Tải bản đầy đủ - 0 (trang)
2 Exercise Is Not Enough

2 Exercise Is Not Enough

Tải bản đầy đủ - 0trang

12 Use It or Lose It



177



little mention of the accompanying ‘cognitive load’, but instead tend to

attribute the effect largely to improvements with the brain’s blood supply

and aspects of the brain’s chemistry. However, at least one recent major

review of this area [6] has been much more guarded about why some

cognitive functions improve with exercise while others are insensitive.

For example, although a year-long indoor walking programme in healthy

older adults [7] pointed to (working) memory improvements, and to better physical fitness, there were no improvements to be seen with measures

of executive function. Here, walking was monotonous, on an indoor circular track and, interestingly, it was noted [7] that with more environmental stimulation, these improvements may well have been greater.

Apparent benefits for the brain of exercise alone, usually soon disappear

when the regimen is ended [8] and exercise taken to excess can be counterproductive, as the brain goes into a protective mode [9] that can be interpreted as a sign of improving brain health, which is not necessarily the

case. On the other hand, brisk walking regimens and jogging can improve

sleep quality and subjectively determined sleep in poor sleepers [10].

Despite physical exercise alone seeming to be able to reverse some detrimental effects of ageing on those aspects of memory that focus on the

hippocampus [11] (Sect. 10.7), the same benefits are seen with a variety

of non-exercise ‘cognitive stimulations’ [11] in normal healthy individuals, in particular, those activities involving novel experiences undertaken

daily over several weeks as, for example, in taxi drivers learning new

routes [12], with these improvements maintained for several months

after training. Although healthy older people usually show obvious associations between their levels of physical fitness and cognitive function,

including executive skills, all of this usually comes with a more mentally

and physically active and outgoing lifestyle as well as with a positive attitude to one’s life.



12.3 Boosting SWS

Sleep, particularly SWS and 1 Hz EEG activities, indicates the enhancing

of brain plasticity [13], and these activities, and probably other (yet to

be determined) aspects of the sleep EEG, can provide useful markers of

the effects of this increased brainwork in terms of ‘use it or lose it’ for the



178



Sleeplessness



ageing brain. However, more needs to be known about how long-term

daily regimens of cognitive stimulation with and without accompanying physical exercise compare with each other. To date, such findings

have been incidental as, for example, seen with a major study [14] of

age-related cognitive decline linked to structural changes within the

frontal cortex, and accompanied by diminished SWS. The investigators

concluded [14] that these findings could be improved by behavioural

interventions. Moreover, there is evidence [15] that three hours of daily

structured but engaging social and physical activity in healthy elderly

people leads to increased SWS, with improvements to memory-oriented

tasks. However, this intervention [15] only lasted for two weeks, and it

is not clear what would happen if this and similar activities were to be

continued in the long term.

Interestingly, we [16] have found that older people who naturally and

habitually have more SWS are more flexible in their thinking, have better executive skills, and thus seem to have a ‘younger brain’ for their age.

But simply using what might be viewed as more artificial methods to

increase SWS in the sleep of the older person, is not necessarily a good

sign of a more active waking brain, unless there is evidence of cognitive improvement. Certain drugs can also elevate SWS, as can shortterm increases in waking brain temperature (thus increasing the brain’s

metabolic rate) but without any improvements to waking behaviour, cf.

[2]. Nevertheless, a 30-minute warm bath in the evening, to increase

both body and brain temperature not only increases SWS that night,

but generally improves nighttime sleep in those healthy elderly with

insomnia [17].

Of course, getting out and about, outdoors, and encountering daylight, will help synchronise the circadian clock and the timing of sleep,

as well as have a daytime alerting effect and reduce the extent of daytime

naps and thus promote better nighttime sleep.

Finally, increased levels of ß-amyloid in the cortex are associated

with dementia. There is new evidence [18] that in older people these

levels in areas of the prefrontal cortex are correlated with diminished

amounts of SWS, especially its 1 Hz component, as well as with impaired

hippocampus-dependent memory consolidation. However the extent to



12



Use It or Lose It



179



which there is any cause and effect, here, remains a matter for speculation, as might the benefits of the ‘getting out and about’ enhancement of

SWS in older age have in offsetting progression of this ß-amyloid. But

clearly this is a potentially worthwhile area of further investigation.



