Download as pdf or txt
Download as pdf or txt
You are on page 1of 26

Accepted Manuscript

Effects of acute morning and evening exercise on subjective and objective sleep
quality in older individuals with insomnia

Yuko Morita, Taeko Sasai-Sakuma, Yuichi Inoue

PII: S1389-9457(17)30150-8
DOI: 10.1016/j.sleep.2017.03.014
Reference: SLEEP 3356

To appear in: Sleep Medicine

Received Date: 12 September 2016


Revised Date: 26 January 2017
Accepted Date: 8 March 2017

Please cite this article as: Morita Y, Sasai-Sakuma T, Inoue Y, Effects of acute morning and evening
exercise on subjective and objective sleep quality in older individuals with insomnia, Sleep Medicine
(2017), doi: 10.1016/j.sleep.2017.03.014.

This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to
our customers we are providing this early version of the manuscript. The manuscript will undergo
copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please
note that during the production process errors may be discovered which could affect the content, and all
legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Effects of acute morning and evening exercise on subjective and objective sleep quality in older individuals with

insomnia

Yuko Morita a, Taeko Sasai-Sakuma b,c, Yuichi Inoue b,d,*


a
Department of Liberal Arts, Faculty of Science and Technology, Tokyo University of Science, Chiba, Japan
b
Department of Somnology, Tokyo Medical University, Tokyo, Japan

PT
c
Department of Life Sciences and Bioinformatics, Division of Biomedical Laboratory Sciences, Graduate

School of Health Sciences, Tokyo Medical and Dental University, Tokyo, Japan

RI
d
Japan Somnology Center, Institute of Neuropsychiatry, Tokyo, Japan

SC
* Corresponding author. Japan Somnology Center, Institute of Neuropsychiatry, 1-24-10 Yoyogi, Shibuya-ku,

Tokyo, Japan. Tel.: +81 3 3374 9112; fax: +81 3 3374 9125.

E-mail address: inoue@somnology.com (Y. Inoue).


U
AN
M
D
TE
C EP
AC

ABSTRACT

Objectives: The aims of this study were to compare the effects of acute morning or evening exercise on

nocturnal sleep in individuals with two subjective insomnia symptoms: difficulty in initiating sleep (DIS), and

early morning awakening (EMA), separately for the first vs the second halves of the night.

Methods: Older individuals (55–65 years old) with DIS (N = 15) or EMA (N = 15) and age- and sex- matched

controls (N = 13) participated in this non-randomized crossover study. Participants were assigned to two

exercise conditions (morning exercise and evening exercise) in counterbalanced order following the baseline

1
ACCEPTED MANUSCRIPT
condition with a 2-week interval between conditions. A single session of aerobic step exercise was performed

during each exercise condition. Nocturnal polysomnography was carried out to evaluate objective sleep quality.

Patient global impression of change scale scores for nocturnal sleep were obtained to subjectively evaluate the

different groups.

Results: Acute physical exercise did not improve subjective sleep quality. Morning exercise decreased the

number of stage shifts over the whole night. The arousal index and the number of stage shifts were decreased

PT
especially during the second half of the night in all groups. Furthermore, morning exercise decreased the

number of wake stages during the second half of the night in the DIS group, but not in the EMA group.

RI
Conclusions: Acute morning exercise can improve nocturnal sleep quality in individuals with difficulty

SC
initiating sleep, especially during the later part of the night.

Keywords:

Insomnia
U
AN
Older adults

Acute exercise
M
D
TE
C EP
AC

2
ACCEPTED MANUSCRIPT

1. Introduction

The prevalence of insomnia increases with age, and no less than 20–30% of older adults from

developed countries report symptoms of insomnia [1–6]. Given that the presence of insomnia may lead to

secondary medical problems, including depression, anxiety disorders, metabolic syndrome, and other

lifestyle-related diseases [7–13], it is desirable to prevent and improve insomnia symptoms in the older

PT
population.

A previous review reported that physical exercise improves not only subjective sleep quality,

RI
but also objective sleep quality among patients with insomnia [14]. Several previous studies have revealed

that chronic afternoon exercise over 16 weeks or longer leads to improved subjective sleep quality, as

SC
evaluated by the Pittsburgh Sleep Quality Index or a sleep diary, as well as improved objective sleep

quality, as evaluated by nocturnal polysomnography (n-PSG) in middle-aged or older adults with

U
insomnia symptoms [15–17]. To the best of our knowledge, however, only one study has explored the
AN
effects of acute exercise. This study revealed that both objective sleep (reduction in sleep onset latency

and total wake time, and increase in total sleep time and sleep efficiency, as assessed using n-PSG) and
M

subjective sleep (reduction in sleep onset latency and increase in total sleep time, as indicated by sleep

logs) were improved after an afternoon of moderate intensity aerobic exercise in young adults with
D

chronic primary insomnia [18]. Thus, the effects of acute exercise on sleep quality in middle-aged and
TE

older adults with insomnia symptoms remain unknown.

Some previous studies have demonstrated that the time of the day of exercise (eg, morning vs
EP

late afternoon) has no impact on the effects of exercise on objective and subjective sleep quality [19,20].

However, the effects of the timing of exercise (either acute or chronic) on different types of insomnia

symptoms have not been investigated. Among the main symptoms of insomnia, such as difficulty
C

initiating sleep (DIS) or early morning awakening (EMA) [21], EMA is more frequently observed in
AC

older adults compared to other symptoms [5]. Furthermore, these symptoms are associated with circadian

core body temperature. DIS has a delayed core body temperature rhythm, while EMA has an advanced

rhythm [22]. Given this observation, it may be speculated that the effects of morning or evening physical

exercise on nocturnal sleep might differ depending on the specific type of insomnia symptoms, as well as

the timing of exercise. These effects may also differ between the first and second halves of the night

depending on difference in intrinsic circadian rhythms between aforementioned types of insomnia

3
ACCEPTED MANUSCRIPT

symptoms. To clarify this issue, nocturnal sleep quality, especially as assessed using n-PSG variables,

should be evaluated separately for the first and second halves of the night in each group and for each

exercise condition.

The aims of this study were (1) to compare the effects of morning and evening exercise on

subjective and objective sleep quality in middle-aged and older adults with insomnia symptoms, and (2)

PT
to compare the effects of morning and evening exercise on objective sleep-related variables in individuals

with two types of insomnia symptoms, EMA and DIS. We analyzed the first and second halves of the

RI
night separately.

2. Materials and methods

SC
2.1. Participants

The ethics committee of the Institute of Neuropsychiatry reviewed and approved the current study.

