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1 John Rankin Laboratory of Pulmonary Medicine, Department Preventive Medicine, University of Wisconsin, Madison, Wisconsin 53705; and 2 Department of Kinesiology, Kansas State University, Manhattan, Kansas 66506
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The
normal respiratory muscle effort at maximal exercise requires a
significant fraction of cardiac output and causes leg blood flow to
fall. We questioned whether the high levels of respiratory muscle work
experienced in heavy exercise would affect performance. Seven male
cyclists [maximal O2 consumption
(
O2) 63 ± 5 ml · kg
1 · min1] each
completed 11 randomized trials on a cycle ergometer at a workload
requiring 90% maximal O2. Respiratory
muscle work was either decreased (unloading), increased (loading), or
unchanged (control). Time to exhaustion was increased with unloading in 76% of the trials by an average of 1.3 ± 0.4 min or 14 ± 5% and decreased with loading in 83% of the trials by an average of
1.0 ± 0.6 min or 15 ± 3% compared with control
(P < 0.05). Respiratory muscle unloading during
exercise reduced O2, caused
hyperventilation, and reduced the rate of change in perceptions of
respiratory and limb discomfort throughout the duration of exercise.
These findings demonstrate that the work of breathing normally incurred
during sustained, heavy-intensity exercise (90%
O2) has a significant influence on
exercise performance. We speculate that this effect of the normal
respiratory muscle load on performance in trained male cyclists is due
to the associated reduction in leg blood flow, which enhances both the
onset of leg fatigue and the intensity with which both leg and
respiratory muscle efforts are perceived.
blood flow distribution; dyspnea; work of breathing
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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RESPIRATORY MUSCULATURE
DURING strenuous exercise in humans can command ~10% of the
total oxygen consumption (O2) in
moderately fit subjects and up to 15% in highly fit subjects
(1). Our laboratory has recently shown, by
unloading the respiratory muscles, that the respiratory muscle work
experienced under normal physiological conditions at maximal exercise
also exerts two types of effects on the cardiovascular response:
1) a substantial portion of the cardiac output (up to
14-16%) is directed to the respiratory muscles to support their
metabolic requirements (11), and 2) blood flow is reduced to working locomotor muscles because of sympathetically mediated vasoconstriction (10). Therefore, given
this high demand for oxygen and blood flow by the respiratory muscles
during maximal exercise and its effects on the cardiovascular system,
both centrally and peripherally, we hypothesized that the work of
breathing normally experienced during strenuous exercise would impair
exercise performance. We tested this hypothesis in highly fit subjects
during high-intensity constant-load exercise by using multiple
randomized trials of control, respiratory muscle unloading, and
respiratory muscle loading conditions.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
Seven male cyclists (nonsmoking; competitive) with resting pulmonary function within normal limits were recruited to participate in this study. None of our subjects experienced significant reductions in arterial PO2 at maximal exercise (10, 11). 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 27.3 ± 3.1 (SD) yr, height 177.9 ± 2.4 cm, and weight 71.3 ± 4.3 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 total bodyO2 and CO2 production were
measured by using equipment and techniques previously reported
(1, 15). Apparatus resistance was
0.80-1.49 cmH2O · l1 · s
at flow rates from 0.5 to 9.0 l/s.
Inspiratory Unloading and Loading
A feedback-controlled proportional-assist ventilator (PAV) was used to reduce the work of the inspiratory muscles during exercise (7, 10, 11, 22). During practice and testing sessions, subjects were verbally coached to relax, reduce their inspiratory effort, and permit the PAV to assist each inspiration as much as possible, as judged by the negativity of mouth pressure at the onset of each inspiration (7). 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. The
ventilation settings and added resistances were chosen to cause
increases and decreases in inspiratory muscle work similar to our
previous studies (Refs. 10, 11; also see DISCUSSION for
values). Subjects participated in practice sessions to familiarize themselves with the inspiratory loading and unloading.
Experimental Protocols
Subjects initially completed a progressive, incremental maximalO2
(O2 max) exercise test on an
electromagnetically braked cycle ergometer (Elema, Solna, Sweden),
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 20 min of recovery, subjects cycled to exhaustion at 5-10% above their peak workload (as determined by the prior progressive test) to verify O2 max. A plateau (<150 ml/min) or
decrease in O2 was observed for each
subject between the final two workloads of the incremental
O2 max test and/or between the final
workload of the incremental test and the workload of the repeat test.
