Sleep plays a pivotal role in recovery and therefore any disruption to sleep or reduction in the quality of sleep will delay recovery and therefore impede overall progress in training.
Sleep is extremely important for numerous biological functions and sleep deprivation can have significant effects on athletic performance, especially sub-maximal, prolonged exercise. From the available evidence it appears that athletes may be obtaining less than 8 h of sleep per night and that increasing sleep (sleep extension) or napping may be useful to increase the total number of hours of sleep and thereby enhance performance.
In normal sleep, the stages follow a structured sequence starting with wake, then light sleep with stages 1 and 2, followed by deep sleep (slow wave sleep) with stages 3 and 4, and then followed by REM sleep. Such a sequence is called a sleep cycle which has a typical duration of 90–110 min. A normal night consists of six sleep cycles where the proportion of deep sleep decreases from the beginning to the end of the night and the proportion of REM sleep increases at the same time. In summary, about 50–60% of time is spent in light sleep, 15–20% of time is spent in deep sleep, 20–25% is spent in REM sleep, and 5% or less is spent in wakefulness.
The autonomous nervous system changes with sleep. Heart rate, blood pressure, and respiratory rate are lowered to adapt to the reduced metabolic needs during normal sleep. Consequently, the mean heart-rate values drop from wakefulness to light sleep and further to deep sleep. During REM sleep heart rate increases again showing a high variability, which may exceed the variability observed during quiet wakefulness
The internal structure of sleep shows clear dynamics that follow a physiological imprinted pattern. This pattern can be described successfully by sleep stages ranging from light sleep to deep sleep and REM sleep. The dynamics of sleep stages can be investigated as such by analyzing the duration of sleep stages in the course of the night. The statistical analysis of sleep-stage durations revealed completely different patterns for the regulation of sleep stages and wakefulness episodes during sleep. This indicates that sleep and wakefulness are not just two parts of a sleep–wakefulness control, but that there exist entirely different mechanisms for their regulation in the brain. This fundamental mechanism is not altered in principle by sleep disorders that have a large impact on sleep fragmentation. Only the parameters of the distributions change.
The analysis of the autonomic nervous system during sleep by the investigation of heart-rate variability gives further insight into the regulation of sleep. We found that when the brain is very active as in the ‘dream’—REM stage, heart rate has long-time correlations, like in the wake phase. In contrast, in deep sleep correlations of the heart rate vanish after a small number of beats. In light sleep finally, the heart rate seems to become uncorrelated as well, but only after an increased number of beats. We also compared the altered autonomic nervous system function in obstructive sleep apnea with the results for normal subjects. We found that the differences between the sleep stages are much clearer than the differences between healthy and sleep apnea subjects. This means that the basic heart-rate control in the different sleep stages is very dominant. Obstructive sleep apnea introduces an additional variation on heart rate with a typical bradycardia/tachycardia pattern corresponding to the apnea events, but leaves the basic autonomous nervous system regulation untouched.
The autonomous nervous system changes with sleep. Heart rate, blood pressure, and respiratory rate are lowered to adapt to the reduced metabolic needs during normal sleep. Consequently, the mean heart-rate values drop from wakefulness to light sleep and further to deep sleep. During REM sleep heart rate increases again showing a high variability, which may exceed the variability observed during quiet wakefulness
The differences between healthy and sleep apnea subjects were much smaller than the differences between sleep stages. This indicates that the basic mechanisms for heart-rate control on an interbeat level did not change very much with sleep apnea. We assume that this basic mechanism is strongly controlled by sleep stages. It seems likely that the long-range correlations during wakefulness and REM sleep are caused by the enhanced influence of the brain on the autonomous nervous system. When this influence is strongly reduced, as is the case during light sleep and deep sleep, the heartbeat intervals behave in a more random fashion. Our studies support the view that there is a strong interaction between the central nervous sleep regulation and the autonomous nervous system regulation. Both systems interact and the measurable parameters cannot be interpreted without the knowledge about the current state of the other system.
The internal structure of sleep shows clear dynamics that follow a physiological imprinted pattern. This pattern can be described successfully by sleep stages ranging from light sleep to deep sleep and REM sleep. The dynamics of sleep stages can be investigated as such by analyzing the duration of sleep stages in the course of the night. The statistical analysis of sleep-stage durations revealed completely different patterns for the regulation of sleep stages and wakefulness episodes during sleep. This indicates that sleep and wakefulness are not just two parts of a sleep–wakefulness control, but that there exist entirely different mechanisms for their regulation in the brain. This fundamental mechanism is not altered in principle by sleep disorders that have a large impact on sleep fragmentation. Only the parameters of the distributions change.
The analysis of the autonomic nervous system during sleep by the investigation of heart-rate variability gives further insight into the regulation of sleep. We found that when the brain is very active as in the ‘dream’—REM stage, heart rate has long-time correlations, like in the wake phase. In contrast, in deep sleep correlations of the heart rate vanish after a small number of beats. In light sleep finally, the heart rate seems to become uncorrelated as well, but only after an increased number of beats. We also compared the altered autonomic nervous system function in obstructive sleep apnea with the results for normal subjects. We found that the differences between the sleep stages are much clearer than the differences between healthy and sleep apnea subjects. This means that the basic heart-rate control in the different sleep stages is very dominant. Obstructive sleep apnea introduces an additional variation on heart rate with a typical bradycardia/tachycardia pattern corresponding to the apnea events, but leaves the basic autonomous nervous system regulation untouched.
Our studies support the view that there is a strong interaction between the central nervous sleep regulation and the autonomous nervous system regulation. Both systems interact and the measurable parameters cannot be interpreted without the knowledge about the current state of the other system.
So, how can sleep be optimised to aid recovery?
- Humans sleep in five phases which repeat themselves every 90 minutes. Five cycles equates to seven-and-a-half hours which is enough for the average adult
- Take naps (up to 1 hour) – ideal time after lunch between 1-3
- The bedroom should be cool, dark and quiet
- Create a good sleep routine by going to bed at the same time and waking up at the same time
- Avoid watching television in bed, using the computer in bed and avoid watching the clock.
- Avoid caffeine approximately 4-5 h prior to sleep (this may vary among individuals)
- Do not go to bed after consuming too much fluid as it may result in waking up to use the bathroom
- Caffeine and liquids high in sugar are off the menu, as are fat-laden meals, which take longer to digest and raise body temperature, which in turn slows the process of falling to sleep
- Begin a pre-sleep routine 90 minutes before bed – start turning off televisions, mobile phones and other electrical devices which give off bright light.
- Have a shower prior to sleeping. Your body temperature will cool after coming out of the shower and ease you naturally into a state of sleep.
- Turn your radiator down – a cool 16-18C is ideal.
- Drink a glass of warm milk before bed. Dairy products are rich in tryptophan, which aids the production of sleep-inducing chemicals serotonin and melatonin.
As well as conditions like sleep apnea, alcohol, work stress and intensive exercise late in the day can limit our amount of deep sleep, whereas aerobic exercise and a regular pre-bed relaxation pattern can facilitate deep sleep. In fact, as summarized in this blog post , higher HRV before bedtime seems to enable a more rapid & effective transition to good quality sleep.