U
Study participants were recruited from members of a private clinical research corporation’s research
AN
panel. Among the members who were motivated to participate in the current study, individuals fulfilling

the following three conditions were eligible: (1) individuals with a primary insomnia complaint of DIS;
M

(2) individuals with a primary insomnia complaint of EMA; and (3) control individuals with no insomnia

symptoms. All participants in the study were Japanese and fulfilled the following inclusion criteria: (1)
D

age of 55–65 years; (2) body mass index of less than 28 kg/m2; (3) systolic arterial pressure less than 180
TE

mmHg and diastolic pressure less than 100 mmHg; (4) less than 30 min per week of physical exercise

according to the Japanese official physical activity guidelines for health promotion established by the
EP

Health, Labour, and Welfare Ministry in Japan; (5) a score of less than 11 on the Epworth Sleepiness

Scale [23], and (6) maintenance of a normal sleep–wake schedule with bed time between 21:00 and 01:00,

and wake time between 05:00 and 09:00. Participants meeting the following exclusion criteria were
C

excluded: (1) current smokers; (2) living alone (to exclude individuals who may have a sleep disorder that
AC

cannot be verified by a family member); (3) history or current morbidity of cardiovascular disease,

diabetes, respiratory disease, cerebrovascular disease, or psychiatric disorders; (4) limit on exercise

imposed by a physician; and (5) subjective symptoms strongly suggestive of sleep disorders other than

insomnia, such as sleep apnea, restless leg syndrome, or rapid eye movement sleep behavior disorder, as

determined using self-administered questionnaires.

4
ACCEPTED MANUSCRIPT

Participants in the DIS group were required to fulfill the following additional inclusion criteria: (1)

score of 6 or higher on the Athens Insomnia Scale (AIS); (2) subjective sleep latency of 30 min or longer

three times or more per week; and (3) answer of “not earlier” or “a little earlier” to the “Final awakening”

subscale on the AIS. Participants in the EMA group were required to fulfill the following criteria: (1)

score of 6 or higher on the AIS; (2) answer of “markedly earlier” or “much earlier or did not sleep at all”

PT
on the “Final awakening” subscale on the AIS; and (3) answer of “no problem” or “slightly delayed” on

the “Sleep induction” subscale on the AIS. The subjects in the control group had scores of less than 6 on

RI
the AIS. In addition, electrocardiography (ECG) and n-PSG were carried out in participants who met the

above inclusion criteria. Participants who had an abnormal ECG or evidence of sleep disorders on PSG,

SC
such as sleep apnea (apnea–hypopnea index [AHI] ≥ 15/h) or periodic leg movements during sleep

(PLMS; PLM index [PLMI] ≥ 15/h), were screened out.

U
Seventy-three participants met the above inclusion criteria. Among these participants, two were
AN
excluded for abnormal ECG findings, 12 were excluded for sleep apnea, and 16 were excluded for

PLMS. Consequently, 43 participants (DIS, N = 15; EMA, N = 15; control, N = 13) participated in the
M

experimental intervention trial (Fig. 1).

2.2. Design and Procedures


D

The current study was conducted using a repeated-measures non-randomized crossover design. All
TE

experimental procedures were conducted at the Yoyogi Sleep Disorder Center. Fig. 2 shows the

experimental protocol. At the first visit (visit 1), all participants who gave informed consent had an ECG
EP

examination. At visit 2, which was performed within 1 week of visit 1, participants underwent a pre-

exercise session followed by n-PSG, which was performed both to adapt the participant to the recording

and to screen for the above-mentioned sleep disorders. At visit 3, which was performed within 1 week of
C

visit 2, participants underwent baseline n-PSG and were asked to respond to the patient global impression
AC

of change (PGI-C) scale, which measures subjective sleep quality (baseline condition).

Scheduled aerobic step exercise was conducted at visits 4 and 5. Visit 4 was scheduled 2 weeks

after visit 3, and visit 5 was scheduled 2 weeks after visit 4. Half of the participants were assigned to the

morning exercise condition at visit 4 and the evening exercise condition at visit 5, and the remaining half

were assigned to the two conditions in the reverse order. The order of these conditions was determined by

the participants’ daily schedules (e.g., jobs, family obligations, etc.). In the morning exercise condition,

5
ACCEPTED MANUSCRIPT

participants performed the step exercise program from 09:30 to 11:00 followed by n-PSG on the same

day. In the evening exercise condition, participants performed the exercise program from 17:30 to 19:00

followed by n-PSG. In both conditions, participants responded to the PGI-C scale just after n-PSG

recording in the next morning.

All participants were instructed not to consume caffeine or alcohol and to avoid naps 24 h prior to

PT
each visit. The participants were instructed to go to bed between 21:00 and 01:00, and to wake up

between 05:00 and 09:00 (according to their usual sleep–wake schedules), and to spend at least 6 h per

RI
night in bed during the experimental period. The participants’ sleep–wake schedules were assessed using

a sleep diary and an activity monitor (ActiSleep BT Monitor; Actigraph LLC, Pensacola, FL, USA) for a

SC
week prior to each visit. Bedtime and wake time were set to 22:00 and 06:00, respectively, on n-PSG

nights in all conditions.

U
2.3. Measurements
AN
2.3.1. Subjective sleep quality

To evaluate subjective sleep quality in each condition, the following seven items on the PGI-C were
M

assessed: subjective sleep latency, wake time after sleep onset, total sleep duration, feeling of deep sleep,

fatigue and sleepiness at the time of awakening, and feeling that sleep was restorative [24]. Each item on
D

the PGI-C is rated on an 11-point numerical rating scale from -5 (much worse) to 5 (much improved)
TE

compared to the participant’s usual condition (with 0 representing the participant’s usual condition).

2.3.2. n-PSG
EP

n-PSG recordings were conducted on adaptation and baseline nights, and on two nights following

exercise using a standard system (Alice 5; Respironics Inc., Murrysville, PA, USA) with video

monitoring. The n-PSG used six scalp electroencephalogram channels (F3/A2, F4/A1, C3/A2, C4/A1,
C

O1/A2, and O2/A1), bilateral electrooculograms, and two electromyograms obtained from the mentalis
AC

muscle. Nasal/oral airflow using sensors, percutaneous oxygen saturation with oximetry, snoring sounds

using a microphone, chest/abdominal respiratory effort, and leg movements (bipolar derivations with two

electrodes placed 3 cm apart on the belly of the anterior tibialis muscle of the right and left legs) were

recorded on the adaptation night to screen for the above-mentioned sleep disorders.

n-PSG data were scored according to the scoring criteria set by the American Academy of Sleep

Medicine (AASM) [25]. The following sleep variables were obtained from each recording: sleep period

6
ACCEPTED MANUSCRIPT

time; total sleep time; sleep efficiency; sleep onset latency; wake after sleep onset; N1, N2, N3, and rapid

eye movement (REM) stage percentages of sleep time; arousal index; number of stage shifts; duration of

early morning awakening (from last epoch scored as sleep to 06:00), AHI, and PLMI.

