The effect of exercise on obstructive sleep apnea: a randomized and controlled trial.

Abstract

The aim of the study was to assess the effect of breathing and physical exercise on pulmonary functions, apnea-hypopnea index (AHI), and quality of life in patients with obstructive sleep apnea syndrome (OSAS).
Twenty patients with mild to moderate OSAS were included in the study either as exercise or control group. The control group did not receive any treatment, whereas the exercise group received exercise training. Exercise program consisting of breathing and aerobic exercises was applied for 1.5 h 3 days weekly for 12 weeks. Two groups were assessed through clinical and laboratory measurements after 12 weeks. In the evaluations, bicycle ergometer test was used for exercise capacity, pulmonary function test, maximal inspiratory-expiratory pressure for pulmonary functions, polysomnography for AHI, sleep parameters, Functional Outcomes of Sleep Questionnaire (FOSQ), Short Form-36 (SF-36) for quality of sleep and health-related quality of health, Epworth Sleepiness Scale for daytime sleepiness, and anthropometric measurements for anthropometric characteristics.
In the control group, the outcomes prior to and following 12-weeks follow-up period were found to be similar. In the exercise group, no change was found in the anthropometric and respiratory measurements (P > 0.05), whereas significant improvements were found in exercise capacity, AHI, and FOSQ and SF-36 (P < 0.05). After the follow-up period, it was shown that improvement in the experimental group did not lead to a statistically significant difference between the two groups (P > 0.05).
Exercise appears not to change anthropometric characteristics and respiratory functions while it improves AHI, health-related quality of life, quality of sleep, and exercise capacity in the patients with mild to moderate OSAS.

Full text

Page 1

ORIGINAL ARTICLE
The effect of exercise on obstructive sleep apnea:
a randomized and controlled trial
Yesim Salik Sengul & Sevgi Ozalevli & Ibrahim Oztura &
Oya Itil & Baris Baklan
Received: 17 July 2009 /Accepted: 14 October 2009 /Published online: 7 November 2009
# Springer-Verlag 2009
Abstract
Purpose The aim of the study was to assess the effect of
breathing and physical exercise on pulmonary functions,
apnea-hypopnea index (AHI), and quality of life in patients
with obstructive sleep apnea syndrome (OSAS).
Methods Twenty patients with mild to moderate OSAS
were included in the study either as exercise or control
group. The control group did not receive any treatment,
whereas the exercise group received exercise training.
Exercise program consisting of breathing and aerobic
exercises was applied for 1.5 h 3 days weekly for 12 weeks.
Two groups were assessed through clinical and laboratory
measurements after 12 weeks. In the evaluations, bicycle
ergometer test was used for exercise capacity, pulmonary
function test, maximal inspiratory-expiratory pressure for
pulmonary functions, polysomnography for AHI, sleep
parameters, Functional Outcomes of Sleep Questionnaire
(FOSQ), Short Form-36 (SF-36) for quality of sleep and
health-related quality of health, Epworth Sleepiness Scale
for daytime sleepiness, and anthropometric measurements
for anthropometric characteristics.
Results In the control group, the outcomes prior to and
following 12-weeks follow-up period were found to be
similar. In the exercise group, no change was found in the
anthropometric and respiratory measurements (P>0.05),
whereas significant improvements were found in exercise
capacity, AHI, and FOSQ and SF-36 (P<0.05). After the
follow-up period, it was shown that improvement in the
experimental group did not lead to a statistically significant
difference between the two groups (P>0.05).
Conclusions Exercise appears not to change anthropomet-
ric characteristics and respiratory functions while it
improves AHI, health-related quality of life, quality of
sleep, and exercise capacity in the patients with mild to
moderate OSAS.
Keywords Mildtomoderateobstructivesleepapnea
syndrome.Breathingexercise.Physicalexercise
Introduction
Obstructive sleep apnea (OSA) can be described as a
condition characterized by repetitive obstruction of the
upper airway resulting in oxygen desaturation and awak-
ening from sleep, loud snoring, and increased daytime
sleepiness [1]. Many studies have shown that a link exists
between OSA and cardiovascular disease, chronic heart
failure ischemia, hypertension, obesity, and impaired
glucose tolerance [2, 3]. A number of factors are likely to
play role in development of clinical OSA syndrome
(OSAS) ranging from upper airway anatomy to central
respiratory control mechanisms. The pathophysiology of
OSA is unclear and complex. Several previous studies have
explored pulmonary function in the OSAS patients [4, 5].
Interestingly, OSAS has been found to be highly correlated
Y. S. Sengul (*):S. Ozalevli
School of Physical Therapy and Rehabilitation,
Dokuz Eylul University,
Inciralti-Izmir TR-35340, Turkey
e-mail: yesim.salik@deu.edu.tr
I. Oztura:B. Baklan
Departments of Neurology, School of Medicine,
Dokuz Eylul University,
Izmir, Turkey
O. Itil
Department of Chest Diseases, Dokuz Eylul University,
Izmir, Turkey
Sleep Breath (2011) 15:49–56
DOI 10.1007/s11325-009-0311-1

