CLINICAL SCIENCES

Inspiratory Muscle Training in Type 2 Diabetes

with Inspiratory Muscle Weakness
ANA PAULA S. CORREA1, JORGE P. RIBEIRO1,2, FERNANDA MACHADO BALZAN1, LORENA MUNDSTOCK1,
ELTON LUIZ FERLIN1, and RUY SILVEIRA MORAES1,2
1
Exercise Pathophysiology Research Laboratory and Cardiovascular Division, Hospital de Clnicas de Porto Alegre,
Porto Alegre, Rio Grande do Sul, BRAZIL; and 2Department of Medicine, Faculty of Medicine, Federal University of
Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, BRAZIL

ABSTRACT
CORREA, A. P. S., J. P. RIBEIRO, F. M. BALZAN, L. MUNDSTOCK, E. L. FERLIN, and R. S. MORAES. Inspiratory Muscle
Training in Type 2 Diabetes with Inspiratory Muscle Weakness. Med. Sci. Sports Exerc., Vol. 43, No. 7, pp. 11351141, 2011. Purpose:
Patients with type 2 diabetes mellitus may present weakness of the inspiratory muscles. We tested the hypothesis that inspiratory muscle
training (IMT) could improve inspiratory muscle strength, pulmonary function, functional capacity, and autonomic modulation in
patients with type 2 diabetes and weakness of the inspiratory muscles. Methods: Maximal inspiratory muscle pressure (PImax) was
evaluated in a sample of 148 patients with type 2 diabetes. Of these, 25 patients with PImax G70% of predicted were randomized to an
8-wk program of IMT (n = 12) or placebo-IMT (n = 13). PImax, inspiratory muscle endurance time, pulmonary function, peak oxygen
uptake, and HR variability were evaluated before and after intervention. Results: The prevalence of inspiratory muscle weakness was
29%. IMT significantly increased the PImax (118%) and the inspiratory muscle endurance time (495%), with no changes in pulmonary
function, functional capacity, or autonomic modulation. There were no significant changes with placebo-IMT. Conclusions: Patients
with type 2 diabetes may frequently present inspiratory muscle weakness. In these patients, IMT improves inspiratory muscle function
with no consequences in functional capacity or autonomic modulation. Key Words: HEART RATE VARIABILITY, PULMONARY
FUNCTION, EXERCISE CAPACITY, CARDIOPULMONARY REHABILITATION

P
atients with diabetes mellitus may present pulmonary
functional abnormalities, which are associated with
chronic hyperglycemia (28). These abnormalities may
include reduction in lung volumes (8) and carbon monoxide
diffusion (12), as well as decreased pulmonary compliance,
lung elastic recoil (38), and inspiratory muscle strength
(4,19). The performance of the inspiratory muscles is of
particular interest because it may influence exercise toler-
ance in some clinical conditions in which inspiratory muscle
weakness (IMW) is present (15,31,32). Indeed, hypergly-
cemic patients with insulin-dependent diabetes mellitus may
present increased ventilatory response to exercise, with pos-
Address for correspondence: Ruy Silveira Moraes, M.D., Sc.D., Cardiology
Division, Hospital de Clnicas de Porto Alegre, Rua Ramiro Barcelos 2350,
90035-007, Porto Alegre, Rio Grande do Sul, Brazil; E-mail: rfilho@
hcpa.ufrgs.br.
Submitted for publication August 2010.
Accepted for publication December 2010.
0195-9131/11/4307-1135/0
MEDICINE & SCIENCE IN SPORTS & EXERCISE!
Copyright " 2011 by the American College of Sports Medicine
DOI: 10.1249/MSS.0b013e31820a7c12
sible consequences to exercise tolerance (28). Moreover, de-
spite some conflicting results, inspiratory muscle training (IMT)
has been shown to improve exercise tolerance in healthy
individuals (3,13,18,21) as well as in patients with chronic
heart failure (32), chronic obstructive pulmonary disease (15),
cerebrovascular disease (36), or neuromuscular disorders (5).
Recently, Kaminski et al. (20) have shown that patients
with type 2 diabetes mellitus (DM) with autonomic neu-
ropathy had reduced inspiratory muscle strength, suggesting
that IMW might be associated with autonomic dysfunction
in these patients. However, the prevalence of IMW in DM is
unknown, neither is the response to IMT. As a corollary to
what happens in other clinical conditions, we raised the
hypothesis that DM with autonomic neuropathy could have
a high prevalence of IMW and that IMT could improve in-
spiratory muscle strength with consequences to functional
capacity and autonomic modulation. The present random-
ized clinical trial was conducted to test these hypotheses.
METHODS
Study design and participants. A prospective, ran-
domized, controlled trial was conducted in patients with
DM, according to the National Diabetes Data Group criteria

