Effects of Imposed Pursed-Lips
Breathing on Respiratory Mechanics
and Dyspnea at Rest and During
Exercise in COPD*
Jadranka Spahija, PhD; Michel de Marchie, MD; and Alejandro Grassino, MD
Study objectives: To investigate the effect of volitional pursed-lips breathing (PLB) on breathing
pattern, respiratory mechanics, operational lung volumes, and dyspnea in patients with COPD.
Subjects: Eight COPD patients (6 male and 2 female) with a mean (ⴞSD) age of 58 ⴞ 11 years and
a mean FEV1 of 1.34 ⴞ 0.44 L (50 ⴞ 21% predicted).
Methods: Wearing a tight-fitting transparent facemask, patients breathed for 8 min each, with and
without PLB at rest and during constant-work-rate bicycle exercise (60% of maximum).
Results: PLB promoted a slower and deeper breathing pattern both at rest and during exercise.
Whereas patients had no dyspnea with or without PLB at rest, during exercise dyspnea was
variably affected by PLB across patients. Changes in the individual dyspnea scores with PLB
during exercise were significantly correlated with changes in the end-expiratory lung volume
(EELV) values estimated from inspiratory capacity maneuvers (as a percentage of total lung
capacity; r2 ⴝ 0.82, p ⴝ 0.002) and with changes in the mean inspiratory ratio of pleural pressure
to the maximal static inspiratory pressure-generating capacity (PcapI) [r2 ⴝ 0.84; p ⴝ 0.001],
measured using an esophageal balloon, where PcapI was determined over the range of
inspiratory lung volumes and adjusted for flow.
Conclusion: PLB can have a variable effect on dyspnea when performed volitionally during
exercise by patients with COPD. The effect of PLB on dyspnea is related to the combined change
that it promotes in the tidal volume and EELV and their impact on the available capacity of the
respiratory muscles to meet the demands placed on them in terms of pressure generation.
(CHEST 2005; 128:640 – 650)
Key words: breathing pattern; breathlessness; end-expiratory lung volume; exercise; respiratory mechanics
Abbreviations: EELV ⫽ end-expiratory lung volume; EILV ⫽ end-inspiratory lung volume; fB ⫽ breathing frequency;
FRC ⫽ functional residual capacity; Pcapi ⫽ maximum static inspiratory pressure-generating capacity;
Pdi ⫽ transdiaphragmatic pressure; Pdimax ⫽ maximum inspiratory transdiaphragmatic pressure; PEEP ⫽ positive
end-expiratory pressure; Pes ⫽ esophageal pressure; Pga ⫽ gastric pressure; Pimax ⫽ maximum inspiratory esophageal
pressure; PLB ⫽ pursed-lips breathing; Ppl ⫽ pleural pressure; Pplmax ⫽ maximum static inspiratory pleural pressure;
Te ⫽ expiratory time; Ti ⫽ inspiratory time; TLC ⫽ total lung capacity; TTdi ⫽ tension-time index of the diaphragm;
Ttot ⫽ total breathing cycle time; V̇ ⫽ airflow; VAS ⫽ visual analog scale; VC ⫽ vital capacity; V̇e ⫽ minute ventilation; Vl ⫽ lung volume; Vt ⫽ tidal volume; Weres ⫽ expiratory resistive work of breathing; Wires ⫽ inspiratory
resistive work of breathing; W(i⫹e)res ⫽ total resistive work of breathing; Ẇlmax ⫽ maximum exercise workload
ursed-lips breathing (PLB) is a technique
P whereby
exhalation is performed through a resistance created by constriction of the lips. Although
the breathing maneuver is often spontaneously
*From the School of Physical and Occupational Therapy (Dr.
Spahija), McGill University, Montreal, QC, Canada; the Department of Adult Critical Care (Dr. de Marchie), Sir Mortimer B.
Davis Jewish General Hospital, Montreal, QC, Canada; and
Centre Hospitalier de l’Université de Montréal (Dr. Grassino),
Notre-Dame Pavillon, Université de Montréal, Montreal, QC,
Canada.
Dr. Spahija was the recipient of a research fellowship award from
the Fonds de la Recherche en Santé du Québec. This study was
supported by the Medical Research Council of Canada.
adopted by COPD patients, it is also routinely taught
as a breathing-retraining exercise in pulmonary rehabilitation programs because it is thought to alleviate dyspnea. It appears, however, that not all patients
obtain symptom benefits from PLB.1 Despite this,
Manuscript received August 31, 2004; revision accepted January
25, 2005.
Reproduction of this article is prohibited without written permission
from the American College of Chest Physicians (www.chestjournal.
org/misc/reprints.shtml).
Correspondence to: Jadranka Spahija, PhD, Hôpital du SacréCoeur de Montréal, L’Axe de Recherche en Pneumologie, 5400
Blvd Gouin Ouest, Montréal, QC, Canada H4J 1C5; e-mail:
[email protected]
640
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Clinical Investigations
unaffected4 or reduced14 when PLB was performed
at rest by patients with COPD, the extent to which
PLB might alter EELV during exercise and might
subsequently affect dyspnea remains unknown.
