Lung (2014) 192:175184
DOI 10.1007/s00408-013-9511-3
SLEEP APNEA
Effects of Exercise Training on Sleep Apnea: A Meta-analysis
Imran H. Iftikhar Christopher E. Kline
Shawn D. Youngstedt
Received: 3 May 2013 / Accepted: 10 September 2013 / Published online: 29 September 2013
 Springer Science+Business Media New York 2013
Abstract
Background Several studies have shown a favorable
effect of supervised exercise training on obstructive sleep
apnea (OSA). This meta-analysis was conducted to analyze
the data from these studies on the severity of OSA (primary
outcome) in adults. Secondary outcomes of interest inclu-
ded body mass index (BMI), sleep efficiency, daytime
sleepiness and cardiorespiratory fitness.
Methods Two independent reviewers searched PubMed
and Embase (from inception to March 6, 2013) to identify
studies on the effects of supervised exercise training in
adults with OSA. Pre- and postexercise training data on our
primary and secondary outcomes were extracted.
Results A total of 5 studies with 6 cohorts that enrolled a
total of 129 study participants met the inclusion criteria.
Electronic supplementary material The online version of this
article (doi:10.1007/s00408-013-9511-3) contains supplementary
material, which is available to authorized users.
I. H. Iftikhar (&)
Division of Pulmonary, Critical Care and Sleep Medicine,
Department of Medicine, University of South Carolina,
One Richland Medical Park, Suite 300, Columbia,
SC 29203, USA
e-mail: Imran.Iftikhar@uscmed.sc.edu
C. E. Kline
Department of Psychiatry, University of Pittsburgh School
of Medicine, Pittsburgh, PA, USA
e-mail: klinec@upmc.edu
S. D. Youngstedt
Departments of Exercise Science and Psychology,
University of South Carolina, Columbia, SC, USA
e-mail: syoungst@mailbox.sc.edu
S. D. Youngstedt
WJB Dorn VA Medical Center, Columbia, SC, USA
The pooled estimate of mean pre- to postintervention
(exercise) reduction in AHI was -6.27 events/h (95 %
confidence interval [CI] -8.54 to -3.99; p \ 0.001). The
pooled estimates of mean changes in BMI, sleep efficiency,
Epworth sleepiness scale and VO2 peak were -1.37 (95 %
CI -2.81 to 0.07; p = 0.06), 5.75 % (95 % CI 2.479.03;
p = 0.001), -3.3 (95 % CI -5.57 to -1.02; p = 0.004),
and 3.93 mL/kg/min (95 % CI 2.445.42; p \ 0.001),
respectively.
Conclusions This meta-analysis shows a statistically
significant effect of exercise in reducing the severity of
sleep apnea in patients with OSA with minimal changes in
body weight. Additionally, the significant effects of exer-
cise on cardiorespiratory fitness, daytime sleepiness, and
sleep efficiency indicate the potential value of exercise in
the management of OSA.
Keywords Exercise
Obstructive sleep apnea

