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Pulmonary Research Laboratory, Veterans Affairs Medical Center, Boise, Idaho 83702; and Division of Pulmonary/Critical Care Medicine, Department of Medicine, University of Washington, Seattle, Washington 98195
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Expiratory resistive loading (ERL) is used by
chronic obstructive pulmonary disease (COPD) patients to improve
respiratory function. We, therefore, used a noninvasive
tension-time index of the inspiratory muscles (TTmus = 
I/PImax × TI/TT, where I is mean
inspiratory pressure estimated from the mouth occlusion pressure,
PImax is maximal inspiratory pressure,
TI is inspiratory time, and TT is total
respiratory cycle time) to better define the effect of ERL on COPD
patients. To accomplish this, we measured airway pressures, mouth
occlusion pressure, respiratory cycle flow rates, and functional
residual capacity (FRC) in 14 COPD patients and 10 normal subjects with
and without the application of ERL. TTmus was then
calculated and found to drop in both COPD and normal subjects
(P < 0.05). The decline in TTmus in both
groups resulted solely from a prolongation of expiratory time with ERL (P < 0.001 for COPD, P < 0.05 for
normal subjects). In contrast to the COPD patients, normal subjects had
an elevation in I and FRC, thus minimizing the
decline in TTmus. In conclusion, ERL reduces the potential
for inspiratory muscle fatigue in COPD by reducing
TI/TT without affecting FRC and
I.
chronic obstructive pulmonary disease; fatigue; mouth occlusion pressure
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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PURSED-LIP BREATHING (PLB) is a technique used by some patients with chronic obstructive pulmonary disease (COPD) as a means of decreasing dyspnea. PLB provides a variable expiratory flow resistive load (ERL) imposed by the subject. Whereas ERL with a fixed resistor and PLB are not equivalent in their effects on breathing pattern, they do induce comparable respiratory muscle recruitment responses (29), making it useful to review both techniques together.
The impact of PLB and ERL on the diaphragmatic tension-time index
(TTdi) and other parameters in COPD and normal subjects has
been studied with conflicting results (6, 11, 15, 21, 22, 29,
30). The TTdi was introduced by Bellemare and
Grassino (3) as a means of identifying the fatigue
threshold of the diaphragm. The parameters that comprise
TTdi include the mean inspiratory transdiaphragmatic
pressure (di) as a fraction of the maximum transdiaphragmatic
pressure (Pdimax), as well as the inspiratory time
(TI) as a fraction of the total respiratory cycle time
(TT) such that TTdi = di/Pdimax × TI/TT,
where TI/TT is the inspiratory muscle duty
cycle. The index was found to be related to the diaphragmatic
electromyogram (4), which has also been used to identify
diaphragmatic fatigue (14). Since its initial description,
TTdi has been used to evaluate diaphragmatic function in
multiple disease states, including COPD (5, 6).
Measurement of TTdi requires placement of esophageal and
gastric balloons, which is moderately invasive, especially for patients who are already dyspneic. A noninvasive tension-time index for all
respiratory muscles [TTmus = I/PImax × TI/TT, where I is mean
pressure developed by the inspiratory muscles, and
PImax is the maximal inspiratory pressure at
functional residual capacity (FRC) generated at the mouth] has been
used in children (11) and adults (25) and
recently has been validated in normal and COPD patients
(24). According to this method, I is
estimated from the airway occlusion pressure at 0.1 s
(P0.1) as I = 5 × P0.1 × TI (11, 24). To make
this estimation of I, the pressure developed by the
inspiratory muscles must be assumed to increase linearly during inspiration.
Ramonatxo, et al. (24) found a highly significant correlation between TTmus and TTdi and thus came to the conclusion that the noninvasive tension-time index is a valid means of evaluating potential inspiratory muscle fatigue in patients with COPD. It has been further argued (24) that, because there is a change in the pattern of ventilatory muscle recruitment in COPD from diaphragmatic predominance to rib cage inspiratory muscle predominance (18), and because rib cage muscles can be fatigued independent of diaphragmatic fatigue (10, 35), the noninvasive TTmus rather than TTdi may better reflect inspiratory muscle fatigue in COPD patients. The effect of PLB on TTdi has been described (6), but the effects of either PLB or ERL on TTmus have not been studied. We, therefore, used TTmus to study the effect of ERL on inspiratory muscle performance in COPD patients.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects.
