SHONA L. HALSON
Department of Physiology, Australian Institute of Sport, Belconnen, ACT, Australia
Halson, Shona L.(2008) 'Nutrition, sleep and recovery', European Journal of Sport Science, 8: 2, 119 —126
Ensuring athletes achieve an appropriate quality and/or quantity of sleep may have significant implications for performance and recovery and reduce the risk of developing overreaching or overtraining. Indeed, sleep is often anecdotally suggested to be the single best recovery strategy available to elite athletes. A number of nutritional factors have been suggested to improve sleep, including valerian, melatonin, tryptophan, a high glycaemic index diet before bedtime, and maintenance of a balanced and healthy diet. Conversely, consumption of alcohol and caffeine and hyper-hydration may disturb sleep. Strategies such as warming the skin, hydrotherapy, and adoption of appropriate sleep hygiene (maintenance of good sleep habits and routines) are other tools to aid in sleep promotion. Ensuring athletes gain an appropriate quality and quantity of sleep may be important for optimal athletic performance.
Keywords: Caffeine, valerian, core temperature, tryptophan
Functions of sleep
The fundamental question of why humans require sleep is largely unanswered. Despite this, scientists are providing more information regarding how humans sleep. As the duration and timing of sleep are tightly regulated, it is assumed that sleep provides a number of important psychological and physiological functions (Beersma, 1998).
In a recent review, Frank (2006) suggested several possible perspectives on sleep function. The first is a somatic theory of function, highlighting the restorative relationship between sleep and the immune and endocrine systems. The second theory is a neurometabolic one, proposing that waking imposes a neural and metabolic cost that is ‘‘paid’’ for via subsequent sleep. This includes both detoxification and restoration of the nervous system. The final theory (cognitive theory) suggests that sleep plays a vital role in learning, memory, and synaptic plasticity.
It is this final theory that carries most scientific support and it has been suggested that sleep is primarily for the brain rather than the body (Frank, 2006). It is probable, however, that sleep has multiple functions across a diverse range of physical and cognitive aspects and that these functions are strongly interrelated.
Sleep and exercise performance
Although the exact function of sleep is unclear, we have some understanding of the effects of sleep deprivation on exercise performance. A summary of postulated effects of sleep loss on various exercise tasks is summarized in Table I. Studies from the laboratory of Reilly and colleagues have demonstrated changes in exercise performance following partial sleep deprivation. Sinnerton and Reilly (1992) measured eight swimmers following 2.5 h of sleep per night over four nights. No effect of sleep loss was observed when investigating back and grip strength, lung function or swimming performance.
However, mood state was significantly altered, with increases in depression, tension, confusion, fatigue and anger, and decreases in vigour. Partial sleep deprivation in the form of three nights of sleep loss followed by one night of recovery (Reilly & Deykin, 1983) resulted in minimal changes in gross motor functions (muscle strength, lung power, and endurance performance), while psychomotor function declined markedly, most of which was evident after only one night of sleep loss. Similar effects on sleep have been observed in both males and females (Reilly & Hales, 1988).
Sustained exercise may be affected to a greater extent than single maximal efforts and thus longer submaximal exercise tasks may be affected following sleep deprivation (Reilly & Edwards, 2007). Decreased performance in submaximal weight-lifting tasks has been demonstrated, with a concomitant increase in perception of effort (Reilly & Piercy, 1994).
In terms of cognitive performance, sleep supplementation in the form of napping has been shown to have a positive influence on cognitive tasks (Postolache & Oren, 2005). Naps can markedly reduce sleepiness and can be beneficial when learning skills, strategy or tactics (Postolache & Oren, 2005).
Sleep and recovery
The suggested recuperative and restorative effects of sleep may have beneficial effects on athletic recovery. In particular, the impairments in the immune and endocrine systems (Reilly & Edwards, 2007) that result from sleep deprivation may impair the recovery process and hence adaptation to training. Appropriate sleep quality and quantity is anecdotally reported to be the single best recovery strategy available to elite athletes.
