Itt írjon a(z) SleepLoss-ról/ről
Cardiovascular Effects
- Sleep deprivation, like smoking is now noted as one of the main causes of developing heart disease. The possible reasoning for this, is that a decrease in sleep results in increased blood pressure, and sympathetic overactivity; known precursors for developing coronary heart disease. Sleep deprivation may be caused by sleep apnea which also can be a factor in developing heart disease (Quan 2009).
Increased Blood Pressure and Sympathetic Overactivity Studies performed on healthy individuals, showed a significantly larger systolic blood pressure following one night of sleep deprivation, compared with non-sleep deprived individuals. One experiment examined the theory of this systolic increase being linked with stress induced reaction. They created a control, where subjects where not exposed to any form of stressful situation following sleep deprivation (Franzen et al., 2011). The same increase in systolic pressure was observed. Therefore highlighting a clear link between sleep deprivation and increased blood pressure.
- Without adequate rest periods sympathetic overactivity results. Normally, heart rate is controlled by a balance between the parasympathetic nervous system and the sympathetic nervous system. The parasympathetic innervation via the vagus nerve causes a decrease in heart rate by having a direct depressor effect on the sympathetic nervous system. Sympathetic nervous system elevates the heart rate by causing an muscarinic Acetylcholine activated elevation in cAMP, which causes elevation in heart rate Sympathetic overactivity, leads to inadequate depression via the parasympathetic vagus nerve and the heart rate remains increased as a result. Figure 1.1 highlights the parasympathetic suppressant effect on the heart rate. Long term sympathetic over-excitability results in hypertension, which leads to cardiovascular disease (Ayas et al., 2003).
Figure 1: Shows the effect of the parasympathetic and sympathetic system on heart rate. Elevation in sympathetic activity counteracts the depressor effect of the parasympathetic system thus, resulting in increased heart rate. Sleep Apnea Obstructive sleep apnea, a cause of sleep deprivation is also linked in patients developing heart disease. During sleep, there is a natural loss in musculature tone including muscles which encapsulate the pharynx. The pharynx and upper airspace is composed of muscles and soft tissue. With this loss of tone, in some patients, it can cause the airway to “collapse” , thus obstructing the airway. This airway occlusion results in decreased intrathoracic pressure, which therefore leads to an increased afterload of venous return, causing right ventricle distention and the interventricular septum to shift. Combination of these invents causes a decrease in left ventricular stroke volume which decreases the cardiac output significantly (Latina et al. 2013).
- Cardiac output decrease causes pulmonary stretch receptors to activate the sympathetic nervous system. Also hypoxia and hypercapnia caused by airway obstruction, stimulate peripheral and central chemoreceptors, also resulting in sympathetic activation. This sympathetic activation increases blood pressure by causing vasoconstriction in an effort to overcome these adverse effects. In a patient suffering with obstructive sleep apnea, they can encounter these surges hundreds of times per night, resulting in huge fluctuations in heart rate and blood pressure. In the long term, hypertension results, which can then lead to heart disease.
Obesity Chronic sleep loss has a huge impact on neuroendocrine function and glucose metabolism, both which are underlying risk factors in obesity development. Sleep deprivation causes alterations in both metabolic and endocrine mechanisms. Such as; Decrease glucose tolerance and insulin sensitivity, Increased cortisol concentrations in the evening, Increased ghrelin concentration, Decreased leptin levels.
These factors result in increased appetite and therefore at a higher risk of developing obesity.
The brain, requires a constant glucose supply, even when food intake that provides the glucose does not occur. During sleep, this supply must be maintained. Studies have found that tolerance to glucose and insulin differed following sleep deprivation. Lack of sleep resulted in an increase in blood glucose level, lower insulin response and a slower glucose tolerance. Prolonged sleep deprivation may result in insulin resistance and development of type 2 diabetes by its affect on mechanisms of blood glucose level regulation. Or it may also indirectly result in type 2 diabetes by causing an increased appetitie (Morsell et al., 2010). Ghrelin is a stomach-derived peptide which has a primary role in energy balance by increasing food intake and bodyweight along with reduction in body fat utilization. Ghrelin has been identified as a sleep inducing factor by inducing slow-wave sleep and night time release of growth hormone, adrenocorticotropic hormone (ACTH) and cortisol. Ghrelin concentration was seen to increase individuals in the morning following sleep deprivation (Leproult, et Cauter, 2010; Russel et al 2012). Leptin, an adipocyte derived hormone is involved in energy metabolism and fat utilization. Under normal circumstances, leptin is involved with reducing feed intake. Leptin is involved in a insulin containing reflex mechanism in which, an increase in insulin following feed intake causes an increase in leptin. Leptin levels decrease following a night a sleep deprivation, which causes an increase in feed intake Sleep derived increase in ghrelin levels and decreased insulin result in a remarkable increase in appetite as there is a strong correlation between increased ghrelin-to-leptin ratio and increased appetite (Sharad et al, 1999). Orexin Neurons Orexin-containing neurons of the lateral hypothalamus have a crucial role in sleep and are involved in the regulation of energy homeostasis. Their site of action is in the same are as the leptin and ghrelin hormone response region, and they partake in its synthesis and secretion. As mentioned above leptin and ghrelin are the main hormones involved in feed intake. Decrease in leptin and increase in ghrelin, following sleep deprivation, suppress the activity of orexin neurons which also leads to increase in feed intake, but orexin also affects energy expenditure. Decreased orexin activity, causes a decrease in energy expenditure, causing an increased body mass index (BMI) from increased fat storage and less fat store energy utilisation.