1135

Copyright 2011 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
 (1), recruited from the Endocrinology Outpatient Clinic of
the Hospital de Clnicas de Porto Alegre, who presented
maximal inspiratory pressure (PImax) G70% of predicted
CLINICAL SCIENCES
(27). This cutoff value has been arbitrarily chosen to define
patients with inspiratory muscle weakness (32). Exclusion
criteria were body mass index 9 33 kgImj2, history of
exercise-induced asthma, infectious disease, osteoarticular
disease, cardiac and pulmonary diseases, as well as regular
alcohol or tobacco consumption in the past 6 months.
Because regular aerobic exercise may improve inspiratory
muscle strength in patients with IMW (42), only sedentary
patients were recruited. The protocol was approved by the
Committee for Ethics in Research of the Hospital de Clnicas
de Porto Alegre, and all subjects signed a written informed
consent form.
Patients were initially evaluated by medical history,
physical examination, and the determination of PImax. Eli-
gible patients were randomly assigned to IMT or to placebo
IMT (P-IMT) for 8 wk. Before and after the intervention,
pulmonary function tests, inspiratory muscle function tests,
cardiopulmonary exercise testing, cardiovascular autonomic
function tests, and 24-h analysis of HR variability were
obtained. All evaluations were performed by investigators
who were unaware of the allocation of patients to different
interventions.
Inspiratory muscle training. Patients received either
IMT or P-IMT for 30 min seven times per week for 8 wk
using the Threshold Inspiratory Muscle Trainer device
(Health Scan Products, Inc., Cedar Grove, NJ) according to
a protocol previously described (7). In short, for the IMT
group, inspiratory load was set at 30% of maximal static
inspiratory pressure, and weekly measures of PImax were
obtained to maintain training loads at 30% of the PImax. The
P-IMT followed the same schedule, using the lowest pres-
sure offered by the device (7 cm H2O). Each week, six
training sessions were performed at home and one training
session was supervised at the hospital.
Pulmonary function. Measurements of forced vital
capacity (FVC), forced expiratory volume in 1 s (FEV1), and
maximal voluntary ventilation (MVV) were obtained with a
computerized spirometer (Eric Jaeger, GmbH, Wurzburg,
Germany), as recommended by the American Thoracic
Society (2), and results were expressed as a percentage of
predicted (30).
Inspiratory muscle function. Inspiratory muscle func-
tion testing was performed using a pressure transducer
(MVD-500 V.1.1 Microhard System; Globalmed, Porto
Alegre, Brazil), connected to a system with two unidirectional
valves (DHD Inspiratory Muscle Trainer, Chicago, IL) as
previously described (7). In short, PImax was determined in
deep inspiration from residual volume against an occluded
airway with a minor air leak. The test was repeated at least
12 times to find si measurements with G10% variation. Pre-
dicted values were corrected for age and gender (27). Inspi-
ratory muscle endurance (Pthmax) was determined by an
incremental test and expressed as a percentage of PImax
1136 Official Journal of the American College of Sports Medicine
Copyright 2011 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
(Pthmax/PImax). Finally, subjects breathed against a constant
inspiratory submaximal load equivalent to 80% Pthmax, and
the time elapsed to task failure was defined as the inspira-
tory endurance time (7). For the endurance tests, a target
inspiratoryexpiratory time ratio of 0.75 was recommended.
Cardiopulmonary exercise testing. Maximal func-
tional capacity was assessed with an incremental exercise
test, on a treadmill (Inbramed 10200, Porto Alegre, Brazil),
using a ramp protocol, as previously described (7). Twelve-
lead ECG tracings were obtained every minute (Nihon
Khoden Corp., Tokyo, Japan), and blood pressure was
measured every 2 min with a standard cuff sphygmoma-
nometer. During the test, gas exchange variables were
measured breath-by-breath by a previously validated system
(Metalyzer 3B, CPX System; Cortex, Leipzig, Germany).
Cardiac autonomic function testing. Autonomic neu-
ropathy was determined by the presence of more than one
abnormal autonomic cardiovascular function test (11), as pre-
viously standardized in our institution (43). The tests used
were the following: HR response during deep breathing (nor-
mal values 96), HR response during the Valsalva maneuver
(normal values 91.2), HR and blood pressure responses to
orthostatic position (normal values 91.06 and G25 mm Hg,
respectively), and blood pressure response to handgrip (normal
values 910 mm Hg).
Heart rate variability. Twenty-four-hour ECG record-
ings were obtained with a SEER Light digital recorder (GE
Medical Systems Information Technologies, Milwaukee,
WI). The recorded data were analyzed using a MARS 8000
analyzer (Marquete Medical Systems, Milwaukee, WI) as
previously described (29). In short, time domain and fre-
quency domain analyses of HR variability (HRV) were per-
formed according to recommendations from the European
Society of Cardiology and North American Society of Pacing
and Electrophysiology (37). For the time domain analysis,
the following 24-h indices were calculated: mean of all nor-
mal RR intervals, SD of all normal RR intervals, root mean
square of successive differences of adjacent RR intervals,
and percentage of successive differences between normal ad-
jacent RR intervals above 50 ms. For the frequency-domain
analysis, the following components of the spectral analysis of
HR were assessed: total power spectrum (0.0031 Hz), low
frequency (0.040.15 Hz), high frequency (0.150.5 Hz), and
low-frequency/high-frequency ratio. The spectral analysis of
HR was calculated at 5-min intervals, during rest, and after a
5-min sympathetic stimulation by passive orthostatism with
a 70% tilt.
Statistical analysis. Data were analyzed on the Statis-
tical Package for Social Sciences (version 14.0 for Windows;
SPSS, Inc., Chicago, IL). On the basis of the results of pre-
vious studies with IMT performed in our laboratory (6,7,42),
we estimated that a sample size of 12 individuals in each
group would have a power of 80% to detect a 20% differ-
ence in PImax, for an > of 0.05. Descriptive data are pre-
sented as mean T SD. Baseline data for the two intervention
groups and the group of patients who were not included in
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FIGURE 1Flow diagram of the study.