12.4 ‘Fresh Air’

Much can be said for the Victorian belief that exercise should be relaxing and not taxing, as advocated, for example by the pronouncements in

1900 by Dr James Sawyer in his article, “Causes and Cure of Insomnia”,

published in the British Medical Journal (8 December 1900, p. 627) that,

“Daily bodily exercise in the open air but always short of great fatigue must

be enjoined. What is called carriage exercise is better than no outdoor change

at all, but walking is far better exercise and cycling better still, and riding

on horseback the best of all. A worn and worrying man habitually wrapt up

in an absorbing torture of self-consciousness and sleeping badly, must come

out of himself with the saving graces when he mounts a cycle or horse’s back.”

And finally, “Gardening in the open air, not in conservatories or hothouses

affords good exercises and it is very efficient in keeping up objective attention.”

As sleeplessness-cum-insomnia was generally thought at the time to be

a problem for those with more cultured and educated minds, one must

sympathise for the horseless, poor worker whose ‘gardening’ comprised

struggling to grow a few vegetables in a meagre plot of land, so as to

supplement the family’s food supply.

We might smile at this naivety and that ‘gardening makes good sport’

but, nevertheless, these words of Dr Sawyer are wiser than they may seem,

as not only does all this outdoor activity also expose one to daylight, but

varied and active gardening will indeed ‘exercise the brain’, to create more

brainwork, and in doing so may further improve sleep and SWS. Hence,

many of us need to be more ‘ecological’ with our sleep and wakefulness,

get out and about more, even commune with nature, take more of those

relaxing baths, contemplate the wisdom of Emerson, and maybe cancel

that subscription to the gym.



180



Sleeplessness



References

1. Halàsz P et al. 2014 Two features of sleep slow waves: homeostatic and reactive aspects. Sleep Med, 15: 1184–1195.

2. Horne JA 2013 Exercise benefits for the aging brain depend on the accompanying cognitive load: insights from sleep electroencephalogram. Sleep Med

14:1208–1213.

3. Fabel K, Kempermann G. 2008 Physical activity and the regulation of neurogenesis in the adult and aging brain. Neuromol Med 10: 59–66.

4. Kraft E. 2012 Cognitive function, physical activity, and aging: possible biological links, implications for multimodal interventions. Neuropsychol Dev

Cogn B Aging Neuropsychol Cogn. 19(1-2):248–263.

5. Lista I, Sorrentino G. 2010 Biological mechanisms of physical activity in

preventing cognitive decline. Cell Mol Neurobiol 30:493–503.

6. Angevaren M et al 2008 Physical activity and enhanced fitness to improve

cognitive function in older people without known cognitive impairment.

Cochrane Database Syst Rev 16: CD005381.

7. Voss MW et al 2012 The influence of aerobic fitness on cerebral white matter integrity and cognitive function in older adults: Results of a one-year

exercise intervention. Hum Brain Mapp. 34:2972–2985.

8. Rhyu IJ et al 2010 Effects of aerobic exercise training on cognitive function

and cortical vascularity in monkeys. Neurosci 167:1239–1248.

9. Secher NH et al 2008. Cerebral blood flow and metabolism during exercise:

implications for fatigue. J Appl Physiol. 104:306–314.

10. Oudegeest-Sander MH et  al 2013 Impact of physical fitness and daily

energy expenditure on sleep efficiency in young and older humans.

Gerontology. 59:8–16.

11. Fotuhi M et al 2012. Modifiable factors that alter the size of the hippocampus with ageing. Nat Rev Neurol. 8:189–202.

12. Woollett K, Maguire EA. 2011 Acquiring “the knowledge” of London’s layout drives structural brain changes. Curr. Biol. 21: 2109–2114.

13. Mander BA et al 2013 Prefrontal atrophy, disrupted NREM slow waves and

impaired hippocampal-dependent memory in aging. Nat Neurosci.

16:357–364.

14. Landsness EC et  al 2009 Sleep-dependent improvement in visuomotor

learning: a causal role for slow waves. Sleep; 32:1273–1284.



12 Use It or Lose It



181



15. Naylor E et al 2000 Daily social and physical activity increases slow-wave

sleep and daytime neuropsychological performance in the elderly. Sleep.

