4 ± 0.8 Torr at 50% of O2 max and 88.0 ± 2.3 and 38.1 ± 1.2 Torr at 75% of
O2 max; arterial and
femoral venous pH were 7.40 ± 0.01 and 7.30 ± 0.01 at 50% of
O2 max and 7.38 ± 0.01 and 7.26 ± 0.01 at 75% of
O2 max; arterial
lactate was 1.34 ± 0.25 mM at 50% of
O2 max and
2.75 ± 0.49 mM at 75% of
O2 max. Arterial
O2 content averaged 19.3 ml/dl at
both work rates, whereas femoral venous
O2 content was 5.0 ml/dl at 50%
of O2 max and decreased
to 3.7 ml/dl at 75% of
O2 max.
Arterial and femoral venous blood-gas values with the respiratory
muscles loaded or unloaded did not differ from those during control.
Effect of Wb on total
O2.
Figure 2 shows individual subject
regression lines for total O2
(O2 tot)
vs. Wb. At 50% of
O2 max, 5 of 10 subjects had a significant positive slope
(P < 0.05). At 75% of
O2 max, 6 of 10 subjects had significant positive slopes. Combining the individual data
revealed that, for a 100% change in
Wb (the approximate difference
between unloaded and loaded conditions),
O2 would change by 4.6 and
6.0% at 50 and 75% of
O2 max, respectively (P < 0.001).
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Effects of changing Wb on
O2 transport.
leg increased in
all subjects from a mean of 11.5 l/min at 50% of
O2 max to
16.6 l/min at 75% of
O2 max (Tables 1 and 2). Figure 3 shows individual subject
regression lines for
leg vs. Wb. None of the slopes of
these regressions were significant, although in two subjects
at 75% of
O2 max the
negative slopes approached significance
(P 
0.06). Mean
leg data were
not different between respiratory muscle loading conditions at 50% of
O2 max, but a trend for
leg to decrease
with increased Wb was evidenced by
a significant decrease in
leg (0.54 l/min,
P < 0.05) for loaded vs.
unloaded conditions at 75% of
O2 max (Table
2).
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5 mmHg
(Fig. 4). Mean femoral venous pressure was
increased 5-8% with unloading and reduced 4-7% with loading
compared with control.
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mean femoral venous pressure) was used in the
calculation for LVR.
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O2 max and for three
subjects at 75% of
O2 max (1 subject had a
significant negative slope at 75% of
O2 max). Mean
HR was significantly higher (3 beats/min) for loaded than for unloaded
and control ventilation at 50% of
O2 max, whereas at 75%
of O2 max the differences were not significant (Tables 1 and 2).
Given the small or absent changes in
leg or
arterial-femoral venous O2 content
with changing Wb at either work
rate, leg O2 was also
unchanged with changing Wb. An
exception to this was found at 75% of
O2 max, where mean leg
O2 was significantly higher
(0.10 l/min) with unloading than with loading (Table 2). By
changing the Wb, leg
O2/O2 tot
ratio increased by 4-5% during respiratory muscle unloading and
decreased by 4-5% during loading at both work rates (Tables 1 and
2).
Effect of Wb on NE spillover.
NE spillover was significantly increased from 50 to 75% of
O2 max
(P < 0.01 for control conditions,
Tables 1 and 2). The increase averaged 91 ± 20% for individual
subjects. There was wide variability in NE spillover between subjects,
and there was no significant change with changes in
Wb at either of the exercise intensities.
Comparison of data with change in Wb at
maximal vs. submaximal exercise.
Figure 6 shows the changes in
O2 tot,
leg, LVR, and NE
spillover vs. the absolute Wb for
the two submaximal work rates (from the present study) and for maximal
exercise (7). Comparing the control values obtained at maximal exercise
with those at submaximal exercise reveals expected increases for
O2 tot
and leg in
response to increasing leg work rate. LVR was highest at 50% of
O2 max, fell
substantially at 75% of
O2 max, and remained at
this low level at maximal exercise. Similarly, NE spillover was lowest
at 50% of O2 max,
increased at 75% of
O2 max, and remained
near this level at maximal exercise.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Summary of findings.