the study were compared by ANOVA, and post hoc com-
parisons were performed with the Tukey test. Categorical
variables were compared with the Fisher exact test. The
effects of interventions were compared by two-way ANOVA
for repeated measures (RM-ANOVA), and post hoc analysis
group had higher PImax when compared with the randomized
patients. There were no differences in PImax, Pthmax/PImax,
and endurance time between the IMT and P-IMT groups.
TABLE 1. Baseline characteristics of randomized and screened patients.

was conducted by the Tukey test to compare weekly values IMT P-IMT Screening
(n = 12) (n = 13) (n = 123) ANOVA
of PImax.
Age (yr) 63 T 7 63 T 7 60 T 9 NS
Sex (F/M) 5/7 8/5 68/55
BMI (kgImj2) 27.3 T 3.2 28.2 T 2.6 28.7 T 4.6 NS
RESULTS Diabetes time (yr) 11.6 T 4.7 13.9 T 8.3 13 T 7 NS
HbA1c (%) 7.5 T 1.4 7.1 T 1.7 8.1 T 2.0 NS
Patients. Figure 1 presents the flow of patients in the Glucose (mgIdLj1) 152 T 49 134 T 72 165 T 68 NS
study. Of the 148 patients with DM evaluated for inspira- Total cholesterol (mgIdLj1) 169 T 53 169 T 37 182 T 48 NS
HDL cholesterol (mgIdLj1) 48 T 8 49 T 11 52 T 16 NS
tory muscle strength, 43 (29%) had PImax G 70% of pre- Creatinine (mgIdLj1) 1.0 T 0.2 0.9 T 0.3 0.9 T 0.3 NS
dicted. Of these patients, two were excluded for obesity, four Potassium (mEqILj1) 4.5 T 0.5 4.8 T 0.4 NS
were excluded for presence of heart failure, and four were Hemodynamics
MAP (mm Hg) 100 T 9 97 T 12 99 T 11 NS
excluded for regular practice of physical exercise. Of the HR (mm Hg) 74 T 8 72 T 14 73 T 11 NS
33 patients randomized to the IMT and P-IMT groups, two Medications, n (%)
Insulin 5 (42) 3 (23) 56 (46)
were excluded from the IMT group because of ischemia on Metformin 8 (67) 10 (76) 87 (71)
the cardiopulmonary test, and one patient in the P-IMT group Sulfonylureas 5 (42) 6 (46) 30 (24)
ACE inhibitor 9 (75) 12 (92)* 73 (59)
died in a car accident. Three patients from the IMT group Diuretics 6 (50) 12 (92)* 63 (51)
and two from the P-IMT group later refused to continue in the Statins 7 (58) 8 (62) 61 (50)
protocol. Therefore, after 8 wk, 13 patients in the P-IMT group A-blockers 1 (8) 6 (46) 34 (28)
Assessment
and 12 patients in the IMT group were analyzed. PImax (cm H2O) 56 T 13 52 T 10 91 T 27** G0.001
Table 1 presents the baseline characteristics of patients PImax (% predicted) 58 T 11 57 T 10 96 T 26** G0.001
Pthmax/PImax (%) 38 T 1 37 T 2 NS
randomized to IMT and P-IMT, as well as the 123 patients Endurance time (s) 376 T 37 245 T 87 NS
screened who did not participate in the protocol. The three
Values are expressed as mean T SD or n (%).
groups presented similar characteristics except for less utiliza- * P-IMT group different from IMT and Screening groups. P G 0.05 on the Fisher
tion of angiotensin-converting enzyme inhibitors in patients exact test.
** Screening group different from IMT and P-IMT groups. P G 0.05, on the Tukey test.
of the screening group and more frequent utilization of ACE, angiotensin-converting enzyme; BMI, body mass index; HbA1c, glycosylated hemo-
diuretics in the P-IMT group. As by protocol, the screening globin; MAP, mean arterial pressure.