The mean O2 max was 63 ± 5 ml · kg1 · min1 (range
55-74 ml · kg1 · min1).
Over a 6- to 8-wk period and by using separate test days for each
trial, subjects were randomly assigned to and completed six trials
under control (3 trials) and respiratory muscle unload (3 trials)
conditions. One to six months later, we added two control trials and
three loaded trials for six of the seven subjects, again using randomly
assigned trials and a separate day for each trial with several days
between trials. After 5-10 min of warm-up with a light work rate
(~40-50% O2 max), subjects were gradually (over 30 s) brought to their prescribed work rate of ~90 O2 max, and this work rate was
held constant for the duration of the test. The work rate averaged
363 ± 48 W (range 300-425 W). Subjects were free to choose
their cadence (between 80 and 100 rpm), and termination of the test was
determined when a cadence of 
50 rpm could not be maintained. Verbal
encouragement and cadence feedback was provided.
Statistical Analysis
Paired t-tests were used to determine treatment differences between group mean values between control and respiratory muscle load or unload. Relationships were determined from simple regression and forward stepwise multiple regression. The intraclass correlation coefficient of reliability (R) (6) was used to evaluate the repeatability of our measures over three trials. As R approaches 1.0, greater repeatability is implied: R < 0.4 indicates poor reliability, 0.4 < R < 0.75 fair to good repeatability, and R 0.75 excellent repeatability. 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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Table 1 shows the reproducibility of
time to exhaustion (Tlim),
O2, dyspnea, and leg rating of
perceived exertion (RPE) during repeat testing under control conditions
(control/unload and control/load). Note that the mean values for
Tlim during control conditions were significantly longer
during the control sessions associated with the unloaded trials than
with the loaded trials, the latter having been conducted later in the
year. No systematic changes were found in any of the variables across
three repeat trials at isotime (minute 5) or end exercise
(P > 0.10). The R value indicated a high
level of reliability in dyspnea and leg RPE ratings across trials, with
poor to good reliability in Tlim and
O2 (see METHODS for
rating scale).
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Effect of Respiratory Muscle Loading and Unloading on Tlim
Table 2 shows mean values in Tlim between experimental conditions. With respiratory muscle unloading, subjects were able to exercise 1.3 ± 2.0 min longer (range
1.2-5.3 min; +14.4 ± 4.9%) than during
control conditions (P < 0.05), whereas, with loading,
Tlim was significantly reduced by 1.0 ± 0.8 min
(range 0.4-4.7 min; 15.1 ± 3.3%; P < 0.05). Individual data for Tlim changes with respiratory
muscle unloading and loading are shown in Fig.
1. Subjects exercised longer with
respiratory muscle unloading in 16 of 21 trials (76%) and shorter with
loading in 15 of 18 trials (83%). The regression line of control vs.
unloaded Tlim was parallel to the line of identity (not
shown), indicating that the effect of unloading on absolute
Tlim was similar across all performance times, whereas,
with loading, the reduction in Tlim tended to be greater
the longer the control performance time.
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Effect of Respiratory Muscle Unloading and Loading on
O2 and E
O2 and minute ventilation
(E)/O2 plotted
against time from the first minute of exercise to exhaustion. All
subjects exercised at least 5 min under all conditions, and, as a
result, continuous data are provided for the initial 5 min of exercise
and for end exercise. Table 3 summarizes
group mean values for all measured variables.
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Figure 2B shows that, under control conditions,
O2 averaged 92 ± 1% (range
91-94%) at the beginning of the prescribed workload and then rose
gradually with exercise duration to achieve 100% of
O2 max at end exercise. With
loading, O2 averaged 6.3 ± 0.2%
greater than control (P < 0.05) for minutes
3-5 but was equal to control at end exercise. With unloading,
O2 averaged 6.9 ± 0.2% lower than
control at all time points throughout exercise, including end exercise
(P < 0.05). Loading resulted in a significantly steeper slope of O2 vs. exercise time
compared with unloading (0.17 vs 0.13; P < 0.05), but
neither of these slopes was different from its respective control.
Table 3 and Figure 2C show that E/O2 was
significantly greater than control with unloading and less than control
with loading, primarily due to changes in tidal volume.