Alternatively, appropriate recovery strategies may aid sleep in several ways. Recovery strategies such as hydrotherapy may influence skin temperature, which, as discussed in a later section, may initiate sleep onset. Furthermore, appropriate recovery may result in a decrease in inflammation and pain, which may increase the ability to sleep, particularly in recently injured athletes.
Increased pain perception and decreased emotional well-being have been reported after several nights of sleep restriction (Dinges et al., 1997; Haack & Mullington, 2005). Haack and Mullington (2005) reported decreased optimism and sociability in individuals who were restricted to 4 h of sleep per night for 12 nights. The authors also reported significantly increased ‘‘bodily discomfort’’, which began after the second sleep-restricted night. Generalized body pain, back pain, and stomach pain contributed to this discomfort across the 12 days in individuals who were pain-free at the beginning of sleep disruption. The results of this study suggest that chronically insufficient sleep may result in the onset or amplification of pain. This fact may have relevance for injured athletes, athletes who are travelling, and/or during periods of competition or stress.
Sleep and overtraining
A few studies have reported alterations in subjective sleep quality during periods of intensified training that resulted in overreaching or overtraining (Halson, Martin, Gardner, Fallon, & Gulbin, 2006; Ju¨ rima¨e, Maestu, Purge, & Ju¨ rima¨e, 2004). Whether poor sleep as a consequence of increased training causes the development of overreaching, or whether sleep disturbances are simply symptoms of overreaching, is unclear. Heightened psychological stress from fatigue, decreased performance or frequent competitions may result in an inability to sleep appropriately.
Nutritional factors that may enhance sleep
Several nutritional substances have traditionally been associated with promoting sleep. Researchers have recently begun to investigate their effectiveness as a substitute for pharmacological interventions.
Valerian (Valeriana officinalis), or valerian root, is a flowering plant that is commonly used to treat insomnia and anxiety (Bent, Padula, Moore, Patterson, & Mehling, 2006; Morin, Jarvis, & Lynch, 2007). It is the most commonly used herbal product to induce sleep in both the USA and Europe (Bent et al., 2006). Over 100 constituents of valerian have been identified, although that responsible for anxiolytic actions remains unknown (Wheatley, 2005). In a recent systematic review and meta-analysis of the efficacy of valerian for improving sleep quality, Bent et al. (2006) suggest that valerian might improve sleep without producing side-effects.
Among the 16 studies assessed, there were a number of methodological issues that limited the ability to draw firm conclusions. Such concerns included different measures of assessing subjective sleep quality and variations in the dose and duration of treatment. However, results suggested that valerian had a statistically significant effect on the relative risk of improved sleep. There were also trends for decreasing subjective sleep onset latency. Furthermore, no significant hangover effect was observed with valerian when compared with placebo, suggesting that valerian may be a useful alternative to some pharmacological agents.
Other sedative herbs
Kava is an extract from the root of Piper methysticum, a Polynesian plant, and has been used for its sedative, aphrodisiac, and stimulatory effects (Wheatley, 2005). Research has shown some positive anxiolytic effects, although several adverse effects have resulted in it being withdrawn from sale in a number of countries (Wheatley, 2005). The limited research on possible benefits of kava on sleep quality and the reported side-effects make the use of this substance questionable for enhancing sleep. Other compounds suggested to have sedative effects include Melissa, passion flower, and hops. However, with the exception of the plant Melissa officinalis (also known as lemon balm), there is a lack of scientific evidence regarding their usefulness. While no research has examined the effect of ingestion of Melissa on sleep quality, a randomized, double-blind, placebo- controlled study reported that it is capable of inducing a mood-state compatible with the induction of sleep (Kennedy, Little, & Scholey, 2003).
Tryptophan is an essential amino acid that is converted to serotonin (5-hydroxytryptamine: 5-HT) in the brain. The conversion occurs when the ratio of free tryptophan to branched-chain amino acids is increased, resulting in an increase in brain tryptophan. Through 5-hydroxytophan, free tryptophan is converted to serotonin, which in turn is converted to melatonin. An imbalance in serotonin has been shown to be involved in the regulation of sleep processes (Markus et al., 2005), and a decrease in plasma tryptophan has been shown to produce sleep disturbances (Markus et al., 2005). This implies that altering the ratio of free tryptophan to branched-chain amino acids may improve sleep function.
