- Sleep Medicine

Sleep Medicine 12 (2011) 1018–1027
Contents lists available at SciVerse ScienceDirect
Sleep Medicine
journal homepage: www.elsevier.com/locate/sleep
Original Article
Effects of moderate aerobic exercise training on chronic primary insomnia
Giselle Soares Passos a, Dalva Poyares a, Marcos Gonçalves Santana b, Carolina Vicaria Rodrigues D’Aurea a,
Shawn D. Youngstedt d,e, Sergio Tufik a,c, Marco Túlio de Mello a,c,⇑
a
Department of Psychobiology, Universidade Federal de São Paulo, São Paulo, SP, Brazil
Universidade Federal de Goiás, Campus Jataí, Goiás, Brazil
c
Researcher Conselho Nacional de Desenvolvimento Científico e Tecnológico - CNPq, Brasília, Brazil
d
Department of Exercise Science, University of South Carolina, Columbia, SC, USA
e
Research and Development, WJB Dorn VA Medical Center, USA
b
a r t i c l e
i n f o
Article history:
Received 5 November 2010
Received in revised form 27 January 2011
Accepted 9 February 2011
Available online 22 October 2011
Keywords:
Insomnia
Physical activity
Sleep
Mood
Quality of life
Polysomnography
a b s t r a c t
Objective: To evaluate the effect of long-term moderate aerobic exercise on sleep, quality of life, and
mood of individuals with chronic primary insomnia, and to examine whether these effects differed
between exercise in the morning and exercise in the late afternoon.
Methods: Nineteen sedentary individuals with chronic primary insomnia, mean age 45.0 (standard error
[SE] 1.9) years, completed a 6-month exercise training protocol, randomized to morning and late-afternoon exercise groups.
Results: Combining polysomnographic data across both time points, this study found a significant
decrease in sleep onset latency (from 17.1 [SE 2.6] min to 8.7 [SE 1.4] min; P < 0.01) and wake time after
sleep onset (from 63.2 [SE 12.8] min to 40.1 [SE 6.0] min), and a significant increase in sleep efficiency
(from 79.8 [SE 3.0]% to 87.2 [SE 1.6]%) following exercise. Data from sleep diaries revealed significant
improvement in sleep onset latency (from 76.2 [SE 21.5] min to 80.3 [SE 7.4] min) sleep quality (from
41.5 [SE 5.2]% to 59.4 [SE 6.6]%) and feeling rested in the morning (from 50.8 [SE 5.3] to 65.1 [SE 5.0]).
There were generally no significant differences in response between morning and late-afternoon exercise.
Following exercise, some quality-of-life measures improved significantly, and a significant decrease was
seen in the following Profile of Mood State measures: tension–anxiety (from 7.2 [SE 1.0] to 3.5 [SE 1.0]),
depression (from 5.9 [SE 1.2] to 3.3 [SE 1.1]) and total mood disturbance (from 9.2 [SE 4.8] to 1.7 [SE
4.8]). These effects did not vary between morning and late-afternoon exercise.
Conclusion: Long-term moderate aerobic exercise elicited significant improvements in sleep, quality of
life and mood in individuals with chronic primary insomnia.
Ó 2011 Elsevier B.V. All rights reserved.
1. Introduction
Chronic primary insomnia is a sleep disorder characterized by
long-term difficulties with initiating and maintaining sleep, waking up too early, non-restorative sleep, and daytime impairment,
including fatigue, poor mood, impaired concentration, and poor
quality of life [1–4]. The prevalence of chronic insomnia worldwide
is between 10% and 15% [5]. In Brazil, a recent study in the city of
São Paulo demonstrated that approximately 35% of the population
complained of insomnia, with the problem being more prevalent
among women (40%) [6].
⇑ Corresponding author at: Universidade Federal de Sao Paulo, Department of
Psychobiology, Francisco de Castro, 93, Vila Clementino, CEP: 04020-050 Sao Paulo,
SP, Brazil. Tel./fax: +55 11 5572 0177.
E-mail addresses: [email protected] (G.S. Passos), [email protected]
(M.T. de Mello).
1389-9457/$ - see front matter Ó 2011 Elsevier B.V. All rights reserved.
doi:10.1016/j.sleep.2011.02.007
Drug therapy is the most commonly prescribed treatment for
insomnia. However, sleep medications may cause side effects and
are not recommended for long-term use [7]. Thus, various nonpharmacological therapies have been proposed in the literature,
especially cognitive and behavioural therapies [8–11].
However, cognitive or behavioural therapies may be very
expensive as frequent treatment is required. As such, physical
exercise as a non-pharmacological, low cost, and easily accessed
treatment alternative has been suggested [10,12,13]. The wellestablished anxiolytic and antidepressant effects of exercise could
help to alleviate psychological comorbidities, which may also be
involved in the aetiology and perpetuation of insomnia [14].
Epidemiological studies have reported an association between
exercise and decreased complaints of insomnia [15,16], as well as
a relationship between low levels of physical activity and a greater
prevalence of insomnia [17]. However, there has been very limited
experimental investigation of the effects of aerobic exercise training on sleep in individuals with insomnia [18,19]. The studies have
G.S. Passos et al. / Sleep Medicine 12 (2011) 1018–1027
been limited primarily to subjective sleep assessments; however,
positive effects of exercise on both subjective and actigraphic measures of sleep have been found.
The optimal time of day for performing exercise to promote sleep
is not clear. Earlier reviews, mainly from literature involving acute
exercise and normal sleepers, suggested a slight advantage for exercise in the late-afternoon [12,13,20], and a recent study by the present authors found a significant improvement in sleep among
insomniacs following acute afternoon exercise [21]. However, it is
plausible that morning exercise may be at least as beneficial for promoting chronic sleep improvement for insomniacs (e.g., by promoting phase advances and stabilization of the circadian system).
The aim of this study was to expand on previous findings by evaluating the influence of long-term aerobic exercise on polysomnographic and subjective sleep measures, and on measures of quality
of life and mood in individuals diagnosed with chronic primary insomnia. Additionally, the authors assessed whether these effects differed
between exercise in the morning and exercise in the late afternoon,
and whether sleep changes were associated with mood changes.
2. Materials and methods
2.1. Recruitment and sample selection
Ethical approval for all experimental procedures was granted by
the University Human Research Ethics Committee and conformed
to the principles outlined in the Declaration of Helsinki. The participants were recruited through advertisements in newspapers,
magazines, and radio shows. The inclusion criteria were: (1) 30–
55 years of age; (2) clinical diagnosis of primary insomnia according to the Diagnostic and Statistical Manual of Mental Disorders
[1]; (3) complaints of insomnia for more than 6 months; and (4)
at least one complaint of daytime impairment due to insomnia
(in mood, cognition, or perceived fatigue). The exclusion criteria
were: (1) evidence that the insomnia was directly related to a
medical condition or to side-effects from medications; (2) use of
medications or psychotherapeutic drugs for insomnia or another
psychiatric disorder; (3) diagnosis of depression or another psychiatric disorder; (4) apnoea–hypopnoea index >15; (5) periodic leg
movement index >15; (6) shift worker or all-night worker; (7) cardiac abnormalities; and (8) regular physical exercise (more than
once per week) over the previous 6 months.