Effect of Respiratory Muscle Unloading and Loading on Leg RPE and Dyspnea Ratings
Figure 3 shows the time course for leg RPE and dyspnea during exercise, and mean changes are shown in Table 3. Leg RPE (Fig. 3A) and dyspneic ratings (Fig. 3B) with respiratory muscle loading were both significantly higher than control for minutes 1-4 but not at end exercise. With unloading, leg RPE and dyspneic ratings were lower during minutes 3-5 but not at end exercise.
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Correlations Among Variables With a Changing Work of Breathing
Interindividual differences with loading and unloading for most variables as measured at isotime (minute 5) or in the slopes of the time-dependent effects were significantly interrelated (see Tables 4 and 5). Of particular relevance were the findings from the multiple-regression analysis that the total variation of changes in Tlim with unloading and loading were best accounted for by 1) the independent effects of changes at isotime in dyspnea perception (r2 = 0.29) and 2) the combination of changes in slope for dyspnea perception plus those inE vs. exercise time
(r2 = 0.35). Changes in both respiratory
and limb discomfort with respiratory muscle loading and unloading were
closely related to each other, especially at the isotime of exercise,
and, in turn, changes in either of these perceptions with loading and unloading were most closely related to changes in
O2.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Major Findings
Our findings demonstrate a significant effect of the work of breathing during strenuous exercise on performance time to exhaustion in healthy, physically trained humans. We observed that decreasing the work of breathing consistently led to significantly longer exercise tolerance, whereas increasing the work of breathing curtailed performance. Respiratory muscle unloading during exercise was also associated with reducedO2,
hyperventilation, and reduced perceptions of respiratory and limb
discomfort. These findings demonstrate that the work of breathing
normally encountered during sustained heavy exercise has a significant
influence on exercise performance. We believe the reason for this
effect is multifactorial and may include the direct effects of high
levels of respiratory muscle work on respiratory muscle fatigue and/or
its "indirect" effects on limiting blood flow distribution to limb
locomotor muscles in very heavy exercise and on the intensity with
which both respiratory and locomotor muscular efforts are perceived.
Limitations
Loading and unloading effects.
We did not directly measure esophageal pressure (Pes) in our study, to
avoid invasive instrumentation that might detract from performance
time. In two previous studies from our laboratory (10,
11), measurements of Pes and Pes-volume loops during exercise at O2 max showed that, under
control conditions, the work of breathing averaged 520-548 J/min
and Pes averaged 28 cmH2O at peak inspiration and 23 cmH2O at peak expiration. Unloading caused the work of
breathing to be reduced, on average, to 37-45% of control and Pes
to be 12-14 cmH2O less negative during inspiration and
6-7 cmH2O less positive at peak expiration, whereas loading caused the work of breathing to increase to 128 and 157% of
control and Pes to be 6-8 cmH2O more negative at peak
inspiration and unchanged in expiration.
O2 with loading and unloading,
respectively, and these changes were similar to those previously
reported (10, 11, 20). Finally,
we also observed that the nadir of mouth pressure (as an estimate of
inspiratory effort) averaged 30-35% less negative than control
with unloading and 40-45% more negative than control with
inspiratory resistive loading throughout exercise. On the other hand,
we also noted previously that the changes in the work of breathing with
unloading during maximal exercise were variable within and between
subjects (see Performance measures). Accordingly, we
believe we can conclude that exercise performance was reduced with
loading and prolonged with unloading, but we are unable to define a
more precise dose-response relationship between the work of breathing
or respiratory muscle force output and performance time.
Performance measures. Performance studies are typically prone to much variability in Tlim because of day-to-day variations in subject motivation, effort perceptions, learning effects, normal biological variability, and so forth. Furthermore, in our study, we also introduced variable amounts of respiratory muscle work with unloading from trial to trial because the resultant amount of work was determined by the combined effects of the set amount of the ventilator's pressure assist plus the subject's ability to "relax" and to reduce the respiratory motor output (or effort) to breathe. Accordingly, we avoided systematic changes within and between trials by randomly assigning experimental (unloading/loading) and control conditions while exposing each subject to several practice trials in addition to multiple trials per condition. Although we did observe random, intrasubject variability in Tlim on repeat testing, no significant systematic learning effects occurred with repeat trials (see Table 2). We attribute the absence of any apparent learning effect to our use of highly trained competitive cyclists who had considerable experience with exhaustive exercise, together with the use of very high-intensity, fairly short-duration exercise trials that did not cause boredom or monotony.
