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Effects of physical exercise on human circadian rhythm


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Bright light is the principal zeitgeber for the biological clock in mammals, including humans. But there is a line of evidence that non-photic stimuli such as physical activity play an important role in entrainment. Scheduled physical activity, such as wheel and forced treadmill running, has been reported to phase-shift and entrain the circadian rhythm in rodent species. In humans, several studies have reported the phase-shifting effects of physical exercise. A single bout of physical exercise at night was demonstrated to phase-delay the circadian rhythm in plasma melatonin. However, for the entrainment of human circadian rhythm, a phase-advance shift is needed. Previously, we demonstrated that scheduled physical exercise in the waking period facilitated the entrainment of plasma melatonin rhythm to the sleep/wake schedule of 23 h 40 min. This result suggested that timed physical exercise produced phase-advance shifts. A regular physical exercise also facilitated entrainment of the circadian rhythms associated with acute phase-delay shifts of the sleep/wake and light/dark schedule. These findings suggest that physical exercise is useful to adjust the circadian rhythm to external time cues, especially for totally blind people and elderly people.
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Sleep and Biological Rhythms 2006; 4: 199– 206 doi:10.1111/j.1479-8425.2006.00234.x
© 2006 The Authors
Journal compilation © 2006 Japanese Society of Sleep Research 199
Blackwell Publishing AsiaMelbourne, AustraliaSBRSleep and Biological Rhythms1446-9235© 2006 The Authors; Journal compilation © 2006 Japanese Society of Sleep ResearchOctober 200643199206Review ArticleExercise and human circadian rhythmsY Yamanaka
et al.
Correspondence: Graduate student Yujiro Yamanaka,
Department of Physiology, Hokkaido University Graduate
School of Medicine, N-15, W-7, Kita-ku, Sapporo 060-8638,
Japan. Email:
*Presented at the World Federation of Sleep Research and
Sleep Medicine Societies 2nd Interim Congress, New Delhi,
India, 22–26 September 2005.
Accepted for publication 17 May 2006.
Effects of physical exercise on human circadian rhythms*
Yujiro YAMANAKA, Ken-ichi HONMA, Satoko HASHIMOTO, Nana TAKASU, Toshihiko MIYAZAKI
and Sato HONMA
Department of Physiology, Hokkaido University Graduate School of Medicine, Sapporo, Japan
Bright light is the principal zeitgeber for the biological clock in mammals, including humans. But
there is a line of evidence that non-photic stimuli such as physical activity play an important role in
entrainment. Scheduled physical activity, such as wheel and forced treadmill running, has been
reported to phase-shift and entrain the circadian rhythm in rodent species. In humans, several stud-
ies have reported the phase-shifting effects of physical exercise. A single bout of physical exercise
at night was demonstrated to phase-delay the circadian rhythm in plasma melatonin. However, for
the entrainment of human circadian rhythm, a phase-advance shift is needed. Previously, we dem-
onstrated that scheduled physical exercise in the waking period facilitated the entrainment of
plasma melatonin rhythm to the sleep/wake schedule of 23 h 40 min. This result suggested that
timed physical exercise produced phase-advance shifts. A regular physical exercise also facilitated
entrainment of the circadian rhythms associated with acute phase-delay shifts of the sleep/wake
and light/dark schedule. These findings suggest that physical exercise is useful to adjust the cir-
cadian rhythm to external time cues, especially for totally blind people and elderly people.
Key words: circadian rhythm, entrainment, human, phase shift, physical exercise.
The performance as well as the effects of physical exer-
cise are known to depend on the time of day when the
exercise is performed.1,2 The biological clock is gener-
ally involved in such time-of-day effects, but the pre-
cise mechanisms for these particular issues are not
The circadian pacemaker, the central structure of the
biological clock, is located in the hypothalamic supra-
chiasmatic nucleus (SCN) in mammals and is entrained
by a light/dark cycle through the photic input from the
retina. The SCN consists of ca 8000 neurons on each
side and most of them show robust circadian oscillations
in neural activity with a period slightly different from
exactly 24 h.3,4
When healthy, sighted people are shielded from a 24-
h light/dark cycle without knowledge of the time of day,
their endogenous circadian rhythms such as plasma
melatonin and core body temperature free run with a
period that is not exactly 24 h. Therefore, to adjust to the
24 h local environmental time, our biological clock must
make a phase-advance shift by about 1 h every day. It has
been demonstrated that natural sunlight is the principal
zeitgeber for the human biological clock, and morning
bright light phase advances and evening bright light
phase delays the circadian clock (Fig. 1).5,6 However,
approximately half of blind people have been reported to
show normal entrainment of the circadian rhythm in
plasma melatonin, but the other half exhibited altered
or free-running rhythms.8 In addition, non-photic
Y Yamanaka et al.
© 2006 The Authors
200 Journal compilation © 2006 Japanese Society of Sleep Research
stimuli such as a forced sleep/wake schedule has been
reported to synchronize the endogenous circadian
rhythms of totally blind individuals with a non-24 h
schedule while living in a constant condition of dim
light.9 This finding supports an idea that the non-photic
stimuli act as a time cue for the human biological clock.
Is physical exercise able to entrain the mammalian
biological clock? It is well known that physical activity,
such as wheel and forced treadmill running, phase shifts
and entrains the circadian rhythms in rodent species.