2.3.3. Pre-exercise session

During the pre-exercise session, the height of the step platform was adjusted to maintain each

PT
participant’s heart rate (HR) reserve (HRR) at 59%, which is considered to be moderate intensity [26].

Participants wore a heart rate monitor (RS800CX; Polar Electro Inc., North New Hyde Park, NY, USA),

RI
and stepped up and down 120 times per minute with the aim of increasing heart rate. The height of the

step platform was set at 10 cm at the beginning of the session and then increased by 2.5 cm every 5 min

SC
until each participant’s HR was increased to the target HR.

Sixty percent of HRR was calculated for each participant based on Karvonen’s formula: target HR

U
= [(maximum HR – resting HR) × % exercise intensity] + resting HR [27]. Maximum HR was calculated
AN
based on a predictive formula reported by Gellish et al.: HR max = 207 0.7 × age [28]. Resting HR

was measured at the time of ECG measurements during the first visit.
M

2.3.4. Exercise intervention

Each exercise condition consisted of four sets of 10-min aerobic step exercise with 5-min rest
D

periods between sets. A previous study reported that only moderate-intensity aerobic exercise improves
TE

sleep quality [18]. Thus, we conducted aerobic step exercise with moderate intensity. During each 10-min

set, the participants were instructed to move up and down a step platform with a height determined in the
EP

pre-exercise session. Prior to the four sets of step exercise, a stretching exercise and a slow-tempo (80

bpm) step exercise were performed as a warm up for 20 min. At the end of the exercise session, a 15-min
C

stretching exercise was performed to cool down. All exercise was performed in a group setting.

2.4. Statistical Analyses


AC

One participant dropped out during the study period due to an orthopedic injury sustained during

routine daily activities. Additionally, two participants who could not follow the study protocol were

excluded from subsequent analyses. Consequently, data from 40 participants (DIS: N = 12, EMA: N = 15,

control: N = 13) were included in the final analyses (Fig. 1).

7
ACCEPTED MANUSCRIPT

Chi-square tests were used for group comparisons of categorical variables and independent t-tests

and one-way analyses of variance (ANOVAs) followed by Bonferroni’s post hoc tests were used for

continuous variables.

To assess subjective sleep quality, scores on the PGI-C were compared among groups using a two-

way repeated-measures ANOVA (groups: DIS, EMA, and control; conditions: baseline, morning exercise,

PT
and evening exercise) followed by Bonferroni’s post hoc test.

To compare n-PSG variables between the two groups (DIS and EMA), a two-way repeated-

RI
measures ANOVA (group × condition) followed by Bonferroni’s post hoc test was conducted. For

exploratory analysis, nocturnal sleep was divided into the first and second half of the night based on time

SC
in bed (240 min per half). To investigate the effects of morning and evening exercise on n-PSG variables

in the first and second halves of the night among the DIS, EMA, and control groups, n-PSG variables in

U
each half were compared using two-way repeated-measures ANOVAs (group × condition). All statistical
AN
analyses were conducted using SPSS software (SPSS, v11.5; SPSS Inc., Chicago, IL, USA). Statistical

significance was indicated by a p-value of less than 0.05.


M

3. Results

3.1. Baseline participant characteristics


D

Baseline participant characteristics are presented in Table 1. No differences in the variables were
TE

found between the three groups, except for the AIS, which was used to select participants for each group.

3.2. Subjective sleep parameters


EP

Table 2 presents the subjective sleep parameters measured using the PGI-C in each group for each

condition. Two-way repeated-measures ANOVA revealed no significant main effect of either group or

condition and no significant interaction on any PGI-C item. Statistical F-values for each item on the PGI-
C

C are as follows: sleep latency (main effect: F(2, 74) = 0.09, interaction effect: F(4, 74) = 0.09), wake after
AC

sleep onset (main effect: F(2, 74) = 0.58, interaction effect: F(4, 74) = 0.11), total sleep duration (main effect:

F(2, 74) = 0.28, interaction effect: F(4, 74) = 0.90), feeling of deep sleep (main effect: F(2, 74) = 1.45,

interaction effect: F(4, 74) = 0.48), fatigue upon awakening (main effect: F(2, 74) = 0.18, interaction effect:

F(4, 74) = 0.68), sleepiness upon awakening (main effect: F(2, 74) = 0.06, interaction effect: F(4, 74) = 0.33),

and feeling that sleep was restorative (main effect: F(2, 74) = 0.59, interaction effect: F(4, 74) = 0.75).

3.3. n-PSG variables

8
ACCEPTED MANUSCRIPT

3.3.1. Effects of morning and evening exercise on n-PSG variables across the entire night

Table 3 presents the n-PSG variable following morning exercise compared to those following evening

exercise across the entire night. There were no significant differences in n-PSG variables among the

groups at baseline. Two-way repeated-measures ANOVA (group × condition) revealed no interaction

effects for any n-PSG variables. A significant main effect of condition was detected in the number of

PT
stage shifts (F(2, 74) = 4.54), such that the number of stage shifts was lower in the morning exercise

condition compared to baseline (P = 0.009).

RI
3.3.2. Effects of morning and evening exercise on n-PSG variables in the first and last halves of the night

Two-way repeated-measures ANOVA revealed no significant main effect or interaction effect for any

SC
n-PSG variable during the first half of the night (Table 4). In the second half of the night, a significant

main effect of condition was found in the number of stage shifts and the arousal index, such that both the

U
number of stage shifts and the arousal index were significantly decreased in the morning exercise
AN
condition (F(2,74) = 3.87 and F(2,74) = 4.67, respectively). Furthermore, a significant interaction was

detected in the number of wake stages (F(2,74) = 2.93, ηn2 = 0.15, p=0.015). Bonferroni’s post hoc analysis
M

revealed that the number of wake stages decreased in the morning exercise condition when compared to

baseline in the DIS group (p<0.001), while this number decreased in the evening exercise condition in the
D

EMA group (p=0.049).


TE

4. Discussion

In the present study, neither acute morning nor acute evening exercise improved subjective sleep
EP

measures in any of the groups. This finding is inconsistent with those of a previous study in patients with

chronic insomnia, which reported that acute moderate-intensity aerobic exercise improves subjective

sleep quality, as evaluated by sleep logs, sleep onset latency, and total sleep time [18]. This discrepancy
C

might be partially ascribed to differences in the populations studied, as the severity of insomnia in our
AC

participants may have been milder than in the participants in the previous study.