Cardiorespiratory fitness
Daytime sleepiness
Introduction
Obstructive sleep apnea (OSA) is a common medical
condition characterized by repetitive upper airway obstruc-
tion during sleep [1, 2]. OSA is linked to a wide range of
adverse health consequences, including daytime sleepiness,
cognitive impairment, and several cardiovascular and
metabolic disorders [3, 4].
The American Academy of Sleep Medicine recom-
mends the use of continuous positive airway pressure
(CPAP) [5] or oral appliances for treating mild to moderate
OSA, whereas CPAP is recommended as the first-line and
oral appliances as second-line treatments for severe OSA
patients [6]. Although highly efficacious when used, the
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176
utility of CPAP is limited by poor patient adherence to
CPAP. Other treatment options for OSA include weight
loss [79] and upper airway surgery [10, 11]. However, the
effects of weight loss on the severity of OSA could be
delayed [12]. Surgical modifications of the upper airway
for the treatment of OSA continue to evolve, and the data
are not as robust due to the relative paucity of randomized,
controlled trials (RCTs) [13].
Exercise training in patients with sleep apnea has
received accelerated attention. Not only has exercise been
shown to be effective in improving OSA, but it also has
been found to decrease the severity of central sleep apnea
in chronic heart failure patients [14, 15]. Moreover, exer-
cise could be uniquely helpful to ameliorate numerous
sequalae of OSA, including cardiovascular disease,
impaired glucose tolerance, and fatigue. Additionally,
analyses from a large community-based cohort showed that
vigorous physical activity was associated with a decrease
in the prevalence of OSA [16]. The mechanisms by which
exercise training leads to improvement in OSA are not
well-understood. Of course, exercise could reduce OSA
indirectly by facilitating decreases in body weight and fat.
However, epidemiologic [17, 18] and experimental studies
[1921] have shown that the effect of exercise on sleep
apnea is independent of body weight reduction. Besides the
beneficial effects on OSA severity, regular physical activity
also has been found to be associated with subjective well
being in patients with OSA irrespective of the severity [22].
The primary purpose of this study was to evaluate the
efficacy of exercise training on OSA severity reduction in
adults with OSA. Secondary objectives were to evaluate
the effects of exercise training on body mass index (BMI),
sleep efficiency, daytime sleepiness, and cardiorespiratory
fitness. In much of the literature on the effects of exercise
on OSA, the degree to which participants indeed exercised
or were encouraged to do so has often been unclear.
Therefore, the present meta-analysis was restricted to
studies that documented exercise training via improve-
ments in cardiorespiratory fitness.
Methods
This meta-analysis was performed according to the
guidelines reported in meta-analysis of observational
studies in epidemiology [23] and preferred reporting items
for systematic reviews and meta-analyses statements [24].
Search Strategy and Selection Criteria
We searched PubMed and Embase databases from their
inception to March 6, 2013. We used combinations of the
following keywords: exercise, obstructive sleep apnea, data were specifically requested from the corresponding
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Lung (2014) 192:175184
and sleep-disordered breathing. The search from PubMed
yielded all the studies included in this meta-analysis. To
ensure a thorough search of the literature, we hand-searched
the reference lists of the included studies and previously
published meta-analyses [25, 26] on lifestyle interventions
and OSA severity. For inclusion in our meta-analysis, we
considered only those studies that reported exercise as a pri-
mary component of an intervention and also reported changes
in cardiorespiratory fitness. Inclusion criteria for RCTs
included a diagnosis of OSA and randomization to exercise
training or to control condition. The control condition could
include individuals who received either stretching exercises or
were left untrained. We excluded studies that reported addi-
tional intervention with CPAP. We also excluded studies that
reported data in median and interquartile range. If the required
data from articles were ambiguous or missing, we contacted
the study authors; after two unanswered attempts, we exclu-
ded these studies from the analysis.
Two investigators (IHI and CEK) independently searched
the studies and performed the final screening. In those
instances when there was a disagreement between the inves-
tigators, a third investigator (SDY) reviewed the article and
disagreements were resolved through discussion. Figure 1
summarizes the results of the selection and exclusion process.
Study Outcomes
Our primary study outcome was OSA severity, as mea-
sured by the apnea hypopnea index (AHI; i.e., number of
apnea or hypopnea events per hours of sleep). Secondary
outcomes included changes in BMI, sleep efficiency, day-
time sleepiness, and cardiorespiratory fitness. As a measure
of body mass, BMI was calculated as weight in kilograms
divided by height in meters squared. As an indicator of
overall sleep quality, sleep efficiency was measured by
overnight polysomnography and expressed as a percentage
of time in bed that was spent asleep. Subjective daytime
sleepiness was measured by the Epworth Sleepiness Scale
[27]. Cardiorespiratory fitness was indicated by peak oxy-
gen consumption (VO2 peak, measured in mL/kg/min)
obtained during a graded cardiopulmonary exercise test.
Data Abstraction
Data were extracted on a prespecified worksheet. This inclu-
ded first authors name, year of publication, number of par-
ticipants, mean of pre- and postexercise training AHI, BMI,
sleep efficiency, Epworth Sleepiness Scale, and VO2 peak
with standard deviations. One study reported separate data for
the two exercise intervention arms (aerobic exercise and
combined aerobic/resistance exercise) [28]; as a result, these
two groups were separately analyzed in our analyses. Some
Lung (2014) 192:175184
Fig. 1 Flow diagram of articles identified and evaluated during the
study selection process
authors of two studies included in our meta-analysis [20, 28].
Kline et al. [20] confirmed that Epworth Sleepiness Scale and
cardiorespiratory fitness data were published separately from
the included study [29, 30]. The authors of two studies pro-
vided additional BMI data for their study populations [19, 26].
One of the studies reported cardiorespiratory fitness data as
metabolic equivalents (METs) [31]. Therefore, we trans-
formed the data to peak relative oxygen consumption using
the following equation: 1 MET = 3.5 mL O2/kg/min. Five of
the study participants in one study [31] used CPAP during the
intervention. Because individual pre- and postexercise train-
ing AHI data were provided, for our meta-analysis on the
effects of exercise training on AHI, we excluded the data of
those who concurrently used CPAP.
Quantitative Data Synthesis
The mean changes in the outcomes from exercise training
along with their 95 % confidence intervals (CIs) were
177
estimated by pooling available data using comprehensive
meta analysis software version 2.2.064. Results are dis-
played in the form of forest plots (Figs. 2, 3, 4, 5, 6).
Similarly, we also conducted separate analyses of the dif-
ference in each outcome between control and exercise
groups in RCTs. We conducted both random-effects
methods and fixed-effects meta-analyses to account for
variance between and within the studies, respectively [32].
However, we chose to include the results from the random-
effects method to account for any heterogeneity within and
between the studies. Statistical heterogeneity was assessed
with the I2 statistic [33]. An I2 [ 60 % indicated significant
heterogeneity. We also performed sensitivity analyses to
assess the influence of each study on estimates of the
overall effect. This was done separately for the pooled
estimates of change in AHI, BMI, sleep efficiency, and
VO2 peak. To check for publication bias, we constructed
funnel plots of effect size and standard error [32, 34] and
also analyzed results by using the Begg and Mazumdar
rank correlation test [35].
Results
We reviewed 498 citations and identified 5 studies [19, 20,
26, 29, 31] for inclusion in our meta-analysis (Fig. 1). Our
search strategy yielded three studies that used exercise as
the sole intervention [20, 21, 28]. In two other studies,
exercise was the primary intervention but study partici-
pants also underwent some dietary intervention [31, 36].
Altogether, these studies enrolled a total of 129 partici-
pants. Table 1 outlines the baseline characteristics of the
population in each study. Table 2 summarizes the exercise
interventions used in each study. On average, study par-
ticipants were [42 years old and had a mean BMI [ 26.
The duration of exercise intervention lasted between 12
and 24 weeks. There were three RCTs [20, 21, 28] and two
single group intervention studies [31, 36]. Two [20, 31] of
the studies were conducted in the United States, one [21] in
Turkey, one [28] in Brazil, and one [36] in Australia.
Effect on Primary Outcome
The effect of exercise training on our primary outcome,
AHI, was assessed by using two approaches. First, the pre-
to postintervention analysis of five studies (six cohorts)
showed a pooled estimate of mean change in AHI of -6.27
events/h (95 % CI -8.54 to -3.99; p \ 0.001) with an
I2 = 0 % (Fig. 2), which reflected a 32 % reduction in
AHI from baseline in the intervention groups. Second, a
separate analysis of the data from three RCTs showed an
AHI reduction of 7.17 (95 % CI -1.86 to -12.48;
p = 0.008) in favor of the exercise groups, with an
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178 Lung (2014) 192:175184