Several studies have assessed the effectiveness of phys-
ical exercise as a phase-resetting cue (non-photic zeit-
geber) in humans as well.10,11
Physical activity such as wheel running and forced
treadmill running phase-shifts the circadian rhythms in
nocturnal rodents.12–14 Briefly, free-running rhythms
under constant dark or light in several rodent species
were phase shifted or entrained by the periodical induc-
tion of running wheels in a cage.15–21 In addition, the
period of free-running rhythms was shortened by access
to a running wheel.17,22,23 A complete phase response
curve (PRC) for a 3-h pulse of novelty-induced wheel
running was demonstrated in the Syrian hamster.15 The
PRC shows a prominent phase-advance portion in the
subjective day (rest phase) and small delay portion in
the late subjective night. These findings indicate that
physical exercise is able to entrain circadian rhythms
in nocturnal rodents. However, the critical variable for
clock resetting associated with wheel running remains
unknown. Possible explanations for clock resetting by
non-photic stimuli in rodent species have been
advanced. For example, physical activity affects the SCN
circadian pacemaker via the geniculo-hypothalamic
tract.24 Neurotransmitters such as neuropeptide-Y
(NPY) and serotonin have been proposed to mediate
non-photic effects of physical activity.25–27 Physical activ-
ity increases an arousal state, which may eventually feed
back though the NPY pathway from the intergeniculate
leaflet to the SCN, and/or through the serotonergic affer-
ents from the raphe nuclei.13,28
It has been suggested that the elevation in body tem-
perature may act as an input to the circadian pacemaker
of mammals, since temperature is a strong zeitgeber for
non-mammalian vertebrates and insects.
Physical activity increases core body temperature, the
level of which is circadian phase-dependent, and the
increment is larger in the rest phase than in active phase
in mammals including humans.29,30 In the PRC for 3-h
wheel running in the Syrian hamster,15 the maximum
phase-advance shift is observed during the middle of the
inactivity phase, which corresponds to the phase of tem-
perature trough and to the phase exhibiting the largest
increment of body temperature by 4-h wheel running.29
These results do not contradict the notion that physical
exercise phase-shifts the pacemaker by changing the
body temperature. On the other hand, injections of
the benzodiazepine, triazolam, induce phase shifts in
the circadian rhythm of hamsters by acutely increasing
their locomotor activity.31,32 The PRC for the triazolam
injection is similar to that for wheel-running31 but the
increase in body temperature is not the signal mediating
the phase-shifting effects of triazolam,32 because triaz-
olam increases body temperature in both restrained and
unrestrained animals but phase-shifts the circadian
rhythms only observed in unrestrained animals.32 Fur-
thermore, Mrosovsky and Biello (1994) suggested that it
is not running per se that is critical for phase shifting the
pacemaker but it may be the motivational context for
running.33 Therefore, at present, there is limited and
small evidence that a change in the body temperature is
the mediator of the phase shift induced by physical
Further studies are needed to fully understand the
mechanism of clock resetting by physical exercise in
rodents and the relation between photic and non-photic
Figure 1 A human phase response curve for bright light
which is measured under free-running conditions. The two
results5,6, represented by open and closed circles,
respectively, are combined (adapted from Beersma and Daan,
Circadian time of mid pulse (h)
(O: Honma & Honma, 1988 and : Minors et al., 1991)
Phase shift (h)
061218 24
Exercise and human circadian rhythms
© 2006 The Authors
Journal compilation © 2006 Japanese Society of Sleep Research 201
A single bout of physical exercise
In hamsters, increased physical activity by 3-h wheel-
running during the rest period is associated with phase-
advance shifts of the biological clock. Van Reeth et al.
(1994) examined whether or not physical exercise
induced phase-advance shifts in humans when carried
out in a usual rest period (nocturnal sleep time).10 In
this study, the circadian rhythms in plasma melatonin
were assessed twice under constant routine conditions,
once in the absence of physical exercise and once with
low intensity physical exercise of 3-h duration [40–60%
of peak oxygen uptake (VO2)]. The light condition was
constant dim light exposure (<300 lux). The phase
shifts were measured on the 1st day after physical exer-
cise. The timing of the physical exercise ranged from
5 to +4 h around the trough of the core body temper-
ature rhythm. A single bout of exercise induced a robust
phase-delay shift. The result was inconsistent with the
rodent data. Using the same protocol, Buxton et al.
(1997) reported that physical exercise with a higher
intensity (75% of peak VO2) and a shorter duration
(1 h) elicited significant phase-delay shifts when exer-
cise were cantered at a clock time of 0100 under dim
light (70–80 lux).11 The timing of the onset of the noc-
turnal elevations of plasma melatonin was used to esti-
mate the circadian phase before and after stimulus. The
mean phase delay shifts were 23 ± SE 10 min without
exercise, 63 ± SE 8 min with low intensity exercise of
3 h, and 55 ± SE 15 min with high intensity exercise of
1 h, respectively. These results suggested that a low
intensity of physical exercise was enough to shift the
human circadian clock. Recently, Buxton et al. (2003)
extended the experiment and demonstrated a PRC for
physical exercise (the data combined with 3-h low
intensity exercise and 1-h high intensity exercise).34 This
PRC revealed phase-advance shifts by physical exercise
in the evening and phase-delay shifts in the subjective
night. In addition, they indicated that physical exercise
in the morning and afternoon had no effect on the cir-
cadian phase.
The question arises as to whether the phase-advance
shift by a single bout of exercise in the evening was
really due to the change in the circadian pacemaker,
since the phase determination was made at 1 to 2 cir-
cadian cycles immediately after the physical exercise.
Indeed, a phase-advance shift was obtained one cycle
after the exercise session (30 ± SE 15 min), but a larger
phase-delay shift (66 ± SE 9 min) occurred on the fol-
lowing day.
