REM Sleep Rebound as an Adaptive Response to Stressful Situations

Abstract

Stress and sleep are related to each other in a bidirectional way. If on one hand poor or inadequate sleep exacerbates emotional, behavioral, and stress-related responses, on the other hand acute stress induces sleep rebound, most likely as a way to cope with the adverse stimuli. Chronic, as opposed to acute, stress impairs sleep and has been claimed to be one of the triggering factors of emotional-related sleep disorders, such as insomnia, depressive- and anxiety-disorders. These outcomes are dependent on individual psychobiological characteristics, conferring even more complexity to the stress-sleep relationship. Its neurobiology has only recently begun to be explored, through animal models, which are also valuable for the development of potential therapeutic agents and preventive actions. This review seeks to present data on the effects of stress on sleep and the different approaches used to study this relationship as well as possible neurobiological underpinnings and mechanisms involved. The results of numerous studies in humans and animals indicate that increased sleep, especially the rapid eye movement phase, following a stressful situation is an important adaptive behavior for recovery. However, this endogenous advantage appears to be impaired in human beings and rodent strains that exhibit high levels of anxiety and anxiety-like behavior.

Sound the alarm: Health and safety risks associated with alarm response for salaried and retained metropolitan firefighters

“…An increased arousal threshold to the alarm is likely to indicate an accumulation of sleep debt (Bruck, 1995). An increased arousal threshold is also consistent with research showing an increased need for sleep following exposure to stress (Sucheki et al, 2012). Paradoxically, high levels of pre-sleep stress have also been associated with difficulty initiating sleep (Wuyts et al, 2012).…”

New hypothesis and treatment targets of depression: an integrated view of key findings

“…Among these, CRH and cortisol produced by the HPA axis, and melatonin secreted by the pineal are most related to biological rhythms and sleep: CRH inhibits slow-wave sleep and triggers the sleep-wake transition; reduced CRH synthesis or CRH receptor blockade increases the duration of non-rapid eye movement (NREM) sleep and suppresses arousal [82] . Moreover, high concentrations of cortisol have effects similar to CRH, which include inhibiting NREM and prolonging arousal time.…”

“…Moreover, high concentrations of cortisol have effects similar to CRH, which include inhibiting NREM and prolonging arousal time. Meanwhile, it also reduces the latency of rapid eye movement (REM) sleep and increases the sleep density in REM sleep [82] . In contrast, melatonin has the opposite effects; it not only shortens the time to fall asleep and improves sleep quality, but also directly regulates the biological rhythms in the suprachiasmatic nucleus, especially the sleep-wake rhythm, through a melatonin receptor-GABA mechanism, thereby improving sleep rhythm disorders and endocrine disorders.…”

Expectation of a loud alarm is not associated with changes in on-call sleep in the laboratory

“…There was a non-significant (p = .051) difference in REM sleep, with participants obtaining 8 min more REM on the on-call night. Recent research has suggested that increases in REM sleep forms part of an adaptive response assisting in recovery from stressful situations, for example car accidents or other traumatic events [25]. Therefore, one possible reason for this result is that, knowing they were going to be woken by loud call overnight participants' stress levels increased, which, in turn, interfered with their REM sleep.…”