Finally, we note that a time trial in which total power output and/or mileage completed in a fixed time is used to measure performance has been shown to be more reproducible than a fixed-work-rate test, at least when the latter requires only 75% ofO2 max and lasts a 1 h or more
(12). Unfortunately, time-trial tests were not feasible in
our study because we found that application of the mechanical
ventilator in the presence of a changing work rate was highly
disruptive to breathing and often inconsistent in unloading the
respiratory muscles.
Although use of the PAV caused subjects to express substantial relief
in their perception of the difficulty of working at high intensities,
it is also important to stress that the use of positive-pressure
ventilation to reduce the work of breathing was not without significant
side effects. Despite several practice sessions, the ventilator was
occasionally disruptive to the subjects who had to concentrate on
relaxing their chest wall while tolerating the foreign sensation of air
being "pushed" into their lungs and the rare asynchrony between the
ventilator breath and the subject's respiratory effort.
Clearly, these procedures often distracted the subject from
concentrating on the main task of completing a maximal cycling
performance to exhaustion. Accordingly, we suspect that the actual
effect of the normally occurring amount of respiratory muscle work, per
se, on high-intensity endurance exercise performance is probably even
greater and more consistent than the 14 ± 5% improvement
presently observed.
Comparison With Other Respiratory Muscle Unloading Studies
Contrary to our findings, several reports have shown no benefits of respiratory muscle unloading on exercise performance. Krishnan et al. (16), Gallagher and Younes (7), and Marciniuk et al. (18) all had subjects perform constant-load exercise at ~70-80% ofO2 max during both control conditions
and with respiratory muscle unloading. These studies found that
respiratory muscle unloading had no effect on ventilation or
Tlim, despite significant reductions (~20-40% less
than control) in respiratory muscle loads during the exercise.
Several factors could account for the difference between these studies
and ours. First, subjects in these studies were only moderately fit
compared with our subjects, whose
O2 max was 168 ± 3% of
predicted. The work of breathing during near-maximal exercise has been
shown to require ~10% of total O2, on
average, for the moderately fit subjects, whereas, in the highly fit
subjects at higher peak work rates and E, the
O2 cost of breathing approaches 15% of
O2 max (1). Therefore, the
effect of reducing the work of breathing during high-intensity exercise
would be most noticeable in the highly fit subject. Second, the
exercise intensity used in previous reports was ~70-80% of
O2 max, whereas our subjects began
exercising at ~90% O2 max and
reached O2 max at end exercise. Our
laboratory has reported that blood flow redistribution between the
respiratory muscles and the legs occurred with loading and unloading at
maximal exercise (10) but not during exercise at 50 or
75% O2 max (20).
Therefore, considering both previous and present studies, we would
predict that endurance performance would not be increased with
respiratory muscle unloading during more moderate-intensity exercise.
Third, our experimental design included several practice trials on the
ventilator and included trained cyclists to eliminate systematic
learning effects on performance. Most importantly, we used multiple,
randomized performance trials in an attempt to reduce the effect of
random variability in performance time (see Limitations).
Previous reports have used fewer trials, which raises the question of
repeatability and their ability to detect significant systematic
changes in performance beyond the "noise" of random variation.
Other attempts to unload the respiratory muscles have used
helium-oxygen gas mixture (13, 21). In these
studies, heliox acts to expand the maximal flow-volume loop and
eliminate expiratory flow limitations that occur in many highly fit
individuals. It was found that heliox did not affect exercise time and
whole body O2 at moderate work
intensities; however, with exercise of >85-90% O2 max, breathing heliox significantly
increased exercise time and reduced O2
(near the end of exercise).
Previous studies of unloading reported either no change in
E or increases that occurred only at lower exercise
intensities or at early stages of prolonged, constant-load exercise
(7, 16). In the present study, however, we
found a significant hyperventilatory response to unloading that
persisted throughout the prolonged heavy exercise (see Fig. 2). We are
not sure why these findings differ. One interpretation of the increased
E/O2 with unloading is that the high level of normal respiratory muscle force exerted in
heavy exercise caused reflex inhibition of central respiratory motor
output and that this inhibition was relieved with unloading. On the
other hand, we cannot rule out behavioral effects on respiratory motor
output and ventilation secondary to application of PAV.
Why Did Unloading/Loading Of The Respiratory Muscles Change Exercise Performance?