23:87–95.

16. Anderson C & Horne JA 2003 Pre-frontal cortex: links between low frequency delta EEG in sleep and neuro-psychological performance in healthy,

older people. Psychophysiology, 40: 349–357.

17. Liao WC. 2002 Effects of passive body heating on body temperature and

sleep regulation in the elderly: a systematic review. Int J Nursing Studies. 32:

803–810.

18. Mander BA et al 2015. ß-amyloid disrupts human NREM slow waves and

related hippocampus-dependent memory consolidation. Nat Neurosci.

Online advance publication.



13

REM Sleep: Food for Thought?



13.1 Phenomena

During our lifespan, REM  sleep (REM) is most prolific 1–2 months

before birth, occupying about half of the roughly 18 hours of the baby’s

daily sleep in utero, where REM probably provides essential, artificial

stimulation for the developing brain in the absence of stimulation from

the outside world. Soon after birth, with the baby being bombarded with

real sensory stimulation, much of REM disappears, much more than

non-REM, to be replaced by wakefulness. However, we adults retain a

higher proportion of REM within sleep than do most other mammals;

this is about 20 % of sleep compared with around 5–15 % for other

mammals. One reason is that we adults resemble our infants more than

any other ape. The retention of marked infant characteristics into adulthood, known as ‘neoteny’, is seen not only in our overall body shape and

general anatomy, but in our remarkable ability to maintain a high degree

of learning, even into old age, and for our cortex to continue adapting

to new experiences and ‘rewire’ itself accordingly. This may help explain

our relatively high amounts of REM in adulthood, to the extent that

some of this REM still falls into the category of ‘dispensability’, like that



© The Editor(s) (if applicable) and The Author(s) 2016

J. Horne, Sleeplessness, DOI 10.1007/978-3-319-30572-1_13



183



184



Sleeplessness



of infants. Our adult REM predominates towards the end of a night’s

sleep, particularly as the usually last REM period (REMP, see hypnogram

in Sect. 6.1) when sleep is less essential, and it is this last REMP which

seems to be most dispensable.

REM is a complex and intriguing aspect of our sleep, and is not simply a platform for dreaming, especially as different parts of the brain are

involved in REM and dreaming, and thus the two phenomena are not

really synonymous. REM can appear in the absence of dreaming, or at

least dreaming as we know it, especially when one considers the predominance of REM in utero.

The eponymous bursts of rapid eye movements (rems), characterising

REM, which are absent from non-REM, typically appear every minute

or so, lasting for about 15 seconds at a time, followed by a period of

inactivity. Although rems are mostly ‘saccadic’, that is with the eyes moving together, darting from side to side as in wakefulness, these bursts are

largely random, seeming to have little or nothing to do with the dream

imagery. The rems per minute, known as ‘REM density’, are greatest during this last REMP, when dreams are also at their most vivid and intense.

In fact, almost half of a whole night’s worth of rems are found here, and

it seems that this overall increased intensity in rems and dreaming may be

a means for maintaining sleep as an alternative to wakefulness when there

is little real need to wake up.

Interestingly, something similar to bursts of rems occurs concurrently

within the ears during rems, called ‘middle ear muscle activity’ (MIMA),

and is also found frequently during wakefulness to ‘tone up hearing’,

and is comparable with ‘pricking up one’s ears’. Bursts of rems and

MIMAs reflect the phasic component of REM, largely emanating from

more ‘basic’ brain structures well below the cortex, where this is seen in

the  ‘sub-cortical’  EEG as bursts of pontine-geniculate-occipital (PGO)

waves. These, together with rems and MIMAs seem to resemble an alerting response, in redirecting attention to a new stimulus.

I liken dreaming to the ‘cinema of the mind’, with what seems to be

increasingly appealing dreams in successive REMPs, when dreams jump

from one intriguing scene to another, maybe distracting us from waking.

Dreams comprise a jumble of waking encounters, thoughts and emotions

and, as Freud noted, ‘we dream as we think’, although I doubt whether



13



REM Sleep: Food for Thought?



