Task 8. Driving to Benidorm(Effect of sleep on performance)
Task 8. Driving to Benidorm
(Effect of sleep on performance)
Sleep deprivation and circadian rhythms
Sleepiness corresponds to a drive to fall asleep, measurable as subjective perception or as physiological and behavioral changes.
Factors contributing to sleepiness: circadian phase, time awake, and prior sleep duration. The main interfering factors for shift worker is the displacement of work to the "window of circadian low" => when metabolism is slow and fatigue in induced.
Countermeasures of misalignment of S and C
: Main problems of shift worker is the misalignment of the sleep-wake pattern and the circadian system. Treaments focus on this misalignments.
(a) rapid shifts rather than slow rotations, so that there is no partial adjustment of the biological clock and recovery after the nigh shifts occurs immediately.
(b) clockwise rotation (morning-evening-night sequence)
(c) Permanent nigh work, allows a more permanent circadian phase that make sleepiness less pronounced.
(d) self-selected work hours are an important factor in coping with shift work
(f) light exposure during early half of the night shift (may delay circadian phase)
we perform worst at night that during the day. As little as 6 h to 10 h wakefulness dramatically impairs a variety of performance measures.
Karolinska Sleepiness Scale: ranges form 1 to 9 sleepiness. Physiological intrussions of sleep in EEG or EOG usually starts at level 7 and dominate the recording at level 9. The relationship is almost exponential and accidents seem to occur only at the highest level of sleepiness. Subjective sleepiness, increased alpha and theta activity, long eye movement, and long eye closure duration are associated with performance impairment.
Sleep performance & Alcohol
Linear correlation between relative performance and hours of wakefulness, as well as mean blood alcohol concentration and mean relative performance.
A 17 hs of sustained wakefulness, cognitive psychomotor performance decreased at level equivalent to the performance impairment observed at a blood level concentration of .05% and iether 25h deficit were equivalent to those observed at a blood alcohol concentration of roughly .10% /legal limit.
Effects of Caffeine on performance
Caffeine act to block adenosine receptors already at low concentrations e.g. 1 cup of coffee
Caffeine counteracts Process S
by blocking adenosine receptors. Adenosine concentration is higher during wakefulness than during sleep. It accumulates in the brain during prolonged wakefulness, and local perfusion and systemic administration of adenosine and its agonists induces sleep and decreases wakefulness.
CNS effects of caffeine are mediated by its antagonistic actions at the A1 and A2a subtypes of the adenosine receptors. A1 are present in almost all brain areas, and A2 receptors are concentrated in dopamine rich regions. Pre-synaptic adenosine A1 receptors mediate the inhibition of transmitter release. The interaction between caffeine in relevant doses and the dopaminergic transmission is based principally on
enhancement of postsynaptic dopamine D2 receptor transmission.
(the antagonist effect of blocking adenosine release dopamine receptors)
: inverted U-shaped dose-response curve (=above 500mg causes a decrease in performance). Lower doses are reliably associated with positive subjective effects, while higher doses increase in measures of anxiety and tension.
: more activation and changes towards higher frequency and lower amplitude activity with increasing arousal.Counteracts sleep loss.
attention :behavioral effect of caffeine indicated that it affects the attention sytem, counteracts low arousal and may have an effect in the response preparation stage (output). Positive effect on attention and perceptual system as well as output related process.
Caffeine and dopamine
: as a result of inhibition of adenosine A2a receptors by caffeine, transmission via dopamine d2 receptors is increased and consequently effects on behavior related to dopamine are expected.The blockade of adenosine receptos is essential for the stimulatory action of caffeine (for thar reason, an intac dopaminergic nt is necessary for the effect)
Scheme / Sleep- Wake Cycle
: wake and/or sleep-promoting signals emerging from or driven from this are thought to impinge on other brain areas, which leads to changes in wake-sleep propensity. It is nearly independent of sleep-wake behavior. Located in SCN; drives melatonin rhythm, and melatonin receptors are present in SCN, which contributes to the rapid dissipation of the drive for wakefulness just after the wake maintenance zone (te mantine dormido una vez que el proceso S se recupera). The excitatory hypocretin/orexin is another mediator.