Study name Statistics for each study Difference in means and 95% CI
Difference Standard Lower Upper
in means error limit limit
Kline 2011 -7.578 2.499 -12.475 -2.681
Sengul 2011 -4.180 1.694 -7.500 -0.860
Servantes 2011 (Aerobic) -8.500 5.405 -19.094 2.094
Servantes 2011 (Aerobic+Strength training) -10.000 3.739 -17.328 -2.672
Barnes 2009 -6.300 3.450 -13.061 0.461
Norman 2000 -10.100 4.687 -19.287 -0.913
-6.272 1.159 -8.544 -3.999

-20.00 -10.00 0.00 10.00 20.00

Decrease in AHI Increase in AHI

Mean difference= -6.272 (95% CI: -8.544 to -3.999), p = 0.000

Fig. 2 Forest plot for the change in AHI following exercise. The diamond reflects the 95 % confidence interval of the pooled estimate of mean
difference. AHI apnea hypopnea index CI confidence intervals

Study name Statistics for each study Difference in means and 95% CI
Difference Standard Lower Upper
in means error limit limit
Kline 2011 -0.294 0.213 -0.711 0.123
Sengul 2011 -0.590 0.913 -2.379 1.199
Servantes 2011 (Aerobic) -0.200 1.091 -2.339 1.939
Servantes 2011 (Aerobic+Strength training) -0.660 1.028 -2.675 1.355
Barnes 2009 -6.000 1.227 -8.405 -3.595
Norman 2000 -1.600 1.501 -4.542 1.342
-1.374 0.737 -2.818 0.070

-9.00 -4.50 0.00 4.50 9.00

Decrease in BMI Increase in BMI

Mean difference= -1.374 (95% CI: -2.818 to -0.070), p = 0.062

Fig. 3 Forest plot for the change in BMI following exercise. The diamond reflects the 95 % confidence interval of the pooled estimate of mean
difference. BMI body mass index CI confidence intervals

Study name Statistics for each study Difference in means and 95% CI
Difference Standard Lower Upper
in means error limit limit
Kline 2011 0.896 1.742 -2.519 4.311
Sengul 2011 5.770 3.831 -1.739 13.279
Servantes 2011 (Aerobic) 5.200 3.015 -0.709 11.109
Servantes 2011 (Aerobic+Strength training) 5.600 2.665 0.377 10.823
Barnes 2009 9.400 2.835 3.844 14.956
Norman 2000 10.700 3.478 3.884 17.516
5.756 1.675 2.474 9.039

-18.00 -9.00 0.00 9.00 18.00

Decrease in SE Increase in SE

Mean difference= -5.756 (95% CI: 2.474 to 9.039), p = 0.001

Fig. 4 Forest plot for the change in sleep efficiency following exercise. The diamond reflects the 95 % confidence interval of the pooled estimate
of mean difference. SE sleep efficiency CI confidence intervals

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Lung (2014) 192:175184 179

Study name Statistics for each study Difference in

means and 95% CI
Difference Standard Lower Upper
in means error limit limit
Kline 2011 -2.444 0.930 -4.266 -0.622
Sengul 2011 -1.200 2.027 -5.173 2.773
Barnes 2009 -2.700 1.371 -5.388 -0.012
Norman 2000 -5.500 0.267 -6.024 -4.976
-3.303 1.161 -5.579 -1.028
-8.00 -4.00 0.00 4.00 8.00
Decrease in ESS Increase in ESS

Mean difference= -3.303 (95% CI: -5.579 to -1.028), p = 0.004

Fig. 5 Forest plot for the change in Epworth Sleepiness Scale following exercise. The diamond reflects the 95 % confidence interval of the
pooled estimate of mean difference. ESS Epworth Sleepiness Scale CI confidence intervals

Study name Statistics for each study Difference in means and 95% CI
Difference Standard Lower Upper
in means error limit limit
Kline 2011 2.246 0.547 1.175 3.317
Sengul 2011 2.100 1.561 -0.959 5.159
Servantes 2011 (Aerobic) 5.200 0.932 3.373 7.027
Servantes 2011 (Aerobic+Strength training) 5.300 0.894 3.548 7.052
Barnes 2009 3.800 1.258 1.334 6.266
Norman 2000 6.650 2.931 0.906 12.394
3.935 0.761 2.444 5.426

