OBJECTIVE: The objective was to evaluate the relationship between the time course of slow wave EEG activity (SWA) during NREM sleep and insulin sensitivity in adolescents. METHODS: Nine normal weight and nine overweight (BMI>85th percentile) adolescents (13-18 years of age) participated. None of the participants had a history of sleep disordered breathing, confirmed by sleep study. Participants maintained a regularized sleep wake cycle for five days followed by overnight polysomnography in the lab or at home. An oral glucose tolerance test (OGTT) was administered after a 12h fast and within two weeks of the sleep study. Whole body insulin sensitivity (WBISI) and homeostasis model assessment (HOMA-IR) determined insulin resistance. Power spectral analysis quantified slow-wave EEG activity (.05-3.9 Hz) and exponential regression evaluated SWA across successive NREM periods. RESULTS: Those who were insulin resistant and had low insulin sensitivity had less Stages 2, 3 and 4 of NREM sleep, more Stage 1, but did not sleep less than those with low resistance and high sensitivity. SWA power was significantly lower in the first NREM period and the decay rate of SWA across NREM sleep was significantly slower in the low insulin sensitivity group. Similar results were obtained after removing the influence of BMI and Tanner score. CONCLUSIONS: Insulin sensitivity in adolescents is related to SWA power and its time course, not total sleep time, regardless of BMI.
OBJECTIVE: The objective was to evaluate the relationship between the time course of slow wave EEG activity (SWA) during NREM sleep and insulin sensitivity in adolescents. METHODS: Nine normal weight and nine overweight (BMI>85th percentile) adolescents (13-18 years of age) participated. None of the participants had a history of sleep disordered breathing, confirmed by sleep study. Participants maintained a regularized sleep wake cycle for five days followed by overnight polysomnography in the lab or at home. An oral glucose tolerance test (OGTT) was administered after a 12h fast and within two weeks of the sleep study. Whole body insulin sensitivity (WBISI) and homeostasis model assessment (HOMA-IR) determined insulin resistance. Power spectral analysis quantified slow-wave EEG activity (.05-3.9 Hz) and exponential regression evaluated SWA across successive NREM periods. RESULTS: Those who were insulin resistant and had low insulin sensitivity had less Stages 2, 3 and 4 of NREM sleep, more Stage 1, but did not sleep less than those with low resistance and high sensitivity. SWA power was significantly lower in the first NREM period and the decay rate of SWA across NREM sleep was significantly slower in the low insulin sensitivity group. Similar results were obtained after removing the influence of BMI and Tanner score. CONCLUSIONS:Insulin sensitivity in adolescents is related to SWA power and its time course, not total sleep time, regardless of BMI.
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