I think we can all agree that sleep is a critical part of our daily lives; it is a restorative function of the brain, to remain healthy and as responsive as we require it to be. Sleep deprivation, therefore, has been found to have detrimental effects on brain function such as impaired brain energy metabolism and cognitive function, but sleep fragmentation is much less understood. Sufferers of sleep fragmentation, unlike sleep deprivation, may actually get a normal amount of sleep, but this sleep cycle is frequently disrupted, and the current research set out to determine if the effects of sleep fragmentation were similar to sleep deprivation, particularly in terms of brain energy metabolism.
When we are awake, our brain metabolizes our energy according to what activities we are pursuing, and adjusts the amount of energy supplied to the neurons to fit our needs, we call this process neurometabolic coupling. During this process, the astrocytes, which are star-shaped glial cells of the central nervous system which regulate the “firing” between neurons, release lactate as a form of energy when glutamate is being released for neuronal activation. This process is called Astrocyte-Neurone Lactate Shuttle (ANLS), and it plays a significant role in the storage of our long-term spatial memories. These lactate secreting astrocytes seem to be impaired by sleep deprivation, as well as glucose uptake; 10-20% less glucose is taken up in all regions of the brain during sleep deprivation in both humans as well as rats, which suggests that neurometabolic coupling is impaired when deprived of sleep, particularly in the hippocampus of the brain, where spatial memories are known to be stored, but it is unknown if this effect occurs when sleep is fragmented.
The current study set out to determine the effects of sleep fragmentation in mice on their brain energy metabolism during “novelty exposure”, simply meaning that the mice were introduced to a new environment for one hour daily, after their sleep was fragmented for a period of 2 weeks. The novelty exposure component was intended to cause increased neuronal activation due to the foreign environment. The fragmentation of sleep was administered once a minute, 12 hours a day, during the “dark” cycle of the controlled 12 hour light, 12 hour dark, environment. Data was collected both at day 1 and day 14, to attempt to see long-term effects of sleep fragmentation.
Compared to the control group, the mice in the experimental fragmented sleep group showed significantly lower glucose uptake both at day 1 and day 14. The specific regions in which the greatest differences were observed were the motor cortex, with a 9% decrease, and the hippocampus, with a 14% decrease. Glycogen levels were not significantly different, glucose levels were only slightly different, but lactate levels were significantly lower in the sleep fragmentation group, specifically in the cortex, where they were 22% lower than the control group. Interestingly, however, the hippocampal EEGs of both groups at both day 1 and day 14 were not significantly different, suggesting that the “online” activation, meaning the in the moment activation of the spatial memory of the hippocampus is not impacted by sleep fragmentation.
Overall, the effects of sleep fragmentation are indeed similar to sleep deprivation, which means that it is not only the quantity of sleep but the quality that are critical in brain function. Although the online function of the hippocampus was not affected, the severe decrease in lactate secreted by the astrocytes which are important in long-term spatial memory suggest that sleep fragmentation will significant impair long-term spatial memory, similar to sleep deprivation. These findings provide insight to the effects sleep fragmentation may have on our cognitive functioning, and perhaps add some severity to sleep disorders that manifest sleep fragmentation.
Baud, M.O., Parafita, J., Nguyen, A., Migistretti, P.J., Petit, J.M. (2016). Sleep fragmentation alters brain energy metabolism without modifying hippocampal electrophysiological response to novel exposure. Journal of Sleep Research, 25(5): 583-590.