-13.00 -6.50 0.00 6.50 13.00

Decrease in VO2 peak Increase in VO2 peak

Mean difference= 3.935 (95% CI: 2.444 to 5.426), p = 0.000

Fig. 6 Forest plot for the change in VO2 peak following exercise. The diamond reflects the 95 % confidence interval of the pooled estimate of
mean difference. VO2 peak cardiorespiratory fitness measured as peak oxygen consumption in mL/kg/min. CI confidence intervals

I2 = 0 %. This effect corresponded to an improvement in significant change in BMI (-1.37; 95 % CI -2.81 to

AHI by 42 % following exercise compared with the control
treatments (Table 3). The I2 statistic for these analyses
showed no significant heterogeneity.
Effect on Secondary Outcomes
Data for the secondary outcomes of BMI, sleep efficiency,
and VO2 peak were available for five studies (6 cohorts),
whereas Epworth Sleepiness Scale data were available for
four studies. The analyses showed significant improvements
following exercise training for sleep efficiency (5.75 %;
95 % CI 2.479.03; p = 0.001, I2 = 53.29 %), VO2 peak
(3.93 mL/kg/min; 95 % CI 2.445.42; p \ 0.001, I2 =
65.89 %) and for Epworth Sleepiness Scale scores (-3.3;
95 % CI -5.57 to -1.02; p = 0.004, I2 = 82.52 %) but no
0.07; p = 0.06, I2 = 76.92 %). These results are shown in
the form of forest plots (Figs. 3, 4, 5, 6). The I2 statistic
for these analyses showed moderate to high heterogeneity.
The results corresponded to an improvement of 8 % in
sleep efficiency, 24.6 % in VO2 peak, and 28 % in Ep-
worth Sleepiness Scale scores compared with baseline
following intervention. Similar results were obtained from
separate analyses of the data from RCTs (Table 3). These
results showed that, compared with the controls, there was
a significant increase in VO2 peak and sleep efficiency in
the exercise groups, but BMI did not decrease signifi-
cantly. These effects corresponded to an improvement in
VO2 peak and sleep efficiency by 17.65 and 5.8 %
respectively, following exercise compared with the control
treatments.

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Sensitivity Analysis

Aerobic exercise: 25.2 (24.7)

Aerobic and resistance
exercise: 26.4 (17.6)
Sensitivity analyses, done by systematically removing one
Exercise: 32.2 (29.0)

Exercise: 15.19 (5.4)

Control: 17.92 (6.4)
Control: 24.4 (22.4)

Control: 22.8 (17.4)

study at a time, demonstrated that no single study changed
AHI, mean (SD)

the statistical significance of the overall results.

24.6 (12.0)

28.0 (17.9)
Publication Bias

The Begg and Mazumdar rank correlation tests of funnel

Aerobic exercise: 26.87 (4.6)

plots for the analyses on AHI, BMI, sleep efficiency, VO2

peak, and Epworth Sleepiness Scale did not show any
Aerobic and resistance
exercise: 27.98 (4.4)

publication bias (see Supplementary Material, only funnel

Exercise: 29.79 (2.6)
Control: 28.42 (5.4)

Control: 27.73 (3.6)

Exercise: 35.5.(6.2)
Control: 33.6 (5.6)

plot for data on pre- and post-AHI is provided).

BMI, mean (SD)

36.1 (4.3)

31.2 (4.6)

Discussion

Our findings indicate that exercise training has a statisti-

Aerobic exercise: 51.76 (9.8)

cally significant effect on AHI that seems to be indepen-

dent of changes in BMI. An important finding of our meta-
Aerobic and resistance
exercise: 50.82 (9.4)

analysis is that the reduction in OSA severity was achieved

Exercise: 47.6 (6.7)

Exercise: 54.4 (6.5)

Control: 45.9 (8.8)

Control: 48.0 (7.4)

Control: 53.0 (8.1)

without a significant reduction in body weight. This sug-

Age, mean (SD)

gests a possible role of exercise in the treatment of sleep

BMI body mass index, SD standard deviation, AHI apnea hypopnea index, RCT randomized controlled trial
42.3 (10.4)

apnea. Using a pre- to postintervention model and pooling

the mean differences in AHI across the studies, we found
48 (9)

that exercise training resulted in a mean AHI reduction of

6.27 events/h. Limiting the results to studies that used
Aerobic exercise: 17 (47.1 %)

exercise as the sole intervention and using change scores to

calculate the difference in AHI between the cohorts that
exercise: 17 (47.1 %)
Number of participants

Aerobic and resistance

received exercise as an intervention and the controls, we

Exercise: 10 (100 %)
Control: 10 (100 %)

Control: 11(45.5 %)
Exercise: 27 (56 %)
Control: 16 (56 %)

found a similar reduction in AHI. Our meta-analysis shows

that BMI did not change with exercise, but there was a
(% of males)

9 (88.8 %)

significant improvement in sleep efficiency and daytime

12 (25 %)

sleepiness.
The AHI reduction seen in our meta-analysis seems
modest compared with similar meta-analyses that evalu-
ated the effects of dietary weight loss, surgery, oral
Duration of

12 weeks

12 weeks

12 weeks

16 weeks

24 weeks

appliances, and CPAP on OSA severity. Anandam et al.

