Categorical sleep stage scoring has traditionally been used to identify SWS. SWS is the deepest stage of sleep and is defined by the presence of low-frequency, high-amplitude waveforms known as slow waves or delta waves on electroencephalogram (EEG) tracings.

1 Importantly, recent work has suggested that some of these effects are related to specific disruption of slow wave sleep (SWS). Consistent with these cross-sectional observations, metabolic abnormalities have also been observed in adults after either acute sleep restriction or sleep fragmentation in a controlled laboratory setting. INTRODUCTIONĮpidemiologic studies have demonstrated that both chronic short sleep and poor sleep quality are associated with an increased risk of obesity and type 2 diabetes mellitus (T2DM) in adults. These results imply that adolescents may have a unique metabolic resiliency to acute sleep disruption follow-up studies will be important in settings of more prolonged SWS restriction or disruption. The current studies, which represent the first SWS disruption studies with metabolic phenotyping to be conducted in children, demonstrate that a single night of SWS disruption does not diminish insulin sensitivity in pubertal children, challenging the existing dogma based on studies in adults. Cross-sectional studies in children and adults and a small number of interventional studies in adults suggest that short slow wave sleep (SWS) duration and SWS fragmentation are risk factors for metabolic syndrome.

No slow wave sleep