Previously we examined the phase-shifting effects of a
single bout of physical exercise.35 In this experiment, the
subjects stayed three nights in the isolation facility. On
Day 1, the pre-exercise circadian phase was obtained.
On the Day 2, a single bout of 2 h of physical exercise
(intensity heart rate at 140 beat/min) was imposed at
one of the three times of day (morning 9:00–11:00,
afternoon 15:00–17:00 and night 00:00–02:00). As a
result, there was a slight but significant phase-delay shift
of circadian rhythm in plasma melatonin when physical
exercise was performed in the afternoon and at night.
However, the amount of the phase shift was not signif-
icantly different from that of the control subjects who
stayed in the same isolation facility for three days with-
out exercise.35
Beersma and Hiddinga (1998) examined the effects of
a single bout of physical exercise on the intrinsic period
(τ) of the human circadian pacemaker using a T-cycle
experimental procedure.36 Using a 20-h forced desyn-
chrony protocol (13.5 h for wakefulness and 6.5 h for
sleep), three experiments were conducted under dim
light conditions (under 10 lux), with and without phys-
ical exercise. The subjects performed two types of phys-
ical exercise using a cycle ergometer, with intermediate
and high intensity for a half hour per 2 h of each waking
time. They did not observe a significant effect of phys-
ical exercise on the τ. In this study, the τ was assessed by
the demasked core body temperature rhythm, which
showed a larger variability in estimating the circadian
phase. Further research is needed to detect the effect
of physical exercise on the τ of human circadian
The mechanism induced a single bout of physical
exercise to phase shift the circadian rhythm is not yet
known. It is well established that the increase of rectal
temperature by physical exercise is greater in the early
morning than in the afternoon and late evening.37–39
Hypothermia after a single bout of physical exercise was
observed longer in the morning than in the afternoon
and night.35
Recently, Kobayshi et al. (2005) examined the effects
of a single bout of physical exercise for 1 h with a
strength of 50–60% VO2 maximum at three different
time of day (morning 07:40–08:40, evening 16:30–
17:30, late evening 20:30–21:30) on the night’s sleep.40
They reported that 1 h physical exercise, when carried
out in the late evening, significantly shortened sleep
latency and increased slow-wave sleep compared with
any other timed exercise. Furthermore, Tanaka et al.
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202 Journal compilation © 2006 Japanese Society of Sleep Research
(2001) have demonstrated that the intervention such as
a short nap after lunch (30 min between 13:00 and
15:00) and moderate intensity of exercise in the evening
(30 min from 17:00) was effective in improving sleep
quality for elderly people who have difficulty in sleep-
ing.41 They have suggested that the quality of the day-
time arousal of the elderly people was improved by
exercise in the evening.41 However, other previous stud-
ies have reported that moderate intensity exercise in
the morning or afternoon improved shorter sleep
latency42–44 and more slow-wave sleep.42,45
Since these studies did not measure the circadian
rhythm maker, it is not known that the subject’s circa-
dian pacemaker would really phase-advance shift as a
result of physical exercise. The precise mechanism of
these time-dependent phenomena is not yet known.
However, a change of body temperature and subjective
arousal by physical exercise cannot be excluded as
a possible factor which may entrain the circadian
Daily bouts of physical exercise
Previously, we reported that daily bouts of physical exer-
cise advanced the human circadian pacemaker.35 In
this experiment, physical exercise was imposed regu-
larly on subjects whose sleep/wake schedule was phase-
advanced by 20 min everyday (Fig. 2). The subjects
performed physical exercise with the bicycle ergometer
for 2 h twice during the waking period. The morning
exercise started at 3 h after wake up and the afternoon
exercise started within 2 h after the end of the morn-
ing exercise (7 h after wake up). In the control experi-
ment, the subjects were sitting in a chair at the same
time of day as physical exercise. The light intensity was
less than 10 lux. The circadian rhythm in plasma mela-
tonin was phase-advanced significantly in the subjects
who took regular physical exercise during the waking
period, whereas the melatonin rhythm was not shifted
in the subjects without taking exercise (Fig. 3). These
findings indicate that regular physical exercise has a
potential to entrain the human circadian pacemaker.
However, it is not known whether the phase shift is due
to the direct effect of physical exercise, or the effect of
some other factors associated with physical exercise,
such as the increase in body temperature.
Possible explanations for the phase-advance shift
observed in a double-session exercise study were; (i) the
physical exercise phase-advanced the circadian rhythm;
or (ii) the physical exercise increased the arousal level,
which resulted in phase-advance shifts.
The question now arises as to why regular exercise
during the waking period induces phase-advance
shifts,35 which is inconsistent with the PRC reported by
Buxton et al. (2003).34 According to the PRC, physical
exercise beginning in the middle of the day produces a
phase delay, rather than a phase-advance shift. There-
fore we constructed a partial PRC using the previous
experiment,35 and found that physical exercise around
8 h after the melatonin peak produced phase-advance
shifts (Fig. 4). Since the time of physical exercise did not
cover the whole circadian phase, we need to complete
the PRC for physical exercise.
Physical exercise facilitate
Shift workers and transmeridian travelers are exposed to
the abnormal light/dark cycles and a change in the phase
Figure 2 Experimental protocol for scheduled sleep/wake
cycle with the period of 23 h 40 min (modified from
Miyazaki et al., 2001).35 Solid bars; rest period, hatched bars;
2 h physical exercise twice a day. The period indicated by the
two arrows is the time of serial blood sampling. The phase
angle difference was calculated between the plasma melato-
nin peak (downward triangles at Day 2 and Day 9) and mid-
point of physical exercise twice a day during a waking period
(upward triangles at Day 2 and Day 9). For calculating the
phase difference, the melatonin peak at Day 1 was used as the
substitute for the melatonin peak at Day 2 (see Fig. 4).