Prospective participants interested in participating in this research were subjected to the following sequence of evaluations:
First, they received an initial screening over the telephone, composed of questions related to the inclusion and exclusion criteria,
such as age, use of medications and the practice of physical exercise. Next, prospective participants who appeared to be qualified
based on the telephone screening were invited to the laboratory
for a further interview and orientation to the study. Those who appeared to be qualified were invited to sign a written informed consent form approved by the Research Ethics Committee. During this
visit, participants also completed the Beck Depression Inventory
[22,23]. Next, prospective participants were assessed by a sleep
medicine physician to diagnose primary insomnia and exclude
other sleep disorders (see above).
Prospective participants who passed these initial screening
stages were randomized to either morning or late-afternoon exercise groups (see below). The Research Ethics Committee at the study
institute strictly prohibits the use of non-effective control or placebo
treatments, so assessments were limited to the effects of exercise
training on sleep and related morbidity in a sample of insomniacs.
Following screening, baseline study assessments were administered. The participants were instructed to refrain from exercise
during the baseline assessments.
1019
2.2. Baseline assessments
Following a 12-h fast, body composition was assessed in the
exercise laboratory of the Center of Psychobiology and Exercise
Studies. After a light breakfast, the participants completed the Profile of Mood States (POMS) and Short Form-36 (SF-36) questionnaires. Following completion of the questionnaires, participants
received a clinical consultation and an electrocardiogram at rest
and under maximal stress during a cardiopulmonary exercise test
(CPET). The CPET was performed on a treadmill (Life Fitness 9500
HR, Illinois, USA) with an initial velocity of 4 km/h and increasing
increments of 0.5 km/h each minute until voluntary exhaustion.
Breath-by-breath assessments were made with a metabolic system
(Quark PFT4, Rome, Italy). The highest pulmonary oxygen uptake
(V_ O2) value obtained during the last 20 s of the test was considered to be peak oxygen uptake (V_ O2peak). Ventilatory threshold
(VT1) was estimated by inspecting the inflection point of V_ CO2
with respect to V_ O2 (modified V slope). A certificate attesting to
the patient’s ability to participate in the exercise protocol was provided by the physician, and served as the final screen for participation in the study.
Forty-eight hours after the completion of exercise testing, participants underwent polysomnographic recording at the Sleep
Institute. This first night served as an adaption night, and participants returned 48 h later for another night of polysomnography.
Participants arrived at the sleep laboratory at 21:00 h and the
examination started and finished according to each participants’s
habitual sleep schedule. Participants left the Sleep Institute with
a 7-day daily sleep diary and instructions for completing the diary
each morning.
2.3. Six-month exercise protocol
Immediately after completion of the 1-week sleep diary, the
participants started the 6-month exercise intervention. Training
was performed in the exercise laboratory 3 days/week on a treadmill (Life Fitness HR 1500, Illinois, USA) for 50 continuous min/session. Participants randomized to the morning group exercised at
10:00 ± 1 h and participants randomized to the late-afternoon
group exercised at 18:00 ± 1 h. All exercise sessions were performed in groups (four or five participants) in the presence of
one or two staff, and were preceded by 5 min of warm-up exercises
and followed by 5 min of active recovery and stretching of the
upper and lower limbs [24]. The participants did not listen to music or watch television while they exercised. The intensity of exercise was determined by the data obtained in the CPET. The speed
relative to VT1 [25,26] was used as the training intensity for both
groups. The intensity was controlled and monitored by means of
heart rate (±5 beats/min), which was measured with a heart rate
monitor (Polar FS1, Kempele, Finland).
Post-treatment assessments of body composition, V_ O2peak,
POMS, and SF-36 were initiated 48 h after the completion of exercise training. As described above, polysomnographic recordings
were made 48 and 96 h after the completion of exercise training,
followed by 1 week of sleep diary assessments. Participants were
instructed not to exercise during this period. Thus, changes can
be attributed to long-term effects of exercise training rather than
acute exercise effects.
2.4. Measures
2.4.1. Body composition
Body composition was obtained through plethysmography with
the Bod Pod Body Composition System (Life Measurement Inc,
Concord, CA USA). This system includes an electronic scale, a plethysmograph, a cylinder for calibration, and a computer with the
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G.S. Passos et al. / Sleep Medicine 12 (2011) 1018–1027
equipment’s software. The Bod Pod body composition system uses
total body densitometry, which is obtained from dividing the body
mass by the body volume of the individual. Through plethysmography, it was possible to obtain the body fat percentage and free
fat mass [27].
2.4.2. Medical outcomes study SF-36 questionnaire
The SF-36 is a multidimensional questionnaire that covers eight
components: physical functioning, role limitations due to physical
health problems, role limitations due to emotional health problems, social functioning, vitality, general health perception, body
pain, and mental health. All scores ranged from 0 to 100, with a
higher score indicating better quality of life [28].
2.4.3. POMS questionnaire
The POMS questionnaire is an instrument to evaluate the acute
profile of mood. It has 65 items and 6 domains: tension–anxiety,
depression, anger–hostility, vigour–activity, fatigue, and confusion–bewilderment. The total mood disturbance score is derived
by subtracting the vigour–activity score from the the sum of scores
from the other subscales [29].
2.4.4. Polysomnography
Polysomnographic recording included an electroencephalogram, an electrooculogram, an electromyogram, and an electrocardiogram. Measurements of air flow (oral and nasal), respiratory
effort (thoracic and abdominal), body movement, and oxygen saturation were also taken. The measured variables included total
sleep time, sleep efficiency (ratio between total sleep time and total recorded time multiplied by 100), sleep onset latency, wake
after sleep onset, arousals, sleep stages (I, II, III, and IV of non-rapid
eye movement [non-REM] sleep and REM sleep), latencies for each
sleep stage (Stage 1, Stage 2, and Stages 3 and 4), and REM sleep
latency. Two researchers who were blinded to the study design
performed the staging and analysed the polysomnographic events
using international criteria [30–32].
2.4.5. Sleep diary
The sleep diary was used to evaluate the subjective perceptions
of sleep. Participants were instructed to complete the diary every
morning after waking for 1 week. The parameters evaluated were
sleep onset latency, wake after sleep onset, total time in bed, number of arousals, sleep quality, feeling rested in the morning, and
sleep efficiency (calculated retrospectively by the researchers as
the ratio of reported total sleep time and reported total time in
bed multiplied by 100 [9]). These data were averaged for each volunteer for pre- and post-treatment assessment weeks.
