Not getting enough sleep, or getting low-quality sleep, leaves most people feeling poorly the next day. It’s common knowledge that a good night’s sleep is important for maintaining mental focus, peak athletic performance, and emotional resilience. But the effects of sleep, or the lack thereof, reach beyond cognition. Over the past several decades, epidemiological research has demonstrated a relationship between chronic inadequate sleep and metabolic disorders, such as obesity, type 2 diabetes, and cardiovascular disease. People who report regularly getting fewer than six hours of sleep per night are at greater risk of becoming overweight, developing insulin resistance (suppressed ability to clear glucose from the blood in response to the hormone insulin) or heart disease, and dying early. Laboratory-based experimental studies, where participant sleep is manipulated and metabolic function recorded, have demonstrated that even one night of short sleep impairs insulin sensitivity such that glucose uptake by the body’s tissues becomes impaired. Over a lifetime of exposure, this is thought to explain part of the links between habitual short sleep and risk of type 2 diabetes.
While research has demonstrated the effects of sleep restriction on glucose metabolism, very little is known about how, or if, sleep restriction affects fat metabolism. We recently performed an 11-day laboratory experiment at Penn State’s Clinical Research Center to assess just that. Participants were screened for good health and regular sleep habits. Eligible participants spent a week at home following a standardized sleep routine to ensure that they were sleep-replete (staying in bed, trying to sleep for 10 hours each night) and abstaining from alcohol, caffeine, and other drugs. Following the week at home, participants moved into the lab for 11 days. For the first three nights, participants maintained the same sleep schedule to allow them to adjust to the laboratory environment and to allow baseline metabolic measures to be taken. For the next five nights, participants were only allowed five hours of sleep opportunity each night, from 12:30 am to 5:30 am, mimicking a workweek of short sleep. For the final two nights of the study, participants resumed the ten hours in bed schedule they had maintained prior to the study and at baseline, mimicking a weekend of catch-up sleep.
We assessed fat metabolism by feeding participants an identical high-calorie, high-fat dinner of chili mac on three occasions, once at baseline, after four nights of short sleep, and after one night of recovery sleep. Prior to the meal and for five hours afterwards we took blood samples from the participants to measure meal absorption, digestion, and clearance of the meal fat.
After four nights of insufficient sleep, our participants had elevated blood insulin levels both before and after the meal, despite no difference in blood glucose levels compared to baseline. This demonstrates, as other studies have shown previously, that with sleep restriction our participants were relatively less sensitive to insulin (their bodies needed to produce more insulin to maintain blood glucose levels). Furthermore, we found that sleep-restricted participants cleared the meal lipids, or fats, from their blood more quickly than they had at baseline, likely driven by the elevated insulin, which stimulates lipid clearance from the blood by adipose (fat) tissue. We also asked participants to rate their hunger and satiety (fullness) before and after the high-fat dinner. When they were sleep restricted, participants reported feeling less full after dinner. One night of recovery sleep, mimicking a weekend or a night of catch-up sleep, partially restored the changes in meal metabolism. Taken together, this means that participants’ bodies more efficiently stored the fat from the meal, they probably would have been inclined to keep eating, and their bodies were working harder to regulate their blood sugar to boot. With regular exposure across a lifetime, these changes could contribute to risk of adiposity, obesity, and type 2 diabetes.
Our study is important for several reasons. First and foremost, for its translatability: we mimicked a workweek of sleep restriction with a weekend of recovery, and we administered the test meal as a high-fat dinner. Prior studies examining the effects of sleep loss on meal digestion have focused on glucose tolerance tests or carbohydrate-rich meals administered in the morning. Yet, many Americans eat their largest, most calorie-laden meal in the evening. Sleep loss is known to affect hormones that fluctuate rhythmically throughout the day (for example, cortisol and melatonin), therefore, the effects of sleep loss on meal digestion and absorption may be different in the morning compared to the evening. Our study is the first to examine the effects of sleep restriction on evening meal digestion. Secondly, we focused on lipid metabolism because abnormal post-meal lipid levels are associated with increased cardiovascular disease risk and chronic short sleep is associated with unhealthy fasting lipid profiles. As a result of our translatable study design, our findings have real-world implications for people who undersleep during the workweek. Our results support the notion that sleep is important for metabolic health and that a weekend of catch up sleep may not fully reverse the impact of a workweek of short sleep.
Read our full results in the Journal of Lipid Research (Ness et al 2019 Four nights of sleep restriction suppress the postprandial lipemic response and decrease satiety).
This complex and intense study would not have been possible without contributions and support from Penn State’s Clinical Research Center, pilot funding from the Clinical and Translational Science Institute and the College of Health and Human Development as well as numerous collaborators. For more about our work and this study, feel free to contact the project principal investigator, Dr. Anne-Marie Chang. See also our first publication from this study in the American Journal of Physiology- Regulatory, Integrative, and Comparative Physiology (Ness et al 2019 Two nights of recovery sleep restores the dynamic lipemic response, but not the reduction of insulin sensitivity, induced by five nights of sleep restriction).
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