The purpose of the present study was therefore to
examine the effect of volitionally performed PLB on
respiratory mechanics, EELV, and dyspnea in a
group of patients with COPD at rest and during
constant-work-rate bicycle exercise. We hypothesized that any possible effect of PLB on dyspnea
would be related to the change that it produced in
ventilatory muscle force-generating capacity.
few studies have tried to determine the actual degree
of dyspnea relief provided, and none, to our knowledge, have examined the effect of PLB on dyspnea
when it is performed volitionally during exercise.
Previous studies of PLB performed volitionally
during resting breathing, have found that it improves
arterial oxygenation1 and saturation2,3 and reduces
arterial carbon dioxide levels4 by promoting a slower
and deeper breathing pattern.1– 4 Despite similar
changes in breathing pattern with PLB performed
during exercise, under such conditions no improvements in the arterial blood gas levels have been
documented.1
Exercise-induced dyspnea has been associated
with the increased intensity and duration of respiratory muscle force generation as well as with an
increased amplitude and velocity of muscle shortening.5,6 More recently, the ratio relating inspiratory
effort (ie, esophageal pressure [Pes], expressed as a
fraction of the maximum Pes at isovolume [maximal
inspiratory pressure (Pimax)], to tidal volume [Vt],
expressed as a fraction of the vital capacity [VC]) was
reported to be the best predictor of the inspiratory
difficulty experienced by patients with COPD during
incremental bicycle exercise.7 Moreover, the (Pes/
Pimax)/(Vt/VC) ratio was shown to be significantly
related to the degree of hyperinflation developed
during exercise.7 Dynamic hyperinflation or an increase in the end-expiratory lung volume (EELV), as
typically occurs during exercise in patients with
COPD,8 –11 can reduce the pressure-generating capacity of the respiratory muscles and has been
associated with increased breathing effort and dyspnea.12,13 Although EELV has been reported to be
Materials and Methods
Subjects
Eight patients (2 women and 6 men) with stable mild-to-severe
COPD15,16 participated in the study (Table 1). Subjects with
known cardiovascular disease, neurologic or psychiatric illness, or
impaired lower extremity function or those requiring supplemental oxygen were excluded from the study. All patients received
their regular treatment of inhaled bronchodilators, and none
received oral steroid therapy. Four of the patients were receiving
inhaled steroid therapy, and one patient was receiving oral
theophylline therapy. No change in the medications was made for
the purpose of the study. Patients were asked to abstain from
smoking on the day of the study and to avoid eating for at least 2 h
prior to undergoing testing. The study was approved by the ethics
committee of the hospital, and all subjects gave written informed
consent.
Protocols and Instrumentation
One week prior to the actual study, subjects underwent
pulmonary function testing (system 1085; Medical Graphics
Table 1—Anthropometric and Lung Function Data on Patients Studied*
Ht, m
Wt, kg
FEV1, L
FVC, L
FEV1/FVC, %
RV, L
TLC, L
FRC, L
1/M/62
1.64
54.4
1.66
70.0
3/M/60
1.75
99.0
4/F/55
1.55
56.7
5/F/46
1.60
63.0
6/M/40
1.68
63.0
7/M/57
1.83
54.5
8/M/72
1.68
72.2
1.67 ⫾ 0.09
66.6 ⫾ 14.7
2.81
(74)
3.27
(87)
3.13
(70)
2.21
(78)
3.29
(100)
2.11
(46)
2.32
(46)
2.91
(77)
2.77 ⫾ 0.48
(72 ⫾ 19)
43
2/M/68
1.22
(45)
1.37
(53)
1.24
(39)
1.56
(74)
2.12
(84)
1.04
(29)
0.73
(21)
1.32
(53)
1.34 ⫾ 0.44
(50 ⫾ 21)
4.13
(208)
5.02
(233)
4.00
(183)
2.62
(151)
2.55
(154)
4.35
(270)
7.48
(326)
3.04
(133)
4.15 ⫾ 1.61
(207 ⫾ 66)
7.56
(128)
8.95
(147)
7.49
(111)
5.06
(97)
5.97
(122)
7.24
(118)
9.85
(133)
6.29
(101)
7.30 ⫾ 1.56
(120 ⫾ 17)
5.31
(176)
6.68
(212)
4.93
(140)
3.15
(123)
3.05
(112)
5.15
(172)
8.38
(217)
4.32
(131)
5.12 ⫾ 1.77
(160 ⫾ 40)
Subject/Sex/Age, yr
Mean ⫾ SD
58 ⫾ 11
42
40
71
64
49
31
45
49 ⫾ 14
*Values in parentheses are percent predicted. RV ⫽ residual volume.