INSPIRATORY MUSCLE TRAINING IN DIABETES Medicine & Science in Sports & Exercised 1137

Copyright 2011 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
 TABLE 2. Pulmonary function, inspiratory muscle function, and cardiopulmonary exercise testing before and after intervention.
IMT (n = 12) P-IMT (n = 13)
Before After Before After
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Pulmonary function
FEV1 (% predicted) 105 T 19 107 T 18 92 T 13 91 T 17
FVC (% predicted) 103 T 19 106 T 18 92 T 10 88 T 13
MVV (% predicted) 80 T 18 82 T 13 79 T 17 76 T 14
Inspiratory muscle function
PImax (cm H2O) 56 T 13 121 T 22 52 T 10 58 T 11*
PImax (% predicted) 58 T 11 125 T 17 57 T 10 63 T 9*
Pthmax/PImax (%) 38 T 1 40 T1 37 T 2 38 T 6*
Endurance time (s) 376 T 37 1863 T71 245 T 87 323 T 53*
Cardiopulmonary exercise test
Peak HR (bpm) 150 T 1 147 T 5 143 T 5 149 T 5
Peak systolic pressure (mm Hg) 189 T 5 176 T 3 180 T 3 178 T 4
VO2peak (mLIminj1Ikgj1) 24.1 T 6.1 23.9 T 5.6 21.2 T 5.9 21.5 T 5.8
VCO2peak (LIminj1) 2 T 0.8 1.9 T 0.6 1.6 T 0.5 1.6 T 0.6
Rpeak 1.1 T 0.1 1.1 T 0.1 1.0 T 0.1 1.0 T 0.0
VE peak (LIminj1) 61 T 20 62 T 19 52 T 18 55 T 23
VE /VO2peak 34.3 T 6.8 34.8 T 10.9 31.9 T 3.1 34 T 7.8
VE /VCO2peak 32.3 T 5.0 31.8 T 8.0 32.4 T 3.0 36.3 T 10.3
Values are expressed as mean T SD.
* ANOVA G 0.01, with group, time, and interaction effects.
Pthmax, inspiratory endurance determined during incremental test; VO2, oxygen uptake; VCO2, carbon dioxide output; R, RER; VE, minute ventilation; VE /VO2, ventilatory equivalent for
oxygen; VE /VCO2, ventilatory equivalent for carbon dioxide.