Patients with COPD were recruited from our pulmonary clinics in the
outpatient department of the Boise Veterans Affairs Medical Center. The
diagnosis of COPD was made based on history of smoking, medical
history, chest X-ray, physical examination, and chronic airflow
obstruction as defined by a forced expiratory volume in 1 s
(FEV1) 
60% of the predicted normal value. Additionally,
normal male volunteers with no history of smoking or lung disease took part in the investigation. After the study protocol was explained to
all subjects, subjects gave verbal and written consent to participate in the protocol. The study protocol was approved by the Human Subjects
Committee of the University of Washington and Research and Development
Committee of the Boise Veterans Affairs Medical Center.
Apparatus for application of ERL.
The apparatus that was used to apply ERL (Fig.
1) consisted of a mouthpiece attached to
a T piece with one-way flap valves such that air was inspired through
one port and exhaled through the other port. An airflow resistor was
placed in-line at the expiratory limb of the T piece, and both the
inspiratory and expiratory limbs of the T piece were attached to a
pneumotachometer. The pressure-flow characteristics of the airflow
resistor are displayed in Fig. 2. The
partial pressure of end-tidal carbon dioxide
(PETCO2) was measured near the
pneumotachometer with an infrared Datex CO2 analyzer
(standard equipment on the MedGraphics critical care management
module). All measurements were taken with and without the
expiratory flow resistor in place. The order of testing with or without
the resistor was alternated from subject to subject, and the subjects
were not aware of what measurements were being taken until after the
testing procedure.
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Instrumentation and measurements. Spirometry was performed according to established guidelines of the American Thoracic Society (1) using a SensorMedics 2200 spirometer (SensorMedics, Yorba Linda, CA). This included measurements of FEV1 and forced vital capacity (FVC). During each session, a minimum of two forced flow-volume loops of reproducible quality was obtained. If the FEV1 and FVC values were not within 5% or 0.100 liter of one another, one additional measurement was taken. The flow-volume loop with the best FEV1 and FVC was used.
FRC with and without ERL was measured by nitrogen washout in all normal volunteers with the SensorMedics 2200 spirometer. To measure the FRC with ERL, the airflow resistor was placed on the expiratory port of the SensorMedics 2200 spirometer while we waited for the subject to reach a steady-state FRC and throughout the nitrogen washout period. In six of the normal subjects and in all COPD patients, a Gould 2800 body plethysmograph (SensorMedics) was used to measure FRC with and without ERL. In this case, the airflow resistor was attached to a one-way valve, which was, in turn, connected to the breathing valve of the body plethysmograph such that the subject could inspire normally through the breathing valve but exhaled through the resistor. The subject was allowed to breathe on this apparatus until steady-state FRC was attained, and subsequently the shutter was closed, allowing measurement of FRC by the pressure plethysmography technique. All airflow and FRC measurements were performed with the subject in the sitting position and were compared with normal predicted values (19). Airway pressures, P0.1, and inspiratory and expiratory flows were measured with the MedGraphics respiratory pressure module (RPM) (Medical Graphics, St. Paul, MN). The triple screen pneumotachometer and the pressure transducer (Validyne) were calibrated according to the manufacturer's specifications. All measurements were taken with the subjects in the sitting position. Subjects breathed through the apparatus (Fig. 1), which included a pneumotachometer for measuring inspiratory and expiratory airflow along with a port at the mouthpiece for simultaneously monitoring the airway pressures. Subjects were asked to breathe at the rate and depth that was most comfortable to them and such that they could maintain the breathing pattern for at least 10-15 min. After steady state was attained in ~5 min, TI, expiratory times (TE), TT, and flow rates were recorded. At steady state, the RPM automatically occluded the balloon shutter valve at the inspiratory port during the expiratory phase of a breath. This would occur randomly on every fifth to eighth respiratory cycle. The balloon shutter valve remained occluded for 200 ms into the inspiratory phase, during which time the P0.1 was measured. After steady state and a uniform breathing pattern were attained, the TI, TE, and TT recorded for each of the P0.1 measurements were taken as the mean values for the four breaths preceding the occlusion. The tidal volumes (VT) of the four breaths preceding the occlusion were calculated by electronic integration of the expiratory flows over time, and the mean was used as the VT for that occlusion. Similarly, the respiratory rate (RR) was calculated as the average frequency in cycles per minute of the four breaths preceding the occlusion. The minute ventilation (
E) for any given
occlusion trial was taken as the product of VT and RR.