Page 2

with lower airway obstruction, although it is originally
defined as an upper airway disease [4]. In the recent
studies, metabolic factors, especially inflammatory cyto-
kines (IL-1, IL-6, and TNF-α) are implicated for leading to
this condition because of its systemic interactions [6, 7].
Another important effect of pro-inflammatory cytokines is
to cause collapse by leading inflammation in dilator
muscles in the upper airway. Thus, the observed hyper-
cytokinemia, hyperleptinemia, and hyperinsulinemia/viscer-
al adiposity, through central and peripheral effects, may
lead to a collapse of the upper airway during sleep [7, 8].
The most commonly accepted interventions in the
treatment of OSA include administration of continuous
positive airway pressure (CPAP) and oral appliances during
sleep and surgery [9–11]. American Sleep Apnea Associ-
ation considers exercise as a non-pharmacological treatment
modality of sleep disorders [12]. Theoretical reviews and
hypotheses on the effects of exercise in OSA have
suggested thermoregulatory, metabolic, and biochemical
mechanisms although clinical trials on the topic are
inadequate [6, 7, 12, 13].
Hargens et al. [14] indicated that alteration in chemo-
reflex sensitivity and breathing efficiency exists in patients
with OSA. Exercise studies showed that an improvement
occurs in respiratory drive (and chemoreceptor sensitivity)
after physical exercise in athletes. Netzer et al. [15] reported
a significant improvement in apnea-hypopnea index (AHI)
following a 6-month exercise program in the patients with
moderate to severe OSAS. They suggested that improve-
ment of OSA severity might be due to a possible rise in the
respiratory drive or a stabilized muscle tonus in the upper
airway after exercise. Nevertheless, Norman et al. [16]
noted that regular exercise training provided improvement
in sleep by decreasing body weight. Consequently, the
studies have shown that regular physical activity reduces
severity of OSA symptoms either by decreasing body
weight or through positive effects on the respiratory
muscles and sufficiency of breathing (ventilatory abilities)
[13, 15–17].
Our study was planned to assess the effects of physical
and breathing exercise training on pulmonary function,
AHI, and quality of life in order to investigate the place of
exercise in management of OSAS.
Methods
Subjects
Study protocols and written informed consents were
approved by the institutional review committee on clinical
research of the Dokuz Eylul University School of Medi-
cine. The inclusion criteria for this study included men 40
to 65 years of age, in good general health (stability of clinic
state), with OSAS symptoms (snoring, breathing cessations,
and daytime sleepiness), and polysomnographic evidence
(AHI, sleep efficiency percentage, minimum saturation
percentage, and total sleep time) consistent with mild (5<
AHI<15) to moderate (16<AHI<30) OSAS. Medical
conditions that would make exercise dangerous such as
angina pectoris, congestive heart failure, cardiomyopathy,
emphysema, lung cancer, recent upper respiratory surgery,
chronic obstructive pulmonary disease, or other serious
medical problems such as neurological, psychological, and
cooperation problems that would prevent successful partic-
ipation in and completion of the protocol by the subject
served as exclusion criteria.
The participants were divided into control and study
groups according to the table of random numbers. The
control group did not receive any treatment, the study group
received exercise training. Both groups underwent similar
clinical and physiotherapeutic assessment. In addition, the
control group was not advised any information and/or
exercise apart from routine clinical treatment and proposals.
In contrast to the control group, the study group received
breathing exercise (approximately; 15–30 min) and aerobic
exercises (approximately; 45–60 min) lasting progressively
1–1.5 hour three times weekly for 12 weeks.
Exercises were given by a single physiotherapist at the
same time and place for 12 weeks. Exercises were taught to
the patients repetitively until they said "I understood". The
patients were enabled to get used to the exercises by giving
them exercise booklets and requiring them to participate
with sports outfits. Several data such as the patients'
respiration rates, heart rates, and blood pressures were
recorded before and after the exercises. Participants'
dyspnea severity and leg tiredness were evaluated with
Modified Borg Scale [18]. The exercises were maintained
under the control of a physiotherapist.
Breathing exercises Exercises were started with the pursed
lips breathing training in which the patient is taught to
inhale the air through the nose and exhale slowly by
slightly opening his/her lips. During entire breathing
exercises, relaxation training and its importance were
explained to the patients in order to minimize contribution
on the shoulder girdle and neck muscles to breathing. The
patients were placed in appropriate position during dia-
phragmatic and thoracic expansion exercises. For kines-
thetic stimulation, the patient was asked to place his/her
hand on the relevant pulmonary areas to increase the
amount of expiration through resistance in the inspiration
period and through pressure in the expiration period. All
exercises were combined with postural exercises. Exercise
program was progressed according to fatigue severity of
patients. Breathing exercises, which had been done in
50 Sleep Breath (2011) 15:49–56