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CHEST / 128 / 2 / AUGUST, 2005
641
Corp; St. Paul, MN) and performed an incremental exercise test
on a bicycle ergometer (model 400L; Medical Fitness Equipment; Maarn, the Netherlands) to determine their maximum
exercise workload (Ẇlmax). Subjects maintained a mean (⫾ SD)
pedaling rate of 60 ⫾ 5 revolutions per minute, and workload was
increased by 10 W every minute until subjects could no longer
continue. During this initial session, a physiotherapist instructed
subjects on how to perform the PLB technique (ie, nasal
inspiration followed by expiratory blowing against partially closed
lips avoiding forceful expiration17), and subjects also practiced
the technique while pedaling and wearing a tight-fitting facemask
in order to familiarize them with the study protocol. None of the
subjects had difficulty in learning the breathing technique.
On the day of the study, while seated on the bicycle ergometer,
each subject first performed maximal inspiratory maneuvers (ie,
the Mueller maneuver) and combined maneuvers consisting of a
Mueller maneuver and abdominal expulsive maneuvers with the
glottis open18 to determine their maximum static inspiratory
pleural pressure (Pplmax) and maximum inspiratory transdiaphragmatic pressure (Pdimax), respectively. Pdimax was measured at functional residual capacity (FRC), and the highest value
obtained from three or more attempts was used in the subsequent analysis. For Pplmax, subjects performed the maximal
inspiratory maneuvers at several lung volumes ranging from FRC
to total lung capacity (TLC). While still seated on the bicycle,
patients then breathed for 8 min using PLB and 8 min without
using PLB (ie, control breathing). This was followed by 8-min
periods of control breathing and PLB during constant-work-rate
exercise at 60% of Ẇlmax. The order of control breathing and
PLB were alternated among subjects, whereas exercise always
followed the resting condition. Subjects were allowed to rest for
at least 10 to 15 min between the two exercise runs.
The breathing circuit consisted of a tight-fitting facemask
(dead space, 90 mL) that was connected to a heated pneumotachograph (model No. 3; Fleisch; Lausanne, Switzerland), which
permitted the measurement of inspiratory and expiratory airflow
(V̇). Vt was obtained by integrating the flow signal. The facemask
was transparent, enabling investigators to verify that subjects
were performing the PLB maneuver appropriately and when
requested. Pleural pressure (Ppl) and gastric pressure (Pga) were
measured using two balloon-tipped catheters that were passed
transnasally, and transdiaphragmatic pressure (Pdi) was obtained
by subtracting Ppl from the Pga.
EELV was estimated by having subjects perform inspiratory
capacity maneuvers every minute during the last 4 min of each
experimental condition. EELV was obtained by subtracting the
inspiratory capacity values from measures of TLC that had been
previously obtained with whole-body plethysmography.19
Subjects were asked to rate the sensation of “breathlessness”
that they perceived every minute during each of the conditions
studied using a visual analog scale (VAS). The VAS was displayed
on a 10-cm oscilloscope screen with the verbal anchors “no
breathlessness” and “maximal breathlessness” corresponding to
the numerical values of 0 and 10, respectively, positioned at the
bottom and top of the scale. Subjects were able to control the
position of the line representing their breathlessness by means of
a variable potentiometer attached to the bicycle handlebar.
end-expiratory and end-inspiratory zero flow. The tension-time
index of the diaphragm (TTdi) was calculated as the product of
the ratio of the delta mean inspiratory Pdi to the Pdimax and the
inspiratory duty cycle.
Resistive work of breathing was determined by measuring the
area enclosed by plots of Ppl vs Vt (see A panels in Fig 2) and was
partitioned into inspiratory resistive work of breathing (Wires)
and expiratory resistive work of breathing (Weres) components.20
The individual average loops presented for each subject were
obtained by combining ensemble averaged inspiratory and expiratory data sections, with each normalized to mean Ti and Te
values, respectively.
The maximum static inspiratory pressure-generating capacity
(Pcapi) was determined first by plotting the Pplmax values along
with their corresponding lung volumes, normalized to TLC, on a
pressure-volume diagram and fitting a polynomial curve through
these data points. For each subject, individual Ppl vs lung volume
(Vl) loops were then positioned on this pressure-volume diagram, using the EELV values obtained under each of the
experimental conditions and normalized to TLC. For every data
point comprising the inspiratory portion of the individual Ppl-Vl
loops, the corresponding Pplmax values were then adjusted for
flow by applying a correction that reduced Pplmax by 5% for
every liter per second increase in inspiratory V̇ according to the
following equation21:
Pcapi ⫽ Pplmax ⫺ [Pplmax ⫻ 0.05 V̇ (L/s)].
For each data point in the inspiratory Ppl-Vl loop, Ppl was then
expressed as a percentage of Pcapi, and an average value for
inspiration was calculated. The ratio of Ppl to Pcapi (percent) was
also determined at the point at which Ppl was at the peak value
during inspiration.