L-Tryptophan ingestion has previously been shown to decrease sleep onset latency by 45% (Hartmann, 1982). It has also been shown that tryptophan reduces sleep onset latency without changing other variables associated with sleep (Dollander, 2002; Hartmann, 1982). Arnulf and colleagues (2002) reported increased sleep fragmentation, increased sleep REM (rapid eye movement) latency, and increased REM density following daytime tryptophan depletion. Tryptophan depletion occurred through the ingestion of a tryptophan-free amino acid mixture and resulted in a 77% decrease in plasma tryptophan. Thus lowering plasma free tryptophan can have the opposite effects on sleep as increasing it.
Markus et al. (2005) investigated the effects of evening ingestion of tryptophan on subsequent morning alertness and attention. The source of tryptophan was a-lactalbumin, which is reported to contain the highest tryptophan content of all foodprotein sources (Heine, Radke, Wutzke, Peters, & Kundt, 1996). The high a-lactalbumin diet resulted in a 130% increase in the plasma ratio of free tryptophan to branched-chain amino acids 2 h after evening intake, compared with placebo. This resulted in reduced sleepiness and higher task-related brain activity the following morning.
The results of the above studies suggest that the intake of tryptophan may improve sleep onset latency and alter REM sleep onset latency. Tryptophan- containing foods include milk, meat, fish, poultry, eggs, beans, peanuts, cheese, and leafy green vegetables. Further research is required to accurately prescribe timing and dosage of tryptophan.
High glycaemic index meals
Another possible method of altering serotonin is through the intake of high glycaemic index (GI) meals. High GI carbohydrates may increase the ratio of free tryptophan to branched-chain amino acids facilitated through the release of insulin, which promotes the uptake of branched-chain amino acids into the muscle. Thus as plasma branched-chain amino acids decrease, the ratio of free tryptophan to branched-chain amino acids increases, resulting in an increase in brain free tryptophan and serotonin (Afaghi, O’Connor, & Moi Chow, 2007). Alternatively, high GI meals may reduce free fatty acids, also through the release of insulin. In a recent study, standard isocaloric meals were provided to participants, with the only difference being the GI of 200 g of steamed rice [Mahatma long grain rice (GI=50) or Jasmine aromatic long grain rice (GI=109)] (Afaghi et al., 2007). High GI meals were provided at 1 and 4 h before bedtime and low GI meals were consumed 4 h before bedtime. The results showed that the high GI meal provided 4 h before bedtime shortened sleep onset latency by 48.6% compared with the low GI meal. The high GI meal resulted in a shortened sleep onset latency (38.3%) when consumed 4 h before bedtime compared with consumption 1 h before bedtime.
The results of this study support the suggestion that manipulations of dietary intake may reduce
sleep onset latency and that the timing of meals may be important. The timing may be important when considering the peak in the ratio of free tryptophan to branched-chain amino acids, which usually occurs 2_4 h after ingestion of a high carbohydrate meal (Afaghi et al., 2007). Insulin may also play a role through decreasing free fatty acids, thereby decreasing competition for albumin transport and lowering free tryptophan.
The effect of altering plasma glucose concentrations has also been suggested to influence sleep, although the data here are less clear. Scheen and colleagues (Scheen, Byrne, Plat, Leproult, & Van
Cauter, 1996) reported an increase in periods of non-REM sleep following a constant infusion of glucose during early nocturnal sleep. However, Driver and co-workers (Driver, Shulman, Baker, & Buffenstein, 1999) manipulated the energy content of meals for a single day and reported markedly different levels of insulin without changes in plasma glucose. In this study, there was no influence of dietary intake and the associated metabolic changes on markers of sleep. The authors suggested there may be a degree of plasticity in the sleep response to changes in total energy intake (Driver et al., 1999).
