This chapter discusses the effects of biologic rhythms and sleep on athletes’ performance and health. Specific operational concepts of chronobiology and the science of biological rhythms are presented in the first section. Sleep and sleep disorders are discussed in the second section, and the role and goals of chronobiology consultation to promote peak athletic performance are presented in the third section.
Biologic day and night is represented internally as “biologic day” or “biological night” to anticipate rather than only react to the temporal environment. Our bodies have clocks that maintain endogenous rhythms in constant conditions and adjust our internal time to the external time through light input to the retina. In this way, light is not just a vehicle for sight but is also the main synchronizer between the internal, approximately 24-hour (i.e., circadian) rhythms in physiologic states and the exact 24-hour cycles in environmental conditions. Chronobiology describes the field of science that systematically studies the timing processes in organisms.
Terminology of Circadian Rhythms
Circadian rhythms represent periodic phenomena within a period of about 24 hours. The circadian timing system generates and regulates these endogenously generated circadian rhythms. Fluctuations of approximately 24 hours occur in parameters that are inherently related to athletic performance, such as attention and other cognitive functions ( Fig. 29-1 ), self-chosen work rate, body flexibility, and pulmonary function. A rhythm that is not in sync with the 24-hour day because of a longer or shorter period is termed free-running . A rhythm that has been reset to the 24-hour period of the earth’s rotation is termed entrained .
To entrain an organism, the endogenous rhythms must be exposed to a zeitgeber, or “ time giver, ” which could be any environmental variable that can reset the body’s clock. The most potent zeitgeber is light, but other zeitgebers (e.g., time of food availability, exercise, ambient temperature, and social contact) also may play a role. Exposure to light changes the period and phase of the circadian pacemaker.
Melatonin is secreted during the biologic (internal) night, a period associated with and operationally defined by hormonal, electrophysiologic, and behavioral parameters. The timing and duration of melatonin secretion reflects prior exposure to light and dark cycles and is limited to the biologic night, which begins, in most cases, about 2 hours before one’s habitual bedtime.
Cortisol reaches peak levels in the early morning, after which the level begins to decline, with a trough during the evening. An elevated cortisol level is noted in persons with interrupted sleep.
The level of prolactin is higher during the internal night, is particularly elevated during rapid eye movement sleep, and in turn promotes rapid eye movement sleep. One study showed that nocturnal prolactin secretion is elevated by late afternoon exercise.
Nocturnal testosterone elevation results in peak concentrations during the early morning, with trough levels during the early evening hours. McMurray et al. suggest that the early morning peak of testosterone might be increased by engaging in heavy resistance exercise in the early evening of the previous day. In contrast, fragmented sleep can disrupt the rhythm of testosterone secretion, and the nocturnal rise in testosterone may be attenuated.
The suprachiasmatic nucleus (SCN) of the hypothalamus, known as the “body clock” or the primary circadian pacemaker, is in charge of regulating endogenous circadian rhythms. Light reaches the SCN from the retina through the neuronal connection of the retinohypothalamic tract. In the retina, light interacts with photosensitive retinal ganglion cells that contain a novel photoreceptor called melanopsin, which, in humans, is more intensely stimulated by short-wavelength blue light (420 to 440 nm).
Sleep and Sleep Disorders
Regulation of the sleep-wake cycle is accomplished by the interaction of two endogenous systems: sleep homeostat (process S) and the circadian process (process C) ( Fig. 29-2 ). Process S can be perceived as sleep pressure (urgency to go to sleep), sleep debt (accumulated effect of not getting enough sleep), or simply the ability to fall asleep. It can be estimated by measuring the delta power during sleep and may be mediated by soluble neurotransmitters (somnogens) such as adenosine.
Process C is the circadian process, which generates a signal of wakefulness with a temporal trajectory that is approximately a mirror image of process S. It increases the threshold for falling asleep during the day as process S accumulates, peaks in the late afternoon and evening (consolidating wakefulness), and decreases during the night (consolidating sleep). The underlying neurologic structure of process C is the SCN, also known as the “master clock” or the “master circadian pacemaker.” The physiologic state of sleep inertia refers to the time lag necessary to reach full arousal and psychomotor abilities after awakening.