2.5. Data analysis
STATISTICA Version 6.0 (Statsoft, Inc., Tulsa, USA) was used for
the analyses. For the variables that did not present normal distributions in the Shapiro-Wilk’s test, a logarithmic transformation
(log 10) was performed. Data were analysed via group x time
(two groups two times) repeated-measures analysis of variance
(ANOVA). Analysis of covariance was used for variables that differed significantly between groups at baseline, with covariate control for baseline. Student’s t-test for independent groups was used
to compare the mean age of drop-outs and those who completed
the study.
Cohen’s effect size (d) was calculated for all variables for the
morning, late-afternoon, and combined data by subtracting the final value from the initial value and dividing by the pooled standard
deviation. According to convention, effect sizes of 0.2–0.3, 0.5, and
P0.8 are considered small, medium, and large, respectively [33].
Spearman rank-order correlations were conducted to assess
whether changes in sleep between morning and late-afternoon
exercise were associated with changes in POMS measures and fitness level (V_ O2peak and maximum heart rate [HRmax]). The data
are presented as mean (SE). P < 0.05 was taken to indicate
significance.
3. Results
3.1. Recruitment, drop-outs, and adherence to the exercise protocol
Two hundred and sixty-seven people were interested in taking
part in the study, and contacted the researchers by telephone or email. Of these, 229 did not meet the initial inclusion criteria and
were excluded (Fig. 1). Thirty-eight participants (29 women, 9
men) passed the initial screening and were randomized to the
morning exercise group (n = 19) or the late-afternoon exercise
group (n = 19). However, 3 men and 5 women withdrew from
the study during the baseline period before commencing exercise
training.
Thus, the exercise protocol began with 14 participants in the
morning exercise group and 16 participants in the late-afternoon
exercise group. However, during the protocol, 4 participants in
the morning exercise group (3 women, 1 man) and 7 participants
in the late-afternoon exercise group (6 women, 1 man) withdrew
from the study. Of these 11 participants (36.6%), 9 (30%) withdrew
due to problems with the programme schedule, which could not be
changed during the protocol. 6 (66.6%) of these nine drop-outs
were in the late-afternoon exercise group. In addition, one participant withdrew after moving to a different city, and one participant
withdrew because of health problems. The mean age of drop-outs
was 42.5 (SE 3.1) years and the mean age of participants who completed the study was 45.0 (SE 1.9) years; the difference was not significant (P = 0.47). As a result, the final sample size was 10
participants in the morning exercise group and 9 participants in
the late-afternoon exercise group.
These 19 participants exhibited good adherence to the study
protocol (>90%), based on class attendance and spending >90% of
exercise time working at the prescribed intensity. Descriptive data
for these participants are displayed in Table 1. There were no significant differences between the morning exercise group and the
late-afternoon exercise group for any of these measures.
3.2. Physiological parameters
No significant differences in body composition were observed
following exercise training (Table 2). Significant increases in V_
O2peak (P < 0.01, d = 1.30) and walking velocity (P < 0.001,
d = 3.32) were observed after the intervention. No significant group
x time interaction was found for these physiological variables.
3.3. Quality of life
After exercise training, there were significant increases and
large associated effect sizes for the following SF-36 measures: social functioning (P < 0.01, d = 1.95), general health perception
(P < 0.01, d = 1.46), and role limitations due to emotional health
problems (P < 0.001, d = 1.39). However, no significant group x
time interaction was found for any of these variables. No significant time or group x time effects were found for the other SF-36
variables (Table 3), although there were large and moderate effect
sizes for improvement in bodily pain (d = 1.07) and mental health
(d = 0.74), respectively. Moreover, Chi-squared analyses revealed
no significant differences between the morning-exercise group
G.S. Passos et al. / Sleep Medicine 12 (2011) 1018–1027
1021
Patients assessed for
elegibility (n=267)
Patients excluded (n=229)
– 47 reported a previous diagnosis of depression
– 20 reported a diagnosis of other psychiatric disorders
– 39 practised systematic physical exercise
– 16 were shift workers
– 15 had AHI or PLMI >15
– 70 reported regular use of medication for insomnia
– 22 did not present evidence of insomnia at the time of
evaluation
Patients randomized
(n=38)
Morning group (n=19)
Late-afternoon group (n=19)
Drop-outs (n=5)
Drop-outs (n=3)
Pre-intervention (n=14)
Pre-intervention (n=16)
Drop-outs (n=4)
Drop-outs (n=7)
Post-intervention (n=10)
Post-intervention (n=9)
Fig. 1. Participant flowchart. AHI, apnoea–hypopnoea index; PLMI, periodic leg movement index.
Table 1
Baseline characteristics of the sample.
Variable
Morning exercise
(n = 10)
Late-afternoon exercise
(n = 9)
Gender (male/female)
Age (years)
Duration of insomnia
(years)
Body mass index (kg/m2)
Beck Depression Inventory
(score)
2/8
42.3 (2.6)
10.2 (2.8)
2/7
48.0 (2.5)
11.1 (3.2)
24.9 (1.7)
9.5 (0.7)
24.8 (1.4)
9.1 (1.4)
Student’s t-test; P > 0.05; data presented as mean (standard error).
and the late-afternoon exercise group for any of the SF-36
measures.
3.4. Mood
After exercise training, there were significant improvements
and large associated effect sizes in the following POMS measures:
tension–anxiety (P < 0.01, d = 1.98), depression (P = 0.04,
d = 1.18), anger–hostility (P = 0.03, d = 0.94), and total mood
disturbance (P = 0.04, d = 1.18) (Table 4). There were no signifi-
cant group x time interactions for any of these variables, nor were
there any significant Chi-squared results comparing the percentage
improvement between groups. No significant time, group x time, or
Chi-squared effects were found for the other POMS measures,
although moderate to large effect sizes showed improvement for
fatigue (d = 1.34) and confusion–bewilderment (d = 0.94).
3.5. Polysomnography
After exercise training, significant reductions and large associated effect sizes were observed in the following polysomnographic
measures: sleep onset latency (P < 0.01, d = 0.96), Stage 2 latency
(P < 0.04, d = 1.21), and REM sleep latency (P < 0.001, d = 2.89).
In addition, exercise resulted in a significant decrease in wake after
sleep onset (P = 0.04, d = 1.66), and a significant increase in sleep
efficiency (P < 0.01, d = 1.91). No significant group x time effects
were found for any of these variables. A group x time interaction
was observed in Stage 1 sleep, demonstrating that the percentage
of sleep in this stage was reduced in the morning exercise group
and increased in the late-afternoon exercise group (Table 5). However, when the percentage of change was compared with Chisquared analysis, no significant difference was found between
the groups. No significant time, group x time, or Chi-squared effects were found for any of the other polysomnographic variables,
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G.S. Passos et al. / Sleep Medicine 12 (2011) 1018–1027
Table 2
Physical evaluation and physiological parameters.