Acute morning exercise decreased the number of stage shifts during the entire night in all three

groups, although the n-PSG results revealed no major improvements in objective sleep measures, such as

reduction of sleep latency in the DIS group or reduction of early morning wake time in the EMA group,

following exercise [18,29]. The aforementioned modest effect of morning exercise in all groups was

observed especially during the later part of nocturnal sleep. The decreased arousal index and stage shifts

9
ACCEPTED MANUSCRIPT

were observed during in the second half of the night. However, modest improvements in n-PSG

parameters did not lead to improvements in subjective sleep quality. Although the improvements

observed in our study were not as dramatic as those observed in previous studies, which included

reductions in both sleep onset latency and wake after sleep onset, as well as improvements in sleep

efficiency, reductions in the arousal index, and stage shifts during the second half of the night, morning

PT
exercise is speculated to induce stabilization of nocturnal sleep.

Our results raise the possibility that morning exercise increases sleep pressure, which in turn leads

RI
to maintenance of stable sleep throughout the night, when compared to evening exercise. Another

possibility is that exercise influences the autonomic nervous system during sleep. A recent study

SC
demonstrated that morning exercise enhanced parasympathetic nervous activity during subsequent

nocturnal sleep, whereas evening exercise enhanced sympathetic nervous activity [30]. The change in

U
autonomic balance toward parasympathetic dominance is known to promote the transition from
AN
wakefulness to sleep [31,32]. Inconsistent with the present results, several previous studies have reported

a positive effect of evening exercise on sleep variables. For example, evening exercise has been reported
M

to cause a steeper decline in core body temperature before bedtime, resulting in a greater amount of slow-

wave [33,34], shorter sleep latency, and increased sleep efficiency [18,34]. One possible reason for the
D

inconsistency between our study and the previous studies is differences in the ages of participants across
TE

the studies. In general, compared to young adults, middle-aged or older adults are known to have

difficulty alternating from the sympathetic nervous system predominance to the parasympathetic one.
EP

This may result in a slower response to change in core body temperature after evening physical exercise

[35]. Thus, in the present study of middle-aged and older adults, slow recovery from the elevated core

body temperature after evening exercise may have diminished the sleep-promoting effects of evening
C

exercise.
AC

In this study, the mild positive effect of morning exercise on objective sleep variables was observed

only during the second half of the nocturnal sleep period. The reason for this phenomenon is unclear.

However, it is possible that the aforementioned autonomic nervous response occurs at a later time after

sleep onset in the middle-aged and older participants in our study. In general, the autonomic balance

shifts toward parasympathetic predominance just after sleep onset in young adults. In contrast, in middle-

aged and older adults, the parasympathetic predominance during sleep is weaker and occurs later than it

10
ACCEPTED MANUSCRIPT

does in younger adults due to the delayed onset of slow-wave sleep [36,37]. This is why the mild impact

of morning exercise was observed only on the second half of the nocturnal sleep episode in older

individuals.

Morning exercise decreased the number of wake stages during the second half of the night only in

the DIS group. This may be due to increased sleep pressure, as discussed above. That is, increased sleep

PT
pressure following morning exercise maintains the subjects’ sleep propensity until early morning. In

contrast, we did not observe an effect of morning exercise during the later part of the night in the EMA

RI
group. One possible reason for this finding may be a difference in intrinsic sleep–wake rhythms between

the DIS and EMA groups. Individuals with DIS have a delayed core body temperature rhythm and those

SC
with EMA have an advanced rhythm [22]. Therefore, in the EMA group, the wake propensity in the early

morning diminishes the effects of morning exercise during the later part of the night. The observed

U
increase in the number of wake stages might support the fact that morning exercise can bring about sleep
AN
stabilization, especially during the later part of the night. These small but significant changes may

indicate mild improvements in objective sleep quality following acute morning exercise. In addition, in
M

clinical settings, feedback from changes in objective parameters following acute exercise is necessary for

patients to maintain their motivation to improve their nocturnal sleep by performing physical exercise. An
D

accumulation of this effect on objective sleep quality following regular morning exercise is expected to
TE

lead to more significant improvements in subjective and objective sleep quality. Future studies should

explore the effect of long-term morning exercise on objective and subject sleep quality in older
EP

individuals. Furthermore, these results provide evidence that the effects of acute physical exercise differ

both among individuals with different types of insomnia and between earlier and later sleep periods. This

study therefore suggests the establishment of practical physical exercise as a therapy for insomnia,
C

although the specific type of insomnia symptoms and the timing of the exercise should be considered.
AC

The current study has several limitations. First, the severity of insomnia symptoms was relatively mild

in our participants because participants were selected on the basis of the AIS score only. We did not

conduct a clinical interview to assess daytime dysfunction, which are listed in the International

Classification of Sleep Disorders – Third Edition (ICSD-3) criteria for chronic insomnia [39]. A possible

reason that these changes in objective sleep parameters were not large enough to improve the

participants’ subjective sleep quality may be that the participants’ symptoms of DIS and EMA were not

11
ACCEPTED MANUSCRIPT

so severe as to be differentiated by objective sleep parameters at baseline. We need to determine whether

a positive effect of physical exercise on nocturnal sleep is observed in participants with more severe

insomnia symptoms (eg, worsened objective sleep variables or clinical insomnia). Second, neither core

body temperature nor heart rate variability was evaluated in the current study. These physiological

markers should be measured in a future study to clarify the impact of physical exercise on autonomic

PT
nervous system activity and sleep quality during the night following exercise. Third, we used a single-

session exercise protocol. Thus, we were unable to assess the impact of physical exercise on the subjects’

RI
circadian rhythms. To determine the optimal exercise timing for patients with different insomnia

symptoms, the impact of exercise on circadian rhythms should be explored using long-term exercise

SC
interventional trials.

5. Conclusion

U
Acute morning exercise moderately improved objective sleep variables, as determined by n-PSG, in
AN
all groups. Although these improvements were not dramatic, reductions in the arousal index and stage

shifts during the second half of the night following acute morning exercise may manifest as mild
M

improvements in objective sleep quality. Furthermore, in the DIS group, the number of wake stages

during the second half of the night decreased following morning exercise. This effect was not observed in
D

the EMA group. These results indicate that the effects of acute physical exercise differ in individuals with
TE

different types of insomnia and during earlier vs later sleep periods. This study thus contributes to the

establishment of practical physical exercise as a therapy for insomnia.


EP

Conflict of interest

This study was supported by The Ministry of Education, Culture, Sports, Science and Technology
C

KAKENHI Grant-in-Aid for Research Activity Start-up No. 25882030. This study was supported by the
AC

industry. Dr Inoue provided expert testimony for and payment for lectures from Takeda Pharmaceutical

Company Limited and MSD K.K. The other authors have indicated that they have no financial conflicts

of interest.

References

12
ACCEPTED MANUSCRIPT

[1] Leger D, Guilleminault C, Dreyfus JP, Delahaye C, Paillard M. Prevalence of insomnia in a

survey of 12,778 adults in France. J Sleep Res 2000;9:35–42.