Pulmonary function. Table 2 shows the results of
pulmonary function tests. After 8 wk of intervention, there
were no changes in FVC, FEV1, and MVV in the IMT and
P-IMT groups.
Inspiratory muscle function. Figure 2 shows the
weekly values of PImax, demonstrating that IMT induced
marked improvement in PImax, which was apparent after the
second week of training and reached an increment of 108%
after 8 wk, whereas in the P-IMT group, there was no sig-
nificant change. Likewise, inspiratory muscle endurance,
evaluated by the Pthmax/PImax, and endurance time increased
only after IMT (Table 2).
Cardiopulmonary exercise testing. Table 2 shows that
there were no significant changes in any of the cardiopul-
monary exercise testingderived variables after IMT or P-IMT.
Cardiac autonomic function testing. At baseline,
all randomized patients presented more than one abnormal
cardiovascular autonomic test. In the IMT group, 10 patients
presented two abnormal test results and 2 patients presented
three abnormal test results. In the P-IMT group, seven patients
presented two abnormal tests and six presented three abnor-
mal tests.
HR variability. Table 3 shows time- and frequency-domain
indices of HRV before and after intervention. Twenty-four-
hour indices of HRV as well as power spectral components of
HRV at rest and after sympathetic stimulation by passive
orthostatism were unaffected by IMT or P-IMT.
These findings were obtained in a placebo-controlled ran-
domized trial, with blind evaluation of outcomes, conducted
in DM with autonomic neuropathy and IMW.
The mechanisms responsible for the development of IMW
in DM are still poorly understood. Experiments have identi-
fied respiratory muscle weakness in rats with streptozotocin
induced diabetes, with evidence of phrenic nerve neuropathy,
characterized by axonal atrophy and significant reduction
in myelin (33). Wanke et al. (41) assessed respiratory muscle
strength in DM patients and healthy controls by measur-
ing transdiaphragmatic pressures and PImax during bilateral
stimulation of the phrenic nerve and from voluntary muscle
contraction. Although only patients with more accentuated
polyneuropathy presented reduced respiratory muscle strength,
phrenic nerve latencies were normal, suggesting that im-
paired diaphragm function was not caused by phrenic neu-
ropathy (40). In contrast, Kabitz et al. (19) demonstrated an

DISCUSSION
The major findings of the present study were that IMW is
frequent in DM, occurring in 29% of screened individuals,
and that IMT is able to reverse the loss of inspiratory muscle
strength in these patients. However, the improvement in in-
FIGURE 2Mean T SD weekly PImax during the training period.
spiratory muscle strength after training was not accompanied *RM-ANOVA: P G 0.001 time effect; P G 0.001 training effect; P G 0.001
by changes in functional capacity or autonomic modulation. interaction.

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TABLE 3. Twenty-four-hour indices of HR variability and spectral analysis of HR at rest and during passive orthostatism before and after intervention.
IMT P-IMT
Before After Before After

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24-h time-domain indices
Mean RR interval (ms) 777 T 116 781 T 105 786 T 125 748 T 84
SDNN (ms) 106 T 33 109 T 37 113 T 31 115 T 31
RMSSD (ms) 20 T 8 23 T 9 21 T 5 23 T 9
PNN50 (%) 3.6 T 4.7 6.3 T 7.4 3.5 T 2.4 5.5 T 5.2
Spectral analysis
Rest
LF (nu) 0.57 T 0.19 0.58 T 0.2 0.59 T 0.16 0.56 T 0.16
HF (nu) 0.31 T 0.21 0.34 T 0.19 0.30 T 0.13 0.33 T 0.14
LF/HF (ratio) 2.52 T 1.41 2.4 T 1.6 2.45 T 1.52 2.2 T 1.7
Total power 444.6 T 333 442.2 T 250.4 715.5 T 381.7 810.7 T 500
Passive orthostatism
LF (nu) 0.58 T 0.11 0.59 T 0.19 0.63 T 0.18 0.60 T 0.21
HF (nu) 0.26 T 0.73 0.30 T 0.19 0.25 T 0.14 0.26 T 0.16
LF/HF (ratio) 2.3 T 1.0 2.7 T 1.8 3.6 T 2.3 3.4 T 2.7
Total power (ms2IHzj1) 292.1 T 171.1 322.6 T 265.7 702.6 T 540.1 479.7 T 362.3
Values are expressed as mean T SD.
HF, high frequency; LF, low frequency; LF/HF, low-frequency/high-frequency ratio; Mean RR interval, mean of all RR intervals; nu, normalized units; SDNN, SD of all normal RR intervals;
RMSSD, root mean square of successive RR interval differences; PNN50, percentage of successive differences between normal adjacent intervals 950 ms.