exercise

[25], in a meta-analysis of studies on dietary weight loss

intervention showed a reduction in AHI by 23.1 events/h
(95 % CI 8.937.3, p = 0.001) corresponding to a 44 %
Table 1 Baseline characteristics of studies

intervention study

intervention study

reduction compared with baseline. In another meta-ana-

lysis, oral appliances were found to reduce AHI by 12.07
Study design

Single group

Single group

events/h (95 % CI -9.7 to -14.3, p \ 0.01), suggesting an

improvement of 60.25 % postintervention [37]. Finally,
RCT

RCT

RCT

Greenburg et al. [38] showed that bariatric surgery reduced

AHI by 38.2 events/h (95 % CI 31.9-44.4), possibly sug-
2011

2011

2011

2009

2000
Year

gesting a 71.11 % improvement compared to baseline.

An important finding of our meta-analysis is that the
Norman et al.
Sengul et al.

Barnes et al.

reduction in OSA severity was achieved without a signif-

et al. [28]
Kline et al.

Servantes

icant reduction in body weight. This is an important dis-

Author

[20]

[21]

[36]

[31]

tinction, as epidemiologic research estimates that a

reduction in body weight of approximately 10 % would be

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 Table 2 Characteristics of exercise intervention used in studies
Study Description of study intervention Level of supervision
Lung (2014) 192:175184

Kline et al. [20] 150 min/week of aerobic exercise (treadmill, elliptical trainer, or recumbent bicycle), All exercise sessions were supervised by staff trained in exercise
performed at 60 % of heart rate reserve, spread across 4 days/week for 12 week physiology
On 2 days/week for 12 week, aerobic exercise was followed by resistance exercise,
consisting of 2 sets of 1012 repetitions for 8 different exercises
Sengul et al. [21] Breathing exercises (1530 min/session) on 3 days/week for 12 week All exercise sessions were supervised by a single physiotherapist
Aerobic exercise (treadmill, bicycle ergometer) performed at 6070 % of VO2 peak
for 6090 min/session on 3 days/week for 12 week
Servantes et al. [28] Group I (aerobic exercise only): First three sessions were supervised by a physiotherapist and a
3045 min of aerobic exercise each session, performed at a heart rate corresponding cardiologist; remaining 12 week of sessions were home-based
to the anaerobic threshold for 12 week (3 sessions/week for weeks 18, 4 sessions/
week for weeks 912)
Group II (aerobic exercise and resistance exercise):
3045 min of aerobic exercise each session, performed at a heart rate corresponding
to the anaerobic threshold for 12 week (3 sessions/week for weeks 18, 4 sessions/
week for weeks 912)
Resistance exercise, consisting of 1 set of 1216 repetitions for 7 different exercises,
performed for 12 week (3 sessions/week for weeks 18, 4 sessions/week for weeks
912)
Barnes et al. [36] Resistance exercise, consisting of 3 sets of 812 repetitions for 7 different exercises During weeks 18, 3 sessions/week were supervised by an exercise
performed at 80 % of 1repetition maximum, conducted on 3 days/week for 16 week physiologist, with an additional 24 unsupervised home sessions/
Beginning in week 5, aerobic exercise (cycling, walking, or jogging) up to 40 min/ week being expected; during week 916, at least 1 session/week was
session at 80 % of VO2peak on 5 days/week for 12 week supervised, with 45 home sessions/week expected
Very low calorie diet for 16 week, consisting of a meal-replacement program that
initially replaced 3 meals/day and gradually reduced to 1 daily meal replacement
Norman et al. [31] 3045 min of aerobic exercise (primarily treadmill or stationary cycle) performed at During months 14, all exercise sessions were supervised in university
6085 % of heart rate reserve on 3 days/week for 24 week wellness center; during months 56, 1 session/week was supervised
Instructed on different resistance exercises that could be incorporated into their
conditioning program
Received a single individual dietary consultation with a dietitian at study entry
181

