REVIEW

CURRENT
OPINION Sleep disturbance at altitude
Jeremy S. Windsor a and George W. Rodway b

Purpose of review
The aim is to describe the impact of altitude upon sleep, the physiology that underpins these changes and
the therapeutic solutions that are currently in place.
Recent findings
On ascending to altitude, lowland residents commonly experience some degree of sleep disturbance.
Occasionally, this can prove very uncomfortable and impact upon daytime activities. Historically, the
underlying cause of sleep disturbance was thought to be due to the effect of periodic breathing. However,
recent research has shown that the link between periodic breathing, lighter stages of sleep and arousals is
far from convincing. Instead, it appears that hypoxia has a far wider effect upon sleep at altitude than was
previously thought. A number of new approaches to the treatment of sleep disturbance at altitude have
recently been identified. Whereas some treat the underlying hypoxia through pharmacological or
technological means, others seek to address the symptoms of sleep disturbance more directly.
Summary
Many of the current approaches to treating sleep disturbance at altitude have been shown to be well
tolerated and successful, although few comparisons have been made. Future research is likely to focus
upon matching the safest and most successful approach to the individual and their environment.
Keywords
acetazolamide, altitude, oxygen, periodic breathing, sleep

INTRODUCTION 34.4–68.1%) from four successful summiteers [3].

Sleep disturbance is a common feature that affects
many of those who ascend to altitude. The eminent
high altitude physician and physiologist Professor
John West once wrote: ‘On ascending to altitude,
unacclimatized lowlanders typically complain that
they take longer to get to sleep, wake frequently,
often have unpleasant dreams and do not feel
refreshed in the morning. The resultant difficulties
are not confined to the night because, as a result of
poor sleep, people often feel somnolent and fatigued
during the following day, their productivity is
reduced and they are more liable to make errors’ [1].
The effect of altitude upon sleep stems largely
from falling barometric pressure and the subsequent
decline in the partial pressure of inspired oxygen
(PO2) (Fig. 1). This is seen most dramatically on
the summit of Mount Everest. At 8850 m, the PO2
is approximately 53 mmHg – a value that is just
one-third of that found at sea level [2]. This has
a profound effect upon oxygenation. At a point
known as ‘The Balcony’, situated at 8400 m on
Mount Everest, researchers from the Caudwell
Xtreme Everest Research Group obtained a mean
arterial oxygen saturation (SaO2) of 54% (range:
Although these effects are somewhat less at lower
altitudes, the steady decline in barometric pressure
and PO2 nevertheless has a significant physiological
impact upon those who ascend to even moderate
heights. In this review, we will explore what occurs
to sleep at altitude, the physiology that underpins
these changes and the therapeutic solutions that are
currently in place.
SUBJECTIVE CHANGES IN SLEEP AT
ALTITUDE
Lowland residents who ascend to altitude frequently
complain of poor sleep. In a study of 130 trekkers
a
University College London, Institute of Human Health Performance,
Highgate Hill, London, UK and bUniversity of Utah, College of Nursing
and School of Medicine, Salt Lake City, Utah, USA
Correspondence to Dr Jeremy S. Windsor, University College London,
Institute of Human Health Performance, Charterhouse Building, Archway
Campus, Highgate Hill, London, UK. Tel: +44 7960 879340; e-mail:
jswindsor@doctors.org.uk
Curr Opin Pulm Med 2012, 18:554–560
DOI:10.1097/MCP.0b013e328359129f

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KEY POINTS

Sleep disturbance is a common feature in those who
ascend to altitude.

Field and hypobaric chamber studies demonstrate a
shift from deep to light non-REM sleep and a decrease
in REM sleep.

Periodic breathing is a common feature during sleep at
altitude. Although it is thought to cause arousals, it is
not entirely responsible for sleep disturbance at altitude.