Insomnia includes the inability to fall asleep within 15 minutes of retiring to bed, the tendency to wake up during the night, the inability to return to sleep after undesired awakening during the night, the inability to remain asleep for the desired full duration with awakening more than 1 hour before the intended time of arousal, and consequent feelings of anxiety about being able to fall asleep. Insomnia is often temporary and is commonly associated with stress and anxiety, levels of which tend to increase with pending competitive performances. The workup and treatment of insomnia in athletes are beyond the scope of this chapter. The effects of exercise on persons with insomnia are discussed in an article by Youngstedt. For a more in-depth discussion of nonpharmacologic interventions for sleep induction, the reader is directed to an article by Cole.
Obstructive sleep apnea (OSA) is the consequence of repeated episodes of either partial or complete pharyngeal airflow obstruction during sleep despite continued respiratory effort, resulting in oxygen desaturation, increased sympathetic tone and arousals, and ultimately concluding with fragmented and nonrestorative sleep with daytime sleepiness. Snoring, although extremely common, is insufficient to make a diagnosis of OSA. Certain athletes are predisposed to OSA based on the physical characteristics of the player. George and colleagues studied sleep-disordered breathing in a sample of 302 professional football players from eight different teams. The rate of sleep-disordered breathing in these professional football players was greatly increased, especially in offensive or defensive linemen, who are easily the largest and strongest players on the gridiron. Excessive daytime sleepiness was present in a high percentage of players.
Diagnosis and treatment of OSA, which is expected to improve performance and overall health by restoring regular breathing during sleep, reducing loud snoring, and minimizing daytime sleepiness, is discussed in detail by Emsellem and Murtagh. Agents that increase alertness such as stimulants have been used to counteract excessive daytime sleepiness, which is a major symptom and often a chief complaint of persons with OSA. In a recent year-long study, Hirshkowitz and Black examined the effects of modafinil, a psychostimulant agent used in conjunction with continuous positive airway pressure in patients with OSA. The results included a reduction in daytime sleepiness as measured by the Epworth Sleepiness Scale (ESS), an increase in functional status as assessed by the Functional Outcomes of Sleep Questionnaire, and an improvement in overall health as shown by the Short Form-36 Health Survey. Because of its capability of enhancing rather than just restoring performance, modafinil was added to the prohibited list of the World Anti-Doping Agency in 2004.
Sports Chronobiology Consultation: “Toward Peak Athletic Performance”
Minimizing Adversity to Maximize Athletic Performance
The goals of a sports chronobiology consultation are to reduce (or avoid altogether) possible hindrances to athletic performance as a result of circadian misalignments and sleep abnormalities. Such a consultation includes addressing early morning, early afternoon, or very late evening decline in athletic performance along with jet lag or seasonal adversity and minimizing or preventing the effects of a less-than-optimal quantity or quality of sleep. Peak performance is achieved during certain intervals and durations of wakefulness, such as during the late afternoon and early evening period of alertness known as the wake-maintenance zone . In particular, the loftier objective of a sports chronobiology consultation includes using natural means (e.g., timely light avoidance or exposure and naps) to align the endogenous circadian peak in athletic performance to the timing of the competitive event, while aiming to avoid sleep inertia and minimizing “sleep debt.”
Measurement of Sleepiness and Alertness
Subjective Scales of Sleep, Sleepiness, and Alertness
A number of scales have been used to assess sleepiness (defined as the urge to sleep), such as the Karolinska Sleepiness Scale. The Karolinska Sleepiness Scale is a 9-point scale ranging from 1 (very alert) to 9 (very sleepy, having difficulty staying awake, or fighting sleep). The Epworth Sleepiness Scale (ESS), for which normative data are available, is a self-report of sleepiness over a period, varying from several weeks to a month. The ESS is particularly useful for quickly assessing sleepiness and can be used to support a suspicion of certain sleep conditions such as sleep apnea, which may be more common than appreciated in football players.
The Pittsburgh sleep quality index, which includes 19 questions grouped in seven component domains (i.e., sleep quality, latency, duration, efficiency, disturbance, medication, and daytime dysfunction), is a validated questionnaire that provides a global score of sleep quality. Cutoff points for disturbed sleep vary between 5 and 8. Samuels provides an example of the use of the Pittsburgh sleep quality index in athletes.