Page 3

sitting position, were done resistively in flat position by the
help of gravity and 250-g weights [19, 20].
Aerobic exercises The height of the bicycle was adjusted
specifically for each patient. After the breathing exercises,
thepatients didwarmupexercisesconsisted ofslowjogging,
calisthenics, and stretching. Then they did aerobic exercises,
resistance, and duration of which were increased according
to the patients' tolerance on bisergo and treadmill. The
training program began at a low to moderate intensity over
the first 1–2 weeks and progressed to a moderate intensity
program. During the treadmill and bicycle exercises, which
were applied at submaximal intensity at 60–70% of
maximal oxygen consumption, it was ensured that the
intensity of fatigue that the patients perceived is at the
interval of 4–5 according to the Modified Borg scale.
During the exercises, the Palco Laboratories Model 400
pulse oxymeter has been used in order to observe the heart
rate and peripheral oxygen saturation. After the bicycle and
treadmill exercises, the exercise program was finished with
the cooling down period which was consisted of low-tempo
walking, posture, and stretching exercises. It was ensured in
all exercises to maintain respiration control [21, 22].
Patients suitable for inclusion criteria were asked if they
had smoking and exercise habits. Anthropometric measure-
ments, pulmonary functions, exercise capacity, quality of
sleep, and health-related quality of health were repeatedly
measured at the end of week 12 in order to describe the
effects of exercise treatments in patients with OSA.
Anthropometric data
Anthropometric measurements including height, weight,
and circumference measurements were obtained before and
after the study. From the height (m) and weight (kg)
measurements, the body mass index (BMI) was calculated
(kg/m2). Circumference measurements were made with a
flexible tape and included neck, upper chest, waist, and hip
circumferences. The waist and hip girths were used to
calculate the waist-to-hip ratio for each individual. A single
investigator performed all measurements.
Skinfold thickness were measured on the right side of
the body with a caliper (Holtain Tanner/Whitehouse
skinfold caliper; Holtain Ltd, UK) to the nearest millimeter.
To assess subcutaneous fat, the skinfold thickness of the
following sites was measured: subscapular, triceps, and
chest in accordance with procedures described by The
American College of Sports Medicine. From the skinfold
thickness, body density was calculated using the predictive
equations proposed by Jackson and Pollock. Relative body
fat was estimated from the equations proposed by Brozek
and colleagues [21].
Pulmonary function testing
Subjects underwent pulmonary function testing to evaluate
the lung functions. Spirometry was performed by an expert
using a Sensormedics Vmax 22 machine (SensorMedics
Inc., Anaheim, CA, USA) conforming to the American
Thoracic Society criteria [23]. Forced vital capacity, first
second forced expiratory volume (FEV1), and FEV1/FVC
values were recorded.
Respiratory muscle strength Mouth pressures were mea-
sured by Sensormedics Vmax 22 (SensorMedics Inc.,
Anaheim, CA, USA) using a previously reported technique
[24]. Inspiratory muscle strength (Pimax) was measured
from functional residual capacity, whereas expiratory
muscle strength (PEmax) was measured near total lung
capacity. Tests were run three times (at the beginning of the
study period, after 3 months, and at the end of the study
period), and three measurements were made in each testing
session.
Exercise testing
The subjects exercised on an electronically braked cycle
ergometer (ercometrics 800, ergoline, Germany) by "Max-
imal incremental cycle ergometry protocols". This protocol
consists of 3 min of rest, followed by 3 min of unloaded
pedaling and by incremental load (3 W per 10 s) until
reaching maximal load [25]. Criteria for terminating
exercise testing include the patient reaching volitional
exhaustion or the test has been terminated by the medical
monitor. Pretest and posttest dyspnea severity and leg
tiredness were evaluated with Modified Borg Scale [18].
Quality of life and sleep
Quality of life was assessed by two questionnaires as OSA
specific measures and a general health-related quality of life
questionnaire. Functional Outcomes of Sleep Questionnaire
(FOSQ), which has been developed specifically for patients
with sleep disorders leading to excessive sleepiness. FOSQ-tr
was applied in a decreased 26-item Turkish version without
the sexual functioning subscale [26].
The general health-related quality of life was assessed
using the Short Form-36 (SF-36) questionnaire. As well as
a transition question, the SF-36 consists of eight multi-item
dimensions, which are physical functioning, role physical
(role limitations due to physical problems), vitality, social
functioning, role emotional (role limitation due to emotion-
al problems), bodily pain, general health, and mental health.
Each of the dimensions is scored from 0 to 100, with higher
scores indicating better health-related quality of life. The
Sleep Breath (2011) 15:49–56 51