[2] Morphy H, Dunn KM, Lewis M, Boardman HF, Croft PR. Epidemiology of insomnia: a

longitudinal study in a UK population. Sleep 2007;30:274–80.

PT
[3] Ohayon MM, Sagales T. Prevalence of insomnia and sleep characteristics in the general

population of Spain. Sleep Med 2010;11:1010–8.

RI
[4] Roth T, Roehrs T. Insomnia: Epidemiology, characteristics, and consequences. Clin Cornerstone

2003;5:5–12.

SC
[5] Kim K, Uchiyama M, Okawa M, Liu X, Ogihara R. An epidemiological study of insomnia among

U
the Japanese general population. Sleep 2000;23:41–7.
AN
[6] Ford ES, Cunningham TJ, Giles WH, Croft JB. Trends in insomnia and excessive daytime

sleepiness among U.S. adults from 2002 to 2012. Sleep Med 2015;16:372–8.
M

[7] Neckelmann D, Mykletun A, Dahl AA. Chronic insomnia as a risk factor for developing anxiety

and depression. Sleep 2007;30:873–80.


D

[8] Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders. An
TE

opportunity for prevention? JAMA 1989;262:1479–84.

[9] Baglioni C, Battagliese G, Feige B, Spiegelhalder K, Nissen C, Voderholzer U, et al. Insomnia as


EP

a predictor of depression: A meta-analytic evaluation of longitudinal epidemiological studies. J

Affect Disord 2011;135:10–9.


C

[10] Buysse DJ. Insomnia, depression and aging. Assessing sleep and mood interactions in older
AC

adults. Geriatrics 2004;59:47–51; quiz 52.

[11] Sivertsen B, Lallukka T, Salo P, Pallesen S, Hysing M, Krokstad S, et al. Insomnia as a risk

factor for ill health: results from the large population-based prospective HUNT Study in Norway.

J Sleep Res 2014;23:124–32.

13
ACCEPTED MANUSCRIPT

[12] Lewis PE, Emasealu O V., Rohrbeck P, Hu Z. Risk of type II diabetes and hypertension

associated with chronic insomnia among active component, U.S. Armed Forces, 1998-2013. Med

Surveill Mon Rep 2014;21:6–13.

[13] Akbaraly TN, Jaussent I, Besset A, Bertrand M, Barberger-Gateau P, Ritchie K, et al. Sleep

PT
Complaints and Metabolic Syndrome in an Elderly Population: The Three-City Study. Am J

Geriatr Psychiatry 2015;23:818–28.

RI
[14] Passos GS, Poyares DLR, Santana MG, Tufik S, Mello MT De. Is exercise an alternative

treatment for chronic insomnia? Clinics (Sao Paulo) 2012;67:653–60.

SC
[15] 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.

[16]
U
King AC, Pruitt L a, Woo S, Castro CM, Ahn DK, Vitiello M V, et al. Effects of moderate-
AN
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.


M

[17] King AC, Oman RF, Brassington GS, Bliwise DL, Haskell WL. Moderate-intensity exercise and
D

self-rated quality of sleep in older adults. A randomized controlled trial. vol. 277. 1997.
TE

[18] Passos GS, Poyares D, Santana MG, Garbuio S a, Tufik S, Mello MT. Effect of acute physical

exercise on patients with chronic primary insomnia. J Clin Sleep Med 2010;6:270–5.
EP

[19] Passos GS, Poyares D, Santana MG, D’Aurea CVR, Youngstedt SD, Tufik S, et al. Effects of

moderate aerobic exercise training on chronic primary insomnia. Sleep Med 2011;12:1018–27.
C

[20] Benloucif S, Orbeta L, Ortiz R, Janssen I, Finkel SI, Bleiberg J, et al. Morning or evening activity
AC

improves neuropsychological performance and subjective sleep quality in older adults. Sleep

2004;27:1542–51.

[21] Lichstein KL, Durrence HH, Taylor DJ, Bush a. J, Riedel BW. Quantitative criteria for insomnia.

Behav Res Ther 2003;41:427–45.

[22] Lack LC, Gradisar M, Van Someren EJW, Wright HR, Lushington K. The relationship between

insomnia and body temperatures. Sleep Med Rev 2008;12:307–17.

14
ACCEPTED MANUSCRIPT

[23] Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep

1991;14:540–5.

[24] Hurst H, Bolton J. Assessing the clinical significance of change scores recorded on subjective

outcome measures. J Manipulative Physiol Ther 2004;27:26–35.

PT
[25] Iber C, Ancoli-Israel S., Chesson A. QSF for the AA of SM. The AASM Manual for the Scoring

of Sleep and Associated Events Rules, Terminology and Technical Specifications. Westchester,

RI
Illinois Am Acad Sleep Med 2007.

[26] Howley ET. Type of activity: resistance, aerobic and leisure versus occupational physical activity.

SC
Med Sci Sports Exerc 2001;33:364–9.

U
[27] Karvonen J, Vuorimaa T. Heart rate and exercise intensity during sports activities. Practical

application. Sports Med 1988;5:303–11.


AN
[28] Gellish RL, Goslin BR, Olson RE, McDonald A, Russi GD, Moudgil VK. Longitudinal modeling

of the relationship between age and maximal heart rate. Med Sci Sports Exerc 2007;39:822–9.
M

[29] Chennaoui M, Arnal PJ, Sauvet F, Léger D. Sleep and exercise: A reciprocal issue? Sleep Med
D

Rev 2015;20:59–72.
TE

[30] Yamanaka Y, Hashimoto S, Takasu NN, Tanahashi Y, Nishide S, Honma S, et al. Moring and

evening physical exercise differentially regulate the autonomic nervous system during nocturnal
EP

sleep in humans. Am J Physiol - Regul Integr Comp Physiol 2015;309:R1112–21.

[31] Trinder J, Kleiman J, Carrington M, Smith S, Breen S, Tan N, et al. Autonomic activity during
C

human sleep as a function of time and sleep stage. J Sleep Res 2001;10:253–64.
AC

[32] Meerlo P, Sgoifo A, Suchecki D. Restricted and disrupted sleep: effects on autonomic function,

neuroendocrine stress systems and stress responsivity. Sleep Med Rev 2008;12:197–210.

[33] McGinty D, Szymusiak R. Keeping cool: a hypothesis about the mechanisms and functions of

slow-wave sleep. Trends Neurosci 1990;13:480–7.

[34] Youngstedt SD, O’Connor PJ, Dishman RK. The effects of acute exercise on sleep: a quantitative

synthesis. Sleep 1997;20:203–14.

15
ACCEPTED MANUSCRIPT

[35] Ferreira JJA, Mendonça LCS, Nunes LAO, Andrade Filho ACC, Rebelatto JR, Salvini TF.