Time of day (hours)
Exercise and human circadian rhythms
© 2006 The Authors
Journal compilation © 2006 Japanese Society of Sleep Research 203
relationship between sleep and the endogenous circa-
dian rhythm. The internal and external desynchroniza-
tions induce various symptoms including fatigue,
headaches, irritability, loss of concentration, gastrointes-
tinal disorders and sleep problems (sleep loss, premature
awakening). In addition, the maximum performance of
physical exercise also declines as a result of jet lag.46
There is a question as to whether physical exercise
facilitates the resynchronization of the circadian rhythm
to a new time zone. In the animal study using Syrian
hamsters, Mrosovsky and Salmon (1987) revealed that a
single pulse of 3-h wheel running in the middle of the
rest period facilitated resynchronization to an 8-h
phase-advance shift of the light/dark cycle.47 In humans,
Klein and Wegman (1974) and Shiota et al. (1996) have
reported that outdoor exercise had some effect on the
resynchronization of circadian rhythms in urinary 17-
hydroxy corticosteroids and catecholamine exertion to a
new time zone. However, the light condition was not
controlled in these studies.48,49 Recently, Barger et al.
(2004) have examined whether physical exercise of
moderate intensity (65–75% heart rate maximim) facil-
itated resynchronization to a new sleep/wake cycle (9-h
delay of the subject’s habitual sleep episode).50 Subjects
carried out physical exercise for seven days following
the 9-h phase delay of the sleep/wake schedule, while
the control subjects were just sitting on the bicycle. The
light intensity was strictly controlled to 0.65 lux at
the standing position (angle of gaze). The mean phase
shift of the rising phase of plasma melatonin was signif-
icantly greater in the subjects doing physical exercise
(3.17 ± SE 00.49 h) than in the control (1.67 ± SE
00.45 h). In this experiment, physical exercise was done
4.2–6.7 h after the rising phase of plasma melatonin.
Thus, daily bouts of physical exercise facilitated the
resynchronization of the melatonin rhythm after a
phase-delay shift of sleep/wake cycle.
On the other hand, physical exercise was reported to
have no or a very small effect on the resynchronization
of circadian rhythms to a shift schedule.51,52 Both studies
simulated shift work with consecutive day/night shift
work (9-h delay from habitual sleep time). In one
study,51 during the 8 days of night work, physical exer-
cise at 50–60% of maximal heart rate was imposed for a
15-min duration in the first three days. A larger phase
delay shift was observed in the temperature rhythm of
the subjects doing physical exercise, but it was not sig-
nificantly different from that in the control subjects
(6.6 ± SD 2.5 vs 4.2 ± SD 3.4 h). In the other study,52
intermittent physical exercise (6 bouts, 15-min long
each, at 50–60% of maximal heart rate) occurred during
Figure 3 Plasma melatonin rhythms on Day 1, Day 8 and
Day 14 of the experiment of the scheduled sleep/wake cycle.
The circadian rhythm in plasma melatonin was phase
advanced significantly in subjects doing physical exercise
(), whereas the melatonin rhythm did not shift in the sub-
jects not doing exercise () (adapted from Miyazaki et al.
Day 8
Day 14
Plasma melatonin (%)Plasma melatonin (%)Plasma melatonin (%)
Time of day (hours)
16 0816
16 0816
16 0 8 16
Day 1
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204 Journal compilation © 2006 Japanese Society of Sleep Research
the first 6 h of the first three night shifts. Exercise nei-
ther facilitated nor inhibited the phase shift induced by
bright light. In both experiments, physical exercise was
performed in the subjective night when the phase-delay
shift was expected.34 Similarly, Youngstedt et al. (2002)
failed to find an additive effect of physical exercise on
bright light-induced phase shifts.53
Almost all studies examining the effects of physical exer-
cise on circadian rhythms have been conducted in
young, healthy subjects. In elderly people, the circadian
rhythms in entrainment tend to phase advance as com-
pared with those in young subjects.54–58 In addition, the
amplitude of circadian melatonin and core body tem-
perature rhythms are low in elderly people.54–56,59,60
Notably, the phase relationship between sleep and the
circadian rhythm of minimum core body temperature
was reported to change in elderly people. The mecha-
nisms for these changes are not well understood. One
study addressed the issue and found that nocturnal
physical exercise induced phase-delay shifts of the cir-
cadian rhythm in plasma melatonin in elderly male and
female subjects.61 Phase shifts were also observed by a
single bout of physical exercise. Although the phase
shift in elderly people was not consistent in direction
[(phase advance (n = 2), phase delay (n = 5), no phase
shift (n = 1)], the result suggests that physical exercise is
useful in elderly people to adjust circadian rhythms to
the environmental cycle.
Nocturnal physical exercise induces significant phase
delay shifts in the human circadian pacemaker. How-
ever, the effects of a single bout of physical exercise in
the daytime were not consistent among studies. On the
other hand, daily bouts of physical exercise facilitated
re-entrainment of the circadian melatonin rhythm to
advance or delay the sleep/wake cycle. These results
suggest that timed and regular physical exercise is useful
for the entrainment of the circadian rhythms in blind
people, shift workers, and jet-lagged travelers. However,
the optimal conditions of physical exercise still remain
to be clarified.
