Summary: A new study reports on how endocannabinoids are affected by sleep deprivation and whether exercise can modulate the effect.
Source: Uppsala University.
A research group at Uppsala University has investigated how levels of endocannabinoids – which target the same receptors as cannabis – are affected by short sleep duration, and whether acute exercise can modulate this effect.
Chronic lack of sleep has been linked to an increased risk of overweight and obesity and previous studies have demonstrated that healthy participants who are sleep deprived eat more, make unfavorable food choices and crave more high-calorie foods. Now, a research group at Uppsala University has investigated how levels of endocannabinoids – which target the same receptors as cannabis – are affected by short sleep duration, and whether acute exercise can modulate this effect.
‘Previous studies have shown alterations in the levels of some hunger hormones after sleep loss, but the results have been mixed and hormones that drive hedonic food intake have been less investigated. Furthermore, whereas exercise has many beneficial effects, whether exercise can modulate the effects of sleep loss on various hormonal pathways is currently unknown,’ says lead author of the new study Jonathan Cedernaes, M.D., Ph.D, at Uppsala University.
In the new study, published in the journal Psychoneuroendocrinology, the researchers invited healthy normal-weight participants to a sleep laboratory on two separate occasions, to be studied after three consecutive nights of normal sleep, and after three nights of only sleeping four hours each night. Meals and activity patterns were kept standardized while participants were in the lab, and blood was drawn repeatedly to assess endocannabinoid levels in blood. This was also done on the last day both before and after a short bout of intensive exercise.
The researchers found that the levels of 2-arachidonoylglycerol – the most abundant endocannabinoid in the brain – was about 80 percent higher after the nights of short sleep compared with after the normal sleep session. When the participants exercised, the levels of 2AG still went up almost by half, regardless of whether participants had been allowed to sleep for three normal nights, or to only sleep four hours each night.
‘As previously shown by us and others, sleep loss increased subjective hunger compared with the well-rested state. Given the role of endocannabinoids for promoting hunger and hedonic eating, this could offer an explanation as to why. Meanwhile, we instead saw lower stress ratings after exercise in the sleep deprivation condition, which could also possibly be attributed to the observed endocannabinoid levels following our exercise intervention,’ says senior author associate professor Christian Benedict.
‘It is noteworthy that when sleep-deprived, the participants saw the same amount of increase in endocannabinoid levels following the acute exercise. Endocannabinoids are thought to confer both the “runner’s high” as well as at least some of the neuroprotective effects of exercise. Therefore, this may suggest that even under conditions of chronic sleep loss, exercise may exert similar centrally active, and possibly neuroprotective, properties as under conditions of sufficient sleep. This is an important area for future research as we and others have found that short sleep duration by itself may be harmful to the brain, and in the long run increase the risk of e.g. Alzheimer’s disease’, says Jonathan Cedernaes.
Source: Uppsala University
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Original Research: Full open access research for “Sleep restriction alters plasma endocannabinoids concentrations before but not after exercise in humans” by Jonathan Cedernaes, MD, PhD, Flaminia Fanelli, PhD, Alessia Fazzini, PhD, Uberto Pagotto, PhD, Jan-Erik Broman, PhD, Heike Vogel, PhD, Suzanne L. Dickson, PhD, Helgi B. Schiöth, PhD, and Christian Benedict, PhD in Psychoneuroendocrinology. Published online September 21 2016 doi:10.1016/j.psyneuen.2016.09.014
Sleep restriction alters plasma endocannabinoids concentrations before but not after exercise in humans
Following binding to cannabinoid receptors, endocannabinoids regulate a variety of central nervous system processes including appetite and mood. Recent evidence suggests that the systemic release of these lipid metabolites can be altered by acute exercise and that their levels also vary across the 24-h sleep-wake cycle. The present study utilized a within-subject design (involving 16 normal-weight men) to determine whether daytime circulating endocannabinoid concentrations differ following three nights of partial sleep deprivation (4.25-h sleep opportunity, 2:45–7 a.m. each night) vs. normal sleep (8.5-h sleep opportunity, 10:30 p.m.–7 a.m. each night), before and after an acute bout of ergometer cycling in the morning. In addition, subjective hunger and stress were measured. Pre-exercise plasma concentrations of 2-arachidonoylglycerol (2AG) were 80% higher 1.5 h after awakening (vs. normal sleep, p < 0.05) when participants were sleep-deprived. This coincided with increased hunger ratings (+25% vs. normal sleep, p < 0.05). Moreover, plasma 2AG was elevated 15 min post-exercise (+44%, p < 0.01). Sleep duration did not however modulate this exercise-induced rise. Finally, subjective stress was generally lower on the day after three nights of short sleep vs. normal sleep, especially after exercise (p < 0.05). Given that activation of the endocannabinoid system has been previously shown to acutely increase appetite and mood, our results could suggest that behavioral effects of acute sleep loss, such as increased hunger and transiently improved psychological state, may partially result from activation of this signaling pathway. In contrast, more pronounced exercise-induced elevations of endocannabinoids appear to be less affected by short sleep duration.
“Sleep restriction alters plasma endocannabinoids concentrations before but not after exercise in humans” by Jonathan Cedernaes, MD, PhD, Flaminia Fanelli, PhD, Alessia Fazzini, PhD, Uberto Pagotto, PhD, Jan-Erik Broman, PhD, Heike Vogel, PhD, Suzanne L. Dickson, PhD, Helgi B. Schiöth, PhD, and Christian Benedict, PhD in Psychoneuroendocrinology. Published online September 21 2016 doi:10.1016/j.psyneuen.2016.09.014