Metabolic and Hormonal Effects of 'Catch-up' Sleep in Men With Chronic, Repetitive, Lifestyle-Driven Sleep Restriction

Roo Killick; Camilla M. Hoyos; Kerri L. Melehan; George C. Dungan II; Jonathon Poh; Peter Y. Liu

Disclosures

Clin Endocrinol. 2015;83(4):498-507. 

In This Article

Abstract and Introduction

Abstract

Objective Acutely restricting sleep worsens insulin sensitivity in healthy individuals whose usual sleep is normal in duration and pattern. The effect of recovery or weekend 'catch-up' sleep on insulin sensitivity and metabolically active hormones in individuals with chronic sleep restriction who regularly 'catch-up' on sleep at weekends is as yet unstudied.

Design 19 men (mean ± SEM age 28·6 ± 2·0 years, BMI 26·0 ± 0·8 kg/m2) with at least 6 months' history (5·1 ± 0·9 years) of lifestyle-driven, restricted sleep during the working week (373 ± 6·6 min/night) with regular weekend 'catch-up' sleep (weekend sleep extension 37·4 ± 2·3%) completed an in-laboratory, randomized, crossover study comprising two of three conditions, stratified by age. Conditions were 3 weekend nights of 10 hours, 6 hours or 10 hours time-in-bed with slow wave sleep (SWS) suppression using targeted acoustic stimuli.

Measurements Insulin sensitivity was measured in the morning following the 3rd intervention night by minimal modelling of 19 samples collected during a 2-h oral glucose tolerance test. Glucose, insulin, c-peptide, leptin, peptide YY (PYY), ghrelin, cortisol, testosterone and luteinizing hormone (LH) were measured from daily fasting blood samples; HOMA-IR, HOMA-β and QUICKI were calculated.

Results Insulin sensitivity was higher following three nights of sleep extension compared to sustained sleep restriction. Fasting insulin, c-peptide, HOMA-IR, HOMA-β, leptin and PYY decreased with 'catch-up' sleep, QUICKI and testosterone increased, while morning cortisol and LH did not change. Targeted acoustic stimuli reduced SWS by 23%, but did not alter insulin sensitivity.

Conclusions Three nights of 'catch-up' sleep improved insulin sensitivity in men with chronic, repetitive sleep restriction. Methods to improve metabolic health by optimizing sleep are plausible.

Introduction

Chronic, lifestyle-driven sleep restriction is common in many modern '24/7' societies, with about 40% of individuals relying on discretional time on weekends to 'catch-up' on sleep curtailment during the working week.[1,2] The prevalence of obesity and type 2 diabetes mellitus is increasing to epidemic proportions, particularly in developing nations, in line with increasing globalization, changes in nutrition and sedentary lifestyles.[3] Epidemiological, interventional and molecular experiments provide a strong rationale linking sleep restriction with these metabolic disorders. Recent large epidemiological studies have associated sleep loss to the development of both obesity[4] and diabetes mellitus,[1] and short sleep duration to increased subcutaneous fat.[5] Experimentally restricting or perturbing sleep for 1–14 nights in duration worsens insulin sensitivity in healthy individuals whose usual sleep is normal in duration and pattern.[1] Molecular experiments show that adipocytes from sleep-restricted individuals are resistant to insulin's effects on phosphorylated Akt, a mediator in the insulin-signalling pathway.[6] Together, these data indicate that acute sleep restriction is metabolically harmful.

Although 40% of individuals 'catch-up' on sleep over the weekend, the metabolic effects of catch-up sleep are relatively understudied with no interventional studies to date. Cross-sectional epidemiological studies in children show that weekend 'catch-up' sleep is associated with a decreased risk of being overweight compared to perpetual short sleepers.[7–9] In adults, an hour of weekend 'catch-up' sleep was associated with a 39% decreased risk of hypertension.[10] Given these epidemiological data, we therefore examined whether three nights of a saturating amount of 'catch-up' sleep following regular weekday sleep curtailment would improve insulin sensitivity in those with a history of such sleep patterns, compared to sustained sleep restriction. We also tried to unravel mechanisms. An exploratory aim was to examine the effect of targeted acoustic perturbation of slow-wave sleep (SWS) on insulin sensitivity as SWS has been implicated mechanistically in glucose homoeostasis.[11] Finally, we also explored the effect of both sleep restriction and experimental perturbation of SWS on other hormones known to modify insulin sensitivity and food intake.

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