1Atkinson G, Reilly T. Circadian variation in sports per-
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Figure 4 A partial phase-response curve to physical exercise twice a day during the waking period and control condition with-
out physical exercise from the shortened T cycle experiment.35 The phase shift derived from melatonin data from Day 1 to Day
8 and from Day 9 to Day 15 are plotted vs the mid-point of timing of stimulus relative to estimated timing of melatonin peak
for each subject on Day 2 and on Day 9. By convention, phase advances are defined as positive numbers and phase delays as
negative numbers. The right panel shows the phase response to control conditions studied in the absence of physical exercise.
Open circles () represent the timing of the mid-point of rest conditions on Day 2 vs the phase shift of plasma melatonin from
Day 1 to Day 8, and open triangles () represent the timing of rest conditions on Day 9 vs the phase shift from Day 9 to Day
15. The left panel shows the phase response to 2 h of physical exercise twice a day. The filled circles () indicate the timing
of exercise twice on Day 2 vs the phase shift of plasma melatonin from Day 1 to Day 8, and the filled triangles () indicate
the timing of exercise on Day 9 vs the phase shift from Day 9 to Day 15.
Timing of physical exercise (hours after melatonin peak)
Phase shift (hours/ 7day)
02468101214 024681012 14
(a) (b)
Exercise and human circadian rhythms
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Journal compilation © 2006 Japanese Society of Sleep Research 205
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... Aside from genetic influences, non-genetic factors such as physical exercise seem to also benefit the organization and development of some cerebral systems (Killgore et al., 2013), and even to adjust the circadian rhythm to external time cues (Yamanaka et al., 2006). ...
... Both, animal (Yamanaka et al., 2008;Wolff and Esser, 2012) and human studies (Yamanaka et al., 2006;Okamoto et al., 2013;Basti et al., 2021) have also found that exercise can alter circadian rhythms in behaviour and gene expression. In addition, the circadian clock seems to also have an influence on the benefits of exercise interventions pertaining to cognitive and physical performance (Atkinson and Reilly, 1996;Drust et al., 2005;Waterhouse et al., 2005;Facer-Childs and Brandstaetter, 2015b;a;Facer-Childs et al., 2018). ...
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A variety of organisms including mammals have evolved a 24h, self-sustained timekeeping machinery known as the circadian clock (biological clock), which enables to anticipate, respond, and adapt to environmental influences such as the daily light and dark cycles. Proper functioning of the clock plays a pivotal role in the temporal regulation of a wide range of cellular, physiological, and behavioural processes. The disruption of circadian rhythms was found to be associated with the onset and progression of several pathologies including sleep and mental disorders, cancer, and neurodegeneration. Thus, the role of the circadian clock in health and disease, and its clinical applications, have gained increasing attention, but the exact mechanisms underlying temporal regulation require further work and the integration of evidence from different research fields. In this review, we address the current knowledge regarding the functioning of molecular circuits as generators of circadian rhythms and the essential role of circadian synchrony in a healthy organism. In particular, we discuss the role of circadian regulation in the context of behaviour and cognitive functioning, delineating how the loss of this tight interplay is linked to pathological development with a focus on mental disorders and neurodegeneration. We further describe emerging new aspects on the link between the circadian clock and physical exercise-induced cognitive functioning, and its current usage as circadian activator with a positive impact in delaying the progression of certain pathologies including neurodegeneration and brain-related disorders. Finally, we discuss recent epidemiological evidence pointing to an important role of the circadian clock in mental health.
... Daily routines and social rhythms are also linked to good human sleep, for example, self-reported good sleepers have more daily activities, earlier daily scheduling of their social rhythms, social rhythms characterized by greater regularity, and are involved in more activities with active social engagement than poor sleepers (156). Overall, exercise has been described as a robust zeitgeber of sleep acting via skeletal muscle clocks (157) that have an important role in regulating the mammalian circadian system generally (158). In horses, groups of animals will demonstrate both rest and locomotory synchrony (159,160) and this can be significantly affected by stabling and social conditions. ...
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Sleep is a significant biological requirement for all living mammals due to its restorative properties and its cognitive role in memory consolidation. Sleep is ubiquitous amongst all mammals but sleep profiles differ between species dependent upon a range of biological and environmental factors. Given the functional importance of sleep, it is important to understand these differences in order to ensure good physical and psychological wellbeing for domesticated animals. This review focuses specifically on the domestic horse and aims to consolidate current information on equine sleep, in relation to other species, in order to (a) identify both quantitatively and qualitatively what constitutes normal sleep in the horse, (b) identify optimal methods to measure equine sleep (logistically and in terms of accuracy), (c) determine whether changes in equine sleep quantity and quality reflect changes in the animal's welfare, and (d) recognize the primary factors that affect the quantity and quality of equine sleep. The review then discusses gaps in current knowledge and uses this information to identify and set the direction of future equine sleep research with the ultimate aim of improving equine performance and welfare. The conclusions from this review are also contextualized within the current discussions around the “social license” of horse use from a welfare perspective.
... In this regard, students in this field are exposed to adverse conditions similar to those of athletes: for example, physical fatigue (12), pain that is caused by many physical and athletic activities (13), and even high pressure on the lumbar spine (14,15). Similarly, the student is also exposed to mental fatigue (16,17), circadian rhythm disruption (18), sleep disturbance, and insomnia related to high activity levels (19). ...