Exercise-associated thermographic changes in young and elderly subjects. Ann Biomed Eng

2008;36:1420–7.

[36] Bonnemeier H, Wiegand UKH, Brandes A, Kluge N, Katus H a., Richardt G, et al. Circadian

PT
profile of cardiac autonomic nervous modulation in healthy subjects: Differing effects of aging

and gender on heart rate variability. J Cardiovasc Electrophysiol 2003;14:791–9.

RI
[37] Brandenberger G, Viola AU, Ehrhart J, Charloux A, Geny B, Piquard F, et al. Age-related

changes in cardiac autonomic control during sleep. J Sleep Res 2003;12:173–80.

SC
[38] Dffy uJ F, Dijk DJ, Klerman EB, Czeisler CA. Later endogenous circadian temperature nadir

relative to an earlier wake time in older people. Am J Physiol 1998;275:R1478–87.

[39]
U
American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd ed.
AN
Darien, IL: American Academy of Sleep Medicine, 2014; p.182-186. n.d.
M

Fig. 1. Flow chart of participants through the study. The order of exercise conditions was determined by
the participants’ daily schedules. BL, baseline condition; ME, morning exercise condition; EE, evening
D

exercise condition.
Fig. 2. Experimental protocol. Half of the participants were assigned to the morning exercise condition
TE

followed by the evening exercise condition, and the remaining half were assigned to the two conditions in
reverse order. EEG, electroencephalogram; PGI-C, patient global impression of changes.
C EP
AC

16
ACCEPTED MANUSCRIPT

Table 1. Baseline participant characteristics


Control DIS EMA
N = 13 N = 12 N = 15 ES p
Sex [male/female] 6/7 4/8 5 / 10 0.12 0.765
Age [years] 58.8 (2.9) 58.9 (3.6) 57.7 (2.9) 0.00 0.539
BMI [m/kg2] 22.9 (2.0) 22.2 (2.3) 21.1 (1.8) 0.02 0.069
SBP [mmHg] 117.5 (9.2) 115.4 (10.3) 124.5 (12.5) 0.02 0.083

PT
DBP [mmHg] 73.3 (8.1) 73.4 (11.0) 77.8 (10.6) 0.00 0.484
Resting heart rate [bpm] 64.9 (10.3) 71.2 (12.5) 68.2 (12.6) 0.00 0.429
Bedtime 23:21 (1 h 16 min) 23:55 (58.4 min) 23:38 (53.0 min) 0.00 0.403
Rise time 06:25 (1 h 09 min) 06:40 (51.7 min) 06:18 (54 min) 0.00 0.626
AHI [events/hour] 4.3 (4.2) 2.7 (2.1) 2.2 (1.9) 0.01 0.151

RI
PLMI [events/hour] 1.0 (2.0) 2.7 (5.2) 1.8 (3.6) 0.00 0.495
AIS score 1.7 (1.7) 10.2 (2.9)* 9.1 (2.4)* 0.53 <0.001
ESS score 3.2 (3.4) 4.1 (2.7) 4.5 (3.2) 0.00 0.512

SC
Employee 3 (23.1) 3 (25.0) 4 (26.7) 0.04 0.976

Continuous variables are expressed as mean (standard deviation), and categorical variables are expressed
as number of subjects (percent). AHI, apnea–hypopnea index; AIS, Athens Insomnia Scale; BMI, body

U
mass index; DBP, diastolic blood pressure; DIS, difficulty in initiating sleep; EMA, early morning
awakening; ES, effect size; ESS, Epworth Sleepiness Scale; PLMI, periodic limb movements index; SBP,
AN
systolic blood pressure. Effect size is expressed as ηp2 (one-way analysis of variance) following Cramer’s
V (2 × 3 chi-square test).
*p<0.05 vs control.
M
D
TE
C EP
AC

17
ACCEPTED MANUSCRIPT

Table 2. Subjective sleep parameters assessed using the patient global impression of change in each
condition.
Main effects
Morning Evening of conditions Interaction
Baseline
exercise exercise
ES p ES p
Sleep latency
Control 0.5 (2.5) -0.2 (3.0) 0.1 (3.4)

PT
DIS -0.8 (2.6) -0.2 (3.0) -0.2 (2.9) 0.00 0.919 0.03 0.707
EMA -0.7 (2.4) -0.1 (2.7) -0.9 (2.8)
Number of awakenings

RI
Control -1.2 (2.8) -0.8 (2.4) -0.8 (2.8)
DIS -1.2 (2.3) -0.7 (2.7) -0.3 (1.8) 0.02 0.561 0.01 0.980
EMA -1.5 (2.0) -1.2 (1.9) -1.3 (2.1)

SC
Total sleep duration
Control 0.0 (3.2) -0.8 (2.2) -0.1 (2.7)
DIS -0.3 (2.5) 0.9 (3.0) 0.3 (2.9) 0.00 0.759 0.05 0.466

U
EMA -0.4 (2.1) 0.2 (2.6) -0.4 (2.9)
Feeling of deep sleep
AN
Control -0.7 (2.9) -0.6 (2.5) -0.1 (2.8)
DIS -0.8 (2.6) -0.1 (3.1) -0.4 (2.9) 0.04 0.24 0.03 0.751
EMA -1.4 (2.3) 0.1 (2.8) -0.5 (2.8)
M

Fatigue upon awakening


Control -1.4 (1.9) -0.9 (2.3) -0.3 (2.0)
DIS 0.0 (2.0) -0.3 (2.4) -0.5 (2.7) 0.01 0.833 0.04 0.611
D

EMA -0.9 (1.6) -0.7 (2.3) -0.7 (1.8)


Sleepiness upon awakening
TE

Control -0.7 (1.0) -0.9 (2.1) -0.2 (2.1)


DIS -0.2 (1.3) -0.1 (2.3) -0.4 (2.4) 0.00 0.944 0.02 0.854
EMA -0.7 (1.4) -0.6 (2.5) -0.6 (2.2)
EP

Feeling that sleep was restorative


Control -1.4 (1.6) -1.2 (2.4) -0.4 (2.8)
DIS 0.1 (1.9) -0.5 (3.0) -0.2 (2.6) 0.02 0.559 0.04 0.562
EMA -1.3 (1.6) -0.6 (2.6) -0.8 (2.2)
C

DIS, difficulty in initiating sleep; EMA, early morning awakening; ES, effect size. ES is expressed as ηp2.
AC

18
ACCEPTED MANUSCRIPT

Table 3. Effects of morning and evening exercise on nocturnal polysomnography variables over the entire

night.

