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This paper presents a modification of the quantitative "three-process model of alertness regulation" to predict sleep latency in connection with irregular sleep/wake patterns. This model uses a circadian and a homeostatic component(sleep loss) that are summed to yield predicted alertness (on a scale of 1 to 20) across a specified time span. The timing of sleep from two studies of irregular sleep were used as input to the model. The predicted alertness at bedtime was regressed on empirical sleep latency from two studies. The maximum R[SUP2] (0.88) was reached for an exponential function, with the model acrophase set to 2048. The predictions were cross validated on another set of sleep latency data from an irregular sleep study and a maximum R[SUP2] of 0.65 was obtained. In both studies, the prediction from the model explained more variance that did self-rated alertness at bedtime. Cross validation was also carried out successfully with published data from two studies of shift work. It was concluded that sleep latency on irregular schedules may be predicted with accuracy from knowledge of the prior sleep/wake pattern. This may have practical consequences for rest/activity management. [ABSTRACT FROM AUTHOR]

Recent concepts of sleep/wake regulation have emphasized circadian influences and largely disregarded homeostatic ones. The present experiment was designed to study sleep loss homeostasis while minimizing confounding circadian influences. Eight male subjects participated in the study. Night sleep was curtailed across four conditions to yield 0, 2, 4, or 8 hrs of sleep. The effects were studied on subsequent day sleep begun at 1100h and spontaneously terminated. Total sleep time (TST), Stage 2 (S2), and Stages 3 + 4 (SWS) showed very strong dose-dependent increases with increasing loss. REM sleep did not respond. After maximum sleep loss TST and S2 doubled whereas SWS increased fivefold. Sleep did not terminate until the prior loss of SWS had been recovered. The total SWS recovery approximately matched the loss. TST, S2, and REM failed to recover more than limited amounts of the loss. The results show that homeostatic influences on sleep may be much larger than usually acknowledged and that SWS closely, although not perfectly, reflects the "active component" of sleep homeostasis. [ABSTRACT FROM AUTHOR]

Twelve subjects were kept awake 64 hrs. During baseline and recovery sleep, subjects were given a simple memory task. The subjects were awakened 3 times each night during slow-wave sleep and shown 4 playing cards. Approximately 90 mm later the subjects were again awakened and tested for retention of the previous cards and given 4 new cards to learn. This procedure was repeated 3 times each night and upon awakening the following morning. On the recovery night recall was reduced, slow-wave sleep was lengthened, sleep latency was shortened, and body motility was reduced. It was suggested that the reason for the poorer recall was deeper sleep induced by the sleep deprivation. [ABSTRACT FROM AUTHOR]

Understanding the association between autonomic nervous system [ANS] function and brain morphology across the lifespan provides important insights into neurovisceral mechanisms underlying health and disease. Resting‐state ANS activity, indexed by measures of heart rate [HR] and its variability [HRV] has been associated with brain morphology, particularly cortical thickness [CT]. While findings have been mixed regarding the anatomical distribution and direction of the associations, these inconsistencies may be due to sex and age differences in HR/HRV and CT. Previous studies have been limited by small sample sizes, which impede the assessment of sex differences and aging effects on the association between ANS function and CT. To overcome these limitations, 20 groups worldwide contributed data collected under similar protocols of CT assessment and HR/HRV recording to be pooled in a mega‐analysis (N = 1,218 (50.5% female), mean age 36.7 years (range: 12–87)). Findings suggest a decline in HRV as well as CT with increasing age. CT, particularly in the orbitofrontal cortex, explained additional variance in HRV, beyond the effects of aging. This pattern of results may suggest that the decline in HRV with increasing age is related to a decline in orbitofrontal CT. These effects were independent of sex and specific to HRV; with no significant association between CT and HR. Greater CT across the adult lifespan may be vital for the maintenance of healthy cardiac regulation via the ANS—or greater cardiac vagal activity as indirectly reflected in HRV may slow brain atrophy. Findings reveal an important association between CT and cardiac parasympathetic activity with implications for healthy aging and longevity that should be studied further in longitudinal research. Impact Statement: Understanding which brain areas are associated with autonomic function has important clinical implications. Previous research was limited to small samples. Aiming for a thorough and large replication, we investigated n = 1,218 healthy subjects in a pooled mega‐analysis. We found unique associations between vagal activity and cortical thickness of frontal brain areas. It is suggested that greater integrity of prefrontal brain areas may be vital for the maintenance of adaptive autonomic nervous system activity in aging. [ABSTRACT FROM AUTHOR]