ANOVA (P)
Variable
Groups
Pre-intervention
Post-intervention
Body mass (kg)
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
63.0
63.0
63.0
31.2
31.4
31.1
68.8
68.6
68.9
29.2
26.0
27.7
176.6
162.9
170.1
5.6
4.9
5.3
16.8
15.3
16.1
118.9
111.6
115.4
62.2
62.3
62.2
33.1
31.9
33.0
66.9
68.1
67.0
31.6
30.7
31.1
178.8
167.8
173.6
6.5
6.2
6.4
17.7
17.5
17.6
117.4
122.9
120.0
Body fat (%)
Free fat mass (%)
V_ O2peak (ml/kg/min)
HRmax (beats/min)
Speed at VT1 (km/h)
V_ O2 at VT1, (ml/kg/min)
HR at VT1 (beats/min)
(4.4)
(4.6)
(3.1)
(3.6)
(3.6)
(2.3)
(3.6)
(3.6)
(2.3)
(2.0)
(1.8)
(1.2)
(3.3)
(3.5)
(2.8)
(0.2)
(0.2)
(0.2)
(1.1)
(1.2)
(0.8)
(4.6)
(4.8)
(3.3)
(4.1)
(4.0)
(2.9)
(3.0)
(3.0)
(2.1)
(3.0)
(3.0)
(2.1)
(2.3)
(2.2)
(1.5)
(4.5)
(4.7)
(3.4)
(0.2)
(0.2)
(0.1)
(1.3)
(1.3)
(0.9)
(3.7)
(3.9)
(2.7)
Effect size Cohen’s d
0.14
0.12
0.13
0.46
0.44
0.46
0.46
0.45
0.46
0.8
2.06
1.3
0.41
0.87
0.57
2.76
4.44
3.32
0.48
1.59
0.93
0.33
1.69
0.78
Group
Time
Group x time
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
<0.01
ns
ns
ns
ns
ns
<0.001
ns
ns
ns
ns
ns
ns
ns
Repeated-measures analysis of variance (ANOVA).
V_ O2, pulmonary oxygen uptake; V_ O2peak, peak oxygen uptake; CF, cardiac frequency; HR, heart rate; HRmax, maximum heart rate; VT1, ventilatory threshold 1; ns, not
significant.
Morning exercise, n = 10; late-afternoon exercise, n = 9.
Data are displayed as mean (standard error). P < 0.05 taken to indicate significance.
Table 3
Quality of life evaluated by the Short Form-36 Questionnaire.
ANOVA (P)
Variable
Groups
Pre-intervention
Post-intervention
Physical functioning
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
87.5
92.8
90.0
87.5
83.3
85.5
62.7
74.0
68.0
74.8
88.8
81.4
66.5
69.4
67.9
80.6
69.4
75.0
69.9
70.4
70.1
76.4
76.0
76.2
88.5
92.8
90.0
82.5
80.5
80.5
68.8
91.7
78.5
89.1
90.8
89.5
68.0
71.7
69.7
86.2
94.4
89.6
86.7
91.6
88.9
79.6
83.1
81.3
Role–physical
Body pain
General health perception
Vitality
Social functioning
Role–emotional
Mental health
(4.0)
(4.2)
(2.9)
(7.8)
(8.2)
(5.5)
(6.2)
(6.5)
(4.6)
(3.7)
(3.9)
(3.1)
(6.0)
(6.4)
(4.3)
(6.0)
(6.7)
(4.7)
(11.4)
(12.0)
(8.0)
(4.5)
(4.7)
(3.2)
Repeated-measures analysis of variance (ANOVA).
ns, not significant.
Morning exercise, n = 10; late-afternoon exercise, n = 9.
Data are displayed as mean (standard error). P < 0.05 taken to indicate significance.
(2.6)
(2.7)
(1.9)
(10.4)
(11.0)
(7.7)
(6.7)
(7.1)
(5.6)
(3.6)
(3.8)
(2.7)
(4.6)
(4.8)
(3.4)
(4.0)
(4.2)
(3.1)
(8.1)
(8.5)
(6.0)
(5.4)
(5.7)
(4.0)
Effect size Cohen’s d
0.19
0.24
0
0.48
0.35
0.39
0.64
1.86
1.07
2.71
0.24
1.46
0.16
0.5
0.25
0.81
3.59
1.95
1.32
1.56
1.39
0.4
1.29
0.74
Group
Time
Group x time
ns
ns
ns
ns
ns
ns
0.04
ns
ns
ns
<0.01
<0.01
ns
ns
ns
ns
<0.01
ns
ns
<0.001
ns
ns
ns
ns
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G.S. Passos et al. / Sleep Medicine 12 (2011) 1018–1027
Table 4
Profile of Mood States questionnaire.
ANOVA (p)
Variable
T–A (score)
Depression (score)
A–H (score)
V–A (score)
Fatigue (score)
C–B (score)
TMD (score)
Groups
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Pre-intervention
7.7 (1.4)
6.2 (1.5)
7.2 (1.0)
5.1 (1.8)
6.5 (2.0)
5.9 (1.2)
3.1 (2.3)
8.5 (2.5)
5.9 (1.7)
18.7 (1.6)
19.9 (1.8)
19.3 (1.1)
6.4 (1.3)
6.5 (1.4)
6.5 (0.9)
3.9 (1.4)
3.6 (1.6)
3.6 (1.0)
6.3 (7.0)
11.5 (7.8)
9.2 (4.8)
Post-intervention
4.8 (1.2)
1.7 (1.4)
3.5 (1.0)
4.1 (1.4)
2.0 (1.4)
3.3 (1.1)
4.8 (1.2)
1.4 (1.3)
3.5 (1.0)
17.6 (1.6)
18.6 (1.8)
18.1 (1.2)
5.1 (1.2)
3.4 (1.3)
4.2 (0.9)
1.7 (1.2)
2.9 (1.4)
1.94 (0.9)
2.9 (6.1)
7.2 (6.8)
1.7 (4.8)
Effect size Cohen’s d
1.39
3.61
1.98
0.45
2.68
1.18
0.58
4.94
0.94
0.47
0.47
0.52
0.66
2.64
1.34
1.08
0.7
0.94
0.33
3.14
1.18
Group
ns
Time
<0.01
Group x time
ns
ns
0.04
ns
0.02
0.03
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
0.04
ns
Repeated-measures analysis of variance (ANOVA).
T–A, tension–anxiety; A–H, anger–hostility; V–A, vigour–activity; C–B, confusion bewilderment; TMD, total mood disturbance; ns, not significant.
Morning exercise, n = 10); late-afternoon exercise, n = 9.
