The homeostatic and circadian processes operate together in a complementary manner that normally optimizes the ability of people to sleep effectively for about 8 hours and remain awake and alert for about 16 hours. The ability to fall asleep at one’s typical bedtime is enhanced by the homeostatic sleep pressure that has accumulated from being awake throughout the daytime. The intrinsic circadian sleepiness drive normally peaks toward the end of sleep period, typically about two hours before one’s habitual spontaneous awakening time. Since homeostatic sleepiness is being discharged during the first few hours of sleep, later circadian sleepiness enhances continued sleep during the last few hours of the night. The opposite occurs during the daytime. Alertness during earlier daytime is facilitated by the low homeostatic sleepiness drive during this period. Conveniently, the circadian pattern of alertness peaks in the evening, just a few hours before one’s habitual sleep-onset time. Low sleep propensity in the evening helps promote sustained alertness during the typical 16hour wakeful period. On the other hand, attempts to sleep during this circadian phase may be frustrating and contribute to an insomnia complaint.
A common exception to the dichotomy of nighttime sleepiness and daytime alertness is midafternoon sleepiness that may result in a dip in alertness or even regular sleep episodes (e.g., siestas, “power naps”). This afternoon sleepiness is not inevitable, as adequate nightly sleep normally allows sustained daytime alertness. When people are even mildly sleep deprived, however, it is during the midafternoon that they are most likely to experience some difficulty remaining alert and awake. This vulnerability of increased afternoon sleepiness seems to be an intrinsic characteristic of the circadian system and is not primarily due to a midday meal (as the term postprandial sleepiness incorrectly would suggest). Although afternoon napping is facilitated by the circadian system, it may have significant homeostatic consequences. A nap may be beneficial in promoting alertness and improved performance during the next several hours; however, it may reduce the sleepiness necessary for rapid sleep onset at one’s desired bedtime. A nap that is relatively early and short, perhaps about 20 minutes, is less likely to have detrimental effects. On the other hand, in the context of sleep deprivation, a longer nap will be beneficial. One additional potential problem with longer naps is the risk of feeling worse due to sleep inertia (see below, under “Electrophysiological Measurements”).
Experimentally differentiating the respective sleep-promoting influences of the homeostatic and circadian processes is rather challenging, as both always are present. Evidence of the intrinsic circadian sleepiness drive can be derived from several different strategies. Studies of repeated opportunities for brief naps offer one reflection of the intrinsic sleepiness pattern. Another clever approach involves ultrashort day lengths that still allow one-third of the total time available for sleep. For instance, a “20minute day” allows about 7 minutes for sleep (Lavie, 1989). The successive 13 minutes of waking and 7 minutes of sleep opportunity can be repeated over a 24-hour period or longer. The pattern of sleep amounts during the brief sleep opportunities will be influenced by the circadian sleep propensity. Roger Broughton (1994) demonstrated how the sleepiness patterns from very different research protocols tend to coincide. This composite pattern of the circadian sleep propensity is demonstrated in figure 2.2. The major nighttime and minor afternoon sleepiness peaks are evident, as is the low point in sleepiness in the early evening. The influence of this underlying circadian sleepiness pattern is consistent with typical real-life experiences, particularly the experience of an afternoon “slump” and then a “second wind” in the early evening.
This discussion of sleep-wake cycle regulation assumes maturity. The sleep propensity pattern of the human newborn lacks temporal organization. The average daily sleep of about 16 to 17 hours occurs relatively randomly. Very gradually over the first few months of life, sleep is more likely to occur during the nighttime. Some daytime sleep in the form of napping typically does continue during the first few years. Although the SCN is thought to be functional at birth, the entire circadian system, with its necessary input and output mechanisms, evolves only gradually during the first few months of life. This maturing circadian system is apparent from the increasing day-night differentiation of such parameters as the infant’s core body temperature and melatonin secretion pattern. The sleep that occurred initially just from the homeostatic drive eventually is shaped by the significant influence of the circadian system, which, in turn, is influenced by the photoperiod.
Fundamentally, the homeostatic and circadian processes of sleepwake regulation are presented as heuristic constructs. Although there are not yet precise explanations of how physiological mechanisms connect each process with the experience of sleepiness, these constructs are quite valuable in theoretical modeling, developing experimental protocols, explaining common experiences, and helping to identify the cause of many sleep-related clinical problems. The appreciation of this pronounced circadian sleep propensity pattern and the influence of homeostatic sleep pressure creates an important broad context for the complaints of sleepiness or sleeplessness at any particular time of the day or night.
Source: David N. Neubauer, “Understanding Sleeplessness: Perspectives on Insomnia,” The Johns Hopkins University Press, Baltimore 2003
Republished by Health Care Programs