185



attempts at dream interpretation are the ‘royal road to unconsciousness’

as he believed. As dreams are largely a mixture of personal experiences

and thoughts, one must be sceptical about attempts by others to ‘interpret’ them, without knowledge of these experiences. Nevertheless, dreams

are quite emotive, and may somehow help consolidate waking memories

having particular emotional significance [1]. However, as we typically

dream for about 90 minutes in total during the course of a night’s sleep,

and as much of dreaming seems to be nonsense, there is little opportunity

to remember a dream unless we immediately wake up out of one, when

little more than the previous few minutes can usually be recalled, even

then, and is soon forgotten.

Recently, there has been much interest in what is known as the ‘default

mode network’ of linked areas within the waking brain, largely identified by fMRI findings, with this network becoming most active during

daydreaming [2] as well as during REM, but being less active during

non-REM.

As noted earlier (Sect. 6.3), by extending sleep, as with a lie-in, and

when not making up for previously lost sleep, the next, hitherto usually absent REMP (at around 7 hours’ sleep), is even longer albeit not

so intense in terms of REM density, suggesting that sleep has probably

reached saturation. Nevertheless, if after waking up in the morning at

the normal time, feeling refreshed and sleep satiated, we then decide to

return to sleep, it is likely that another REM will reappear within 10

minutes of any sleep onset. This is known as a ‘SOREMP’—sleep onset

REM period. These otherwise absent examples of ‘extra REM’ seem to

help sleep ‘coast along’, especially as this extra REM does not subtract

from the ensuing night’s amount of REM, nor change rem density. Thus,

this particular REM seems quite surplus to requirements.

Another notable characteristic of REM is its associated atonia, a temporary paralysis of limb, trunk and facial muscles, preventing us from

moving and thus physically enacting a dream. Sometimes, when woken

up suddenly from a frightening nightmare, this atonia remains for a short

while, often causing further alarm, especially as this also prevents speech.

Known as ‘isolated sleep paralysis’, it is unlikely to be symptomatic of

narcolepsy (see Sect. 9.5). This atonia may well have roles other than just

safeguard the dreamer, as there may be a need for the brain to generate



186



Sleeplessness



this physical movement during REM, to be blocked by the paralysis.

Interestingly, if healthy sleepers are woken as soon as they enter REM,

then get up and quietly walk around for about 15 minutes to return to

sleep, and if this process is repeated whenever REM reappears that night,

then there is little recovery of this lost REM (‘REM rebound’) the following night and, perhaps surprisingly, there is little by way of increased

daytime sleepiness, cf. [3]. However, it is not known to what extent all

this could be replicated into a second night and beyond. Nevertheless,

substitution of REM by waking movement, with no subsequent REM

rebound, has also been reported by several animal studies, cf. [3].



13.2 REM Wakefulness

REM is both a light and deep form of sleep, inasmuch that during REM we

can hear what is going on around and unconsciously determine whether

to wake up and respond to a noise or ignore it. This mechanism centres

on the limbic system of the brain, most notably the amygdala, which in

wakefulness is largely concerned with assessing the emotional significance

of whatever is sensed. Throughout REM the amygdala  remains active

and can ‘decide’ whether a sound warrants a rapid awakening with full

alertness or being blocked out. In this latter respect, REM seems to be a

‘deep’ form of sleep, allowing sleep to continue, and this is why a familiar

train thundering by on a nearby railway is unlikely to cause an awakening during REM, whereas whispering a familiar name or the whimper of

a child will cause an immediate awakening and rapid alertness. On the

other hand, during SWS such arousals are largely a matter of the loudness of the sound rather than its meaning, requiring much more stimulation for an awakening, followed by grogginess and ‘sleep inertia’ lasting

for several minutes (see Sect. 11.5). ’Light sleepers’ are more reactive to

sounds, especially during REM, and as they are more liable to wake up,

so are they more likely to know they have been dreaming, unlike the

‘sounder sleeper’ who slumbers on, unable to remember their dreams.

Brain imaging using fMRI during REM also shows the activities of

several other major brain areas to be similar to those of wakefulness, apart

from the default mode network and the amygdala, which are in contrast



13



REM Sleep: Food for Thought?



187



with non-REM and quite different from SWS [4]. This similarity is also

apparent in the EEGs of REM and relaxed wakefulness, where for many

mammals REM is also known as ‘paradoxical sleep’ as the EEG appears to

be like that of wakefulness, while the animal is clearly asleep.