Data are displayed as mean (standard error). P < 0.05 taken to indicate significance.
although there were large effect sizes for increases in total sleep
time (d = 0.97), reduction in Stage 4 sleep (d = 0.97), and reduction in latency for Stages 3 and 4 (d = 1.35).
3.6. Sleep diary
After exercise training, there was a significant decrease and a
large associated effect size in the sleep diary measure of sleep onset latency (P < 0.01, d = 1.25), and a significant increase in the
sleep diary measures of sleep quality (P = 0.02, d = 1.92) and feeling
rested in the morning (P < 0.01, d = 1.70). No significant group x
time effects were found for these variables. Chi-squared analysis
indicated that the proportion of improvement in sleep quality
was significantly greater following morning exercise compared
with late-afternoon exercise (P = 0.03); the proportion of improvement in feeling rested in the morning was also marginally greater
after morning exercise compared with late-afternoon exercise
(P = 0.06). No significant effects were found for the other sleep
diary parameters (Table 6).
3.7. Correlation of POMS and fitness level with sleep data
Significant correlations were found between a decrease in
POMS-depression and improvements in the following sleep diary
measures: sleep quality (r = 0.58, P < 0.05), sleep onset latency
(r = 0.56, P < 0.05), and feeling rested in the morning (r = 0.81,
P < 0.05). However, there were no other significant correlations between changes in POMS measures with changes in subjective or
objective sleep, or between the changes in sleep and changes in fitness level (V_ O2peak and HRmax).
4. Discussion
This study showed significant improvements in objective and
subjective sleep, as well as quality of life and mood measures, following exercise training in individuals with chronic primary
insomnia. The results are consistent with other research showing
the benefits of exercise training for individuals with disturbed
sleep.
Much of the research on the effects of exercise training on sleep
has focused on older adults, often under the assumption that exercise may have the greatest potential to benefit age-related sleep
disturbance. King et al. [34] found a reduction in self-reported
sleep onset latency and an increase in reported sleep duration in
older adults with sleep complaints following a 16-week programme of moderate aerobic exercise. Another study of older
adults with sleep complaints performed by King et al. demonstrated an increase in morning feeling of restfulness and a reduction in subjective sleep onset latency after a long-term exercise
intervention (12 months) [35]. Reid et al. [19] recently observed
improvements in self-reported sleep quality, depressive symptoms, and daytime sleepiness following a moderate 16-week aerobic exercise programme in individuals with primary insomnia.
Studies that have focused on nursing home or assisted living
residents, who typically have disrupted sleep, have reported mixed
results. For example, Alessi et al. [36] found that 9 weeks of exercise had no effect on actigraphic sleep in nursing home residents.
Ferris et al. [37] found improvements in subjective sleep compared
with baseline following 3 months of circuit weight training, but not
following 6 months of training. However, exercise has helped to reduce fragmentation of the rest–activity rhythm [38] as well as
mood disturbance in this population [39].
The present study found differences between subjective sleep
reports and polysomnographic measures, particularly for sleep onset latency and total sleep time. These data are consistent with
other studies which have reported that people diagnosed with primary insomnia often report worse sleep than can be verified with
objective sleep recordings [40,41].
Compared with the objective data, the subjective data are in
better agreement with the participants’ anecdotal accounts. The
anecdotal accounts indicated that the participants felt there had
been a remarkable improvement in sleep. It is worth noting that
subjective complaints are the primary means of defining insomnia,
and subjective feelings of improvement remain the primary means
of determining improvement clinically. Moreover, a limitation of
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G.S. Passos et al. / Sleep Medicine 12 (2011) 1018–1027
Table 5
Sleep variables obtained with polysomnography.
ANOVA (P)
Variable
Group
Pre-intervention
Post-intervention
Effect size Cohen’s d
Group
Time
Group x time
TST (min)
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
352.5 (17.6)
316. 5 (18.6)
335.5 (13.1)
16.8 (3.7)
17.4 (4.4)
17.1 (2.6)
100.0 (15.8)
122.4 (18.4)
110.6 (11.4)
83.8 (4.1)
75.4 (4.9)
79.8 (3.0)
52.5 (17.7)
75.2 (20.6)
63.2 (12.8)
10.9 (2.7)
19.6 (3.8)
15.0 (2.2)
4.6 (0.6)
2.8 (0.6)
3.7 (0.5)
53.8 (2.3)
60.1 (1.5)
56.8 (1.8)
4.2 (0.6)
4.6 (0.5)
4.4 (0.4)
15.4 (1.5)
15.1 (1.2)
15.2 (1.1)
22.0 (1.9)
17.3 (0.8)
19.8 (1.4)
8.5 (2.8)
10.0 (3.0)
9.2 (1.9)
1.8 (1.5)
2.6 (1.6)
2.2 (1.1)
84.5 (36.2)
115.0 (44.2)
98.9 (25.8)
19.3 (7.3)
29.8 (10.6)
24.3 (5.3)
43.2 (16.5)
73.4 (23.4)
57.5 (12.2)
355.3
351.5
353.5
10.5
6.7
8.7
68.7
72.8
70.6
89.6
84.6
87.2
30.7
50.5
40.1
13.8
17.5
15.5
3.1
4.1
3.6
57.7
57.5
57.8
3.9
4.9
4.4
13.1
13.8
13.3
22.1
19.8
21.0
9.1
10.1
9.6
0.5
3.7
1.9
62.1
71.5
66.3
11.4
16.2
13.7
28.5
39.4
33.7
0.16
1.71
0.97
1.67
2.46
2.06
2.23
3.56
2.89
1.68
2.16
1.91
1.45
1.82
1.66
1.36
0.31
0.18
1.86
1.28
0.16
1.04
0.84
0.31
0.4
0.07
0
0.98
0.9
0.97
0.02
2,02
0.51
0.15
0.28
0.21
1.24
0.31
0.09
0.5
0.82
0.68
2.07
1.04
1.21
1.52
1.4
1.35
ns
ns
ns
ns
<0.01
ns
ns
<0.001
ns
ns
<0.01
ns
ns
0.04
ns
ns
ns
ns
ns
ns
<0.01
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns
0.04
ns
ns
ns
ns
SOL (min)
LREM (min)
SE (%)
WASO (min)
Arousals (events/h)
S1 (%)
S2 (%)
S3 (%)
S4 (%)
REM (%)
AHI (events/h)
PLMI (events/h)
L1 (min)
L2 (min)
L3–4 (min)
(11.0)
(11.6)
(7.7)
(1.9)
(1.8)
(1.4)
(5.8)
(6.3)
(3.7)
(2.1)
(2.7)
(1.6)
(7.8)
(10.5)
(6.0)
(2.3)
(3.2)
(1.7)
(0.7)
(0.9)
(0.5)
(2.3)
(2.2)
(1.6)
(0.5)
(0.4)
(0.4)
(1.4)
(1.3)
(1.0)
(1.4)
(0.9)
(1.0)
(3.1)
(3.9)
(2.2)
(2.0)
(2.1)
(1.5)
(32.8)
(38.3)
(24.2)
(4.6)
(6.7)
(3.3)
(6.9)
(9.2)
(5.1)
Repeated-measures analysis of variance (ANOVA).