For each subject, 10 P0.1 measurements were taken, and the
resultant RR, VT, E, TI,
TE, and TT were calculated. The mean values of
these measurements were used for each subject.
The PImax at FRC was measured with the
MedGraphics RPM as well. Subjects breathed comfortably on the
experimental apparatus without the airflow resistor in place. After a
steady-state FRC was attained, the inspiratory and expiratory ports
were occluded at end exhalation with a balloon shutter valve, and the
subject was asked to perform a maximal inspiratory effort. The shutter valve opened automatically after 5 s, and the highest inspiratory pressure that was sustained for at least 1 s was taken as the PImax. To reduce the variability that resulted
from technique, the measurement was repeated three times, and the mean
of the three measurements was considered to be the subject's
PImax at FRC.
The hemoglobin saturation (SaO2) of the COPD patients
was measured with an Ohmeda Biox 3700 oximeter (Ohmeda, Boulder, CO) while they breathed on the MedGraphics RPM apparatus. The mean of the
saturations recorded at the time of each P0.1 measurement was taken as the SaO2 for that trial. For each of the
COPD patients, the PETCO2 was measured
through a port at the mouthpiece (Fig. 1). The mean
PETCO2 for the four breaths preceding each
P0.1 measurement was taken as the
PETCO2 for that P0.1 value.
The mean of the PETCO2 values for each of
the 10 P0.1 determinations was used to characterize each
COPD patient.
Calculations.
According to the method of Gaultier et al. (11), we
estimated the I as I = 5/s × P0.1 × TI. In doing so, it was assumed that inspiratory pressure rises linearly from time 0 to
TI. Therefore, this equation can be rewritten as
I = 0.5 × k × TI,
where k = 10/s × P0.1. Subsequently,
TTmus was calculated as TTmus = I/PImax × TI/TT (25).
Statistical analysis. Means, SDs, and Student's unpaired t-test were used to describe and compare the baseline data, as well as the measured ventilatory parameters, for the COPD patients and normal volunteers. Means, SEs, and paired t-tests were used to compare the measured values with and without the ERL in both the normal subjects and COPD patients. Paired t-tests were also used to compare the FRC values of the normal subjects, who had the measurements done by both nitrogen washout and plethysmography. All data were analyzed with a database and statistical package (SigmaStat, Jandel Scientific, San Raphael, CA).
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects.
One female and 13 male patients with COPD were recruited for the study
and gave informed consent (Table 1). In
addition, 10 normal male volunteers were studied. The COPD group
differed from the normal subjects in that they were significantly older (age range 56-80 yr old for the COPD group and 21-49 yr old
for the normal subjects), had a history of smoking [61 ± 18 (SD)
yr], had marked airflow obstruction with a mean FEV1 of
0.97 ± 0.59 (SD) liter, and had a significantly lower
PImax.
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TTmus.
The effect of ERL on TTmus in COPD patients is demonstrated
in Table 2. Specifically,
TTmus decreased by 12% (P = 0.02) with ERL. Whereas most subjects had a drop in TTmus, there was
some variability, and some actually had an increase in
TTmus with ERL (Fig. 3).
Figure 3 also demonstrates the TTmus isopleths of 0.27 and
0.33, which, in validation studies (24), correlate with Bellemare and Grassino's critical TTdi of 0.12 for COPD
patients (5) and 0.15 for normal subjects
(3). These critical values represent the fatigue
thresholds above which subjects cannot persistently maintain their
breathing pattern. Several of the COPD patients were breathing near or
above the fatigue threshold at baseline, and in general ERL tended to
move these subjects to a more favorable TTmus. The drop in
TTmus was the result of a prolongation of TE and a reduction in TI/TT. Otherwise,
TI, P0.1, and I did not change with ERL (Table 2).