We used multiple trials of submaximal exercise and measurements of limb
blood flow in 10 subjects to test the effects of changing the
Wb on LVR,
leg, and
O2 tot.
Our findings at these submaximal exercise levels show that
O2 tot
increased with increasing Wb and
decreased with decreasing Wb;
however, leg,
LVR, and NE spillover did not change significantly with changing
Wb. These findings at submaximal
exercise intensities differ from those previously described at maximal
exercise, where
O2 tot
(and CO) and LVR were affected by changing
Wb. We believe that the lack of
effect of loading or unloading respiratory muscles on LVR at submaximal
exercise is a consequence of too small a load placed on (or removed
from) the cardiovascular system to disturb whatever variable(s)
activate(s) the sympathetic nervous system to cause vasoconstriction in
active locomotor muscle. Furthermore, the large effect of changing the
Wb on LVR (and
leg) during exercise at O2 max is a
consequence of the high O2 and
blood flow demand of the respiratory muscles occurring at a time when total available blood flow is limited. The major physiological implication of the new findings at submaximal exercise is that the
normal Wb incurred at moderate
exercise intensities does not contribute to the tonic vasoconstrictor
activity present in working leg muscles. Our findings also suggest that
even substantial increases in Wb
(at least in the range of 50-70% above normal) will raise whole
body O2 but do not cause
alterations in LVR or
leg during submaximal exercise.
Sensitivity of measurements.
Our protocol involved making multiple
leg measurements
for each subject. Because we randomly assigned respiratory muscle load
and unload conditions and analyzed within-bout measurements for trends,
we are confident that the results are not obscured by time-dependent
effects. Previously, at maximal exercise, we also used multiple
exercise trials and measurements of
leg and demonstrated an ability to detect systematic changes of <10% in leg that
corresponded with changes in Wb,
even on an individual-subject basis (7). The reproducibility of
leg measurements
within trials at O2 max
was very good [coefficient of variation (CV) ± 3.9%].
This reproducibility was comparable at 75% of
O2 max (CV ± 5.5%
for leg
measurements under control conditions) and was lower at 50% of
O2 max (CV ± 9.9%). Thus a relative mean change in
leg over the
range of the change in Wb similar
to that seen at O2 max
(11%) would have been slightly more difficult to detect at the
submaximal work rates.
Effect of changing Wb on
O2 tot.
By increasing Wb at submaximal
work rates (50 and 75% of
O2 max), we were able
to show a relatively small but significant increase in
O2 tot;
similarly, by reducing Wb via PAV,
O2 tot decreased compared with control. Although these changes in
O2 tot are relatively small, they are what would be predicted on the basis of
previous measurements of the O2
cost of mimicking the mechanics and breathing pattern of exercise
hyperpnea in normal subjects at rest (1). Given the regression equation
developed by Aaron et al. (respiratory muscle
O2 = 0.081 + 0.001 × Wb, where
Wb is measured from
pressure-volume loops and is in J/min), we estimate from our
measurements 1) that the total
O2 cost of breathing at 50 and
75% of O2 max is 0.18 and 0.30 l/min, respectively and 2)
that the O2 cost of the change in
the Wb between unloaded and loaded
conditions is 0.11 l/min at 50% of
O2 max and 0.20 l/min
at 75% of
O2 max. These
latter estimates were nearly identical to the group mean
O2 tot
differences of 0.12 and 0.21 l/min found in the current study. On the
basis of this same equation, corresponding values at
O2 max were estimated
to be 0.61 l/min for the total O2
cost of breathing during control conditions and a change in
O2 of 0.54 l/min over the
range of Wb between unloaded and
loaded breathing.
O2 change
with changing Wb during exercise.
