Abstract

Abstract Introduction Poor sleep in early childhood is linked to reduced school readiness. This study examined the role of acute sleep loss in behavioral self-regulation using a delay of gratification task. We hypothesized that after acute nap deprivation, toddlers would have worse inhibitory control and resort to more maladaptive self-regulation strategies than after a nap. Methods 25 healthy children (11 males, 34.1±2.3 months-old) followed a strict sleep schedule for ≥5 days before a baseline (nap) and an acute nap deprivation condition (no-nap). After being introduced to an age-appropriate toy, children were instructed not to touch the toy and left alone for 3-minutes. To assess inhibitory control, videos of the waiting period were behaviorally coded for latency to touch and 11 self-regulation strategies. We combined strategies into adaptive and maladaptive composites; higher scores on each composite indicated greater use. Results During the nap condition, 19 children touched the toy (latency to touch=70.0±60.7 sec); during the no-nap condition, 18 children touched the toy (latency to touch=65.4±71.6 sec). The adaptive composite score was 1.58±0.25 for the nap condition and 1.17±0.27 for the no-nap condition. The maladaptive score was 0.92±0.17 for the nap condition and 0.83±0.19 for the no-nap condition. We found no differences between conditions in the number of children who touched the toy (X2=0, p=0.50), mean latency to touch (t=0.27, p=0.39), or the composite scores of adaptive (z=0.35, p=0.12) and maladaptive strategies (z=0.09, p=0.69). Conclusion Findings indicate that acute nap deprivation may not have an immediate impact on inhibitory control and self-regulation in toddlers. 30-36 months old children may not have sufficient cognitive resources to exert inhibitory control and self-regulate whether or not they have obtained adequate daytime sleep. Future research should examine developmental changes in the effects of acute sleep restriction on behavioral self-regulation. Support Research support from NIH R01-MH086566 to MKL.

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