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I were significantly
elevated by ERL (Table 2).
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I) were not significantly different between the two
groups (Table 2).
Breathing pattern.
ERL decreased RR and E while raising VT
in COPD patients. However, it had no significant effect on these
parameters in normal subjects (Table 2). Whereas VT went up
slightly and TI remained unchanged with ERL, the mean
average inspiratory flow (VT/TI) for the COPD
patients showed a tendency to rise but did not meet statistical
significance (0.66 ± 0.04 without ERL, 0.70 ± 0.05 with
ERL, P = 0.12). Given the number of subjects studied,
the SD of the VT/TI values seen, and the
observed difference of 0.04 l/s, the power of this test was only 0.36, raising the real possibility that a significant difference in
VT/TI could have been missed.
P0.1 and I.
P0.1 and its corresponding I were
unchanged by ERL in the COPD patients. In contrast, P0.1
increased by 33% (P = 0.01) and I
increased by 17% (P = 0.04) in the normal volunteers.
The difference between the I values for COPD and
normal subjects was not significant. However, when the
PImax is considered, there is a marked
difference between the
I/PImax values of the two groups (P < 0.001).
FRC. FRC was significantly larger in the COPD patients compared with the normal subjects (P < 0.001). In response to ERL, the FRC remained constant in COPD patients, whereas it increased in normal subjects (P < 0.05) (Table 2). This increase in normal subjects was seen when FRC was measured by nitrogen washout in all normal subjects (Table 2) and when it was measured by plethysmography in 6 of 10 normal subjects (3.45 ± 0.45 liters without ERL, 4.07 ± 0.46 liters with ERL, P < 0.001). The FRC measurements done by both plethysmography and nitrogen washout in six of the normal subjects were not significantly different from each other (3.36 ± 0.43 liters by nitrogen washout, 3.45 ± 0.45 liters by plethysmography, P = 0.52).
Gas exchange. Peripheral oximetry (SaO2) was monitored only in the COPD patients and remained unchanged with ERL. PETCO2 measured in these patients also did not significantly change with ERL.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In this study, we found that ERL in COPD patients and normal subjects reduces the noninvasive TTmus. The baseline indexes obtained without ERL are similar to those found in the validation studies done in normal subjects and COPD patients (24). Ramonatxo et al. (25) also used the technique to demonstrate the absence of any difference in TTmus with and without ERL in normal subjects exercising at 40% of their maximum O2 consumption. However, this is the first use of this method to ascertain the effect of ERL in COPD patients. These noninvasive measurements are similar to Breslin's (6) more invasive measurements of TTdi in COPD patients using PLB techniques. However, because the TTmus does not require the placement of esophageal and gastric balloons, it is a technique that may better lend itself to the study of subjects with more severe, acute airflow obstruction.
When comparisons are made between TTmus and TTdi, the issue of whether or not one is better than the other must be raised. In fact, Spahija and Grassino (29) looked at the effect of ERL on the TTdi of normal subjects and found that the TTdi remains unchanged, a result that would appear to be different than our finding of a decline in TTmus in normal subjects. Alternatively, the two indexes may better be thought of as measurements of two different muscle groups. The TTdi is an index of diaphragmatic function, whereas TTmus is a better indicator of the output of all inspiratory muscles. Thus a drop in TTmus without a significant change in TTdi in normal subjects treated with ERL may be an indication of improved efficiency of the rib cage muscles without a concomitant improvement in the diaphragmatic efficiency. Others have shown that rib cage muscles and diaphragm function can be partially uncoupled and have concluded that the two muscle groups can be fatigued independently, depending on inspiratory recruitment patterns (10, 35). Martinez et al. (18) have also shown that the pattern of ventilatory recruitment in COPD is one of rib cage inspiratory muscle rather than diaphragmatic predominance, thus leading some (24) to suggest TTmus rather than TTdi as the better indicator of inspiratory muscle fatigue in COPD patients. TTmus may actually be much closer to the rib cage tension-time index (35) with similar fatigue thresholds (24).
