Laverne C. Johnson

Bio: Laverne C. Johnson is an academic researcher from United States Department of the Navy. The author has contributed to research in topics: Sleep Stages & Non-rapid eye movement sleep. The author has an hindex of 28, co-authored 55 publications receiving 2125 citations.

Effects of Exercise, Bedrest and Napping on Performance Decrement During 40 Hours

Abstract: : Young male Naval volunteers were denied normal nocturnal sleep and maintained on a 60-min treatment-160-min testing schedule for 40 consecutive hours Ten subjects bicycled, 20 subjects controlled EEG activity during bedrest, and 10 subjects napped Eight measures of addition, auditory vigilance, mood, and oral temperature were obtained The Bedrest group showed significant impairment on all eight measures, and thus, gave no support to the forced rest theory of sleep function The exercise group was worse than the Nap and Bedrest groups for all measures In spite of fragmented, reduced sleep (about 37 hours per 24 hours), the Nap group had no impairment on six of the measures The results suggest that exercise increases the impairment due to sleep loss, and naps reduce or remove this impairment

Bispectrum analysis of electroencephalogram signals during waking and sleeping

Abstract: The degree of interaction of component waves making up a single electroencephalogram trace was strongly correlated with alpha activity, lead placement, and state of consciousness. Significant quadratic coupling of the waves was found only for awake subjects with high alpha activity. For these subjects about 50 percent of beta activity can be attributed to harmonic coupling with the alpha peak. During sleep, the degree of interaction was of borderline significance and did not follow a consistent pattern with respect to subject, frequency, state, or lead.

Performance and mood during and after gradual sleep reduction.

Abstract: Long-term gradual sleep reduction effects were investigated on 4 young adult collegiate couples. The battery of assessment tools included a sleep log, Stanford Sleepiness Scale, Profile of Mood States, Feeling Tone Checklist, a measure of circadian oral temperature, Williams Word Memory test, Digit Span test, Wilkinson Auditory Vigilance task, Wilkinson Addition task, Minnesota Multiphasic Personality Inventory, Rapid Alternation task, psychiatric and medical examinations, and a subjective effects questionnnaire. It was concluded that 6–8 months of gradual sleep restriction, down to 4.5–5.5 hrs per night, does not result in behavioral effects measurable by the instruments used. Subjective fatigue appears to be the limiting factor in determining tolerability of gradual sleep restriction. At the end of an additional 12-month follow-up period, total sleep time was still 1–2.5 hrs below baseline, but measures of well-being had returned to baseline levels.

Racial Differences in Skin Resistance.

Abstract: In two laboratories utilizing different age subjects and recording techniques, Negro subjects had higher skin resistance than a comparable white population. There was no difference in other autonomic variables or autonomic reactivity. Reasons for this racial difference may offer a better physiological explanation for galvanic skin resistance.

The Cumulative Cost of Additional Wakefulness: Dose-Response Effects on Neurobehavioral Functions and Sleep Physiology From Chronic Sleep Restriction and Total Sleep Deprivation

Abstract: OBJECTIVES: To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation. DESIGN: The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days. SETTING: Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring. PARTICIPANTS: A total of n = 48 healthy adults (ages 21-38) participated in the experiments. INTERVENTIONS: Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited. RESULTS: Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness were near-linearly related to the cumulative duration of wakefulness in excess of 15.84 h (s.e. 0.73 h). CONCLUSIONS: Since chronic restriction of sleep to 6 h or less per night produced cognitive performance deficits equivalent to up to 2 nights of total sleep deprivation, it appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults. Sleepiness ratings suggest that subjects were largely unaware of these increasing cognitive deficits, which may explain why the impact of chronic sleep restriction on waking cognitive functions is often assumed to be benign. Physiological sleep responses to chronic restriction did not mirror waking neurobehavioral responses, but cumulative wakefulness in excess of a 15.84 h predicted performance lapses across all four experimental conditions. This suggests that sleep debt is perhaps best understood as resulting in additional wakefulness that has a neurobiological "cost" which accumulates over time.