Our findings speak to three types of influences that have a potential bearing on why changes in respiratory muscle loading may have affected exercise performance. These include influences on O2 transport to (and CO2 transport from) locomotor muscles, on respiratory muscle fatigue, and on the perception of respiratory and/or locomotor muscle effort.Effects of respiratory muscle loading on O2 transport
to locomotor muscles.
In view of previous findings (see Comparison With Other
Respiratory Muscle Unloading Studies; Refs. 10, 11) we would
expect that, under the near-maximal and maximal conditions of
exhaustive exercise encountered in the present study, the appropriate
increases and decreases in limb vascular conductance, blood flow, and
O2 transport occurred with respiratory muscle unloading and
loading, respectively. However, we emphasize that, with
respiratory muscle unloading and less negative intrathoracic pressure,
the stroke volume and cardiac output (and
O2) are also reduced, and, therefore, the effects on local limb blood flow, although consistent and significant, are relatively small (in the range of 5-7% increase from control). Nevertheless, limb muscle force output and fatigue have
been shown to be highly responsive to even small changes in limb muscle
blood flow under conditions of high intensities of muscle contraction
(5). In contrast to these relatively small effects on limb
blood flow with unloading of respiratory muscles, the effects are
substantially greater with loading because the cardiac output remains
unchanged from control and also because slightly greater changes are
elicited in limb vasoconstriction. Consistent with these findings, we
also found in the present study that unloading reduced total body
O2 throughout our prolonged exercise at
>90% O2 max, whereas loading
increased the O2 up to end exercise, at
which point O2 in control and loaded conditions was equal and equivalent to
O2 max. The absence of an effect of
added respiratory muscle load on O2 at
end exercise was because cardiac output had also achieved maximal
levels (10). Presumably then, with loading, the observed
reduction in limb blood flow was closely matched by an increase in
blood flow to the respiratory muscles.
Was respiratory muscle fatigue affected by loading and unloading and what were the consequences? Diaphragm fatigue is consistently caused by heavy sustained exercise when exercise intensity exceeds 85% of maximum (14). Furthermore, diaphragm fatigue is prevented when PAV is used to reduce diaphragmatic work during heavy, exhaustive exercise (3). On the basis of these findings, we presume that, in our study, diaphragm fatigue did occur during prolonged heavy exercise and that it was likely worsened by inspiratory resistive loading and relieved and delayed by unloading.
We must also ask how or even whether diaphragm or respiratory muscle fatigue actually influences endurance exercise performance. Theoretically, respiratory muscle fatigue could lead to alveolar hypoventilation (and reduced systemic O2 transport and CO2 elimination) if either "pump failure" occurred or a tachypneic breathing pattern caused high dead space and, therefore, reduced alveolar ventilation. However, cases of arterial hypoxemia are rare during prolonged submaximal exercise (9). Apparently, even though maximal force output of the diaphragm is reduced (in response to supramaximal phrenic nerve stimulation), and the relative contribution of the diaphragm to total inspiratory pleural pressure is reduced over the duration of heavy exercise (14), this is not sufficient to cause "task failure" or hypoventilation. In fact, hyperventilation commonly occurs over time during prolonged heavy exercise because of the extensive array of "accessory" respiratory muscles that are progressively recruited (Refs. 4, 14; see Fig. 2). Therefore, by itself, exercise-induced diaphragm fatigue probably did not influence the adequacy of alveolar ventilation or systemic O2 transport. Indirectly, diaphragm fatigue may have influenced performance by reducing the relative contribution of the diaphragm and promoting greater use of accessory respiratory muscles (14). This change in muscle recruitment patterns may have led to chest wall distortion, mechanical inefficiency of breathing, and, therefore, a greater work of breathing and increased metabolic and blood flow demand by the respiratory muscles (see above). This fatigue-induced increase in respiratory muscle work would also be expected to increase sensory input to the central nervous system, and, therefore, heighten awareness and perception of respiratory muscle effort (also see Role of changing perception of effort with respiratory muscle loading/unloading).Role of changing perception of effort with respiratory muscle loading/unloading. Loading and unloading of the respiratory muscles during heavy exercise had substantial effects on the perception of both respiratory and limb effort; in turn, changes in Tlim correlated significantly with changes in both types of effort perception. The changes in these perceptions with changing loads on the respiratory muscles were usually similar for both respiratory and limb discomfort, both in time and amplitude, especially during unloading (see Fig. 3 and Table 5). Perhaps the influence of reducing respiratory muscle work on the perception of dyspnea is especially significant in our well-trained subjects, because, under near-maximal exercise conditions, their high ventilatory demand requires that inspiratory muscle force output commonly reach 90% of the capacity available for pressure generation (15).