At maximal exercise, unloading resulted in a decreased stroke volume
and CO (HR and arterial-mixed venous
O2 difference did not change),
which we associated with increases in inspiratory intrathoracic
pressure (8). It is also likely during submaximal exercise that our observed decrease in O2
corresponded with a decrease in CO. With respiratory muscle loading, CO
(or
O2 tot)
did not change at maximal exercise, probably because the limits of the
pericardium had been reached (8). At submaximal exercise, loading did
increase O2, and it is likely
that stroke volume and CO were also increased by the more negative
intrathoracic pressures with loading.
Respiratory muscle work and changes in LVR. Why did adding and removing respiratory muscle work at maximal exercise cause changes in LVR, and why were these changes not seen during the current study at submaximal exercise? Our basic premise during maximal exercise was that the work and/or aerobic status of the respiratory muscles stimulated type III-IV afferents in the diaphragm and other respiratory muscles, which then caused reflex vasoconstriction of limb vasculature during control or loaded conditions and reflex vasodilation with respiratory muscle unloading (9). Indirect evidence in support of this postulate and a discussion of other possible mechanisms (i.e., baroreflexes) were presented previously (7).
Unloading the respiratory muscles.
These unloading data are especially important, because they speak
directly to the cardiovascular role of respiratory muscle work and/or
intrathoracic pressure normally incurred at the various exercise
intensities. Why did respiratory muscle unloading result in decreases
in LVR at maximal but not submaximal exercise? One possibility is that,
during submaximal exercise, tonic vasoconstrictor sympathetic nerve
activity to locomotor muscles is not normally present (during control
conditions), and thus there would be no activity to relieve with
respiratory muscle unloading. This does not appear to be likely, since
there is overwhelming evidence that tonic vasoconstrictor activity is
present in leg vasculature during moderate exercise (20). Furthermore,
in our experiment, under control exercise conditions, we observed a
measurable level of NE spillover at 50% of
O2 max and a
63% increase in this mean level at 75% of
O2 max. In
fact, at 75% of O2 max
the NE spillover approximated that at
O2 max. LVR followed
similar trends, showing a decrease from 50 to 75% of
O2 max and comparable values at 75% of
O2 max and
O2 max. Accordingly, we
would suggest that substantial sympathetic vasoconstrictor activity did
indeed exist at these submaximal workloads, which potentially could
have been relieved with respiratory muscle unloading. Therefore, we
must conclude that in our healthy subjects the work of breathing normally incurred during these submaximal exercise intensities does not
contribute to the vasoconstrictor tone present in working locomotor muscles.
Loading the respiratory muscles.
Why did additional respiratory muscle loading result in increases in
LVR at maximal but not submaximal exercise? Perhaps the load placed on
the respiratory muscles at submaximal exercise was simply insufficient
to cause a change. Although we did increase the
Wb substantially (50-70%),
the absolute increase in Wb was less than that achieved during maximal exercise. However, even had we
increased the Wb to the same level
attained during maximal exercise, it is likely that an increase in
O2 and CO that would enhance
O2 transport to meet the increased
metabolic requirements of the respiratory muscles would have occurred.
This compensatory response at submaximal exercise is different from the
case of maximal exercise, where increasing blood flow and
O2 transport to meet the increased
work of the respiratory muscles were not accomplished by an augmented
CO (8). Thus, at maximal exercise, increased LVR and diversion of blood
flow from working leg muscle was necessary. Our present experimental
design did not provide a sufficiently large increase in
Wb during submaximal exercise to
distinguish between these possibilities.
Relevance of findings.
