Review article
Sleep, sleep deprivation, autonomic nervous system and cardiovascular diseases

https://doi.org/10.1016/j.neubiorev.2016.07.004Get rights and content

Highlights

  • Sleep deprivation (SD) can be due to lifestyle habits and sleep disorders.

  • SD alters several mechanisms, i.e. autonomic nervous system, inflammation, endothelial dysfunction.

  • SD are associated with increased risk of cardiovascular and metabolic diseases.

  • An early diagnosis of sleep disorders is essential to prevent detrimental effects on health.

Abstract

Sleep deprivation (SD) has become a relevant health problem in modern societies. We can be sleep deprived due to lifestyle habits or due to sleep disorders, such as insomnia, obstructive sleep apnea (OSA) and neurological disorders.

One of the common element of sleep disorders is the condition of chronic SD, which has complex biological consequences. SD is capable of inducing different biological effects, such as neural autonomic control changes, increased oxidative stress, altered inflammatory and coagulatory responses and accelerated atherosclerosis.

All these mechanisms links SD and cardiovascular and metabolic disorders. Epidemiological studies have shown that short sleep duration is associated with increased incidence of cardiovascular diseases, such as coronary artery disease, hypertension, arrhythmias, diabetes and obesity, after adjustment for socioeconomic and demographic risk factors and comorbidities.

Thus, an early assessment of a condition of SD and its treatment is clinically relevant to prevent the harmful consequences of a very common condition in adult population.

Section snippets

Sleep physiology and autonomic nervous system (ANS)

Mammals spend around one-third of their lifetime sleeping. Although the biological meanings of sleep process is still debated, we know that sleep is a complex physiological event, which involves several different biological pathways, from neural cortical circuits to the heart (Saper et al., 2005, Tononi and Cirelli, 2006).

Most of the biological functions of the body changes during sleep compared to wake, such as heart rate (HR), arterial blood pressure (ABP), temperature, as well as hormonal

Sleep deprivation: general aspects

In the last decades, several studies have investigated the effects of sleep deprivation (SD) on cardiovascular morbidity.

We know that we sleep less than in the past: in 1900 estimated adult average sleep in US was nine hours, in 1980 seven hours, in 2000 six and a half hours (Schoenborn and Adams, 2010). National Institutes of Health recommends at least 10 h of sleep for children, 9–10 h for teenagers, and 7–8 h for adults. It has been reported that in 2014 almost 1/3 of the adults slept less than

Experimental sleep deprivation

Several epidemiological evidences suggest a link between short sleep duration and an increased risk of developing cardiovascular diseases, i.e. coronary artery diseases, congestive heart failure and hypertension (Cappuccio et al., 2010), as well as infections (Patel et al., 2012) and metabolic diseases (Tasali et al., 2008a, Tasali et al., 2008b).

These clinical consequences are due to the activation of different biological pathways, such as a disregulation of the autonomic cardiovascular

Pathological sleep deprivation

As stated before, pathological SD can be the consequence of several sleep disorders. In this review, we will focus on three main categories of sleep disturbances: sleep disordered-breathing (SDB), such as obstructive sleep apnea syndrome (OSA), insomnia and neurological disorders such as PLM and RLS. In fact, although the pathophysiological differences, one of the most important common element of these sleep disorders is the condition of chronic SD, which has a complex series of biological

Conclusions and perspectives

SD is a growing health problem in the whole world. This condition is related to changes in lifestyle habits and an increased prevalence of sleep disorders, such as insomnia and OSA. Independently of its primary cause, SD can impinge upon several biological pathways, such as cardiovascular autonomic control, oxidative stress, inflammatory responses and endothelial function. All these pathophysiological mechanisms are resposible for the link between SD and increased risk of cardiovascular

Acknowledgments

This work was partly supported by a European Regional Development Fund—Project FNUSA-ICRC (No. CZ.1.05/1.1.00/02.0123) to N.M

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