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Table 3 Difference in outcomes between control and exercise groups
in randomized, controlled trials
Outcomes Mean difference p value
AHI (events/h) -7.174 (95 % CI: -1.867 to 0.008
-12.482)
BMI (kg/m2) -0.573 (95 % CI: -1.34 to 2.486) 0.557
Sleep efficiency % 6.188 (95 % CI: 2.021 to 10.354) 0.004
VO2 peak 5.695 (95 % CI: 1.698 to 9.692) 0.005
(mL/kg/min)
AHI apnea hypopnea index, BMI body mass index, VO2 peak car-
diorespiratory fitness, CI confidence interval
necessary to achieve the 2530 % reduction in OSA
severity that we documented with exercise [7]. Further-
more, complete amelioration of OSA is not necessary to
obtain significant health benefits; even modest differences
in OSA severity have been associated with significantly
reduced risk of adverse health outcomes (e.g., hyperten-
sion) [37]. Finally, whereas CPAP and oral appliances are
dependent upon nightly use to obtain the effects, evidence
indicates that exercise training elicits chronic reduction in
the severity of OSA [19].
Besides changes in OSA severity, the improvements in
secondary outcomes following exercise training are note-
worthy. The improvement in cardiorespiratory fitness has
unique health and longevity benefits [39]. Moreover, the
improvement in sleep efficiency with exercise is similar to
what is typically achieved with CPAP [40, 41]. Likewise,
the effects on daytime sleepiness (as measured by the
Epworth Sleepiness Scale) with exercise training is similar
to that seen with CPAP [42, 43]. Therefore, although based
upon a small number of studies, these preliminary findings
suggest that the effects of exercise in adults with OSA
extend past AHI reduction.
Although converging evidence suggests beneficial
effects of exercise training on the severity of sleep apnea,
the current body of evidence remains inconclusive on the
exact mechanisms of these effects. Different theories have
been proposed. An earlier study in canines found increased
tone in the genioglossus muscle when the gastrocnemius
muscle and sciatic nerve were stimulated [44]. Later, two
studies in humans raised some interest in the possible role
of strength of respiratory muscles in relation to exercise
[31, 45]. However, contrary to this hypothesis, Sengul et al.
[21] found no change in the strength of respiratory muscles
in OSA patients who received breathing and aerobic
exercise training.
Some authors have also suggested that exercise can
lead to decreased leg fluid accumulation and, hence,
prevent the nocturnal rostral fluid shift that may be
implicated in upper airway collapse [4650]. This mech-
anism would more likely be associated with a potential
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Lung (2014) 192:175184
acute effect of exercise rather than a training effect,
which could nevertheless be important if repeated fre-
quently. However, a recent study by Jafari and Mohsenin
[51] casts some doubt on this study, as they found no
progressive worsening in OSA despite a demonstrable
fluid shift overnight.
Slow wave sleep (SWS) has been found to be associated
with decreased severity of sleep apnea [52, 53]. In the
study by McSharry et al. [53] this effect was thought to be
related to the increased genioglossus single motor unit
activity during SWS, making the airway more stable and
resistant to collapse. It also is known that exercise training
is associated with increased SWS [15]. Is it possible that
the effects of exercise on reducing sleep apnea severity
could be related to the protective effects of SWS that it
induces?. Proving such a relationship in a well designed
study would indeed be more insightful. However, it is
possible that no single mechanism is responsible and per-
haps there is a complex interplay of factors associated with
exercise training that leads to improvement in the severity
of sleep apnea.
Our meta-analysis has numerous strengths. First, our
analysis had enough power to detect an effect of exercise
intervention in the included studies. Given a total of 87
participants that received exercise intervention, we esti-
mate that our meta-analysis had a power of 100 % to detect
a change in AHI of 12.8 assuming a standard deviation of
nine. Second, there was no evidence of publication bias by
funnel plots. Third, our sensitivity analyses showed no
significant change in the overall statistical significance of
the results. Fourth, the analysis for the change in AHI
based on the pre- and postintervention effects of exercise
showed no significant heterogeneity. Finally, our study
showed that significant effects from exercise training
occurred despite the fact that studies differed in the mode,
frequency, intensity, compliance, and levels of supervision
of the exercise interventions.
However, there also are limitations to our study. Most of
the studies had a small sample size and the length of
intervention in most studies ranged from 12 to 24 weeks.
Therefore, this meta-analysis does not address the long-
term efficacy of exercise training on OSA severity. With so
few studies thus far, it was not possible to evaluate which
exercise characteristics were associated with more favor-
able OSA outcomes. It also is a limitation of our study that
the data on secondary outcomes had moderate to high
heterogeneity.
In conclusion, our meta-analysis demonstrates that
exercise training leads to a significant reduction in AHI,