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Background Grit is a key concept in positive psychology and educational science. The construct measures two related constructs that are interest and effort. Several instruments have been developed to measure this construct in professional and educational contexts, but no tools have been developed considering specific contexts such as physical education and sport.Objectives The objective of this study is to develop and test a measurement scale to assess Grit in the context of physical education and sport.Methods Two exploratory (Phase 1) and confirmatory (Phase 2) samples were administered the 16-item PE-Grit scale in Arabic. In addition, the confirmatory sample also was administered the R-SPQ-2F two-factor learning approaches scale. The factor structure was examined first by exploratory factor analysis on the first sample and then by confirmatory factor analysis on the second sample. Reliability testing was performed by checking internal consistency simultaneously by the three indices: McDonald's ω, Cronbach's α and Gutmann's λ6. Concurrent validity was checked by Pearson's correlation between the PE-Grit and the two dimensions of the SPQ-2F.ResultsAfter the exploratory factor analysis, which identified the factors and gave a preliminary validation of the designed instrument, confirmatory factor analysis was performed on three hierarchical models to be able to identify the best fitting model. A third-order hierarchical model with two physical and academic components each formed by interest and effort presented the best fit indices: chi X2 = 192.95 (p < 0.01), and the X2/DF = 1.36; GFI = 0.99; AGFI = 0.99; CFI and TLI close to 1; RMSEA = 0.025. In addition, McDonald's ω, internal consistency, and Gutmann's λ6 ranged from 0.78 to 0.86 for all four scale dimensions.Conclusion The PE-Grit scale displays adequate factor structure, good reliability, and acceptable concurrent validity and can be administered to assess Grit in physical education and sport students.
... Besides other non-pharmaceutical treatment options for sleep problems in older adults (such as hygiene education, cognitive behavioural therapy and relaxation [5,13,14], also PA has been shown to benefit sleep outcomes in older adults, such as wake time after sleep onset (WASO), sleep quality, sleep latency, sleep efficiency and sleep disturbances [5,15,16]. The biological mechanisms that underlie the positive effects of regular PA on sleep include relaxation which helps to prepare body and mind for a good night sleep; and an increased energy expenditure that increases sleep pressure and in turn creates physiological tiredness [16][17][18]. Being physically active outdoors may also increase exposure to bright day light, which helps to reset the circadian rhythm and can in turn enhance sleep [19,20]. ...
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Study objectives Age related changes in sleep result in an increasing prevalence of poor sleep in mid-aged and older adults. Although physical activity has shown to benefit sleep in studies in controlled settings, this has not yet been examined in a real-life lifestyle program. The aims of this study were to: 1) examine the effects of a lifestyle program on moderate-to-vigorous physical activity and objective and subjective sleep in adults aged 55+ years; and 2) examine if the effects differed between good and poor sleepers. Methods This controlled pretest-posttest trial examined the effects of the 12-week group-based real-life lifestyle program ‘Lekker Actief’ on moderate-to-vigorous physical activity (measured using accelerometers) and sleep (measured using accelerometers and the Pittsburgh Sleep quality Index, PSQI). The main component of the program was a 12-week progressive walking program, complemented by an optional muscle strengthening program and one educational session on healthy nutrition. Of the 451 participants who were tested pre-intervention, 357 participants completed the posttest assessment (200 in the intervention group and 157 in the control group). Effects on moderate-to-vigorous physical activity and on objective sleep (sleep efficiency, total sleep time, wake time after sleep onset (WASO) and number of awakenings) as well as subjective sleep (sleep quality) were examined in crude and in adjusted multiple regression models. An interaction term between program (control versus intervention) and sleep category (good and poor) was included in all models. Results Moderate-to-vigorous physical activity levels significantly increased in the intervention group compared with the control group (43,02 min per day; 95%CI: 12.83–73.22; fully adjusted model). The interaction terms revealed no differences between good and poor sleepers regarding the effect of the intervention on moderate-to-vigorous physical activity. There were no significant effects on sleep, except for good sleepers who showed an increase in number of awakenings/night by 1.44 (CI 95% 0.49; 2.24). Conclusions Although this program was effective in increasing physical activity, it did not improve sleep. Lifestyle programs should be promoted to increase physical activity, but more is needed to improve sleep as well. This trial was registered at (Trial registration NCT03576209).
... These data are also supported by Miyazaki and colleagues who studied the timing of daily aerobic exercise on phase shifts exercise in participants who followed a 23 h 40 min sleep-wake cycle for 15 days 34 . A phase advance was observed when exercise was performed 6-9 h after the peak of plasma melatonin 35 . Given that plasma melatonin peak coincides with CBT min around 5 am 33 , these data would predict a phase advance of CBT when exercise was performed between 11 am and 2 pm. ...
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With NASA’s plans for the human exploration of Mars, astronauts will be exposed to mission durations much longer than current spaceflight missions on the International Space Station. These mission durations will increase the risk for circadian misalignment. Exercise has gained increasing interest as a non-pharmacological aid to entrain the circadian system. To assess the potential of exercise as a countermeasure to mitigate the risk for circadian disorders during spaceflight, we investigated the effects of long-term head-down tilt bed rest (HDBR) with and without exercise on the circadian rhythm of core body temperature. Core body temperature was recorded for 24 h using a rectal probe in sixteen healthy men (age: 30.5 ± 7.5 years (mean ± SD)) after 7 days and 49 days of HDBR. Five participants underwent HDBR only (CTR), five participants underwent HDBR and performed resistive exercises (RE), and six participants underwent HDBR and performed resistive exercises superimposed with vibrations (RVE). The exercise was scheduled three times per week. CTR showed a phase delay of 0.69 h. In contrast, both exercise groups were characterized by a phase advance (0.45 h for RE and 0.45 h for RVE; p = 0.026 for interaction between time and group). These findings suggest that resistive exercise (with or without vibration) may also serve as a countermeasure during spaceflight to mitigate circadian misalignments. The results could also be important for increasing awareness about the role of circadian disorders in long-term bedridden patients.