The sources of both respiratory and limb discomfort perceptions have much in common because force output of respiratory and limb muscles increases with time, especially with the onset and development of muscle fatigue. For example, increased central motor command to the locomotor and to the respiratory muscles may be directly perceived via central corollary discharge as an increased sense of muscle effort (8). Furthermore, discomfort of limb and respiratory muscles may also arise from the periphery via activation of muscle type IV afferents as muscle metabolites accumulate with the onset of fatigue. Accordingly, we observed significant correlations between the change in perception of either limb or respiratory discomfort and changes inO2 vs. exercise time with
unloading and loading. Therefore, these findings would predict that,
during heavy, fatiguing exercise, subjects cannot discriminate with
much sensitivity between the two different noxious sensations because
both are expressions of similar internal perceptions.
O'Donnell et al. (19) have also reported a significant
effect of respiratory muscle unloading on reducing limb discomfort perceptions and prolonging exercise in heart failure patients, even in
the absence of measurable effects on dyspnea. These authors suggested
that respiratory muscle work, per se, was not a major determinant of
dyspnea in these patients, but, rather, their respiratory discomfort
may originate in the expiratory flow limitation and hyperinflation they
experience during even moderate-intensity exercise (19).
This apparently specific effect of changes in the work of breathing,
via pressure assist, on the perception of limb discomfort may have a
physiological basis in the redistribution of cardiac output away from
or to the exercising limb vasculature (10). This was
apparently not the case in our study of prolonged heavy exhaustive
exercise in healthy trained subjects, in whom reductions in respiratory
muscle work and their associated energy expenditure had major effects
on the perception of dyspnea throughout the exercise.
Summary and Relevance
In summary, we believe our findings, obtained during respiratory muscle unloading, have demonstrated a consistent, significant effect of the work of breathing that is normally achieved during very heavy exercise in trained subjects on endurance exercise performance. We speculate that the major links between respiratory muscle work and endurance exercise performance lie in a combination of the reflex sympathetic vasoconstrictor influences exerted by respiratory muscle work on limb vasoconstriction and blood flow, and, therefore, on limb muscle fatigability, together with its feedback effects on the intensity of effort perception. Furthermore, the influence of ventilatory work on dyspneic perceptions was also substantial and likely added significantly to the total perception of discomfort, which caused the performers to slow their pace. Finally, the diaphragm fatigue that accompanies heavy endurance exercise does not compromise an adequate alveolar ventilation but may indirectly curtail exercise performance if the excessive use of accessory respiratory muscles causes a mechanically inefficient ventilation.Under what conditions is respiratory muscle work likely to influence
exercise performance? Given our stated reasons for the link between
respiratory muscle work and performance (see above), we propose that
the exercise conditions must be sufficient to elicit a significant
vasoconstrictor effect from the diaphragm to the limb muscle
vasculature. This would occur in healthy subjects but only
during very heavy exercise (i.e., >80-85% of
O2 max) in which the work of breathing
is sufficiently high and the cardiac output limited in its ability to
distribute flow adequately to both respiratory and locomotor muscles
(10). The appropriate conditions might also occur even at
more moderate intensities of submaximal exercise when cardiac output is
abnormally low and ventilatory work is high. This is likely to occur in
exercising heart failure patients (17, 19) or
during exercise in healthy subjects after acclimatization to the
hypoxia of high altitudes (2).
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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 acknowledge our subjects for their willing participation in these studies.
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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 and T. J. Wetter were supported by a NHLBI training grant. C. A. Harms was additionally supported by a Parker B. Francis Foundation Fellowship.
Address for reprint requests and other correspondence: C. A. Harms, Dept. of Kinesiology, 8 Natatorium, Kansas State Univ., Manhattan, KS 66506 (E-mail: caharms{at}ksu.edu).
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.
Received 9 September 1999; accepted in final form 25 February 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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 N. Ambrosino and S. |
, Control load; 
, load;
, control unload; 
, unload. Group mean
data are shown for minutes 1-5 of exercise, which was
achieved for all subjects for all conditions, and for end exercise.
* Significantly different from control, P < 0.05.