Several approaches have been used successfully to
treat sleep disturbance at altitude. At present, oral
acetazolamide, 250 mg twice daily, is amongst the
most popular.
ascending the popular Marangu route on
Kilimanjaro, between 26 and 54% complained of
poor sleep during the 5-day climb to the summit [4].
Following a night at Horombo Hut (3720 m), 25%
‘did not sleep as well as usual’, 21% ‘woke many
times’ and 5% ‘could not sleep at all’. Recently,
standardized scales have been used to identify
the specific subjective changes that occur at altitude
[5]. Using the Pittsburgh Sleep Quality Index
and Athens Insomnia Scale (AIS-8), 38 volunteers
climbing Lobuche East (6119 m) and Lenin Peak
(7134 m) felt that they took longer to fall asleep,
that they woke more frequently at night and
they woke earlier the next day (all P < 0.05). Overall,
the AIS global score rose from 2.09 to 5.59 (P < 0.05).
This, the authors argue, is striking as a value of 6
or more is often used as a guide in the diagnosis of
insomnia [6]. Poor sleep can impact upon daytime
activities too. Using a comprehensive battery of
tests and questionnaires, researchers found that
mmHg
800
700
600
500
400
300
200
100
0
0 1000 2000 3000 4000 5000 6000 7000 8000 9000 10000
Altitude (m)
FIGURE 1. The barometric pressure (light grey) and partial
pressure of oxygen (dark grey) calculated between 0 m and
10000 m in 1000 m increments.
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Sleep disturbance at altitude Windsor and Rodway
measures of fatigue and alertness amongst 12
participants differed significantly after a night
at the Cosmiques Hut (3613 m) (P < 0.01 and
P < 0.001) [7]. Similar findings have been identified
in healthy volunteers who undergo sleep depri-
vation studies at sea level. Here, functional neuro-
imaging has consistently found abnormal activity
in the prefrontal cortex, thalamus, parietal and
temporal lobes that has been linked to the wide-
spread cognitive decline that is often seen in those
who are sleep deprived [8].
OBJECTIVE CHANGES IN SLEEP AT
ALTITUDE
Over the last four decades, changes in sleep
architecture have been extensively studied in a
range of hypoxic chamber and high-altitude field
experiments. In the majority of polysomnographic
studies, there is a movement away from the
deep stages of non-rapid eye movement (REM) sleep
(III and IV) to lighter stages (I and II) [9]. In a recent
study of 19 trekkers ascending to altitudes of more
than 5000 m, the percentage of time spent in non-
REM sleep fell from 24 to 18% (P < 0.001) [10].
While the duration of stage II non-REM sleep
did not change, stage I non-REM sleep increased
from 3 to 11% (P < 0.001). Findings like these
agree with the results of the landmark Operation
Everest II (OEII) hypobaric chamber study in
which the percentage of time spent in stage I
non-REM increased from 10% at sea level to
16.7% at 4572 m and 21.4% at 6100 m [11]. Mean-
while, REM sleep is reduced at altitude, with some
studies reporting a reduction by as much as 50%
[12,13].
In keeping with the shift towards lighter sleep
at altitude, studies have consistently demonstrated
an increase in the number of arousals that occur [9].
Using the definition adopted by the former
American Sleep Disorders Association (now renamed
the American Academy of Sleep Medicine),
researchers stationed at the Regina Margerita Hut
(4559 m) identified an increase in arousals amongst
&
the 14 healthy participants studied [14 ]. On the
fourth night at altitude, the mean arousal index
was 6.0 per hour compared with just 1.7 per hour
&
at 490 m above sea level (P < 0.05) (Fig. 2) [14 ].
This increase is even more noticeable at higher
altitudes. During the simulated ascent to the summit
of Mount Everest, OEII researchers found a fall
in mean oxygen saturation of 44% and an eight-
fold increase in the arousal index [11]. This had a
dramatic effect on the time spent asleep, with sleep
efficiency falling from 89% at sea level to 52% at
an equivalent altitude of 7620 m.
www.co-pulmonarymedicine.com 555
 Sleep and respiratory neurobiology
awake
S1
S2
S3
S4
REM
22:00 23:00 24:00 22:00 01:00 02:00 03:00 04:00 05:00
awake
S1
S2
S3
S4
REM
22:00 23:00 24:00 22:00 01:00 02:00 03:00 04:00 05:00
awake
S1
S2
S3
S4
REM
22:00 23:00 24:00 22:00 01:00 02:00 03:00 04:00 05:00