Objective Tests of Sleep, Sleepiness, and Alertness
Laboratory tests include multiple sleep latency tests, polysomnography, and the maintenance of wakefulness test.
Polysomnography is overnight monitoring of an electroencephalogram, eye movements, a chin electromyogram, limb movements, airflow (nasal and oral), an electrocardiogram, chest and abdominal movements, and oxygen saturations. The polysomnograph assesses stages of sleep (“sleep architecture”), arousals, and severity of disordered breathing, oxygen desaturation, and limb movements.
Used in diagnosing sleep disorders since the mid 1970s, the Multiple Sleep Latency Test is an objective measure of daytime sleepiness and assesses how long it takes a person to fall asleep (sleep latency) at predetermined times throughout the day.
Ambulatory tests include actigraphy and the psychomotor vigilance task (PVT). Activity monitors (e.g., actigraphs and actiwatches) are small devices that accurately record body movement; they are similar in concept to the seismograph. The PVT is usually administered at 2-hour intervals and measures the changes in reaction time and sustained attention resulting from sleep loss and circadian rhythmicity. With a standard duration of 10 minutes, PVT can quantify the effects of sleep deprivation and measure the effectiveness of naps or recovery sleep.
Homeostatic and Circadian Impairments: Role in Alertness, Sleep Appetite, and Sports Performance
The homeostatic hardship is a function of the appetitive nature of sleep; it increases during prolonged wakefulness and decreases as the need for sleep is fulfilled. The circadian hardship describes the possible misalignment between the circadian rhythm–dictated ideal performance time (measured historically as the hours in which the athlete’s performance peaks) and the timing of the competition.
Many athletes who have practices in the early morning do not go to bed early enough to allow for an adequate duration of sleep, often because of academic, occupational, or family/social demands. With prolonged wakefulness, the homeostatic pressure for sleep continually builds in intensity following a saturating curve, but with the occurrence of sleep, the dissipation is very steep and is observable even after a short nap of 10 to 20 minutes. In a study conducted to examine neurobehavioral functioning in sleep-deprived compared with sleep-restricted groups, the 4- and 6-hour chronic sleep restriction groups showed cumulative performance deficits after 2 consecutive weeks that matched those of the group with total sleep deprivation. The potential of sleep extension for improved athletic performance was suggested by Dement and confirmed in a recent study that reported an improved shooting accuracy and sprint performance in parallel to improved PVT and score reduction on the ESS.
Naps are an effective tool to address homeostatic adversity in athletes, although no consensus appears to exist regarding the appropriate duration of the nap. In a recent study, Waterhouse and coworkers reported that a 30-minute postlunch nap between 1 pm and 1:30 pm , after a night of partial sleep restriction of 4 hours, improved sprint time, alertness, wakefulness, and short-term memory compared with persons who underwent identical sleep restriction but did not take a nap. Brief naps as short as 10 minutes have been shown to be effective in countering sleep restriction as measured by sleep latency, fatigue, alertness, and cognitive performance. A nap longer than 30 minutes may encroach on the deep sleep phase, after which abrupt awakening results in considerably more subjective grogginess (than before the nap) and places the person in the physiologic state of sleep inertia. Reilly and Edwards suggest that the subjective improvement following a “power nap” in athletes is greater in persons who habitually power nap than in persons who are unfamiliar with this practice.
Sleep Gates, Wake Maintenance Zones, and Performance
Humans have predictable “windows” of time when it is relatively easy to fall asleep that alternate with windows of time when it is difficult to fall asleep. The two intervals during which falling asleep is greatly enhanced are called sleep gates . The first sleep gate, called the postprandial dip, occurs during the early afternoon ( Fig. 29-3 ) and is more frequently seen in morning-type persons; it is further intensified by a high-carbohydrate meal. Monk associates the dip with an innate human propensity for sleep during the early afternoon hours. The term “postprandial dip” is a misnomer, however, because this circadian dip occurs regardless of food intake and likely represents metabolic anticipation of a main meal rather than reaction to the meal.