improvement in sleep efficiency, and daytime sleepiness,
independent of the effects on BMI. Although the effect size
in AHI reduction seems smaller compared with CPAP and
oral appliances, exercise training may be an ideal adjunct
Lung (2014) 192:175184
therapy, especially considering its effects on sleep effi-
ciency and daytime sleepiness. Given the preliminary
nature of our findings, RCTs involving a larger number of
participants and longer duration of intervention are needed
to determine whether the beneficial effects of exercise
training in patients with sleep apnea can be sustained over a
longer period of time.
Acknowledgment This work was supported in part by HL78566 (to
SDY) and HL082610 (to CEK).
Conflict of interest The authors report no potential conflicts of
interest with any companies/organizations whose products or services
may be discussed in this article.
References
1. Young T, Peppard PE, Gottlieb DJ (2002) Epidemiology of
obstructive sleep apnea: a population health perspective. Am J
Respir Crit Care Med 165(9):12171239
2. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S (1993)
The occurrence of sleep-disordered breathing among middle-aged
adults. N Engl J Med 328(17):12301235
3. Parish JM, Somers VK (2004) Obstructive sleep apnea and car-
diovascular disease. Mayo Clin Proc 79(8):10361046
4. Levinson PD, McGarvey ST, Carlisle CC, Eveloff SE, Herbert
PN, Millman RP (1993) Adiposity and cardiovascular risk factors
in men with obstructive sleep apnea. Chest 103(5):13361342
5. Kushida CA, Littner MR, Hirshkowitz M, Morgenthaler TI,
Alessi CA, Bailey D et al (2006) Practice parameters for the use
of continuous and bilevel positive airway pressure devices to treat
adult patients with sleep-related breathing disorders. Sleep 29(3):
375380
6. Kushida CA, Morgenthaler TI, Littner MR, Alessi CA, Bailey D,
Coleman J Jr et al (2006) Practice parameters for the treatment of
snoring and obstructive sleep apnea with oral appliances: an
update for 2005. Sleep 29(2):240243
7. Peppard PE, Young T, Palta M, Dempsey J, Skatrud J (2000)
Longitudinal study of moderate weight change and sleep-disor-
dered breathing. JAMA 284(23):30153021
8. Schwartz AR, Gold AR, Schubert N, Stryzak A, Wise RA, Per-
mutt S et al (1991) Effect of weight loss on upper airway col-
lapsibility in obstructive sleep apnea. Am Rev Respir Dis 144(3
Pt 1):494498
9. Smith PL, Gold AR, Meyers DA, Haponik EF, Bleecker ER
(1985) Weight loss in mildly to moderately obese patients with
obstructive sleep apnea. Ann Intern Med 103(6 Pt 1):850855
10. Bridgman SA, Dunn KM (2000) Surgery for obstructive sleep
apnoea. Cochrane Database Syst Rev 2:CD001004
11. Sundaram S, Bridgman SA, Lim J, Lasserson TJ (2005) Surgery
for obstructive sleep apnoea. Cochrane Database Syst Rev
4:CD001004
12. Morgenthaler TI, Kapen S, Lee-Chiong T, Alessi C, Boehlecke
B, Brown T et al (2006) Practice parameters for the medical
therapy of obstructive sleep apnea. Sleep 29(8):10311035
13. Aurora RN, Casey KR, Kristo D, Auerbach S, Bista SR, Chow-
dhuri S et al (2010) Practice parameters for the surgical modifi-
cations of the upper airway for obstructive sleep apnea in adults.
Sleep 33(10):14081413
14. Yamamoto U, Mohri M, Shimada K, Origuchi H, Miyata K, Ito K
et al (2007) Six-month aerobic exercise training ameliorates
183
central sleep apnea in patients with chronic heart failure. J Card
Fail 13(10):825829
15. Ueno LM, Drager LF, Rodrigues AC, Rondon MU, Braga AM,
Mathias W Jr et al (2009) Effects of exercise training in patients
with chronic heart failure and sleep apnea. Sleep 32(5):637647
16. Quan SF, OConnor GT, Quan JS, Redline S, Resnick HE, Shahar
E et al (2007) Association of physical activity with sleep-disor-
dered breathing. Sleep Breath 11(3):149157
17. Awad KM, Malhotra A, Barnet JH, Quan SF, Peppard PE (2012)
Exercise is associated with a reduced incidence of sleep-disor-
dered breathing. Am J Med 125(5):485490
18. Peppard PE, Young T (2004) Exercise and sleep-disordered
breathing: an association independent of body habitus. Sleep
27(3):480484
19. Giebelhaus V, Strohl KP, Lormes W, Lehmann M, Netzer N
(2000) Physical exercise as an adjunct therapy in sleep apnea: an
open trial. Sleep Breath 4(4):173176
20. Kline CE, Crowley EP, Ewing GB, Burch JB, Blair SN, Durstine
JL et al (2011) The effect of exercise training on obstructive sleep
apnea and sleep quality: a randomized controlled trial. Sleep
34(12):16311640
21. Sengul YS, Ozalevli S, Oztura I, Itil O, Baklan B (2011) The
effect of exercise on obstructive sleep apnea: a randomized and
controlled trial. Sleep Breath 15(1):4956
22. Hong S, Dimsdale JE (2003) Physical activity and perception of
energy and fatigue in obstructive sleep apnea. Med Sci Sports
Exerc 35(7):10881092
23. Stroup DF, Berlin JA, Morton SC, Olkin I, Williamson GD,
Rennie D et al (2000) Meta-analysis of observational studies in
epidemiology: a proposal for reporting. Meta-analysis of obser-
vational studies in epidemiology (MOOSE) group. JAMA
283(15):20082012
24. Liberati A, Altman DG, Tetzlaff J, Mulrow C, Gotzsche PC,
Ioannidis JP et al (2009) The PRISMA statement for reporting
systematic reviews and meta-analyses of studies that evaluate
health care interventions: explanation and elaboration. Ann Intern
Med 151(4):W65W94
25. Anandam A, Akinnusi M, Kufel T, Porhomayon J, El-Solh AA
(2013) Effects of dietary weight loss on obstructive sleep apnea: a
meta-analysis. Sleep Breath 17(1):227234