Statistical analysis for the comparison of variables between
control breathing and PLB during rest and exercise was performed using the Student t test for paired data. Associations
between the changes in the dyspnea scores and the changes
promoted to breathing pattern variables, operational lung volumes, FEV1 (percent predicted), and the ratio of the mean Ppl to
Pcapi, were assessed by computing the Pearson product moment
correlation coefficient. Significance for all tests was considered to
be p ⬍ 0.05.
Results
Effect of PLB on Dyspnea
Whereas none of our subjects claimed to have
dyspnea at rest, during control exercise at 60% of
Ẇlmax, dyspnea scores ranged between 3.5 and 9.
With PLB, breathlessness increased in four of the
eight patients, was relatively unaltered in two patients, and decreased in two patients (Fig 1).
Data Analysis
All signals were acquired online at a sampling rate of 100 Hz.
Offline breath-by-breath analysis was performed on the last 4 min
of each 8-min data segment. Timing parameters including inspiratory time (Ti), expiratory time (Te), total breathing cycle
time (Ttot), and duty cycle were determined from the flow
signal.
Mean pressure swings were calculated between points of
Effect of PLB on Breathing Pattern
Individual and average values for breathing pattern variables at rest and during exercise are shown
in Tables 2 and 3, respectively. PLB prolonged total
breath duration, slowed breathing frequency (fB),
and increased Vt both at rest and during exercise.
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Clinical Investigations
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*p ⬍ 0.05 vs rest control breathing.
Ttot, s
Ti, s
EELV, L
Vt/Ti, L/s
V̇e, L/min
Vt, L
Ttot, s
1.16
2.98
0.63
20.13
12.68
0.54
5.85
2.56
9.02
1.41
6.65
9.38
0.55
5.45
1.39
4.02
0.86
14.93
12.84
0.60
6.36
1.93
5.84
1.33
10.27
13.66
0.70
6.34
4.13
9.74
1.21
6.16
7.45
0.30
5.01
4.28
11.55
1.49
5.19
7.74
0.35
5.35
1.02
2.57
0.38
23.35
8.87
0.38
3.51
0.93
2.09
0.86
28.71
24.69
0.94
3.76
0.97
2.56
0.84
23.44
19.69
0.86
3.35
0.89
2.48
0.99
24.19
23.95
1.12
3.19
3.30
7.07
1.24
8.49
10.52
0.39
4.38
3.30
9.77
2.00
6.14
12.28
0.62
4.30
1.12
2.76
0.69
21.74
15.00
0.61
7.98
1.98
4.97
1.27
12.07
15.33
0.64
7.64
1.22
3.12
0.76
19.23
14.16
0.63
4.49
1.09
3.37
0.80
17.80
14.24
0.74
4.42
Mean ⫾ SD 1.79 ⫾ 1.22 4.35 ⫾ 2.64 0.83 ⫾ 0.29 17.18 ⫾ 6.69 12.71 ⫾ 3.87 0.54 ⫾ 0.18 5.12 ⫾ 1.56 2.12 ⫾ 1.21 6.14 ⫾ 3.58* 1.27 ⫾ 0.39* 13.88 ⫾ 8.83 15.16 ⫾ 6.19 0.71 ⫾ 0.24 5.06 ⫾ 1.45
1
2
3
4
5
6
7
8
EELV, L
Vt/Ti, L/s
V̇e, L/min
fB, breaths/
min
fB, breaths/
min
Vt , L
PLB
Control Breathing
Ti, s
Whereas EELV increased on average by approximately 350 mL with exercise alone, it was variably
altered by PLB at rest and during exercise across
patients (Tables 2 and 3). On average, the increased
Vt and unaltered EELV caused the end-inspiratory
lung volume (EILV), which was 81% of TLC at rest
without PLB, to increase to 86% of TLC with PLB
(p ⬍ 0.05). Furthermore, due to a combined dynamic hyperinflation and increased Vt values, EILV
during exercise increased to 91% of TLC without
PLB and was 92% of TLC with PLB. Changes in the
dyspnea scores promoted by PLB were significantly
Subject
Effect on End-Expiratory and End-Inspiratory
Lung Volumes
Table 2—Ventilatory Parameters in Eight Patients With COPD During Resting Breathing
Figure 1. Average breathlessness scores (VAS) from the last 4
min of constant-work-rate exercise in each of the eight COPD
patients during control breathing (E) and PLB (F). Lines of
asterisks represent the average dyspnea scores for the group.
CHEST / 128 / 2 / AUGUST, 2005
643
Effect of PLB on Respiratory Mechanics
As shown in Table 4 and also illustrated by the
respective horizontally lined and hatched areas of the
average plots of Vt vs Ppl shown for two representative subjects in Figure 2 (panel A in upper and
lower panels) because PLB promoted larger Vt
values, Wires and Weres were significantly increased
with PLB at rest and during exercise. However, the
total resistive work of breathing [W(i⫹e)res] per
minute was not significantly altered by using PLB
during exercise.