In this study, the amount of protein did not differ in the diets, possibly suggesting a role for the composition of the diet rather than total energy content. More extreme dietary conditions may result in more significant alterations in sleep. Ramadan, observed by millions of Muslims, involves abstaining from eating, drinking, and smoking from dawn to sunset for a period of one month. In eight Muslims assessed during Ramadan, there was a significant delay in sleep onset, which was associated with an increase in nocturnal body temperature (Roky, Chapotot, Hakkou, Benchekroun, & Buguet, 2001). Slow wave sleep and REM sleep were also decreased, which may be related to increased cortisol concentrations and/or an increased body temperature (Roky et al., 2001). A decrease in thermoregulatory responses has been shown during energy restriction lasting 4 weeks (Karklin, Driver, & Buffenstein, 1994), although the negative influence on sleep was similar.
The results of the two studies mentioned above have several implications. First, restricted energy intake over prolonged periods may influence sleep onset latency and REM sleep. Second, as the two studies had similar effects on sleep but with different thermoregulatory effects, the decreased sleep during Ramadan may be related to the inversion of the drinking and meals schedule more than the low energy intake. Finally, athletes in weight-restricted sports may have poorer sleep quantity and/or quality, and methods of improving sleep in these athletes may be necessary.
Melatonin (N-acetyl-5-methoxytryptamine) is a pineal hormone that is suggested to be associated with the control of circadian rhythms (Atkinson, Drust, Reilly, & Waterhouse, 2003). As described earlier, melatonin is converted from serotonin and its precursor tryptophan. As light is a powerful inhibitor of melatonin, almost all daily excretion of melatonin occurs at night (Atkinson et al., 2003). In addition, some foods are naturally high in melatonin, most notably ‘‘montmemary tart cherries’’, or it can be taken as a supplement. Apart from a role in the control of circadian rhythms, melatonin also induces a hypothermic effect, with reductions in core temperature ranging from 0.01 to 0.38C (Atkinson et al., 2003).
Few studies have investigated the use of melatonin in the treatment of insomnia (Morin et al., 2007). Generally, melatonin has been found to decrease subjective estimates of sleep latency and to increase total sleep time (Atkinson et al., 2003). As melatonin is thought to act as a chronobiotic, it has been successful in regulating normal sleep_wake cycles in a variety of illnesses and disorders where this is a concern (Atkinson et al., 2003). It is also for this reason that melatonin has been used with some success in shift-workers and individuals experiencing jetlag.
Other dietary factors
Most ‘‘self-help’’ advice on dietary factors that may improve sleep include eating a balanced diet containing vegetables and whole grains and consuming Bvitamins, iron, magnesium, zinc, calcium, and copper. While this advice may be nutritionally sound, there is little scientific evidence to support these recommendations in the context of enhancing sleep.
Nutritional factors that may decrease sleep
Alcohol can be viewed as having both positive and negative influences on sleep, although overall the consumption of alcohol before sleep is considered to be detrimental to sleep quality and quantity. Due to the relatively fast metabolism of alcohol, the effects of alcohol on sleep can differ between the first and second half of the night. Research has demonstrated a decrease in sleep latency, a reduction in REM sleep, and an increase in non-REM sleep, which typically occurs in the first half of sleep (MacLean and Cairns 1982; Rundell, Lester, Griffiths, & Williams, 1972; Williams, MacLean, & Cairns, 1983). Sleep during the second half of the night can be interrupted with frequent wakings, increased dreaming, and increased REM sleep (Rundell et al., 1972). In a recent study, Feige et al. (2006) examined the effects of alcohol consumption that resulted in a blood alcohol level of 0.03% (considered normal consumption) or 0.1% (considered abuse of alcohol) on polysomnographically recorded sleep. Results suggested a minimal effect of a 0.03% blood alcohol level on sleep parameters, but decreased sleep latency was observed when the participants’ blood alcohol level was 0.1%. When examining the night’s sleep in two halves, the higher alcohol dose resulted in a significant suppression of sleep stage 1 (light sleep), a reduced number of wakings, increased slow wave sleep, and decreased REM density. However, during the second half of sleep, this dose resulted in an increase in light sleep (Feige et al., 2006). The authors concluded that these results viewed alongside previous data support the hypnotic-like effects of alcohol intake at high doses before sleep and subsequent sleep disturbance during the second half of the night. For this reason, alcohol should not be viewed as a suitable hypnotic and indeed is likely to cause an overall impairment in sleep quality and quantity.