Page 4

SF-36 was administered during a face-to-face interview by
the physiotherapist [27].
Daytime sleepiness evaluation
The subjective sleepiness was assessed using Turkish
Epworth Sleepiness Scale (ESS). The ESS is a question-
naire containing eight items that shows the likelihood of
dozing during typical daytime activities. The dozing
probability ranges from 0 (never) to 3 (high probability).
Normal values range from 2 to 10, with scores >10
indicating daytime sleepiness [28].
Polysomnography
Polysomnography (PSG) evaluation of at least 8 h was
performed on Embla A 10 (Flaga, Reyjavick, Iceland) and
Schwarzer Comlab 32 polysomnographic device (Comlab 32;
Schwarzer Medical Diagnostic Equipment, Baermannstr,
Germany) sleep systems. The following variables were
monitored: four channel EEG (C3/A2-C4/A1-O1/A2-O2/A1
according to the 10–20 international electrode placement
system), right and left electrooculogram, chin electromyo-
gram, and electrocardiogram. Airflow was monitored by nasal
pressure cannula. Respiratory movements were assessed by
thoracic and abdominal strain gauges. Snoring was evaluated
with neck microphone. The oxygen saturation during sleep
was measured continuously using a pulse oxymetry. Leg
movements were recorded by left and right tibial electromyo-
grams. PSG recordings were scored according to the standard
criteria of Rechtschaffen and Kales in 30-s epochs [29].
Data analysis
Statistical analyses of data obtained before and after the
treatment were performed with "SPSS for Windows Ver
11.0" software. Wilcoxon signed rank test was used to
compare the pre- and post-treatment data of the study
groups and chi-square test to compare determined changes
and Mann–Whitney U test to compare the groups.
Statistical significance level was chosen as p values less
than 0.05.
Results
Twenty-five patients were randomized as exercise and
control group and were screened. Twenty patients complet-
ed the trial. Data were presented for the control group (CG;
n=10 patients) and exercise group (EG; n=10 patients). All
of the ten patients in the exercise group participated the
training. No problems occurred during the exercises.
Characteristics of the subjects
Baseline characteristics of the subjects for each group are
presented in Table 1. There were no significant differences
in height and weight (P>0.05). Patients in CG (48.0±
7.49 years) were slightly younger than those in the EG
(54.40±6.57 years; P<0.05).
In regard to exercise habits of the subjects, seven subjects
in the exercise group (70%) and nine subjects in the control
group (90%) were found not to physically exercise at all. No
statistically significant difference was found between the
control and exercise groups in exercise and smoking habits
(χ2=1.25, P=0.26; χ2=2.80, P=0.25; Table 1).
Physical changes
BMI, body fat percentage (BF percentage), skinfold
thickness, neck and waist girth measures, and waist-to-hip
ratios were similar in both groups at the baseline and the
end of the 12-week program (P>0.05). The patients'
anthropometric parameters did not change significantly
during the exercise period (P>0.05; Table 2).
Respiratory parameter results
At the baseline, there were no significant differences in all of
the pulmonary function tests, except FEV1/FVC ratio, Pimax,
Exercise group n=10Control group n=10P value
Age (year)
Height (cm)
Weight (kg)
Percentage of current smoker
Percentage of Never
Percentage of former Smoker
Regular exercise
Not regularly exercise
54.40 (6.57)
170.40(6.17)
86.40(8.04)
30.0
60.0
10.0
30
70
48.0 (7.49)
176.60(5.40)
88.47(16.24)
30.0
30.0
40.0
10
90
0.04a
0.40a
0.70a
0.25b
0.26b
Table 1 Baseline subject
characteristics of patients with
OSAS
Data are presented as mean±
standard deviation
BMI body mass index
aP values were derived by
Mann–Whitney U test
bP values were derived by chi-
square test
52 Sleep Breath (2011) 15:49–56