FIGURE 2. Hypnograms obtained at 490 m and 4559 m.
The hypnogram obtained in a subject during a night at
490 m (top panel) shows a normal distribution of sleep
stages. In contrast, the hypnogram recorded during the first
night at 4559 m (middle panel) reveals predominantly
superficial sleep stages with frequent awakenings, very
rare deep sleep stages 3 and 4, and no REM sleep. The
hypnogram from the third night at 4559 m (bottom panel)
reveals a partial restoration of normal sleep architecture
[14 ]. REM, rapid eye movement.
&
THE PHYSIOLOGICAL CHANGES
RESPONSIBLE FOR SLEEP DISTURBANCE
AT ALTITUDE
I stretched myself upon a composite couch of
snow and granite, and immediately fell asleep.
My friend, however, soon aroused me ‘You quite
frighten me’ he said, ‘I listened for some minutes
and have not heard you breathe once’ [15] (p. 71).
Historically, the subjective and objective
changes that occur during sleep have largely been
attributed to the presence of periodic breathing
(Fig. 3) [16]. During sleep at altitude, the normal
cyclical breathing pattern is lost [16]. Hypoxic
exposure triggers peripheral and central chemore-
ceptors that prompt an increase in ventilation.
Although this results in an increase in the partial
pressure of alveolar oxygen, this subsequently
causes a decline in the partial pressure of carbon
dioxide (PaCO2). As carbon dioxide is a powerful
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respiratory stimulant, this dampens the urge to
breathe and suppresses ventilation. At altitude, this
normally reduces the rate and depth of breathing
(hypopnea) but can, in some instances, cause a
complete cessation in ventilation (apnea). An apnea
of 44 s was once recorded at Mount Everest
Base Camp (5300 m) in an otherwise healthy moun-
taineer who subsequently went on to reach the
summit [17]! As the apnea lengthens, the PCO2
climbs and the PO2 starts to fall, leading eventually
to the resumption of ventilation (Fig. 4) [9].
The frequency and duration of periodic
breathing varies from individual to individual.
On the summit of Pike’s Peak (4300 m), the duration
of periodic breathing amongst six healthy
volunteers ranged between 0 and 93% of the total
time spent asleep [18]. This variation is thought to be
due to the differences in the sensitivity of peripheral
chemoreceptors to changes in oxygen and carbon
dioxide tension at altitude. Those with a pronounced
hypoxic ventilatory response (HVR) have been found
to have more prolonged periods of periodic breathing
[19,20]. Moreover, it is likely that in increasingly
hypoxic environments in which peripheral chemo-
receptors become more important ‘drivers’ of respir-
ation, coordination between peripheral and central
chemoreceptor activity is imperfect, and hence
exacerbates periodic breathing [9].
Despite variation between individuals, periodic
breathing tends to increase with each successive
gain in height. Amongst 19 healthy mountaineers
ascending Muztagh Ata (7546 m), the percentage of
time spent in periodic breathing increased from 0%
at sea level to 21% at base camp (4497 m) to 71% at
camp 1 (5533 m) and 85% at camp 2 (6265 m) [16].
Findings like these have tended to encourage the
belief that periodic breathing is responsible for the
shift towards lighter sleep stages and the increasing
frequency of arousals. However, recent studies have
been unable to demonstrate this association.
Amongst 14 trekkers at 5000 m, the frequency of
periodic breathing episodes measured by the apnea–
hypopnea index (AHI) was 68 per hour, however,
the mean number of arousals was just 30 per hour
(P < 0.05) [10]. Similarly, at the Reginna Margerita
hut (4559 m), the greatest AHI was measured on
the first night at 88.1 per hour and then fell over
the course of the next three nights to 42.4 per hour,
but nevertheless the number of arousals remained
largely unchanged [21]. In 16 mountaineers
who spent three nights at the same altitude, AHI
increased from 60.9 per hour on the first to 86.5 per
hour on the third night (P < 0.05), yet the number of
arousals fell and a shift towards deeper non-REM
and REM sleep occurred [22]. Although even the
most sceptical observers will accept that periodic
Volume 18
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November 2012
 Sleep disturbance at altitude Windsor and Rodway