Other alcohol-related factors, including tachycardia, perspiration, stomach complaints, headaches or a full bladder, may also disturb sleep (Feige et al., 2006). Previous research has also shown that alcohol can impair daytime performance and increase fatigue as a consequence of disturbed sleep (Roehrs, Yoon, & Roth, 1991).
Caffeine is considered a mild central nervous system stimulant and is the most commonly used methylxanthine (Hindmarch et al., 2000). Caffeine can be found in a range of products, with coffee and tea being the most common sources. There is a widely held belief that caffeine may impair sleep, although individual differences in tolerance are commonly reported.
In a review of the effects of caffeine on sleep, Bonnet and Arand (1992) suggest that caffeine administered within 2 h of bedtime can increase sleep latency, decrease slow wave sleep, and decrease total sleep time. These effects can occur with doses of 100 mg or greater.
Several authors have examined the effect of caffeinated coffee on sleep onset latency and sleep quality and quantity, with negative influences reported on each of these sleep variables (Penetar et al., 1993; Smith, Maben, & Brockman, 1994). A dose response relationship was observed by Karachan et al. (1976) with a one-cup equivalent of coffee (1.1 mg caffeine per kilogram of body weight) taken 30 min before bedtime having little effect on sleep.
The two-cup equivalent (2.3 mg _ kg_1) resulted in changes in the early part of the night, with the four cup equivalent (4.6 mg _ kg_1) showing impairments in all major measures of sleep (Karacan et al., 1976). Shilo et al. (2002) compared sleep variables and 6- sulphoxymelatonin (6-SMT), a measure of melatonin excretion, between caffeinated (130 mg per cup, times 5.391.6 across 24 h) and decaffeinated beverages. Caffeine consumption resulted in decreased sleep quality and decreased estimated secretion of melatonin.
In a naturalistic investigation of day-long consumption of tea and coffee, Hindmarch et al.
(2000) provided participants with equal-volume drinks equivalent to either one or two cups of tea (containing 37.5 or 75 mg caffeine) or one or two cups of coffee (containing 75 or 150 mg of caffeine), or water in a randomized cross-over design, four times per day. In this study, there was a dose-dependent relationship between caffeine and sleep onset, sleep time, and sleep quality.
There was some indication that the individuals with the lowest habitual intake of caffeine were most influenced by the caffeine intake, evidenced by greater disturbances in sleep.
The negative influence of caffeine on sleep is of particular concern for those athletes who use relatively high doses of caffeine for performance enhancement, particularly for events in the late afternoon/evening. Anecdotal evidence suggests that this is a concern, with athletes reporting significantly increased sleep onset latencies following caffeine ingestion. A possible strategy to counteract this effect is to encourage athletes to use caffeine only for major competition (finals as opposed to heats and not in routine training).
Another nutritional factor involved with sleep quantity and quality may be hydration. In a recent survey of sleep habits of athletes at the Australian Institute of Sport, a major reason for sleep disturbances was waking during the night several times to urinate. One reason for this is the need for rehydration following afternoon or evening training sessions or competition, possibly resulting in hyper-hydration in some individuals. It may also be related to the intake of high volumes of low-sodium fluids (i.e. water) in the period between cessation of exercise and bedtime.
Other factors to enhance sleep
Sleep onset tends to occur when core body temperature is declining and sleep ends when it is rising Raymann, Swaab, & Van Someren, 2005). Prescription sleep medications such as Temazepan and the ingestion of melatonin result in vasodilation of distal skin regions, which results in heat loss. This lowers core temperature (Kra¨uchi and Wirz-Justice, 2001) and thus in turn initiates sleep onset.