Cumulative sleepiness, mood disturbance, and psychomotor vigilance performance decrements during a week of sleep restricted to 4-5 hours per night

Abstract: To determine whether a cumulative sleep debt (in a range commonly experienced) would result in cumulative changes in measures of waking neurobehavioral alertness, 16 healthy young adults had their sleep restricted 33% below habitual sleep duration, to an average 4.98 hours per night [standard deviation (SD) = 0.57] for seven consecutive nights. Subjects slept in the laboratory, and sleep and waking were monitored by staff and actigraphy. Three times each day (1000, 1600, and 2200 hours) subjects were assessed for subjective sleepiness (SSS) and mood (POMS) and were evaluated on a brief performance battery that included psychomotor vigilance (PVT), probed memory (PRM), and serial-addition testing, Once each day they completed a series of visual analog scales (VAS) and reported sleepiness and somatic and cognitive/emotional problems. Sleep restriction resulted in statistically robust cumulative effects on waking functions. SSS ratings, subscale scores for fatigue, confusion, tension, and total mood disturbance from the POMS and VAS ratings of mental exhaustion and stress were evaluated across days of restricted sleep (p = 0.009 to p = 0.0001). PVT performance parameters, including the frequency and duration of lapses, were also significantly increased by restriction (p = 0.018 to p = 0.0001). Significant time-of-day effects were evident in SSS and PVT data, but time-of-day did not interact with the effects of sleep restriction across days. The temporal profiles of cumulative changes in neurobehavioral measures of alertness as a function of sleep restriction were generally consistent. Subjective changes tended to precede performance changes by 1 day, but overall changes in both classes of measure were greatest during the first 2 days (P1, P2) and last 2 days (P6, P7) of sleep restriction. Data from subsets of subjects also showed: 1) that significant decreases in the MSLT occurred during sleep restriction, 2) that the elevated sleepiness and performance deficits continued beyond day 7 of restriction, and 3) that recovery from these deficits appeared to require two full nights of sleep. The cumulative increase in performance lapses across days of sleep restriction correlated closely with MSLT results (r = -0.95) from an earlier comparable experiment by Carskadon and Dement (1). These findings suggest that cumulative nocturnal sleep debt had a dynamic and escalating analog in cumulative daytime sleepiness and that asymptotic or steady-state sleepiness was not achieved in response to sleep restriction.

Publication recommendations for electrodermal measurements.

Abstract: This committee was appointed by the SPR Board to provide recommendations for publishing data on electrodermal activity (EDA). They are intended to be a stand-alone source for newcomers and experienced users. A short outline of principles for electrodermal measurement is given, and recommendations from an earlier report (Fowles et al., ) are incorporated. Three fundamental techniques of EDA recording are described: (1) endosomatic recording without the application of an external current, (2) exosomatic recording with direct current (the most widely applied methodology), and (3) exosomatic recording with alternating current-to date infrequently used but a promising future methodology. In addition to EDA recording in laboratories, ambulatory recording has become an emerging technique. Specific problems that come with this recording of EDA in the field are discussed, as are those emerging from recording EDA within a magnetic field (e.g., fMRI). Recommendations for the details that should be mentioned in publications of EDA methods and results are provided.

Timing of human sleep: recovery process gated by a circadian pacemaker

Abstract: A model for the timing of human sleep is presented. It is based on a sleep-regulating variable (S)--possibly, but not necessarily, associated with a neurochemical substance--which increases during wakefulness and decreases during sleep. Sleep onset is triggered when S approaches an upper threshold (H); awakening occurs when S reaches a lower threshold (L). The thresholds show a circadian rhythm controlled by a single circadian pacemaker. Time constants of the S process were derived from rates of change of electroencephalographic (EEG) power density during regular sleep and during recovery from sleep deprivation. The waveform of the circadian threshold fluctuations was derived from spontaneous wake-up times after partial sleep deprivation. The model allows computer simulations of the main phenomena of human sleep timing, such as 1) internal desynchronization in the absence of time cues, 2) sleep fragmentation during continuous bed rest, and 3) circadian phase dependence of sleep duration during isolation from time cues, recovery from sleep deprivation, and shift work. The model shows that the experimental data are consistent with the concept of a single circadian pacemaker in humans. It has implications for the understanding of sleep as a restorative process and its timing with respect to day and night.