TST, total sleep time; SOL, sleep onset latency; LREM, REM sleep latency; SE, sleep efficiency; WASO, wake after sleep onset; S1, Stage 1; S2, Stage 2; S3, Stage 3; S4, Stage 4;
REM, rapid eye movement; AHI, apnoea–hypopnoea index; PLMI, periodic leg movement index; L1, Stage 1 latency; L2, Stage 2 latency; L3–4, Stages 3 and 4 latency; ns, not
significant.
Morning exercise, n = 10); late-afternoon exercise, n = 9.
Data are displayed as mean (standard error). P < 0.05 taken to indicate significance.
the polysomnographic data in this study, and many other studies,
was that it was only assessed on one night, whereas the sleep diary
data were averaged over 1 week. Considering the high nightly variability in sleep, particularly among individuals with insomnia
[42,43], several nights of assessment with actigraphic assessment
may be preferable for the detection of treatment effects.
Nonetheless, as subjective sleep data may be more susceptible
to various behavioural confounds (e.g., demand and expectancy
biases) than objective sleep data, demonstration of significant
improvements in both objective and subjective sleep measures
provides perhaps the most compelling evidence of improvements
in sleep following exercise training. Previous studies of the effects
of exercise training on insomnia have generally been limited to
subjective measures. One notable exception by Guilleminault
et al. [18] examined changes in actigraphic and diary measures
of sleep following 4 weeks of moderate aerobic exercise in middle-aged adults with sleep complaints. The effects of exercise on
actigraphic measures were not significantly different from the effects of a control sleep hygiene treatment, and the associated exercise effect sizes (e.g., d for sleep onset latency = 036, d for wake
after sleep onset = 0.16) were smaller than those observed in
the present study, perhaps due to the relatively short duration of
this study.
The lack of a significant increase in objective or subjective measures of total sleep time in the present study is inconsistent with
some [18,34], but not all, other research showing elevations in total sleep time following exercise training [35]. Notwithstanding
these ANOVA results, the large Cohen’s effect sizes observed for
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G.S. Passos et al. / Sleep Medicine 12 (2011) 1018–1027
Table 6
Sleep variables obtained from the sleep diary (mean 7 days).
ANOVA (P)
Variable
Groups
Pre-intervention
Post-intervention
TST (h)
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
Morning
Late afternoon
Combined
4.8
5.5
5.1
6.5
7.3
6.8
59.5
83.0
76.2
79.1
76.9
78.5
1.4
1.8
1.6
38.9
43.8
41.5
41.9
58.5
50.8
6.2
5.5
5.7
7.1
7.0
6.9
25.9
39.6
35.2
86.3
80.3
83.1
1.3
1.8
1.5
65.9
54.4
59.4
62.9
67.1
65.1
TTB (h)
SOL (min)
SE (%)
Arousals (events/h)
SQ (%)
FRM (%)
(0.7)
(0.6)
(0.5)
(0.6)
(0.5)
(0.4)
(31.7)
(27.5)
(21.5)
(8.0)
(7.0)
(5.4)
(0.5)
(0.5)
(0.3)
(7.9)
(7.3)
(5.2)
(7.3)
(6.7)
(5.3)
(0.7)
(0.6)
(0.4)
(0.4)
(0.4)
(0.2)
(17.7)
(15.3)
(12.1)
(8.5)
(7.4)
(5.9)
(0.5)
(0.4)
(0.3)
(9.9)
(9.2)
(6.6)
(7.7)
(7.1)
(5.0)
Effect size Cohen’s d
1.65
0.00
0.56
1.03
0.42
0.00
3.09
1.24
1.25
1.1
0.24
0.5
0.19
0.22
0.18
2.9
0.49
1.92
2.23
0.71
1.7
Group
Time
Group x time
ns
ns
ns
ns
ns
ns
ns
<0.01
ns
ns
ns
ns
ns
ns
ns
ns
0.02
ns
ns
0.01
ns
Repeated-measures analysis of variance (ANOVA).
TST, total sleep time; TTB, total time in bed; SOL, sleep onset latency; SE, sleep efficiency; SQ, sleep quality; FR, feeling rested in morning; ns, not significant.
Morning exercise, n = 10); late-afternoon exercise, n = 9.
Data are displayed as mean (standard error). P < 0.05 is taken to indicate significance.
both objective (d = 0.97) and subjective (d = 0.96) total sleep time
following exercise training is noteworthy.
The effects of exercise on sleep in the present study were similar to the effects reported in studies of other long-term, non-pharmacological treatments for chronic insomnia, such as paradoxical
intention therapy [44], phototherapy and sleep hygiene [18], progressive relaxation [45], and cognitive behavioural therapy [46].
The participants of the present study presented a similar quality
of life as reported in previous studies of people with mild–severe
insomnia [19,47–49]. Improvements in mood and quality-of-life
measures are consistent with a vast literature showing the psychological benefits of exercise training [50–53]. Moreover, the data are
consistent with studies that have shown psychological benefits of
exercise in individuals with sleep disorders [19,54]. For example,
following exercise training, individuals with obstructive sleep apnoea showed similar reductions in POMS-total mood disturbance
and similar improvements in quality of life as reported in the present study [54]. Likewise, compared with the results of the present
study, Reid et al. [19] observed similar improvements in SF-36
measures and depression following 16 weeks of moderate aerobic
exercise in patients with primary chronic insomnia. Singh et al.
[55] observed improvements in subjective sleep quality, depression, and quality of life following a supervised weight-training programme three times a week.
It has been posited that exercise training may promote sleep via
its anxiolytic or antidepressant effects. The authors found some
support for this hypothesis insofar as decreases in POMS-depression scores were significantly correlated with improvements in
the following sleep diary measures: sleep quality (r = 0.58,
P < 0.05), sleep onset latency (r = -0.56, P < 0.05), and feeling rested
in the morning (r = 0.81, P < 0.05). Moreover, in post-hoc analyses
in which change in POMS-depression was controlled as a covariate,
only the changes in the sleep diary measure of feeling rested in the
morning remained statistically significant. The association between sleep improvement and improved mood is particularly
noteworthy in light of the fairly low levels of baseline depression
scores, which were the result of exclusion for a high score on the
Beck Depression Inventory or clinical depression.
Reid et al. [19] observed a significant association between
improvements in depressive symptoms and improvements in subjective sleep quality in insomniacs. However, in contrast with the
results of the present study, improvements in sleep persisted after
controlling for changes in depression in the study by Reid et al.,
suggesting an independent sleep-promoting effect of exercise in
their study. Further exploration of this issue is warranted.