The extent of heat loss from the skin of the hands and feet has been shown to be the best predictor of a fast sleep onset (Krauchi, Cajochen, Werth, & Wirz-Justice, 1999, 2000). Raymann et al. (2005) examined whether minute changes in skin temperature could influence sleep onset latency to determine if skin temperature changes were the cause of sleep onset or if a common mechanism caused both the decrease in skin temperature and sleep onset.
Eight healthy individuals with no history of sleep complaints were monitored under several conditions of altered core and skin temperatures. Core temperature was manipulated through hot and cold food and drinks, and skin temperature through the use of a thermosuit. Results indicated that the process of falling asleep is accelerated through warming of the proximal skin. This occurred despite the participants reporting less comfort in this condition. Therefore, heat loss mechanisms that cause the much reported decrease in core temperature are strongly related with sleep onset (Raymann et al., 2005). The authors concluded that changes in skin temperature may be both an output signal of the circadian timing system as well as an input signal to sleep-regulating brain areas (Raymann et al., 2005).
Cole (2005) suggests that if skin is cool when going to bed and skin warming strategies are not available, an inverted posture may be of benefit. This posture may stimulate baroreceptors, thereby resulting in reflex vasodilation, and can be achieved through elevation of the legs (Cole, 2005).
There is limited scientific evidence to suggest that water therapy of some kind may elevate skin temperature and thus may result in enhanced sleep. Shortened sleep latency and increased sleepiness have been observed following warm baths and/or foot baths that increased skin temperature (Horne & Reid, 1985; Horne & Shackell, 1987; Kanda, Tochihara, & Ohnaka, 1999; Sung & Tochihara, 2000).
Other forms of hydrotherapy typically used to enhance athlete recovery will result in changes in skin and core temperature. Cold water immersion, contrast water therapy, and hot water immersion (spa baths), all have the potential to change both skin and core temperature. While speculative, it is possible that the enhanced feelings of recovery and well-being typically experienced by athletes the day following hydrotherapy recovery may in part be related to enhanced sleep.
Sleep hygiene refers to behaviours that are believed to promote improved quality and quantity of sleep (Stepanski & Wyatt, 2003). Typically, this involves avoiding behaviours that interfere with sleep patterns and/or engaging in behaviours that promote good sleep. Table II includes a list of sleep hygiene recommendations (Stepanski & Wyatt, 2003).
Empirical evidence for the use of sleep hygiene recommendations as a treatment for insomnia is limited, mainly due to a lack of research and methodological limitations (Stepanski & Wyatt, 2003). However, it is generally regarded that poor sleep hygiene is not the primary cause of insomnia, although it may contribute to it.
In addition to skin warming and inverted posture, Cole (2005) suggests several non-pharmacological techniques for enhancing sleep. Motor relaxation in the form of relaxation of skeletal muscles or stretching to reduce muscle tone can inhibit sleep active neurons in the brain. Sensory withdrawal, through reducing sensory stimuli in the form of noise, light, touch, and body discomfort, may aid in sleep. Breathing techniques in the form of spontaneous exhalation has also been suggested in addition to cognitive relaxation (relaxation and biofeedback).
While these techniques lack rigorous scientific examination, there is underlying physiological rationale as to why they may be beneficial.
Based on the information presented above, several potential non-pharmacological methods may be used to enhance sleep. It is important to recognize that much sleep research has not been conducted on elite athletes; indeed, most research has been on non-athletes. However, until research has been conducted on elite athletes, these guidelines remain appropriate.
For athletes with persistent poor sleep, it is essential that medical advice is sought to ensure there is no underlying medical condition causing disturbed sleep. Depression and anxiety are common causes of insomnia and it is vital that conditions such as these are treated appropriately.
There is limited scientific information regarding sleep requirements and characteristics in elite athletes.
However, from the available evidence it would appear that sleep disturbances may have an influence on athletic performance, particularly if they occur over a prolonged period. Identifying athletes who are experiencing poor sleep is critical, as it may lead to overtraining, illness or precipitate injury. There are a number of nutritional factors that may positively or negatively influence sleep, as well as sleep hygiene recommendations that may aid sleep promotion in athletes. Finally, maximizing sleep may be one method of enhancing performance that has gained little scientific attention.
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