As evidenced by the higher expiratory Pga values
observed in the average Vt-Pga loops presented in
Figure 2 (panel B in upper and lower panels), PLB
performed at rest promoted an increased abdominal
expiratory muscle recruitment compared to control
breathing. This was a consistent finding in all subjects. As presented also in Figure 2 (panel B in upper
and lower panels), exercise without PLB promoted
greater clockwise looping in all patients compared to
control breathing at rest, indicating the presence of
more expiratory abdominal muscle activity. However, PLB during exercise further increased abdominal muscle recruitment in only three of the patients.
In general, neither mean Pdi nor TTdi were
altered by PLB at rest or during exercise (Table 4).
However, as shown in the individual exercise Vt-Pdi
loops of Figure 2 (panel C in upper and lower
panels), end-expiratory Pdi was increased as a result
of Pdi increasing prior to the onset of inspiratory
flow, which was a consistent finding in all COPD
patients breathing with and without PLB during
exercise, and was observed in four of the eight
patients during control breathing at rest. The mean
end-expiratory Pdi, which was 2.5 ⫾ 1.6 cm H2O
during control breathing at rest and increased to
8.0 ⫾ 3.6 cm H2O with exercise, was not significantly
altered by PLB under either condition.
Effect of PLB on Inspiratory Muscle Capacity
*p ⬍ 0.05 vs exercise control breathing.
†p ⬍ 0.01 vs exercise control breathing.
1
2
3
4
5
6
7
8
0.78
2.15
0.89
27.91
24.84
1.14
5.92
1.06
3.76
1.30
15.96
20.74
1.24
6.05
0.86
2.01
0.98
29.85
29.25
1.14
7.56
0.94
2.72
1.15
22.06
25.37
1.23
7.48
1.06
2.81
1.24
21.35
26.47
1.18
5.32
1.57
4.34
1.72
13.82
23.78
1.10
5.50
0.65
1.35
0.84
44.44
37.33
1.29
3.57
0.72
1.52
0.89
39.47
35.13
1.25
3.68
0.57
1.31
1.40
45.80
64.12
2.48
3.31
0.58
1.42
1.67
42.25
70.56
2.89
3.24
0.89
2.37
1.71
25.32
43.29
1.92
5.17
0.93
2.59
1.87
23.17
43.32
2.05
5.05
0.75
2.10
1.11
28.57
31.71
1.50
8.31
0.97
2.68
1.32
22.39
29.55
1.36
7.98
0.81
2.18
1.18
27.52
32.48
1.47
4.76
0.80
2.23
1.17
26.91
31.48
1.47
4.72
Mean ⫾ SD 0.80 ⫾ 0.15 2.04 ⫾ 0.50 1.17 ⫾ 0.29 31.35 ⫾ 8.89 36.19 ⫾ 12.75 1.52 ⫾ 0.47 5.49 ⫾ 1.75 0.95 ⫾ 0.30 2.66 ⫾ 1.00* 1.39 ⫾ 0.34† 25.75 ⫾ 10.22† 34.99 ⫾ 16.03 1.57 ⫾ 0.61 5.46 ⫾ 1.67
EELV, L
Vt/Ti, L/s
V̇e, L/min
fB, breaths/min
Subject
T i, s
Ttot, s
V t, L
fB, breaths/
min
V̇e, L/min
Vt/Ti, L/s
EELV, L
Ti, s
Ttot, s
V t, L
PLB
Control Breathing
Table 3—Ventilatory Parameters in Eight Patients With COPD During Exercise
correlated with changes in EELV (as a percentage of
TLC; r2 ⫽ 0.82; p ⫽ 0.002).
The mean Pcapi at FRC was ⫺67.5 ⫾ 18.4 cm
H2O, where the mean FRC for the group was
69.1 ⫾ 8.2% of TLC, while at TLC the mean Pcapi
was ⫺24.2 ⫾ 9.5 cm H2O. Individual and average
group values of the mean inspiratory ratio of Ppl/
Pcapi (in percent) are presented in Table 4. The
ratio was increased significantly with PLB at rest but
was inconsistently altered by PLB during exercise.
Changes occurring in the Ppl/Pcapi ratio with PLB
during exercise were significantly correlated with
changes in EELV (as a percentage of TLC;
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Clinical Investigations
Discussion
The present study shows that PLB can have a
variable effect on dyspnea when performed volitionally by patients with COPD during exercise, and that
the effect of PLB is dependent on changes promoted
to the Vt, the EELV, and, ultimately, to respiratory
muscle function. Patients who experience increases
in breathlessness with PLB have the greatest combined increases in EELV and/or Vt, forcing the
inspiratory muscles to operate close to the limits of
their pressure-generating capacity, whereas patients
who experienced reductions in dyspnea had reductions in EELV and greater reserves in inspiratory
muscle pressure-generating capacity.