Main effects
Morning Evening of Interaction
Baseline
exercise exercise conditions
ES p ES P

PT
SPT (min)
Control 471.7 ± 16.1 471.8 ± 12.2 475.0 ± 6.8
DIS 469.0 ± 8.7 468.2 ± 20.3 474.3 ± 7.1 0.01 0.828 0.05 0.456
EMA 471.9 ± 13.3 469.9 ± 13.8 466.1 ± 21.1

RI
TST (min)
Control 431.7 ± 29.9 433.0 ± 31.1 430.7 ± 38.2
DIS 425.3 ± 25.0 427.6 ± 50.6 434.0 ± 28.7 0.00 0.866 0.01 0.906
EMA 429.3 ± 34.4 434.3 ± 23.6 428.3 ± 32.4

SC
SE (%)
Control 91.5 ± 4.9 91.8 ± 5.7 90.7 ± 7.6
DIS 90.7 ± 4.5 91.1 ± 8.0 91.5 ± 5.2 0.01 0.639 0.02 0.879
EMA 90.9 ± 6.6 93.1 ± 4.2 91.8 ± 4.1

U
Sleep onset latency (min)
Control 6.7 ± 10.7 4.2 ± 3.3 4.8 ± 6.9
AN
DIS 9.5 ± 8.4 6.5 ± 6.6 3.4 ± 2.2 0.06 0.105 0.08 0.185
EMA 3.2 ± 2.1 3.5 ± 2.8 4.0 ± 3.0
REM sleep onset latency
(min)
M

Control 74.5 ± 25.0 82.1 ± 48.9 106.2 ± 57.8


DIS 120.1 ± 45.3 96.1 ± 29.5 86.8 ± 17.0 0.01 0.587 0.10 0.094
EMA 86.6 ± 39.2 80.5 ± 19.0 91.3 ± 50.9
Time of early morning
D

awakening (min)
Control 1.6 ± 5.5 4.0 ± 9.9 0.7 ± 1.7
TE

DIS 1.5 ± 3.5 5.3 ± 16.5 2.3 ± 7.3 0.02 0.467 0.03 0.655
EMA 4.9 ± 13.8 6.7 ± 13.3 9.9 ± 19.8
WASO (%)
Control 8.5 ± 4.9 8.2 ± 5.8 9.3 ± 7.6
EP

DIS 9.3 ± 4.5 8.9 ± 8.0 8.5 ± 5.2 0.01 0.776 0.10 0.941
EMA 9.1 ± 6.6 7.5 ± 4.9 8.2 ± 4.1
N1 stage (%)
Control 13.9 ± 6.9 11.5 ± 4.9 12.1 ± 5.1
C

DIS 11.4 ± 4.7 11.1 ± 5.9 11.6 ± 3.8 0.03 0.286 0.02 0.762
EMA 11.2 ± 5.5 10.2 ± 5.6 11.2 ± 4.1
N2 stage (%)
AC

Control 59.1 ± 7.8 59.3 ± 9.6 59.9 ± 10.1


DIS 61.6 ± 6.7 60.3 ± 8.3 61.1 ± 5.0 0.00 0.980 0.02 0.877
EMA 61.7 ± 9.1 62.5 ± 7.8 60.6 ± 7.5
N3 stage (%)
Control 0.5 ± 0.8 0.5 ± 1.0 0.9 ± 1.5
DIS 0.9 ± 2.0 0.3 ± 0.6 0.8 ± 1.3 0.07 0.057 0.07 0.279
EMA 0.7 ± 1.2 0.4 ± 1.1 0.5 ± 0.6
REM stage (%)
Control 18.0 ± 7.0 20.5 ± 5.9 17.9 ± 6.1
0.08 0.050 0.02 0.767
DIS 16.8 ± 4.7 19.3 ± 3.9 18.1 ± 6.0

19
ACCEPTED MANUSCRIPT

EMA 17.3 ± 4.6 19.3 ± 4.1 19.5 ± 3.9


Stage shift (number)
Control 164.6 ± 35.8 139.5 ± 32.4 146.0 ± 33.4
DIS 149.0 ± 33.7 131.0 ± 41.5 148.5 ± 35.9 0.11 0.014 0.03 0.758
EMA 143.7 ± 47.2 131.1 ± 39.5 139.0 ± 22.2
Arousal index (events/h)
Control 11.2 ± 4.4 10.2 ± 4.4 10.1 ± 2.9
DIS 16.5 ± 21.5 9.4 ± 4.5 9.7 ± 3.9 0.06 0.109 0.05 0.450

PT
EMA 10.2 ± 3.9 8.1 ± 2.6 10.0 ± 2.9
Shifting to wake stage
(number)
Control 33.3 ± 10.3 31.2 ± 11.1 29.8 ± 9.9

RI
DIS 32.2 ± 12.2 25.9 ± 10.4 32.4 ± 11.8 0.04 0.213 0.05 0.460
EMA 30.5 ± 17.7 29.1 ± 11.2 28.8 ± 8.5

SC
DIS, difficulty in initiating sleep; EMA, early morning awakening; ES, effect size. REM, rapid eye

movement;SE, sleep efficiency; SOL, sleep onset latency; SPT, sleep period time; TST, total sleep time;

WASO, wake after sleep onset. ES is expressed as ηp2.

U
AN
M
D
TE
C EP
AC

20
ACCEPTED MANUSCRIPT

Table 4. Effects of morning and evening exercise on nocturnal polysomnography (PSG) variables in the first and second halves of the night.
First half of the night Second half of the night

PT
Main Main
Morning Evening effects of Interaction Morning Evening effects of Interaction
Baseline Baseline
exercise exercise conditions exercise exercise conditions

RI
ES p ES p ES P ES P
SPT (min)
Control 233.2 ± 10.7 235.8 ± 3.3 235.2 ± 6.9 238.2 ± 5.5 236.0 ± 9.9 239.3 ± 1.7

SC
DIS 230.6 ± 8.4 234 ± 6.0 236.5 ± 2.2 0.07 0.066 0.07 0.274 238.5 ± 3.5 234.7 ± 16.5 237.7 ± 7.3 0.03 0.371 0.01 0.985
EMA 236.8 ± 2.1 236.6 ± 2.8 236.7 ± 2.6 235.1 ± 13.7 233.3 ± 13.3 234.6 ± 11.9
TST (min)

U
Control 217.3 ± 16.2 218.5 ± 13.1 217.2 ± 25.0 214.3 ± 22.6 214.5 ± 22.9 213.6 ± 19.9
DIS 211.5 ± 14.4 218.6 ± 16.1 222.5 ± 8.8 0.02 0.576 0.05 0.383 215.5 ± 25.1 209.0 ± 45.6 211.5 ± 24.9 0.00 0.921 0.01 0.906