... However, Roveda et al. (2017) showed a protective effect where physical activity may be beneficial against the detrimental health effects typically associated with sleep disruption. Such studies are not uncommon as found in Yamanaka et al. (2006), Montaruli et al. (2017) and Nohara et al. (2015). ...
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The UK Biobank dataset follows over 500,000 volunteers and contains a diverse set of information related to societal outcomes. Among this vast collection, a large quantity of telemetry collected from wrist-worn accelerometers provides a snapshot of participant activity. Using this data, a population of shift workers, subjected to disrupted circadian rhythms, is analysed using a mixture model-based approach to yield protective effects from physical activity on survival outcomes. In this paper, we develop a scalable, standardized, and unique methodology that efficiently clusters a vast quantity of participant telemetry. By building upon the work of Doherty et al. (2017), we introduce a standardized, low-dimensional feature for clustering purposes. Participants are clustered using a matrix variate mixture model-based approach. Once clustered, survival analysis is performed to demonstrate distinct lifetime outcomes for individuals within each cluster. In summary, we process, cluster, and analyse a subset of UK Biobank participants to show the protective effects from physical activity on circadian disrupted individuals.
The circadian clock participates in various biological activities like hormone excretion, body temperature control, sleep–wake cycle, cardiac arrhythmias, and glucose homeostasis. The circadian clock is the foremost controller of metabolism. It plays a vital role in determining the summary of the bidirectional response of circadian rhythm on both energy balance and metabolic activities. Several factors affect circadian rhythms, for instance, molecular clock, physical movement, metabolic regulation, and various synchronizers. This chapter discusses various synchronizers (e.g., light, arousal stimuli, time-restricted feeding, temperature, chemical factors, mechanical stimuli, oxidative stress, chronic centrifugation, and serum shock) that play a crucial role in synchronizing the circadian rhythm. Further, it also envisaged monitoring of circadian rhythm along with detecting techniques and influence of circadian rhythms on the pharmacokinetics of the drugs.
The adaptation of organisms to a rhythmic environment is mediated by an internal timing system termed the circadian clock. In mammals, molecular clocks are found in all tissues and organs. This circadian clock network regulates the release of many hormones, which in turn influence some of the most vital behavioural functions. Sleep-wake cycles are under strict circadian control with strong influence of rhythmic hormones such as melatonin, cortisol and others. Food intake, in contrast, receives circadian modulation through hormones such as leptin, ghrelin, insulin and orexin. A third behavioural output covered in this review is mating and bonding behaviours, regulated through circadian rhythms in steroid hormones and oxytocin. Together, these data emphasize the pervasive influence of the circadian clock system on behavioural outputs and its mediation through endocrine networks.
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Aging is a multifactorial process likely stemming from damage accumulation and/or a decline in maintenance and repair mechanisms in the organisms that eventually determine their lifespan. In our review, we focus on the morphological and functional alterations that the aging brain undergoes affecting sleep and the circadian clock in both human and rodent models. Although both species share mammalian features, differences have been identified on several experimental levels, which we outline in this review. Additionally, we delineate some challenges on the preferred analysis and we suggest that a uniform route is followed so that findings can be smoothly compared. We conclude by discussing potential interventions and highlight the influence of physical exercise as a beneficial lifestyle intervention, and its effect on healthy aging and longevity. We emphasize that even moderate age-matched exercise is able to ameliorate several aging characteristics as far as sleep and circadian rhythms are concerned, independent of the species studied.
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We studied the relationship between the phase and the amplitude of the circadian temperature rhythm using questionnaires that measure individual differences in personality variables, variables that relate to circadian rhythms, age and sex. The ambulatory core body temperature of 101 young men and 71 young women was recorded continuously over 6 days. The temperature minimum (Tmin) and amplitude (Tamp) were derived by fitting a complex cosine curve to each day’s data for each subject. Participants completed the Horne–Ostberg Morningness–Eveningness Questionnaire (MEQ), the Circadian Type Inventory (CTI) and the MMPI-2, scored for the Psychopathology-5 (PSY-5) personality variables. We found that the average Tmin occurred at 03.50 h for morning-types (M-types), 05.02 h for the neither-types and 06.01 h for evening-types (E-types). Figures were presented that could provide an estimate of Tmin given an individual’s morningness–eveningness score or weekend wake time. The Tmin occurred at approximately the middle of the 8-h sleep period, but it occurred closer to wake in subjects with later Tmin values and increasing eveningness. In other words, E-types slept on an earlier part of their temperature cycle than M-types. This difference in the phase-relationship between temperature and sleep may explain why E-types are more alert at bedtime and sleepier after waking than M-types. The Tmin occurred about a half-hour later for men than women. Another interesting finding included an association between circadian rhythm temperature phase and amplitude, in that subjects with more delayed phases had larger amplitudes. The greater amplitude was due to lower nocturnal temperature.
This chapter focuses on the role of retinal afferents, serotonin, and melatonin in circadian entrainment in the Syrian hamster. The Syrian hamster (Mesocricetus auratus) has been used extensively in the studies of the formal properties and the neurobiology of circadian and seasonal timing. The chapter also discusses some recent studies that have used the Syrian hamster to investigate the neurochemical mechanisms by which the circadian clock is entrained. In common with other mammals, including humans, there are three neural inputs to the hamster SCN that are thought to be involved in synchronization of the clock. The powerful resetting effect of light on the circadian clock can be demonstrated by exposing free-running hamsters to brief pulses of light. The phase response curve (PRC), which describes the relationship between the circadian time at which the light is presented and the resulting phase-shift, is well characterized for the Syrian hamster. This interaction between the pathways may be especially significant during early neonatal life when the developing SCN switches from non-photic (maternal) to photic cues as the principal entraining stimuli.
