The Relationship Between Estrogen and the Decline in Delta Power During Adolescence.

Study Objectives: During adolescence, there is a precipitous decrease in slow-wave sleep (SWS) and its spectral correlate, delta power, which may reflect cortical reorganization. The temporal association between the decrease in delta power and puberty suggests that sex steroids may initiate these changes. This association has not been previously investigated. Methods: To determine whether estrogen triggers the adolescent decline in delta power, we compared delta power in 14 girls with central precocious puberty (CPP) and 6 age-matched, prepubertal controls. Five CPP participants were re-studied 7-14 months after pubertal suppression to determine if the changes in delta power are reversible after restoring a prepubertal hormonal milieu. The change in delta power was also compared between CPP participants and five historic controls from a longitudinal polysomnographic study. Results: CPP participants (6.7-10.5 years) spent 30% of the night in SWS. Delta power (3.7 × 106 ± 2.7 × 105 µV2) predominated in the first 2 non-rapid eye movement episodes and decayed exponentially (tau 0.006 minutes). Age-matched controls demonstrated similar sleep staging (24% SWS) and delta dynamics (3.3 × 106 ± 5.1 × 105 µV2, tau 0.004 minutes). Four out of 5 CPP participants had a significant decrease (26%) in delta power after hormone suppression (p < .05), similar to historic controls. Conclusion: Using an innovative model of girls with CPP studied before and after estrogen suppression, the effects of puberty on the decline in delta power were dissociated from those of chronologic age. The current studies suggest that increased estrogen does not cause the adolescent decline in delta power and indicate that neurodevelopmental changes per se or other factors associated with puberty drive these sleep changes.

Effect of Slow Wave Sleep Disruption on Metabolic Parameters in Adolescents.

STUDY OBJECTIVES: Cross-sectional studies report a correlation between slow wave sleep (SWS) duration and insulin sensitivity (SI) in children and adults. Suppression of SWS causes insulin resistance in adults but effects in children are unknown. This study was designed to determine the effect of SWS fragmentation on SI in children. METHODS: Fourteen pubertal children (11.3-14.1 y, body mass index 29(th) to 97(th) percentile) were randomized to sleep studies and mixed meal (MM) tolerance tests with and without SWS disruption. Beta-cell responsiveness (Φ) and SI were determined using oral minimal modeling. RESULTS: During the disruption night, auditory stimuli (68.1 ± 10.7/night; mean ± standard error) decreased SWS by 40.0 ± 8.0%. SWS fragmentation did not affect fasting glucose (non-disrupted 76.9 ± 2.3 versus disrupted 80.6 ± 2.1 mg/dL), insulin (9.2 ± 1.6 versus 10.4 ± 2.0 µIU/mL), or C-peptide (1.9 ± 0.2 versus 1.9 ± 0.1 ng/mL) levels and did not impair SI (12.9 ± 2.3 versus 10.1 ± 1.6 10(-4) dL/kg/min per µIU/mL) or Φ (73.4 ± 7.8 versus 74.4 ± 8.4 10(-9) min(-1)) to a MM challenge. Only the subjects in the most insulin-sensitive tertile demonstrated a consistent decrease in SI after SWS disruption. CONCLUSION: Pubertal children across a range of body mass indices may be resistant to the adverse metabolic effects of acute SWS disruption. Only those subjects with high SI (i.e., having the greatest "metabolic reserve") demonstrated a consistent decrease in SI. These results suggest that adolescents may have a unique ability to adapt to metabolic stressors, such as acute SWS disruption, to maintain euglycemia. Additional studies are necessary to confirm that this resiliency is maintained in settings of chronic SWS disruption.