Effect of PLB on Dyspnea, Breathing Pattern, and
Respiratory Mechanics
*p ⬍ 0.05 vs control breathing.
1
2
3
4
5
6
7
8
36.83
⫺ 16.11
14.58
0.08
7.53
2.49
279.66
43.89
⫺ 16.58
10.64
0.04
10.29
3.77
224.4
41.01
⫺ 11.74
13.26
0.04
7.01
4.80
352.53
49.36
⫺ 13.31
15.20
0.02
7.16
11.76
417.38
29.38
⫺ 14.30
19.80
0.07
12.83
17.81
654.16
43.29
⫺ 15.92
8.26
0.07
12.29
17.99
418.47
25.9
⫺ 13.89
17.86
0.04
4.85
6.50
504.39
37.54
⫺ 18.77
26.23
0.05
10.05
15.37
1003.33
23.76
⫺ 19.00
10.64
0.03
18.64
14.54
1519.64
31.61
⫺ 23.59
14.84
0.04
24.36
27.7
2199.54
36.19
⫺ 18.26
14.22
0.05
25.22
21.05
1171.56
40.49
⫺ 19.43
12.16
0.05
32.82
25.43
1349.65
60.64
⫺ 23.56
26.97
0.03
14.80
27.25
1201.37
54.92
⫺ 22.89
26.04
0.02
16.49
26.13
954.26
41.35
⫺ 15.06
19.48
0.04
9.74
10.89
567.74
40.35
⫺ 15.33
19.75
0.04
10.24
14.02
652.84
Mean ⫾ SD 36.76 ⫾ 11.61 ⫺ 16.48 ⫾ 3.69 17.10 ⫾ 5.10 0.05 ⫾ 0.02 12.58 ⫾ 6.82 13.17 ⫾ 8.60 781.38 ⫾ 454.79 42.68 ⫾ 7.12 ⫺ 18.23 ⫾ 3.64* 16.67 ⫾ 6.82 0.04 ⫾ 0.02 15.46 ⫾ 8.81* 17.77 ⫾ 8.27* 902.48 ⫾ 642.19
Wi⫹eres,
cm H2O䡠L䡠min
Weres,
cm H2O䡠L
Wires,
cm H2O䡠L
TTdi
Subject
Mean Ppl/
Pcapi, %
Mean Ppl,
cm H2O
Mean Pdi,
cm H2O
TTdi
Wires,
cm H2O/L
Weres,
cm H2O/L
Wi⫹eres
cm H2O/L/min
Mean Ppl/
Pcapi, %
Mean Ppl,
cm H2O
Mean Pdi,
cm H2O
PLB
Control Breathing
Table 4 —Respiratory Mechanics in Eight Patients With COPD During Exercise
r2 ⫽ 0.65, p ⫽ 0.016) and EILV (as a percentage of
TLC; r2 ⫽ 0.60; p ⫽ 0.024).
Figure 3 illustrates the relationship between the
concurrent changes occurring in the dyspnea scores
and the ratio of mean inspiratory Ppl to Pcapi with
PLB during exercise. Subjects who experienced less
breathlessness when using PLB exhibited decreases
in the mean inspiratory ratio of Ppl to Pcapi
(r2 ⫽ 0.84; p ⫽ 0.001).
Patients reported having no dyspnea at rest, with
or without PLB, whereas during exercise PLB had a
variable effect on the dyspnea perceived by individual patients, with half of patients experiencing more
dyspnea when using PLB. This is the first study that
objectively corroborated previous anecdotal evidence suggesting that some patients with COPD
obtain relief of dyspnea with PLB, whereas others do
not.1
During both breathing at rest and exercise, PLB
promoted a slower and deeper breathing pattern,
findings that concur with those of previous studies of
volitional PLB.1– 4,14 Mueller et al1 observed that
COPD patients who obtained dyspnea relief with
PLB exhibited larger increases in Vt and greater
reductions in fB than did subjects who failed to
experience any symptom benefit. These investigators
proposed that the relief of breathlessness provided
by PLB was related to its ability to promote a slower
and deeper breathing pattern. In our study, however,
such breathing pattern changes were not found to
correlate with breathlessness. Certain patients who
exhibited large increases in Vt combined with reductions in the respiratory rate experienced increases in breathlessness with PLB (eg, subjects 1
and 2). Likewise, there was no relation between the
changes in breathing pattern promoted and the
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645
Figure 2. Average loops of Ppl (A panels), Pga (B panels), and Pdi (C panels) plotted against Vt and
obtained with breath-by-breath analysis during the last 4 min of resting breathing (upper panels) and
exercise (lower panels) for two representative COPD patients. Dashed lines ⫽ control breathing; solid
lines ⫽ PLB; 䡬 ⫽ points of end-expiration; F ⫽ points of end-inspiration. The loops in the A panels
move in the clockwise direction, the direction of the loops in the B panels are indicated by the arrows,
and the loops in the C panels move in the counterclockwise direction. Error bars represent the SD for
Vt and the respective pressures. Horizontally lined and hatched areas in the A panels represent the
increased Wires and Weres values that occurred in the two subjects with PLB.