Our findings are relevant to several conditions in which ventilatory
work is increased during submaximal exercise. For example, in elderly
fit men, ventilatory work is increased (relative to younger fit men)
throughout exercise. This is due to an enhanced ventilatory response to
compensate for increased dead space ventilation and possibly the
presence of expiratory flow limitation (11). LVR is also increased and
leg is decreased
across a range (mild to heavy) of exercise intensities (17). Present
findings would not predict that most of this decreased limb flow rate
was attributable to increased Wb,
at least at work rates up to 75% of
O2 max. We hasten to
add that the nature of the increase in ventilatory work is quite
different from our experimentally induced increases in
Wb, which were purely increased
inspiratory flow resistive work. The elderly have increased ventilation
rates, expiratory flow limitation, relative hyperinflation, and
increased elastic work, all of which may have some reflex influence on
sympathetic nerve activity (5, 23).
leg. For
example, in heart failure patients, exercise hyperpnea is enhanced and peripheral blood flow is reduced. Although a causal link between these
two factors has not been established, they have been theoretically linked as parts of one underlying process (4). In the rat model with
myocardial infarction, blood flow to the diaphragm is enhanced and limb
muscle blood flow reduced during submaximal exercise (15). A similar
scenario might occur with submaximal exercise in healthy subjects
during short-term exposure to the hypoxia of high altitude, where,
again, hyperventilation and increased ventilatory work are combined
with a reduced CO at any given submaximal O2 (24, 25). Another
exceptional case in this regard may occur in prolonged exercise at
fixed, heavy, submaximal work rates, where a time-dependent tachypnea,
hyperventilation, expiratory flow limitation, and increased ventilatory
work occur and where diaphragmatic fatigue is prevalent (10).
In summary, our present and past results would predict that the
normally occurring Wb with
increasing exercise intensity in healthy subjects at sea level
would require a progressively greater portion of the
increasing CO (and O2) to
be directed to respiratory muscles at all work rates; however, these
effects of increasing ventilatory work on sympathetic vasoconstrictor
outflow and on limb blood flow would not be realized until maximal or
at least very near-maximal exercise intensities. Our present findings
do not allow us to distinguish between increased ventilatory work per
se and a limited blood flow distribution as the primary trigger for
increased vasoconstrictor outflow to locomotor muscle.
Hierarchy of muscle blood flow distribution during exercise.
Because the diaphragm and accessory respiratory muscles have a high
oxidative capacity, their resistance vessels may be especially sensitive to local vasodilator influences (13, 14). The fact that
decreases in leg
were observed with addition of respiratory muscle work (7) but not with
added arm work (18, 19, 22) was interpreted to mean that, at
high-intensity exercise, a hierarchy may exist for blood flow
distribution, with respiratory muscles ranking before leg and arm
musculature (21). However, our present findings show that changing
respiratory muscle work did not cause changes in LVR or
leg during
submaximal exercise. Accordingly, respiratory muscles may not rank
above limb muscles in terms of vasodilatory sensitivity, and the reason
for differences in previous findings may be more related to the
different work intensities used and the limits to available CO imposed
at O2 max. A quite different type of hierarchy might exist among the different skeletal muscle vascular beds in terms of their relative propensity to produce
and accumulate metabolic end products. The higher oxidative capacity
and fatigue resistance of the diaphragm vs. leg vs. arm musculature may
mean, thus, that the respiratory muscles must maintain a much higher
work intensity before incurring sufficient metabolic acidosis to
trigger sympathoexcitatory reflexes.
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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 this study. We also recognize the technical assistance provided by Claudette St. Croix, Kathy Henderson, Annie Gazdag, and Charles Dumke.
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FOOTNOTES |
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This research was supported by National Heart, Lung, and Blood Institute Grant RO1 HL-15469. T. J. Wetter and C. A. Harms were supported by a National Heart, Lung, and Blood Institute training grant.
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 and other correspondence: J. A. Dempsey, 504 N. Walnut, Madison, WI 53705 (E-mail: jdempsey{at}facstaff.wisc.edu).
Received 18 November 1998; accepted in final form 29 March 1999.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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) and 75%
of 
) in 1 subject. None of regression line slopes were significantly different
from zero (P > 0.05).
, data for 75% of