1L
Volume
sum

1L
Volume rib
cage

1L
Volume
abdomen

20
V’E, L/min
0
140
Heart
rate, 1/min
50
90
SpO2, %
50 3 min

FIGURE 3. A nocturnal polygraph recording at 6850 m. The channels show respiratory inductive plethysmographic sum, rib
cage and abdominal tidal volume, minute ventilation (V’E), heart rate and arterial oxygen saturation (SpO2). At altitude, periodic
breathing causes changes in the respiratory rate and subsequent swings in arterial SpO2. In this example, the SpO2 fluctuated
between 64 and 71%. Reprinted with permission of the American Thoracic Society. Copyright ß 2012 American Thoracic
Society [16].

breathing can disturb sleep, the inconsistencies specific solutions are sometimes required, a number
between periodic breathing and arousals demon- of general steps should be taken first. These include
strated in recent studies suggest that this expla- common sea level practices such as avoidance
nation is far from complete. Instead, the effect of of daytime sleeping, going to bed only when tired,
hypoxia upon sleep is likely to be far more pervasive limiting physical and psychological stress before
than has been previously thought. going to bed and abstinence from caffeine, alcohol
and tobacco [23].
In addition to practical solutions, efforts can
TREATING SLEEP DISTURBANCE AT also be made to address the direct effects of hypoxia.
ALTITUDE According to evidence-based clinical guidelines
On ascending to altitude, sleep can be disturbed by issued by the Wilderness Medical Society (WMS),
a number of different factors (Table 1). Although acclimatization is best achieved by a slow ascent.
A gain in sleeping altitude of no more than 500 m
each night is recommended, with a rest day taken
Altitude every 3 or 4 days [24]. Although this is widely
believed to reduce the incidence of conditions such
as acute mountain sickness (AMS), its effects upon
sleep have not been formally studied. Nevertheless,
Hypoxia the improvements seen in sleep architecture over
several nights at moderate altitude suggest that
the WMS’s advice might be of considerable benefit
[16,25,26]. For instance, during a four-night stay
Hypoventilation Hyperventilation at 4559 m, the mean SaO2 increased from 74 to
81% (P < 0.05), whereas the incidence of periodic
breathing fell by more than one half (P < 0.05) [23].
Such results have prompted research into the
Hypocapnia effect of exposing individuals to a program of
hypoxic exposure prior to ascent [27,28]. This
FIGURE 4. Periodic breathing at high altitude. Adapted novel approach has the potential to stimulate the
from [9]. acclimatization process before even setting foot on a

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 Sleep and respiratory neurobiology

Table 1. Common factors that may disturb sleep at altitude

Environmental Personal

Extremes of ambient temperature Acute illnesses (e.g. AMS, high-altitude cough, gastrointestinal infection)
High winds Side effects of drugs (e.g. diuretics, steroids)
Limited or inadequate sleeping equipment Exacerbation of chronic illness (e.g. GORD, musculoskeletal disorders, prostatism)
Loud noise Jetlag
Precipitation Stress reaction
Uneven surface Withdrawal of drugs (e.g. caffeine, antidepressants)
Unsafe location

AMS, acute mountain sickness; GORD, gastroesophageal reflux disease.

mountain [28]. By sleeping for seven nights in a
hypoxic chamber prior to ascent, visitors to 4300 m
had a higher SaO2 (80 versus 76%; P < 0.05) and
a trend towards fewer awakenings (12 versus 17;
P ¼ 0.06) compared with those without previous
hypoxic exposure [27]. Nevertheless, provided
individuals ascend slowly and comply with the
aforementioned WMS guidelines, many argue that
interventions like this are unnecessary. However,
there will remain a small proportion, who for
a number of different reasons, may benefit from
some form of intervention during their time at high
altitude (Table 2).
CARBONIC ANHYDRASE INHIBITORS
For many years, acetazolamide has been used in
the prevention and treatment of AMS [24].
Although its effects are wide reaching, its benefits
at altitude are largely thought to be due to the
formation of a metabolic acidosis that leads to an
increase in ventilation and a subsequent improve-
ment in oxygenation. More recently, acetazolamide
has been shown to improve sleep at altitude [29].
At 3454 m, the mean SaO2 of 30 healthy volunteers
was significantly higher in those taking acetazola-
mide (250 mg twice daily), compared with individ-
uals receiving placebo (86.2 versus 81.0%; P < 0.05)
[30]. Using acetazolamide was also associated with
fewer arousals and a shift from non-REM I and II to III
and IV sleep. Acetazolamide has also been used
successfully in those heading to altitude with
&
preexisting sleep disorders [31 ]. At 2590 m,
45 patients with obstructive sleep apnea enjoyed
a higher SaO2 (88 versus 85%) and lower AHI (61.4
versus 86.2 per hour) following the administration of
acetazolamide (250 mg twice daily) compared with
placebo. Not only did this improve markers of sleep,
but it also dampened the increase in systemic blood
pressure that is commonly seen in newcomers
to altitude.
BENZODIAZEPINE RECEPTOR AGONISTS
The short-term use of benzodiazepines is commonly
employed in combination with behavioural
interventions to treat insomnia in the primary care
setting [23]. The ability of these drugs to suppress
the HVR has encouraged a number of investigators
to examine their effects upon sleep disturbance
at altitude. As expected, small doses of temazepam
(10 mg at bedtime) have been shown to reduce
periodic breathing at a number of altitude locations
[32,33] (Fig. 5) [32]. Although the use of benzo-
diazepines results in fewer arousals, a switch towards
deeper sleep stages and a subjective improvement
in the quality of sleep, the suppression of HVR
has been shown, in some cases, to reduce mean
SaO2 measurements. During two nights spent above
5000 m, the mean SaO2 amongst healthy trekkers
was 2% lower in those taking temazepam compared
with placebo (P ¼ 0.01) [33]. Such a finding suggests
that benzodiazepines modify the body’s response
to hypoxia, but unlike acetazolamide they do not