association between diabetic polyneuropathy and impaired
respiratory neuromuscular function assessed by phrenic nerve
stimulation in DM. In the present study, diabetic poly-
neuropathy was not evaluated; therefore, more studies should
be conducted to elucidate its role on the development of
IMW in DM.
We have consistently shown that the same IMT program
used in the present study improves inspiratory muscle strength,
induces diaphragm hypertrophy, and increases functional
capacity in patients with chronic heart failure and IMW
(6,7,42). Therefore, contrary to what has been proposed
by others (32), the training stimulus of this protocol results
in clear functional and structural adaptations. Our patients
had preserved peak exercise capacity at baseline, and IMT
resulted in no significant change in V O2peak. However,
similar to the present findings, even in chronic obstructive
pulmonary disease patients, IMT may not be associated with
a significant improvement in peak exercise capacity (24).
Likewise, IMT has no significant effect on peak exercise
capacity in healthy individuals, but it may improve perfor-
mance during high-intensity constant workload exercise (3).
Another possible explanation for our findings may be the
activation of the inspiratory muscle metaboreflex, which
controls the competition for blood flow between inspiratory
muscles and skeletal muscles in healthy individuals (9) as
well as in patients with chronic obstructive pulmonary dis-
ease (39) and in chronic heart failure (6). Therefore, it is
conceivable that DM might not improve functional capacity
after IMT because they have an attenuated inspiratory muscle
metaboreflex. However, this hypothesis deserves to be for-
mally tested by controlled experiments.
Patients with DM and autonomic neuropathy may
present abnormal HRV (26) and increased risk of mortality
(25). Whole-body aerobic exercise improves HRV in DM
without autonomic dysfunction or with mild autonomic
neuropathy (16,23). Despite its beneficial effects on func-
tional capacity in chronic heart failure, Laoutaris et al. (22)
found no significant effect of IMT on HRV of these
patients. Likewise, in our study, the increase in inspiratory
muscle strength with IMT did not lead to any change in
HRV in time and frequency domains, and there was no
correlation between PImax and autonomic modulation. All
of our patients showed reduced PImax and evidence of
pronounced autonomic impairment, as indicated by the
presence of abnormal autonomic tests, absence of change in
the spectral components of HR during sympathetic stimu-
lation (Table 3), and reduced indices of 24-h HRV con-
sidering expected values for age (38).
This study has several limitations. Inspiratory muscle
function was evaluated with volitional noninvasive tests
and, therefore, part of the improvement in these measures
could have been related to a learning effect. Hart et al. (14)
evaluated the effects of IMT using the Powerbreathe! de-
vice in healthy individuals, showing that improvement in
PImax after intervention could be due to a learning effect
because it had no influence on diaphragm strength assessed
by magnetic stimulation of the phrenic nerve. However, we
took care to control the breathing strategy in the inspiratory
muscle endurance tests, probably reducing this confounding
factor. Moreover, both the IMT group and the P-IMT had
their PImax measured every week, and despite these repeated
measures, the P-IMT showed no significant learning effect
in the measurement of PImax (Fig. 1). Finally, we cannot
exclude the possibility that higher-intensity IMT could have
resulted in improvement in functional capacity in our
patients, as has been suggested by a meta-analysis in chronic
obstructive pulmonary disease (34) as well as studies in
cystic fibrosis (10) and chronic heart failure (22). However,
the size of the mean increment in PImax in the present study
is remarkably similar to that obtained with the same protocol
in patients with chronic heart failure (7), suggesting that a
training effect on the inspiratory muscles was obtained and
that further increments in training intensity would unlikely
change the outcome.
In conclusion, IMW occurs frequently in DM and can
be reversed by IMT. In these patients, IMT does not

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 improve pulmonary function, functional capacity, and auto-
nomic modulation. These findings may have clinical impli-
cations during situations where pulmonary functional reserve
CLINICAL SCIENCES
may be of clinical relevance. One such a situation is in
the preoperative evaluation for major surgery. For instance,
PImax is associated with functional capacity after coronary
artery bypass surgery (35) and preoperative IMT has been
shown to reduce pulmonary complications after this surgical
intervention (17). Therefore, the measurement of PImax may
be particularly important in the preoperative evaluation of
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1140 Official Journal of the American College of Sports Medicine
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patients with DM, and this should be addressed in future
studies.
A. P. S. Correa was supported by grant from the Coordination for
the Improvement of Higher Education Personnel (CAPES), Brazil.
This study was supported by Fundo de Incentivo a` Pesquisa do
Hospital de Clnicas de Porto Alegre (FIPE HCPA). ClinicalTrials.gov
ID No. NCT00815178.
No potential conflicts of interest relevant to this article are
reported.
The results of this study do not constitute endorsement by the
American College of Sports Medicine.
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