Two nights of recovery sleep restores the dynamic lipemic response, but not the reduction of insulin sensitivity, induced by five nights of sleep restriction

Abstract

Chronic inadequate sleep is associated with increased risk of cardiometabolic diseases. The mechanisms involved are poorly understood but involve changes in insulin sensitivity, including within adipose tissue. The aim of this study was to assess the effects of sleep restriction on nonesterified fatty acid (NEFA) suppression profiles in response to an intravenous glucose tolerance test (IVGTT) and to assess whether 2 nights of recovery sleep (a “weekend”) is sufficient to restore metabolic health. We hypothesized that sleep restriction impairs both glucose and lipid metabolism, specifically adipocyte insulin sensitivity, and the dynamic lipemic response of adipocyte NEFA release during an IVGTT. Fifteen healthy men completed an inpatient study of 3 baseline nights (10 h of time in bed/night), followed by 5 nights of 5 h of time in bed/night and 2 recovery nights (10 h of time in bed/night). IVGTTs were performed on the final day of each condition. Reductions in insulin sensitivity without a compensatory change in acute insulin response to glucose were consistent with prior studies (insulin sensitivity P = 0.002; acute insulin response to glucose P = 0.23). The disposition index was suppressed by sleep restriction and did not recover after recovery sleep ( P < 0.0001 and P = 0.01, respectively). Fasting NEFAs were not different from baseline in either the restriction or recovery conditions. NEFA rebound was significantly suppressed by sleep restriction ( P = 0.01) but returned to baseline values after recovery sleep. Our study indicates that sleep restriction impacts NEFA metabolism and demonstrates that 2 nights of recovery sleep may not be adequate to restore glycemic health.

Sleep–wake-driven and circadian contributions to daily rhythms in gene expression and chromatin accessibility in the murine cortex

“…These perturbations eventually recover, as hinted by the absence of differential expression after 7 d; however, until baseline is reached, this temporary regulatory background could possibly cause the response to another exposure (repeated SD or other) to differ from that under the pre-SD baseline background. While it is debated whether repeated SD on subsequent days alter the homeostatic response at the phenotypic level in rats (EEG) (53, 54), recent studies in humans found that even 2 nights of recovery sleep were insufficient to completely reverse the metabolic perturbations caused by multiple nights of restricted sleep (55, 56). Follow-up experiments at the molecular level will show how such a transient “new baseline” due to only a partial recovery would influence the response to a second event occurring before full recovery.…”

Simple and complex interactions between sleep-wake driven and circadian processes shape daily genome regulatory dynamics in the mouse

“…These perturbations eventually recover, as hinted by the absence of differential expression after 7 days, however until baseline is reached, this temporary regulatory background could possibly cause the response to another exposure (repeated SD or other) to differ from that under the pre-SD baseline background. While it is debated whether repeated sleep deprivation on subsequent days alter the homeostatic response at the phenotypic level in rats (EEG) (49,50), recent studies in humans found that even two nights of recovery sleep were insufficient to completely reverse the metabolic perturbations caused by multiple nights of restricted sleep (51,52). Follow-up experiments at the molecular level will show how such a transient "new baseline" due to partial recovery would influence the response to a second event occurring before full recovery.…”

Four nights of sleep restriction suppress the postprandial lipemic response and decrease satiety

“…We have previously reported the actigraphy-quantified sleep in a subset of participants from this study (10). Actigraphy-assessed habitual sleep was 8.4 ± 0.1 h/night (mean ± SEM).…”

“…Discrepancies between scorers (if any) >15 min were rectified prior to unblinding; device recordings of activity counts, light levels, and wear/non-wear status were used to aid scoring. Actigraphy scoring methods have previously been described (10,61). A registered polysomnographic technologist staged the in-lab PSG recordings in 30 s windows according to American Academy of Sleep Medicine standards (62,63).…”

“…Fasting respiratory quotient, a measure of the relative quantity of carbohydrate oxidation to fat oxidation occurring throughout the body, decreases in response to sleep restriction, indicating increased lipid oxidation (9,(22)(23)(24). NEFA rebound following the suppression induced by an intravenous glucose tolerance test is delayed and impaired during sleep restriction, consistent with elevated NEFA clearance from the plasma, possibly by skeletal muscle (10). Studies investigating the effects of short-term sleep restriction on circulating lipids have had mixed results.…”