Table 2. The pharmacological treatment of sleep disturbance at altitude

Drug category Drug and dose Common side effects

Carbonic anhydrase inhibitor Acetazolamide (125–250 mg bd) Gastrointestinal disturbance; paraesthesia

Benzodiazepine receptor agonist Temazepam (10 mg nocte) Daytime tiredness; somnambulism
GABA receptor agonist Zolpidem (10 mg nocte); zaleplon (10 mg nocte) Daytime tiredness; somnambulism

bd, twice daily; GABA, Gamma aminobutyric acid.

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 Sleep disturbance at altitude Windsor and Rodway

Placebo

100%
SaO2
50%

80 bpm
HR
50 bpm

Temazepam

100%
SaO2
50%

80 bpm
HR
50 bpm

0 10 20 30 40 50 60
Time (min)

FIGURE 5. Nocturnal SaO2 (upper) and heart rate (lower) in one male trekker following placebo (top panel) and temazepam
10 mg (bottom panel). Eight hours of each study is shown, with each line representing a successive hour of the night [32].
bpm, beats per minute; HR, heart rate.

correct the underlying cause of sleep disturbance frequency of arousals, nor did they influence mean
at altitude. SaO2 measurements.

GAMMA AMINOBUTYRIC ACID RECEPTOR OXYGEN

AGONISTS
The effects of the nonbenzodiazepine gamma
aminobutyric acid agonists zolpidem and zaleplon
have both been studied in newcomers to altitude [7].
Over three nights spent at 3613 m, researchers
found that both drugs caused a shift towards
deeper sleep, an increase in sleep efficiency and a
subsequent reduction in the severity of AMS
compared with placebo [7]. The mechanism under-
pinning these benefits is unclear. In contrast to
benzodiazepines and carbonic anhydrase inhibitors,
neither drug influenced periodic breathing or the
Improving PO2 has been shown to be an effective
way of improving sleep at altitude [34]. According
to the scientists taking part in the first ascent of
Mount Everest in 1953, ‘oxygen brought about an
immediate feeling of warmth, sound sleep and
greatly improved recovery from fatigue’ [35]. Using
oxygen supplied through nasal prongs, trekkers
at Mount Everest Base Camp (5300 m) had a higher
SaO2 (81.4 versus 57.5%) and a lower AHI (20.0
versus 51.0) than those breathing ambient air alone
[36]. At lower altitudes, it is possible to pipe supple-
mental oxygen directly into sleeping quarters.

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 Sleep and respiratory neurobiology
By increasing the fraction of inspired oxygen to
0.24, non-REM sleep stages III and IV increased from
13.9 to 17.2% at 3800 m (P < 0.05) [37]. Oxygen-
ation during sleep at altitude can also be improved
by breathing ambient air through a noninvasive
positive pressure ventilation system [38]. Using an
inspiratory positive airway pressure of 9–12 cm H2O
and an expiratory positive airway pressure of 4–6 cm
H2O, the mean SaO2 of seven healthy volunteers
at 3800 m was 4.6% greater than when the mask was
removed (P ¼ 0.002). This, the authors explained,
may have been due to the combined effects of an
increase in alveolar ventilation and the prevention
of airway collapse during exhalation.
CONCLUSION
For the majority of those who make a slow and
gradual ascent to altitude, the changes in sleeping
pattern are unlikely to cause significant disturb-
ances. Nevertheless, for those who ascend quickly
or have underlying sleep difficulties, interventions
may be needed. Whereas the physiologist may
prefer the simplicity of using a drug or device
that treats the underlying hypoxia, trekkers and
mountaineers may opt for familiar drugs that are
used to treat insomnia at low altitude. At present,
both approaches appear to be well tolerated and
successful. Nevertheless, they have limitations
and as new agents become available, these will need
to be investigated and their role in treating sleep
disturbance at altitude clearly established.
Acknowledgements
None.
Conflicts of interest
There are no conflicts of interest.
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Volume 18
Number 6
November 2012