Few differences were found between the benefits of morning
and late-afternoon exercise on sleep, mood, and quality-of-life
measures in this sample of insomniacs. Moderate to large effect
sizes were found for many of the sleep and mood, variables (and
some of the SF-36 variables) following morning and late-afternoon
exercise [33]. The data suggest that either morning or late-afternoon exercise is beneficial for patients with chronic primary
insomnia. There were more drop-outs in the late-afternoon exercise group compared with the morning exercise group, but this
may have been related to logistical features of the study, such as
the fact that the journey to the laboratory took over 1 h for many
of the participants.
The drop-out rate of 30% following commencement of exercise
training, mainly due to scheduling problems, is consistent with
other long-term exercise interventions. The inability to choose
the time of exercise may have hindered adherence, as many individuals have a clear preference for the time of day for exercise. Better adherence may be accomplished with either greater flexibility
in training times or home-based interventions.
The present study had several notable limitations. First, without
a control treatment, it cannot be ascertained whether the results
were influenced by a number of potential confounds associated
with participating in the study, including demand or expectancy
effects associated with recruiting for an exercise study for insomnia, social interaction between the participants and with staff,
and spontaneous remission. Moreover, the exercise training was
performed in front of large windows with a beautiful view of the
city, so the results may be partly explained by increased exposure
to bright light, which can have sleep and mood-promoting effects.
Post-hoc assessments of laboratory light levels at the exercise
times indicated 800 lux in the late afternoon and 500 lux in the
1026
G.S. Passos et al. / Sleep Medicine 12 (2011) 1018–1027
morning. However, it is unclear whether light had any impact on
the dependent variables, as these light levels are far below those
generally prescribed for depression, and it is unclear whether the
intervention had any impact on 24-h light exposure. Future research should explore these issues more carefully.
Second, since interim data were not assessed, it is unclear how
long the intervention needs to be in order to produce these effects.
Third, post-training improvements in sleep may have been attenuated by required inactivity for 13 days after the study, as withdrawal
from regular exercise can elicit sleep impairments [56]. Fourth,
although drop-outs mainly complained about scheduling conflicts,
it is plausible that they also responded less positively to the exercise,
such that their removal from the study resulted in a positive bias.
Fifth, without statistical correction for multiple testing, some of
the significant results may be attributed to Type I error.
Notwithstanding these limitations, the results suggest that
long-term moderate aerobic exercise, performed in the morning
or late afternoon, improves sleep (objective and subjective), mood,
and quality of life in patients with chronic primary insomnia. These
results are consistent with the results of other studies, indicating
that physical exercise may be a good non-pharmacological treatment alternative for patients with chronic primary insomnia.
Conflicts of Interest
The ICMJE Uniform Disclosure Form for Potential Conflicts of
Interest associated with this article can be viewed by clicking on
the following link: doi:10.1016/j.sleep.2011.02.007.
Acknowledgements
The authors would like to thank all participants who volunteered their time to take part in the study. Giselle Soares Passos
had a fellowship from the FAPESP (2008/02862-1). The authors
would like to thank the institutions that made this manuscript possible: AFIP, FAPESP, CEPID/FAPESP, CEPE and FADA/UNIFESP.
References
[1] American Psychiatric Association. Diagnostic and statistical manual of mental
disorders (DSM-IV). Washington: American Psychiatric Press; 1994.
[2] American Academy of Sleep Medicine. The international classification of sleep
disorders: diagnostic and coding manual. Westchester, IL: Diagnostic
Classification Steering Committee; 2005.
[3] Simon GE, VonKorff M. Prevalence, burden, and treatment of insomnia in
primary care. Am J Psychiatry 1997;154:1417–23.
[4] Summers MO, Crisostomo MI, Stepanski EJ. Recent developments in the
classification, evaluation, and treatment of insomnia. Chest 2006;130:276–86.
[5] Ohayon MM. Epidemiology of insomnia: what we know and what we still need
to learn. Sleep Med Rev 2002;6:97–111.
[6] Bittencourt LR, Santos-Silva R, Taddei JA, Andersen ML, de Mello MT, Tufik S.
Sleep complaints in the adult Brazilian population: a national survey based on
screening questions. J Clin Sleep Med 2009;5:459–63.
[7] Ringdahl EN, Pereira SL, Delzell Jr JE. Treatment of primary insomnia. J Am
Board Fam Pract 2004;17:212–9.
[8] Becker PM. Pharmacologic and nonpharmacologic treatments of insomnia.
Neurol Clin 2005;23:1149–63.
[9] Morin CM, Hauri PJ, Espie CA, Spielman AJ, Buysse DJ, Bootzin RR.
Nonpharmacologic treatment of chronic insomnia. An American Academy of
Sleep Medicine review. Sleep 1999;22:1134–56.
[10] Passos GS, Tufik S, Santana MG, Poyares D, Mello MT. Nonpharmacologic
treatment of chronic insomnia. Rev Bras Psiquiatr 2007;29:279–82.
[11] Yang CM, Spielman AJ, Glovinsky P. Nonpharmacologic strategies in the
management of insomnia. Psychiatr Clin North Am 2006;29:895–919;
abstract viii.
[12] Driver HS, Taylor SR. Exercise and sleep. Sleep Med Rev 2000;4:387–402.
[13] Youngstedt SD. Effects of exercise on sleep. Clin Sports Med 2005;24:355–65, xi.
[14] Nowell PD, Buysse DJ. Treatment of insomnia in patients with mood disorders.
Depress Anxiety 2001;14:7–18.
[15] De Mello MT, Fernandez AC, Tufik S. Levantamento Epidemiológico da prática
de atividade física na cidade de São Paulo. Rev Bras Med Esporte
2000;6:119–24.
[16] Youngstedt SD, Kline CE. Epidemiology of exercise and sleep. Sleep Biol
Rhythms 2006;4:215–21.
[17] Morgan K. Daytime activity and risk factors for late-life insomnia. J Sleep Res
2003;12:231–8.
[18] Guilleminault C, Clerk A, Black J, Labanowski M, Pelayo R, Claman D. Nondrug
treatment trials in psychophysiologic insomnia. Arch Intern Med
1995;155:838–44.
[19] Reid KJ, Baron KG, Lu B, Naylor E, Wolfe L, Zee PC. Aerobic exercise improves
self-reported sleep and quality of life in older adults with insomnia. Sleep Med
2010;11:934–40.
[20] Youngstedt SD, O’Connor PJ, Dishman RK. The effects of acute exercise on
sleep: a quantitative synthesis. Sleep 1997;20:203–14.
[21] Passos GS, Poyares D, Santana MG, Garbuio SA, Tufik S, Mello MT. Effect of
acute physical exercise on patients with chronic primary insomnia. J Clin Sleep
Med 2010;6:270–5.
[22] Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J. An inventory for
measuring depression. Arch Gen Psychiatry 1961;4:561–71.