With dreams often being emotional, and as REM can be a light sleep,

it is surprising that we do not wake up more frequently from them.

Despite such dream content, the actual emotional response is blocked,

as there is no physiological arousal such as rapid rises in heart rate and

blood pressure, as would happen in wakefulness. Although, if the dream

develops into a nightmare and an awakening, these responses are triggered immediately. This blocking of responses is, again, largely under the

control of the amygdala which, during wakefulness, also helps us to deal

with threats and fears [5], as do the activities of other parts of the limbic

system, notably the orbitofrontal region (see Fig.  10.1) of the frontal

cortex which tones down more basic emotions into more acceptable ways

[6]. The Appendix also gives examples of the effects on behaviour when

this region is destroyed as a result of trauma, often leading to uninhibited

and impaired social responses. The orbitofrontal region also happens to

be active in REM, but not in non-REM.

Other key brain regions similarly active during both REM and wakefulness are the anterior cingulate cortex (ACC) and the hippocampus

[4, 7]. In wakefulness the ACC helps resolve indecisions or conflicts

between competing behavioural responses and in working out the payoffs, especially in terms of curiosity versus risk [8]. Inasmuch as curiosity

can bring us into threatening situations, the amygdala and orbitofrontal

cortex seem to contribute to the final decision on what to do. The hippocampus, mentioned earlier (Sect. 10.7), within the context of memory,

not only is critical to the formation of long-term (‘episodic’) memories

associated with personal events, experiences and related emotions, but

also enables the navigating around our environment, with the creation of

‘mental maps’ (largely utilising hippocampal ‘place neurones’), as well as

with helping to integrate these memories.

In conjunction with other brain regions also active in REM, these mental maps might be created for the location of places having strong positive

or negative emotional associations. Which brings me back to that atonia

of REM, and the suppression of intended movements, as these might be



188



Sleeplessness



integral to the creation of mental maps during REM.  In wakefulness,

locomotion is indeed integral to brain plasticity (see Sect. 12.1), including this mental mapping [9]. One might even speculate that the atonia

of REM is somehow ‘rehearsing’ the physical movements between these

more emotionally driven mapping points.

Whilst the role of REM in the more ‘standard’ forms of memory,

outlined in Sect. 10.7, remains debatable [7], impressive evidence is

accumulating that REM helps us cope with and stabilise the emotional

memories of wakefulness [7, 10–13], not only in terms of what has happened recently, but also in preparation for the future. The term used is

‘fear extinction’, that is, the lessening of more fearful or apprehensive

events, and maybe their locations, thus enabling one better able to deal

with similar encounters in the future. However, in these respects there

remains the puzzle of explaining the value of what must be the ‘surplus’

REM, seen in extended sleep and those SOREMPs.

Most antidepressant medicines reduce REM by at least 30 % (about

30 minute per night) [14, 15], with more extreme cases [16] of at least

50 % REM reductions for over 6 months. This absent REM seems largely

replaced by interim wakefulness throughout the night, which may well

be compensatory. It should be noted that this form of REM suppression

is diffuse throughout the night, and not just a termination of the last

REMP. Although there is some increase in REM (‘REM rebound’) when

medication ceases, this only lasts a few days and, clearly, only represents

a small fraction of the REM that has been lost. Interestingly, these longterm partial losses of REM do not seem to cause memory impairments.

As REM suppression is immediate when these medications are given,

their beneficial effects on depression tend to take 2–4 weeks before

becoming evident. So, the extent to which REM and dream loss are therapeutic remains a matter for conjecture, and it should be noted that most

antidepressants are associated with changes to non-REM as well as with

REM [15]. On the other hand, when severely depressed patients have

their night sleep reduced to about 4 hours, thus losing the last one or two

REMPs, there is often an immediate but temporary mood-improving

effect the next day, which relapses on the return to normal sleep. But we

cannot be certain that it is the loss of REM itself which is the key to this

temporary mood improvement.



Tài liệu bạn tìm kiếm đã sẵn sàng tải về

2 Exercise Is Not Enough

Tải bản đầy đủ ngay(0 tr)

×