AN
EMA 222.1 ± 15.0 225.4 ± 11.3 216.0 ± 25.1 207.2 ± 32.2 208.9 ± 22.0 212.3 ± 20.7
SE (%)
Control 90.6 ± 6.8 91.0 ± 5.4 90.5 ± 10.4 89.3 ± 9.4 89.4 ± 9.5 89.0 ± 8.3

M
DIS 88.1 ± 6.0 91.1 ± 6.7 92.7 ± 3.7 0.02 0.580 0.05 0.384 89.8 ± 10.4 87.1 ± 19.0 88.1 ± 10.4 0.00 0.921 0.01 0.906
EMA 92.6 ± 5.6 93.9 ± 4.7 90.0 ± 10.5 86.3 ± 13.4 87.0 ± 9.2 88.5 ± 8.6
WASO (%)

D
Control 6.9 ± 4.4 7.3 ± 5.3 7.8 ± 9.6 10.0 ± 9.0 9.2 ± 8.0 10.7 ± 8.3
DIS 8.4 ± 4.3 6.7 ± 5.2 6.0 ± 3.2 0.01 0.674 0.04 0.561 9.7 ± 10.4 11.9 ± 16.4 11.2 ± 9.1 0.00 0.999 0.02 0.820

TE
EMA 6.2 ± 5.4 4.7 ± 4.8 8.7 ± 10.7 12.0 ± 12.3 10.4 ± 8.1 9.5 ± 7.6
N1 stage (%)
Control 12.9 ± 7.3 11.7 ± 5.9 10.8 ± 6.9 14.8 ± 7.9 11.2 ± 6.7 13.3 ± 7.0
EP
DIS 11.4 ± 6.3 11.3 ± 7.0 9.5 ± 5.0 0.01 0.689 0.03 0.644 11.3 ± 5.5 11.0 ± 6.4 13.8 ± 5.9 0.07 0.066 0.09 0.138
EMA 10.5 ± 6.9 9.8 ± 8.3 11.6 ± 4.7 11.9 ± 5.4 10.7 ± 4.2 10.4 ± 4.2
N2 stage (%)
C

Control 64.6 ± 8.1 61.9 ± 9.7 66.3 ± 11.7 53.7 ± 11.3 56.6 ± 15.6 53.5 ± 10.1
DIS 65.9 ± 9.8 67.3 ±11.4 68.1 ± 7.3 0.00 0.961 0.04 0.500 57.4 ± 13.3 52.7 ± 13.8 54.1 ± 9.1 0.01 0.742 0.04 0.557
AC

EMA 67.9 ± 8.8 68.8 ±9.1 65.2 ± 12.9 55.5 ± 11.6 56.0 ± 8.8 55.0 ± 10.6
N3 stage (%)
Control 1.0 ± 1.5 1.0 ± 2.0 1.9 ± 2.9 0.0 ± 0.1 0.0 ± 0.1 0.0 ± 0.1
DIS 1.6 ± 3.8 0.6 ± 1.3 1.5 ± 2.5 0.07 0.083 0.07 0.271 0.2 ± 0.7 0.0 ± 0.0 0.0 ± 0.1 0.01 0.686 0.07 0.224
EMA 1.5 ± 2.5 0.9 ± 2.2 0.9 ± 1.1 0.0 ± 0.1 0.1 ± 0.2 0.2 ± 0.4

21
ACCEPTED MANUSCRIPT

REM stage (%)


Control 14.6 ± 8.9 18.1 ± 6.7 13.3 ± 8.0 20.8 ± 9.6 22.9 ± 7.6 22.4 ± 9.5

PT
DIS 12.6 ± 5.5 14.1 ± 7.4 15.1 ± 7.1 0.04 0.212 0.04 0.588 20.8 ± 5.9 24.5 ± 6.5 21.0 ± 10.0 0.04 0.249 0.03 0.703
EMA 14.0 ± 6.1 15.9 ± 6.0 13.6 ± 7.8 20.7 ± 9.9 22.8 ± 6.3 25.0 ± 5.1
Stage shifts (number)

RI
Control 81.2 ± 26.5 75.2 ± 21.4 74.4 ± 24.2 84.2 ± 20.4 65.2 ± 22.7 72.5 ± 23.8
DIS 76.9 ± 26.0 73.8 ± 26.3 75.7 ± 24.2 0.04 0.190 0.04 0.547 72.9 ± 27.1 58.3 ± 19.0 73.8 ± 21.5 0.11 0.012 0.11 0.070
EMA 75.9 ± 27.0 63.1 ± 24.5 77.5 ± 9.5 68.7 ± 25.1 68.8 ± 20.7 62.2 ± 16.8

SC
Arousal index (h-1)
Control 11.5 ± 5.9 11.5 ± 5.7 10.6 ± 5.1 11.0 ± 4.5 8.9 ± 5.2 9.8 ± 3.8
DIS 11.2 ± 5.7 11.0 ± 7.5 9.4 ± 4.4 0.01 0.721 0.07 0.244 9.7 ± 4.9 8.2 ± 3.2 10.3 ± 5.4 0.10 0.025 0.03 0.728

U
EMA 9.8 ± 4.7 7.9 ± 3.7 10.9 ± 3.2 10.5 ± 3.8 8.4 ± 2.8 9.0 ± 3.7
Number of wake stages

AN
(number)
Control 13.4 ± 5.1 15.3 ± 6.0 11.4 ± 5.7 19.7 ± 7.6 15.8 ± 7.5 18.5 ± 8.8
*
DIS 14.7 ± 7.1 13.4 ± 6.1 14.3 ± 4.0 0.00 0.902 0.07 0.273 17.3 ± 9.7 12.3 ± 6.3 17.9 ± 8.3 0.07 0.060 0.15 0.014

M
EMA 13.6 ± 9.5 11.8 ± 6.2 14.4 ± 4.3 16.8 ± 10.7 17.2 ± 6.3 12.9 ± 4.4*

DIS, difficulty in initiating sleep; EMA, early morning awakening; ES, effect size; REM, rapid eye movement; SE, sleep efficiency; SOL, sleep onset latency; SPT,

D
sleep period time; TST, total sleep time; WASO, wake after sleep onset. ES is expressed as ηp2.

* p<0.05 vs baseline, analyzed by Bonferroni’s post hoc test.


TE
C EP
AC

22
ACCEPTED MANUSCRIPT

PT
RI
U SC
AN
M
D
TE
EP
C
AC
ACCEPTED MANUSCRIPT

PT
RI
U SC
AN
M
D
TE
EP
C
AC
ACCEPTED MANUSCRIPT

Highlights

 Acute morning exercise may moderately improve objective sleep in older adults.

 Effect of acute exercise was observed during later part of nocturnal sleep.

PT
 Effect of acute physical exercise differs between types of insomnia.

RI
U SC
AN
M
D
TE
C EP
AC

You might also like