Thanks for returning to read part IV of this series on sleep and cardiovascular health. So far, we’ve covered the association of sleep with cardiovascular disease (CVD) (Part I), sex-differences in the effects of insufficient sleep on cardiovascular health (Part II), and the role of circadian rhythms in CVD (Part III).
Today, we go a bit deeper — exploring how sleep (or a lack thereof) influences the health of our blood vessels. Specifically, we will be looking at how insufficient sleep impacts the stiffness and function of our arteries.
While a detailed overview of arterial stiffness and vascular function is beyond the scope of this post, I want to briefly touch upon each of these so we can gain a better understanding of what they mean for our overall health.
Arterial stiffness is a measure of how stiff or “inelastic” our arteries are. In general, arteries need to be elastic (think, stretchy) in order to handle the body’s large blood volume and keep blood pressure under control. Age, disease, and other conditions can increase the stiffness of our arteries, and this predisposes to an increased CVD risk.
Vascular function is related to and influenced by (and influences) arterial stiffness. When our arteries function properly, they are able to dilate (relax and increase in diameter) in response to the proper regulatory signals. This is important during everyday life, but especially during exercise and other situations where our demand for blood flow increases. Our arteries need to be able to dilate to increase blood flow where it’s needed.
When arteries don’t function properly, this is known as vascular/endothelial dysfunction. Generally, this means a failure of a blood vessel to properly dilate. Like arterial stiffness, endothelial function declines with age and in many disease states.
With that brief primer out of the way, it’s time to look at how arterial stiffness and endothelial function are associated with sleep.
Several studies report inconsistent findings in regards to arterial stiffness and its association with sleep. Some studies report that certain measures of arterial stiffness are only associated with long sleep duration of >9 hours (Yoshioka 2011), or that people with a short sleep duration have lower arterial stiffness than those with normal or long sleep duration (Logan 2018). Other studies find no significant association (Anujo 2016).
However, one study finds that, in male children, short sleep duration is associated with increased arterial stiffness (Morita 2017). Perhaps early-life sleep deprivation may lead to negative vascular effects later in life? This has yet to be studied.
Vascular function has been more widely studied as it relates to sleep duration, with more consistency in the data.
People who report having a lower sleep quantity as well as those with objectively measured short sleep duration have lower brachial-artery function vs. those who have normal sleep duration (Behl 2014, Hall 2017). Short sleep duration is also associated with worse measures of arterial vasodilation and microvascular function (Bain 2017, Bonsen 2014).
Short sleep duration may also affect biomarkers of vascular function. For instance, Von Willebrand factor, a protein involved in blood clotting, is higher in people with short sleep duration (Zoonoozi 2017). They also have higher levels of endothelin-1 — which is involved in vasoconstriction and endothelial dysfunction (Weil 2010).
Associations are interesting and provide insight into potential causal pathways linking poor sleep to cardiovascular dysfunction. But what tells us more about how sleep might actually influence CVD risk are studies that experimentally manipulate sleep. By measuring arterial stiffness, vascular function, and related biomarkers after sleep-deprivation, we are able to observe a causal influence, rather than a mere correlation.
Restricting sleep for even a single night increases arterial stiffness, blood pressure, cardiac output (Sunbul 2014), and the elasticity of the aorta (Akdemir 2012), even in healthy young adults. In one interesting study, when dark chocolate rich in polyphenols was given to participants after TSD, arterial stiffness was reduced and brought back to normal. (Grassi 2016). In all of these studies, participants were deprived of sleep for a full 24 hours, what is known as total sleep deprivation (TSD).
Sleep deprivation also has consistent, negative effects on vascular function. For example, vascular function is reduced after extended work shifts of 24 and 30 hours (Amir et al, Zheng et al). A single night shift or three-sequential night shifts also reduces vascular function in medical personnel (Tarzia et al, Shimada 2011, Kim 2011).
TSD reduces microvascular function in healthy young men AND rodents (Sauvet 2010, Sauvet 2013), and this has been shown using sleep deprivation periods of 29 and 40 hours (Sauvet 2017, Sauvet 2010). However, just 24 hours of TSD reduces FMD and raises arterial stiffness. Some studies observe that TSD reduces the ratio of two factors in the blood: L-Arginine and Asymmetric dimethylarginine — which is associated with blood vessel dysfunction (Slomko 2018).
There is a single study that fails to report a decrease in vascular function after 24 hours of TSD. However, this investigation did find that shift workers have worse vascular function compared to non-shift workers, which is consistent with what is found in the literature (Wehrens 2012).
Total sleep deprivation is an interesting intervention, but what about sleep restriction — which involves a more moderate yet prolonged reduction in the amount of hours slept? Some say this more accurately represents “real life” and therefore may have a wider generalizability to public health.
Similar to TSD, sleep restriction for 5, and 6, and 8 nights causes reduced arterial function, venous function, and microvascular function (Calvin 2014, Dettoni 2012, Sauvet 2015). In most studies, sleep is restricted to about 3–5 hours per night, which comes close to what many individuals get on a consistent basis (don’t do this!)
Sleep restriction may not have an effect on arterial stiffness, however. One study measured arterial stiffness before and after a 3-week period where sleep was restricted by 1.5 hours/night less than normal, and found no change. (Robertson 2013). It might take a more “intense” stressor like total sleep deprivation to influence arterial stiffness.
Studying the interaction of arterial stiffness and endothelial function with insufficient sleep is important because it tells us a potential pathway through which insufficient sleep mediates cardiovascular disease development and progression. Indeed, arterial stiffness and vascular function are independent predictors of future CVD and CVD events — they tell A LOT about the overall health of your cardiovascular system — perhaps even more than traditional risk factors like blood pressure, cholesterol, or body composition.
In part 5, the final of our series, we will explore some of the physiological mechanisms responsible for the cardiovascular dysfunction that occurs in response to insufficient sleep.
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