The validity of TTmus as a measure of respiratory muscle
function rests, in large part, on the assumption that P0.1
provides an accurate assessment of I
(11). The calculation of I from P0.1 assumes a linear rise in respiratory muscle pressure
from initiation to termination of inspiration. This is not always the case, and, at least in anesthetized animals and humans, the slope of
the inspiratory pressure curve of the occluded airway is often not
linear (28, 33, 34). This is especially true at higher RRs. However, whereas the shape of the occluded airway pressure curve
is quite variable from subject to subject, the shape of the waveform
within any given human or animal subject is quite repeatable (28,
34). Thus, whereas comparisons of repeated measurements of
P0.1, I, and TTmus for any
one individual should be reliable, the use of the absolute values to
compare different subjects may be somewhat limited. Alternatively, the
validation studies of Ramonatxo and colleagues (24) show a
significant correlation between TTmus and TTdi
and various respiratory pressure measurements in both COPD and normal
subjects, suggesting that use of TTmus to compare different
groups and individuals is indeed valid. This should allow the use of
this noninvasive tension-time index to assess the effect of various
disease states and experimental protocols on the respiratory muscles.
The fact that TTmus measurements do not require placement
of esophageal and gastric balloons makes this technique a much easier
tool for assessing subjects who are experiencing acute exacerbation of
their respiratory disease and may not tolerate more invasive
measurements. As with any other index of respiratory muscle function,
it does have its limitations, and the effect on P0.1 of
various disease states, exercise, medications, ERL, FRC, and other
factors must always be considered when evaluating TTmus
values (33).
The tension-time indexes have been used in large part as a predictor of endurance and fatigue in individual muscles or groups of muscles, especially the diaphragm (3, 4, 10). Specifically, the higher the index, especially if near the threshold values, the closer the muscle group is to fatigue. However, it may be more useful to look at the individual components of TTmus to better understand the effect of ERL on inspiratory muscle function.
Analysis of these components that comprise the TTmus shows
that baseline TTmus for COPD patients is significantly
higher than that for normal subjects because of the marked difference
in PImax. In fact, the differences between
baseline TI, TT, and I are not statistically significant. Similar findings have been demonstrated when TTmus and TTdi in COPD patients have been
analyzed (5, 24). When looking at the effect of ERL on the
components of TTmus, it is easily seen that there is a
reduction of TTmus in COPD patients only because
TE and TT are prolonged, whereas the other
components remain unchanged. Breslin (6) found that PLB had a similar effect on TI/TT without changing
Pdi in those with COPD. In contrast, ERL in normal subjects resulted in
not only a prolonged TE but also an elevation in
P0.1 and I. This elevation in
P0.1 and I with ERL has been found by
others (13, 25) and significantly minimizes the reduction
in TTmus seen with ERL in normal subjects. To our
knowledge, this is the first time that this contrast between COPD and
normal subjects in their response to ERL has been noted. It provides a
potential explanation of why PLB is commonly used by some COPD patients
and not by those without any lung disease. It should also be noted that
the difference in response to ERL between COPD and normal subjects in
this study may in part be due to the significant difference in the ages
of the two groups.
RR, VT, and E are also affected by ERL
in COPD patients. The decline in RR and E and the
larger VT with ERL and PLB have been described by
others (6, 30). Reports of the effect of ERL and PLB on
these parameters in normal subjects have been mixed (13, 22, 23,
25, 29). Whereas we found similar trends in RR, VT,
and E, none of the changes with ERL in normal
subjects was statistically significant or as dramatic as those seen in COPD patients. Our baseline E and
VT/TI values were higher than those of others
(24), which was probably a result of the dead space in the
experimental apparatus.
It has been shown that a drop in RR without the use of PLB or ERL
reproduces many of the same effects as PLB and ERL (20, 30). The braking action of the inspiratory muscles during
exhalation probably accounts for a significant slowing of the RR
(12, 27), but PLB and ERL may provide an alternative means
of slowing the RR without placing additional demands on the inspiratory
muscles. This would be most important during the respiratory muscle
fatigue, which can be seen with high levels of ventilation (2, 7, 17), and in COPD patients, who demonstrate lower
PImax and higher TTmus
(8). Whereas this study does demonstrate a decrease in RR,
TTmus, E, and
TI/TT and can, therefore, demonstrate at least some of the potential advantages of PLB and ERL in COPD patients, it
does not address inspiratory muscle function during expiration and
probably does not fully explain the subjective decrease in dyspnea and
objective improvement in gas exchange seen with PLB and ERL. In fact,
the greatest decline in workload on the inspiratory muscles may
come not from the decline in TI/TT, RR, and
E but from their being relieved of their expiratory
braking duties. This study also does not address the increased demands
placed on the expiratory muscles by ERL. How much ERL is adequate to relieve inspiratory muscle fatigue without inducing expiratory muscle
fatigue remains unclear but likely varies dramatically, depending on
the subject and breathing conditions.