: Antomical location unknown. Likely to be a diffuse system, represented by neurochemical factors (e.g. adenosine), accumulating during wakefulness or changes in synaptic weight that may occur as a result of neuronal activiation during wakefulness and the need to be reversed during sleep. Contributes to sleep-wake propensity aslo, and it is driven mainly by sleep-wake behavior (keeps track of sleep history and wakefulness)
a major determinant of sleep-wake behavior, specially affecting timing behavior and do not directly affect the circadian pacemaker or homestat. This can lead to a conflict between socially dictated sleep timing and sleep propensity driven by circadian physiology
: the strongest sychronizer of circadian rhythmicity. Direcly affects many aspects of physiology and behavior in humans. Light synchronizes the pacemaker.
The sleep wake cycle also sends feedback to both processes, the light input reached the SCN via the feedback loop between the cycle and the SCN.
In relation to sleep process.
SWS -principal marker-
Theta activity in waking is an marker of the rising limb of S (rem sleep)
Adenosine: mediates the homesotatic response to prolonged wakefulness
Related to core body temperature and melatonin rhytms
Sleep spindles, mediated by melatonin = lower frequency
8 h sleep and 16 h wake episode
, that recur around the same time every day. During this 16 h wake: alertness and performance on a variety of tasks remain nearly stable. The reduction in performance and increase in sleepiness in the afternoon are minor compared to decrements when wakefulness is extended into the biological night.
Many physiological and endocrine rhythms such as body temperature, heart-rate, cortisol, melatonin and growth hormone change in association with the sleep-wake cycle.
Daily rhythms in human sleep and performance are generated by the interplay of multiple external and internal oscillators
. E.g. in the absence of externally imposed light-dark and social cycles, sleep remain consolidates but desynchronize from the 24h day => dramatic change in the internal phase relationship between the sleep-wake cycle and the body temperature rhythm. The sleep-wake shifts approx 4 to 6 h later. Also, most sleep initiations occur now at the body temperature lowest point.
This change in the internal phase relationship suggests that
separate oscillators drive the sleep-wake cycle and body temperature rhythm.
Two process model of sleep regulation.
Model = sleep propensity = S + C or S - C*
S = homeostatic sleep drive
(= sleep-dependent process) => weak self-sustaining oscillator
Exponential decline in SWA during a sleep period following a regular waking period. During a prolonged vigil slow wave is more predominant. S expresses the
rising level of sleep propensity
C = circadian sleep drive
(=sleep-independent process) => strong self-sustaining oscillator (or pacemaker)
Assumed to be controlled by circadian oscillatory which is unaffected by waking and sleep. The phase position of this process has been derived from the rhythm in vigilance during prolonged sleep deprivation. Minimum = 16 hs, and max at 4 in the morning (inverse of C). It corresponds to circadian body temperature -which is inversely related to sleep propensity. Sleep threshold is highest when circadian sleep propensity is lowest (in the afternoon). -mas temperatura corporal, menos sueño.
Process S + C
= After sleep deprivation, sleep propensity and the level of SWA are higher than after a regular waking period. However, due to the exponential decline of prcess S, sleep duration is not much prolonged.
The circadian rhythm counteracts the steep drop of sleep propensity once you fall asleep so you stay asleep. If you go to sleep in the morning yo do not sleep as much because the circadian rhythm does not counteract the drop anymore. => Lower distance between curves shows lower tendency to fall asleep and shorter duration of sleep.
Implications of the model & shift workers: when sleep occurs during the biological day, not only sleep duration is shorter, but also sleep architure and sleep EEG, are very different from noctural sleep.