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This is the first study to analyze variations in time estimation during 60 h of sleep deprivation and the relation between time estimation performance and the activation measures of skin resistance level, body temperature, and Stanford Sleepiness Scale (SSS) scores. Among 30 healthy participants 18 to 24 years of age, for a 10-s interval using the production method, we found a lengthening in time estimations that was modulated by circadian oscillations. No differences in gender were found in the time estimation task during sleep deprivation. The variations in time estimation correlated significantly with body temperature, skin resistance level, and SSS throughout the sleep deprivation period. When body temperature is elevated, indicating a high level of activation, the interval tends to be underestimated, and vice versa. When the skin resistance level or SSS is elevated (low activation), time estimation is lengthened, and vice versa. This lengthening is important because many everyday situations involve duration estimation under moderate to severe sleep loss. Actual or potential applications of this research include transportation systems, emergency response work, sporting activities, and industrial settings in which accuracy in anticipation or coincidence timing is important for safety or efficiency.

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The present investigation analyzes if the effect of Total Sleep Deprivation (TSD) on depressive mood in normal subjects is related to participants' activation levels. Reaction time (RT), subjective sleepiness, and depressive mood were assessed among 48 normal subjects who were subjected to 60 h of TSD. Subjects were divided into groups based on his/her depressive mood changes following TSD: subjects with worse response (n ϭ 11), subjects with better response (n ϭ 12), and intermediate group (n ϭ 25). We sought to determine if RT and subjective sleepiness were related systematically to depressive mood changes following TSD. TSD produces a general reduction in activation (i.e., a monotonic increase in RT and subjective sleepiness) modulated by circadian oscillations. Baseline activation (RT) was confirmed partially as a predictor of participants' response to TSD. Subjects with high levels of activation (lower RTs at the baseline) experienced a better response (greater reductions in depressive mood) following TSD. There was no relationship between pre-treatment subjective sleepiness levels and the TSD effect on depressive mood. The results partially support the role of the activation level as a differential moderator of TSD effects on depressive mood in normal subjects.