The determinants of diaphragmatic endurance have been reviewed and include not only the tension-time index but also the work rate and lung volume (9, 16, 32). As discussed above, ERL in COPD patients does indeed decrease the tension-time index and, although not directly measured in our study, may decrease the workload on the inspiratory muscles. The third determinant of inspiratory muscle endurance, namely the volume, was evaluated in our study. FRC did not change with ERL in the COPD patients. This finding was similar to that of Thoman et al. (30), who found no change in FRC with PLB or rate-controlled breathing, but was in contrast to the apparent elevation in FRC with ERL and PLB found by others (15, 23). However, Ingram and Schilder (15) did note that, when those COPD patients who routinely used PLB are compared with those who did not, the PLB group had a much smaller degree of FRC elevation with ERL. Like Ingram and Schilder, we also found significant variability in the FRC response to ERL in COPD patients. Thus different FRC findings may be a result of subject selection. Exactly what accounts for the different FRC response to ERL remains unclear. It is interesting to note a trend toward worse FEV1 and/or maximal voluntary ventilation in those who had little to no elevation in FRC in both our study and Ingram and Schilder's study. However, no statistically significant correlation could be found in either of the studies because of the small number of subjects studied. A decrease in end-expiratory alveolar pressure due to the increase in TE would be one potential explanation for a decrease or lack of elevation of FRC with ERL.
As demonstrated by others (15, 25, 29), the mean FRC in
the normal subjects did increase significantly. This could contribute to a reduction in the inspiratory muscle endurance (32).
In addition, the increase in FRC may in itself decrease the
P0.1, thereby decreasing the I and
TTmus, which otherwise might have been seen with ERL if the
FRC had been unchanged in normal subjects. It should also be noted that
PImax was measured only at FRC without ERL.
TTmus calculated with the PImax
measured at the higher FRC would likely be higher, because
PImax tends to decrease with elevated lung
volumes. Thus the TTmus in the normal subjects may not have significantly decreased with ERL if the elevated FRC (and therefore reduced PImax) had been considered.
ERL and PLB have usually been shown to increase arterial PO2/SaO2 (6, 20, 26, 31), whereas their effects on arterial PCO2, PETCO2, and CO2 production have been variable (22, 23, 25, 30). Our study failed to show any significant change in either SaO2 or PETCO2 with ERL in COPD patients. One potential explanation for this is the increased workload placed on the expiratory muscles with the fixed expiratory resistor. This may have resulted in a higher CO2 production and O2 consumption, which, in turn, could have masked any improvement in gas exchange when only SaO2 and PETCO2 were measured. The higher dead space of the experimental apparatus may also have affected the PETCO2.
In summary, we have demonstrated that ERL results in a decline in the
TTmus of COPD patients by reducing the
TI/TT. It has no effect on the
I nor the FRC of these patients. This may, in part,
explain the use of PLB by these patients. We have also shown that the
noninvasive TTmus is well tolerated by patients with
chronic dyspnea and provides a practical means of studying the
tension-time index of these patients at baseline and potentially during
acute exacerbation of their chronic disease.
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ACKNOWLEDGEMENTS |
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This study was supported in part by the Medical Research Service of the Department of Veterans Affairs.
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FOOTNOTES |
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Address for reprint requests and other correspondence: W. H. Thompson, VA Medical Center, 500 West Fort St., Boise, ID 83702 (E-mail: william.Thompson2{at}med.va.gov).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 30 June 1999; accepted in final form 22 June 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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,
pressures measured at given flows.
, values obtained with expiratory resistive
loading.