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Clinical Investigations
Figure 3. Relationship between changes in dyspnea and the
concurrent changes in the ratio of mean inspiratory Ppl to Pcapi
(as a percentage) occurring with PLB during steady-state exercise. The points represent the values for each individual patient
with corresponding patient number.
existing degree of expiratory airflow obstruction (as
FEV1 percent predicted) and/or static hyperinflation
(ie, the ratio of residual volume to TLC [as a
percentage]). Indeed, healthy individuals performing
volitional PLB have also previously been found to
exhibit significant increases in Vt during resting
breathing and exercise, suggesting that the ability of
PLB to promote changes in breathing patterns does
not depend on the presence of expiratory flow
obstruction.22
In our patients, both at rest and during exercise,
PLB had no effect on minute ventilation (V̇e). In
addition, PLB also significantly increased both the
Wires and Weres per breath, the result of joint
increases in Vt and the expiratory flow resistance
(Table 4). Thus, despite a reduction in the respiratory rate, the increased work of breathing was sufficient to offset the former, precluding significant
change in the W(i⫹e)res per minute.
Although the use of PLB by patients in our study
promoted larger mean inspiratory Ppl swings, mean
inspiratory Pdi was not altered, suggesting that PLB
may have the propensity to increase the recruitment
of the rib cage and accessory muscles, as has been
proposed in previous studies.3,23 However, it is not
certain to what extent such changes in respiratory
muscle recruitment ultimately affect dyspnea, given
that dyspnea may not depend on the activation of any
one specific respiratory muscle group but, rather,
may involve the integration of neural afferent information from any number of respiratory muscles. This
premise is supported by previous findings24 of the
existence of a close relationship between respiratory
effort sensation and Ppl swings, irrespective of
whether the rib cage/accessory muscles or the diaphragm are used to generate those pressures.
PLB performed at rest in the present study led to
an increase in the recruitment of the abdominal
muscles, whereas during exercise it had a less consistent effect. The expiratory muscles were already
significantly recruited by exercise alone. While it is
presumed25,26 that abdominal muscle recruitment
during expiration can lengthen the diaphragm, improving its tension-generating capacity during inspiration, it has also been postulated9 that abdominal
muscle recruitment can store elastic and gravitational energy within the diaphragm/abdomen, which,
when released during the initial part of inspiration,
enhances inspiratory pressure generation and lung
inflation. Because our patients exhibited substantial
expiratory muscle recruitment during exercise alone,
PLB may have been unable to further improve on
the existing pattern, thus having little impact in
altering dyspnea. While in some studies,10,27 expiratory muscle recruitment has been associated with a
worsening of dyspnea, the extent to which the
expiratory muscles contribute to the genesis of dyspnea in COPD patients is uncertain, given that
hyperinflation improves the mechanical advantage of
the expiratory muscles while requiring the inspiratory muscles to work at a higher fraction of their
force-generating capacity.
Although it was previously suggested3 that PLB
may act to unload the diaphragm and consequently
may help to protect it against the development of
fatigue, in our study PLB was found to have no effect
on TTdi at rest or during exercise. However, using
TTdi during dynamic exercise may be problematic
due to the static nature of the Pdimax measurement.
Because it can vary with changing lung volumes as
well as with the rate and extent of muscle shortening,
its application under conditions of exercise may be
limited.
Effect of PLB on EELV
Among our subjects, PLB was found to have an
inconsistent effect on EELV both at rest and during
exercise (Tables 2 and 3, respectively). This concurs
with the results obtained by Thoman et al4 for PLB
performed at rest, whereas, to the best of our
knowledge, no other study has examined the effect of
PLB on EELV in patients with COPD during exercise. However, the fact that patients are able to
variably modulate the pressure generated with PLB
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647
from breath to breath and within a breath22 and the
wide range of expiratory flow obstruction exhibited
by patients in our study may explain the variable
effect that PLB was observed to have on EELV.
Studies of positive end-expiratory pressure (PEEP)
have demonstrated that the effect of PEEP on
EELV varies depending on the presence or absence
of dynamic airway collapse. In subjects who are not
limited, expiratory muscle recruitment has been
shown to effectively reduce the normal increase in
EELV that occurs with the addition of PEEP,28
whereas in the presence of expiratory flow limitation
the resulting effect appears to be dependent on the
degree of existing airway collapse, the amount of
expiratory pressure reflected upstream from the
mouth toward the airways, the level of V̇e, and the
extent to which the expiratory muscles are recruited.29
Several studies have elucidated the impact of
dynamic hyperinflation on respiratory muscle function and dyspnea in COPD patients performing
exercise.7,11 O’Donnell and Webb,11 found dynamic
EILV (as a percentage of TLC) to be the strongest
independent predictor of exertional dyspnea, while
combined changes in the EILV, EELV, Vt, and fB
accounted for 61% of the variance in the change in
dyspnea. While such lung volume components may
contribute to the absolute dyspnea experienced by
patients, in the present study 82% of the variance in
the change in dyspnea promoted by PLB was accounted for by the alteration produced in EELV (as
a percentage of TLC).