Page 5

and Pemax between the EG and CG. There were increases in
FVC percentage and FEV1/FVC ratio, but unchanged in
Pimax-Pemax and respiratory parameters after exercise. All
pulmonary parameters were the same in both groups (P<
0.05), while the FEV1/FVC ratio was significantly higher in
the CG on follow-up (P>0.05; Table 3).
Responses to the exercise testing
Dyspnea severity after the test was higher in the exercise
group than in the control group at first exercise test (P<0.05).
Significant improvements in MaxVO2, metabolic equivalent
of task (MET), and maximal work load were noted on
follow-up exercise testing in the exercise group (P<0.05).
The dyspnea and leg fatigue severity was the same before
and after the exercise program. However, after the exercise
test, the dyspnea and leg fatigue severity were significantly
decreased (P<0.05). In the control group, they did not
change after exercise test at week 12 (P>0.05). In control
evaluation of the subjects included and not included in the
exercise program, maximal tolerated load was significantly
higher and dyspnea severity perceived following the test was
significantly lower in the exercise group (P<0.01; Table 3).
Quality of life and sleep outcomes
Baseline SF-36 and ESS scores (Table 4) were same in both
groups (P>0.05). However, activity level scores of the
Table 2 Anthropometric changes
Exercise group Control groupP**
Pre PostP* Pre PostP*
BMI (kg/m2)
Neck circumference (cm)
Waist circumference (cm)
Waist-hip ratio
Body density
Body fat percentage (%)
29.79 (2.66)
41.15 (1.53)
104.25 (5.51)
0.97 (3.33)
1.03 (9.38)
28.41 (4.01)
29.20 (3.07)
42.15 (2.79)
104.45 (6.85)
0.97 (3.24)
1.04 (7.7)
26.87 (3.27)
0.17
0.31
0.88
0.79
0.17
0.17
28.42 (5.42)
41.30 (3.47)
103.5 (14.83)
0.96 (6.30)
1.04 (7.23)
24.84 (3.06)
28.28 (5.52)
41.60 (3.10)
101.25 (11.57)
0.96 (5.59)
1.04 (5.65)
25.81 (2.40)
0.89
0.47
0.21
0.96
0.29
0.29
0.41
0.54
0.16
0.33
0.50
0.53
Data are presented as mean±standard deviation
BMI body mass index
*P<0.05, Wilcoxon signed rank test
**P<0.05, Mann–Whitney U test
Table 3 Results of pulmonary function tests and the exercise test
Exercise groupControl groupP**
Pre PostP* PrePostP*
FEV1% predictive
FVC% predictive
FEV1/FVC%
PE(cmH2O)
Pİ(cmH2O)
MaxVO2(mL/min)
MET
Maximum work load (W)
104.3 (10.65)
108.50 (12.06)
77.0 (4.69)
122.40 (16.60)
91.90 (31.46)
15.38 (3.58)
4.40 (1.00)
112.50 (35.54)
96.60 (17.57)
98.60 (18.90)
78.80 (3.80)
117.40 (23.37)
90.20 (31.51)
17.48 (5.63)
5.37 (1.04)
155.00 (18.11)
0.13
0.05
0.04
0.67
0.88
0.02
0.02
0.02
112.50 (22.03)
105.80 (16.85)
85.50 (4.93)
113.00 (33.40)
89.20 (36.22)
16.6 (4.87)
4.76 (1.40)
141.50 (35.90)
103.40 (25.00)
99.40 (21.92)
83.70 (4.74)
113.00 (33.40)
96.90 (44.88)
18.37 (3.52)
5.27 (1.01)
147.50 (25.50)
0.11
0.11
0.19
0.58
0.14
0.31
0.26
0.31
0.62
0.94
0.05
0.68
0.97
0.47
0.47
0.40
Data are presented as mean±standard deviation
FEV1 forced expiratory volume in 1 s as a percent of the predicted, FVC forced vital capacity as a percent of the predicted, FEV1/FVC forced
expiratory volume in the first second as a percent of the predicted value/forced vital capacity, Pimax maximal inspiratory pressure, Pemax maximal
expiratory pressure, Max VO2 maximal oxygen consumption, MET metabolic equivalents
*P<0.05, Wilcoxon signed rank test
**P<0.05, Mann–Whitney U test
Sleep Breath (2011) 15:49–56 53