[23] Gorenstein C, Andrade L. Validation of a portuguese version of the beck
depression inventory and the state–trait anxiety inventory in Brazilian
subjects. Braz J Med Biol Res 1996;29:453–7.
[24] American College of Sports Medicine Position Stand. The recommended
quantity and quality of exercise for developing and maintaining
cardiorespiratory and muscular fitness, and flexibility in healthy adults. Med
Sci Sports Exerc 1998;30:975–91.
[25] Beaver WL, Wasserman K, Whipp BJ. A new method for detecting anaerobic
threshold by gas exchange. J Appl Physiol 1986;60:2020–7.
[26] Goldberg L, Elliot DL, Kuehl KS. Assessment of exercise intensity formulas by
use of ventilatory threshold. Chest 1988;94:95–8.
[27] Dempster P, Aitkens S. A new air displacement method for the determination
of human body composition. Med Sci Sports Exerc 1995;27:1692–7.
[28] Da Mota FD, Ciconelli RM, Ferraz MB. Translation and cultural adaptation of
quality of life questionnaires: an evaluation of methodology. J Rheumatol
2003;30:379–85.
[29] McNair DM, Lorr M, Droppelman LF. Manual for the Profile of Mood States. San
Diego, CA: Education and Industrial Testing Service; 1971.
[30] EEG arousals: scoring rules and examples: a preliminary report from the Sleep
Disorders Atlas Task Force of the American Sleep Disorders Association. Sleep
1992;15:173–84.
[31] Sleep-related breathing disorders in adults: recommendations for syndrome
definition and measurement techniques in clinical research. Report
of an American Academy of Sleep Medicine Task Force. Sleep 1999;22:
667–89.
[32] Rechtschaffen A, Kales A. A Manual of Standardized Terminology, Techniques
and Scoring System for Sleep Stages of Human Subjects. Washington,
US: Government Printing Office; 1968.
[33] Cohen J. Statistical power analysis for the behavioral sciences. Hillsdale, NJ: L
Erbaum Associates; 1988.
[34] King AC, Oman RF, Brassington GS, Bliwise DL, Haskell WL. Moderate-intensity
exercise and self-rated quality of sleep in older adults. A randomized
controlled trial. JAMA 1997;277:32–7.
[35] King AC, Pruitt LA, Woo S, Castro CM, Ahn DK, Vitiello MV, et al. Effects of
moderate-intensity exercise on polysomnographic and subjective sleep
quality in older adults with mild to moderate sleep complaints. J Gerontol A
Biol Sci Med Sci 2008;63:997–1004.
[36] Alessi CA, Schnelle JF, MacRae PG, Ouslander JG, al-Samarrai N, Simmons SF,
et al. Does physical activity improve sleep in impaired nursing home
residents? J Am Geriatr Soc 1995;43:1098–102.
[37] Ferris LT, Williams JS, Shen CL, O’Keefe KA, Hale KB. Resistance training
improves sleep quality in older adults–a pilot. J Sport Sci Med 2005;4:
354–60.
[38] Martin JL, Marler MR, Harker JO, Josephson KR, Alessi CA. A multicomponent
nonpharmacological intervention improves activity rhythms among nursing
home residents with disrupted sleep/wake patterns. J Gerontol A Biol Sci Med
Sci 2007;62:67–72.
[39] Ruuskanen JM, Parkatti T. Physical activity and related factors among nursing
home residents. J Am Geriatr Soc 1994;42:987–91.
[40] Pinto Jr LR, Pinto MC, Goulart LI, et al. Sleep perception in insomniacs, sleepdisordered breathing patients, and healthy volunteers – an important biologic
parameter of sleep. Sleep Med 2009;10:865–8.
[41] Tang NK, Harvey AG. Time estimation ability and distorted perception of sleep
in insomnia. Behav Sleep Med 2005;3:134–50.
[42] Frankel BL, Coursey RD, Buchbinder R, Snyder F. Recorded and reported
sleep in chronic primary insomnia. Arch Gen Psychiatry 1976;33:
615–23.
[43] Edinger JD, Marsh GR, McCall WV, Erwin CW, Lininger AW. Sleep variability
across consecutive nights of home monitoring in older mixed DIMS patients.
Sleep 1991;14:13–7.
[44] Asher LMTR. Paradoxal intention and insomnia: an experimental investigation.
Behav Res Therapy 1979;17:408–41.
[45] Nicassio PM, Boylan MB, McCabe TG. Progressive relaxation, EMG biofeedback
and biofeedback placebo in the treatment of sleep-onset insomnia. Br J Med
Psychol 1982;55:159–66.
[46] Jacobs GD, Pace-Schott EF, Stickgold R, Otto MW. Cognitive behavior therapy
and pharmacotherapy for insomnia: a randomized controlled trial and direct
comparison. Arch Intern Med 2004;164:1888–96.
[47] Katz DA, McHorney CA. The relationship between insomnia and healthrelated quality of life in patients with chronic illness. J Fam Pract
2002;51:229–35.
G.S. Passos et al. / Sleep Medicine 12 (2011) 1018–1027
[48] Leger D, Scheuermaier K, Philip P, et al. SF-36: evaluation of quality of life in
severe and mild insomniacs compared with good sleepers. Psychosom Med
2001;63:49–55.
[49] Zammit GK, Weiner J, Damato N, Sillup GP, McMillan CA. Quality of life in
people with insomnia. Sleep 1999;22(Suppl. 2):S379–85.
[50] Rand D, Eng JJ, Tang PF, Hung C, Jeng JS. Daily physical activity, its contribution
to the health-related quality of life of ambulatory individuals with chronic
stroke. Health Qual Life Outcomes 2010;8:80.
[51] Savela SL, Koistinen P, Tilvis RS, et al. Physical activity at midlife and healthrelated quality of life in older men. Arch Intern Med 2010;170:1171–2.
[52] Stewart AL, King AC, Haskell WL. Endurance exercise and health-related
quality of life in 50–65 year-old adults. Gerontologist 1993;33:782–9.
1027
[53] Vale F, Reardon JZ, ZuWallack RL. The long-term benefits of outpatient
pulmonary rehabilitation on exercise endurance and quality of life. Chest
1993;103:42–5.
[54] Barnes M, Goldsworthy UR, Cary BA, Hill CJ. A diet and exercise program to
improve clinical outcomes in patients with obstructive sleep apnea – a
feasibility study. J Clin Sleep Med 2009;5:409–15.
[55] Singh NA, Clements KM, Fiatarone MA. A randomized controlled trial of the
effect of exercise on sleep. Sleep 1997;20:95–101.
[56] Hague JF, Gilbert SS, Burgess HJ, Ferguson SA, Dawson D. A sedentary day:
effects on subsequent sleep and body temperatures in trained athletes. Physiol
Behav 2003;78:261–7.