Shorter Sleep Predicts Longer Subsequent Day Sedentary Duration in Healthy Midlife Adults, but Not in Those with Sleep Apnea.

PURPOSE: Sedentary behavior and suboptimal sleep increase risks for chronic diseases. We hypothesized that sedentary behavior and sleep affect each other and that an underlying sleep disorder would alter these relationships. To test these hypotheses, we studied the bidirectional relationships between sedentary behavior and sleep (duration and efficiency) in healthy controls (HC) and people with untreated obstructive sleep apnea (OSA). PATIENTS AND METHODS: Fifty-two volunteers (18 HC, 19 mild OSA [apnea/hypopnea index [AHI] range 5-14.9/hour], 15 moderate OSA [AHI range 15-29.9/hour]) were studied with actigraphy and sleep diaries across ~9 consecutive nights of self-selected consistent ~8-hour sleep episodes at home (range 4-21/nights per person). We analyzed whether total time asleep and sleep efficiency affected the subsequent daytime sedentary duration while controlling for body mass index and whether the severity of OSA altered this relationship. We also tested the reverse relationship, namely whether daytime sedentary duration affected the subsequent night's sleep and if any such relationship differed with OSA severity. RESULTS: Overnight sleep duration and efficiency negatively predicted the subsequent day's sedentary duration in HC (p<0.02), but not in people with mild or moderate OSA (p>0.05). There was no significant reverse relationship between daytime sedentary duration and the subsequent night's sleep duration or efficiency (p≥0.2). CONCLUSION: In healthy adults, short nighttime sleep predicts a longer duration of sedentary behavior on a subsequent day, but we did not observe this relationship in people with OSA. The mechanisms underlying this association in healthy individuals and its disruption in the presence of OSA need to be studied.

Biological pathways underlying the association between habitual long-sleep and elevated cardiovascular risk in adults.

Cardiovascular disease is the leading cause of death in the world. In addition to non-modifiable factors such as age and sex, cardiovascular risk is also driven by behavioral, and therefore somewhat modifiable, factors such as physical activity, diet, and sleep. It is well established that sleep duration has a U-shaped association with mortality and cardiovascular disease, with recent evidence suggesting that this association is observed even while controlling for the effects of comorbid conditions. Whereas several biological mechanisms mediating the association between chronic short sleep duration and cardiovascular risk have been established, the biological mechanisms underlying the relationship between habitual long sleep (≥9 h) duration and cardiovascular risk, in the absence of other chronic diseases, are not well understood. This review will focus on summarizing the literature investigating the mechanisms underlying the association between habitual long sleep duration and cardiovascular risk. We will also propose the mechanistic pathways, distinct from the ones for short sleep, by which habitual long sleep can increase cardiovascular disease.