Appropriately timed exercise can phase shift the circadian rhythms of rodents. The purpose of this study was to determine whether exercise during the night shift could phase delay the temperature rhythm of humans to align with a daytime sleep schedule. Exercise subjects (N = 8) rode a stationary cycle ergometer for 15 min every h during the first 3 of 8 consecutive night shifts, whereas control subjects (N = 8) remained sedentary. All subjects wore dark welder's goggles when outside after the night shift until bedtime, and then slept in dark bedrooms. Sleep was delayed 9 h from baseline. Rectal temperature was continuously measured. There were fewer evening-types and more morning-types in the exercise group than in the control group, which should have made phase delay shifts more difficult for the exercise group. Nevertheless, a majority of the exercise subjects (63%) had large temperature rhythm phase delay shifts (> 6 h in the last 4 days relative to baseline), whereas only 38% of the control subjects had large shifts. An ANCOVA showed that, when morningness-eveningness was accounted for (as the covariate), the exercise group had a significantly larger temperature rhythm phase shift than the control group. As expected, there was a correlation between the temperature rhythm phase shift and morningness-eveningness in the control group, with greater eveningness resulting in larger phase shifts. However, there was no such relationship in the exercise group; exercise facilitated temperature rhythm phase shifts regardless of circadian type. These results suggest that exercise might be used to promote circadian adaptation to night shift work.
Many elderly people complain of disturbed sleep patterns but there is not evidence that the need to sleep decreases with age; it seems rather that the timing and consolidation of sleep change. We tried to find out whether there is a concurrent change in the output of the circadian pacemaker with age. The phase and amplitude of the pacemaker's output were assessed by continuous measurement of the core body temperature during 40 h of sustained wakefulness under constant behavioural and environmental conditions. 27 young men (18-31 years) were compared with 21 older people (65-85 years; 11 men, 10 women); all were healthy and without sleep complaints. The mean amplitude of the endogenous circadian temperature oscillation (ECA) was 40% greater in young men than in the older group. Older men had a lower mean temperature ECA than older women. The minimum of the endogenous phase of the circadian temperature oscillation (ECP) occurred 1 h 52 min earlier in the older than in the young group. Customary bedtimes and waketimes were also earlier in the older group, as was their daily alertness peak. There was a close correlation between habitual waketime and temperature ECP in young men, which may lose precision with age, especially among women. These findings provide evidence for systematic age-related changes in the output of the human circadian pacemaker. We suggest that these changes may underlie the common complaints of sleep disturbance among elderly people. These changes could reflect the observed age-related deterioration of the hypothalamic nuclei that drive mammalian circadian rhythms.
This study investigated the relative potency of melatonin and arousal as Zeitgebers in the non-photic phase shifting of circadian rhythmicity in the adult Syrian hamster. Animals held under dim red light (DD) exhibited robust free-running rhythms of wheel-running activity. Melatonin (1 mg/kg) or ethanolic saline vehicle, delivered manually by subcutaneous injection after removing the animal from its cage, resulted in phase advances of the activity rhythm. This effect was phase dependent, injections at CT 8 and 10 being effective (CT 12 = anticipated activity onset), whereas injection at CT 2, 6, 14 and 20 did not cause a shift. There was no significant difference between the magnitude or timing of phase shifts in response to injections of saline or melatonin. To determine whether the observed shifts were related to arousal of the animals induced by handling, a second group held under DD were fitted with chronic s.c. cannulae so that melatonin solution or vehicle could be delivered remotely at projected CT 10. Neither solution had any effect upon the free-running rhythm. However, when these animals received manual s.c. injection of saline or melatonin solution, they exhibited phase advances similar to those observed in Expt. 1. These results fail to support the hypothesis that melatonin can exert a chemically specific, acute phase-shifting action in the adult Syrian hamster. They do, however, demonstrate the potent effect of arousing stimuli upon the circadian clock in this species.
Treatment with the short-acting benzodiazepine, triazolam (Tz), 6 h before activity onset (CT 6) induces large phase advances in the circadian rhythm of locomotor activity in golden hamsters free-running in constant lighting conditions. These phase shifts are associated with acute increases in locomotor activity. The acute increases in activity appear to be necessary for induction of phase shifts in the activity rhythm by Tz, since suppression of this activity by restraining the animal blocks the phase shifts normally induced by Tz. Furthermore, other stimuli which induce an acute increase in locomotor activity phase shift the circadian clock in a similar manner as does Tz. Since increased locomotor activity is associated with a rise in body temperature in mammals, and changes in temperature have been associated with changes in circadian rhythms, this study was designed to determine whether the phase-shifting effect of Tz on the circadian clock could be mediated by the change in body temperature resulting from the induced acute increase in locomotor activity. Hamsters free-running in constant light (LL) were implanted with Mini-Mitter biotelemetry devices and either injected with Tz at CT 6, injected with Tz at CT 6 and restrained for the next 6 h, or restrained for 6 h beginning at CT 6. Treatment with Tz resulted in large phase advances in the activity rhythm, while the other two treatments did not induce phase advances. Mean body temperature increased over control levels for all 3 groups during most of the 6 h following the beginning of treatment, and there were no significant differences in body temperature changes between any pairs of groups.(ABSTRACT TRUNCATED AT 250 WORDS)