26. Thomasouli MA, Brady EM, Davies MJ, Hall AP, Khunti K,
Morris DH et al (2013) The impact of diet and lifestyle man-
agement strategies for obstructive sleep apnoea in adults: a sys-
tematic review and meta-analysis of randomised controlled trials.
Sleep Breath 17(3):925935
27. Johns MW (1991) A new method for measuring daytime sleep-
iness: the Epworth sleepiness scale. Sleep 14(6):540545
28. Servantes DM, Pelcerman A, Salvetti XM, Salles AF, de Albu-
querque PF, de Salles FC et al (2012) Effects of home-based
exercise training for patients with chronic heart failure and sleep
apnoea: a randomized comparison of two different programmes.
Clin Rehabil 26(1):4557
29. Kline CE, Crowley EP, Ewing GB, Burch JB, Blair SN, Durstine
JL et al (2012) Blunted heart rate recovery is improved following
exercise training in overweight adults with obstructive sleep
apnea. Int J Cardiol 167(4):16101615
30. Kline CE, Ewing GB, Burch JB, Blair SN, Durstine JL, Davis JM
et al (2012) Exercise training improves selected aspects of day-
time functioning in adults with obstructive sleep apnea. J Clin
Sleep Med 8(4):357365
31. Norman JF, Von Essen SG, Fuchs RH, McElligott M (2000)
Exercise training effect on obstructive sleep apnea syndrome.
Sleep Res Online 3(3):121129
32. Sutton AAK, Jones D, Sheldon T, Song F (2000) Methods for
meta-analysis in medical research Wiley series in probability and
statistics. Wiley, New York
123
184
33. Huedo-Medina TB, Sanchez-Meca J, Marin-Martinez F, Botella J
(2006) Assessing heterogeneity in meta-analysis: Q statistic or I2
index? Psychol Methods 11(2):193206
34. Sterne JA, Egger M, Smith GD (2001) Systematic reviews in
health care: investigating and dealing with publication and other
biases in meta-analysis. BMJ 323(7304):101105
35. Begg CB, Mazumdar M (1994) Operating characteristics of a rank
correlation test for publication bias. Biometrics 50(4):10881101
36. Barnes M, Goldsworthy UR, Cary BA, Hill CJ (2009) A diet and
exercise program to improve clinical outcomes in patients with
obstructive sleep apneaa feasibility study. J Clin Sleep Med
5(5):409415
37. Iftikhar IH, Hays ER, Iverson MA, Magalang UJ, Maas AK
(2013) Effect of oral appliances on blood pressure in obstructive
sleep apnea: a systematic review and meta-analysis. J Clin Sleep
Med 9(2):165174
38. Greenburg DL, Lettieri CJ, Eliasson AH (2009) Effects of sur-
gical weight loss on measures of obstructive sleep apnea: a meta-
analysis. Am J Med 122(6):535542
39. Sui X, LaMonte MJ, Laditka JN, Hardin JW, Chase N, Hooker SP
et al (2007) Cardiorespiratory fitness and adiposity as mortality
predictors in older adults. JAMA 298(21):25072516
40. Rodway GW, Weaver TE, Mancini C, Cater J, Maislin G, Staley
B et al (2010) Evaluation of sham-CPAP as a placebo in CPAP
intervention studies. Sleep 33(2):260266
41. McArdle N, Douglas NJ (2001) Effect of continuous positive
airway pressure on sleep architecture in the sleep apnea-hypopnea
syndrome: a randomized controlled trial. Am J Respir Crit Care
Med 164(8 Pt 1):14591463
42. Giles TL, Lasserson TJ, Smith BH, White J, Wright J, Cates CJ
(2006) Continuous positive airways pressure for obstructive sleep
apnoea in adults. Cochrane Database Syst Rev 3:CD001106
43. Marshall NS, Barnes M, Travier N, Campbell AJ, Pierce RJ,
McEvoy RD et al (2006) Continuous positive airway pressure
reduces daytime sleepiness in mild to moderate obstructive sleep
apnoea: a meta-analysis. Thorax 61(5):430434
123
Lung (2014) 192:175184
44. Haxhiu MA, van Lunteren E, Mitra J, Cherniack NS, Strohl KP
(1984) Comparison of the responses of the diaphragm and upper
airway muscles to central stimulation of the sciatic nerve. Respir
Physiol 58(1):6576
45. ODonnell DE, McGuire M, Samis L, Webb KA (1998) General
exercise training improves ventilatory and peripheral muscle
strength and endurance in chronic airflow limitation. Am J Respir
Crit Care Med 157(5 Pt 1):14891497
46. Mirrakhimov AE (2013) Physical exercise related improvement
in obstructive sleep apnea. Look for the rostral fluid shift. Med
Hypotheses 80(2):125128
47. Redolfi S, Yumino D, Ruttanaumpawan P, Yau B, Su MC, Lam J
et al (2009) Relationship between overnight rostral fluid shift and
obstructive sleep apnea in nonobese men. Am J Respir Crit Care
Med 179(3):241246
48. Redolfi S, Arnulf I, Pottier M, Bradley TD, Similowski T (2011)
Effects of venous compression of the legs on overnight rostral
fluid shift and obstructive sleep apnea. Respir Physiol Neurobiol
175(3):390393
49. Redolfi S, Arnulf I, Pottier M, Lajou J, Koskas I, Bradley TD et al
(2011) Attenuation of obstructive sleep apnea by compression
stockings in subjects with venous insufficiency. Am J Respir Crit
Care Med 184(9):10621066
50. Shiota S, Ryan CM, Chiu KL, Ruttanaumpawan P, Haight J, Arzt
M et al (2007) Alterations in upper airway cross-sectional area in
response to lower body positive pressure in healthy subjects.
Thorax 62(10):868872
51. Jafari B, Mohsenin V (2011) Overnight rostral fluid shift in
obstructive sleep apnea: does it affect the severity of sleep-dis-
ordered breathing? Chest 140(4):991997
52. Ratnavadivel R, Chau N, Stadler D, Yeo A, McEvoy RD,
Catcheside PG (2009) Marked reduction in obstructive sleep
apnea severity in slow wave sleep. J Clin Sleep Med 5(6):519524
53. McSharry DG, Saboisky JP, Deyoung P, Matteis P, Jordan AS,
Trinder J et al (2013) A mechanism for upper airway stability
during slow wave sleep. Sleep 36(4):555563