Relationship Between Dyspnea and Inspiratory
Muscle Force-Generating Reserve With PLB
The mean Pplmax at FRC achieved in our patients
at rest was 67.5 ⫾ 18.4 cm H2O, and it declined by
about 1.4 cm H2O for every 1% increase in Vl (as a
percentage of TLC). While the Pplmax was below
normal, which is consistent with previous values
reported in patients with COPD,18,21,30 the rate of
decline in the pressure-generating capacity with
increasing lung volume was similar to that observed
in healthy subjects.21,31 The capacity to generate
pressure also declines with increasing inspiratory
flow,32,33 and increased inspiratory flows during exercise in healthy subjects can result in substantial
reductions in Pcapi.21 In contrast, our patients exhibited significantly smaller peak inspiratory flows
during exercise, and therefore had more modest
reductions in Pcapi. Although patients with COPD
typically demonstrate reduced exercise capacities
and achieve below normal levels of maximum ventilation and V̇, the smaller inspiratory flows seen in our
patients could also be attributed to the fact that they
were exercising at 60% of their Ẇlmax.
In our patients, the mean inspiratory Ppl/Pcapi
ratio accounted for 84% of the variance observed in
the change in dyspnea produced by PLB (p ⫽ 0.001)
[Fig 3]. Those patients who experienced more
breathlessness with PLB demonstrated an increase
in the ratio of mean Ppl to Pcapi, whereas subjects
who reported improvements in dyspnea, exhibited a
reduction in the ratio. Both the changes in EELV
and EILV (as percentages of TLC) were correlated
with the changes promoted in the Ppl/Pcapi ratio by
PLB. Changes in both the EELV and Vt contributed
to altering the EILV and, consequently, had an
impact on the ratio of Ppl to Pcapi (Fig 4). Thus,
PLB was able to modify dyspnea by promoting
changes in the operational lung volumes, which
consequently altered respiratory muscle capacity and
performance. In patients with COPD, mechanical
derangements of the ventilatory system and an increased flow resistance require that such patients
generate larger inspiratory forces to achieve a given
V̇e. Because hyperinflation promotes the shortening
of the inspiratory muscles, a higher than normal
neural motor output, or central neural drive, is
needed.34,35 Although conscious awareness of the
outgoing motor command resulting from corollary
discharges to the cerebral cortex has been suggested
to mediate the sense of effort,12,36,37 it has been
proposed38,39 that the discrepancy between the perceived effort and the actual ventilatory output (ie,
neuroventilatory dissociation) contributes to the
manifestation of dyspnea during exercise in such
patients.
The findings of the current study relate specifically
to volitionally performed PLB and cannot be generalized to spontaneous PLB. Volitional PLB may
involve greater focusing of the individual’s attention
on breathing pattern, which could have affected the
results. It should also be noted that we did not ask
whether our patients had used PLB prior to enrollment in the current study. Although none of the
patients had previously participated in any formal
pulmonary rehabilitation program, it is not known
how many patients may have discovered the breathing technique on their own. Future studies of patients who naturally incorporate PLB into their
breathing pattern may provide added information
regarding this breathing technique.
In summary, the present study shows that volitionally performed PLB by patients with COPD promotes a slower and deeper breathing pattern both at
rest and during exercise, while prolonging expiratory
and total breath durations, particularly at rest. Although PLB during exercise is capable of relieving
dyspnea by decreasing EELV in some patients, it can
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Clinical Investigations
Figure 4. Average loops of Ppl plotted against Vl expressed as a percentage of the TLC (%TLC) in
two representative patients during exercise. Dashed lines ⫽ control breathing; solid lines ⫽ PLB;
䡬 ⫽ points of end-expiration; F ⫽ points of end-inspiration. Loops move in the clockwise direction.
The dotted line to the left of the loops indicates the Pplmax values that could be generated at a given
Vl, and the corresponding curves represent the available inspiratory pressure generating capacity of the
inspiratory muscles once adjusted for V̇ (Pcapi).
likewise be ineffective or even detrimental to dyspnea in others when Vt values increase. The effect
that PLB has on dyspnea seems to be related to the
combined changes that it promotes in EELV and Vt,
and the impact that this has on the available capacity
of the respiratory muscles to meet the demands that
are placed on them in terms of pressure generation
to achieve a given ventilation.
7
8
9
ACKNOWLEDGMENT: The authors thank Dr. Heberto
Ghezzo for his helpful advice on the statistical analysis.
10
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