Growth Hormone The release of growth hormone from the adenohypophysis is stimulated by hypothalamic derived Growth Hormone Releasing Factor (GHRF) and is inhibited by somatostatin (growth hormone inhibition factor, GHIF). GHRF is also involved with inducing slow-wave-sleep, but its release is highly dependent upon the duration and quality of sleep (Redwine et al., 2000). GH has a circadian rhythm, meaning the majority of GH pulses occur shortly after the onset of sleep (figure 2). GH exerts its effects on various organs and tissues, while also stimulating release of further hormones in the liver. It is referred to as an anabolic hormone, as its involved in increasing amino acid uptake, protein synthesis which leads to increased growth.
Figure 2: The Ciracadian Pattern of Growth Hormone. Diurinal levels are minimal in comparison with nocturnal levels. Sleep deprivation results in decreased growth hormone levels, affecting the circadian rhythm of growth hormone.
A decrease in sleep, leads to a decrease release in growth hormone, which has been linked with dwarfism in younger animals and people. A lack of GH is also linked with increased weight gain, as GH is involved lipolysis of adipose tissue, to mobilize fatty deposits for energy need during anabolic processes. It also has a insulin suppressant effect by decreasing insulin-dependent uptake of glucose by adipose tissues (Maurovich et Sonka, 2008). GH stimulates liver synthesis of Insulin-like growth factor (IGF-I), involved in bone growth and metabolism.
The Corticotropin Axis
Figure 3: The Corticotropin Axis.
The corticotropin axis, involves Adrenocorticotropic Hormone (ACTH)released from the adenohypophysis in response to corticotropin releasing hormone (CRH) from the hypothalamus. ACTH then causes the adrenal cortex to release cortisol, and this collectively is refereed to as the corticotropin axis (Figure 3). Sleep deprivation is associated with alterations in the 24hour cortisol release pattern, with elevated levels in the evening and the morning. As opposed to the regular diurnal rhythm of cortisol elevation on occurring during the evening (figure 4) (Redwine et al., 2000;Maurovich et Sonka, 2008). Cortisol is involved in gluconeogenesis, which is the use of glycerol, lactic acid and amino acids in the liver to form glucose. It also has an important role in glycogenolysis which also results in an increased blood glucose concentration.
Thyrotopin (TSH) TSH normally shows decreased diurnal levels which then rapidly increase during the evening and reaching the maximum levels at night at the start of sleep onset. Sleep deprivation results in a significant decrease in this night peak of TSH and the overall 24hr concentration of TSH shows a decrease as a result. TSH stimulates the thyroid gland to release Thyroxine (T4), which is later converted into Triiodothyronine (T3). T3 is one of the main hormones involved in metabolism; including protein, lipid and carbohydrate metabolism. It increases lipolysis, gluconeogensis, and protein break down all of which are involved with decreasing BMI (Leproult et Cauter, 2010).
- Conclusion
Decrease in sleep can lead to elevations in blood pressure which over time can lead to cardiovascular disease. There is also a strong correlation identified between sleep apnea and hypertension. Cardiac output decrease causes pulmonary stretch receptors to activate the sympathetic nervous system. This results in increased blood pressure. Chronic sleep deprivation also has an impact on neuroendocrine function and glucose metabolism. The sleep deprivation caused alterations in metabolism and endocrine function result in obesity.
AYAS, N. T., WHITE, D. P., MANSON, J. E. & ET AL. 2003. A prospective study of sleep duration and coronary heart disease in women. Archives of Internal Medicine, 163, 205-209. FOUNDATION, T. N. S. 2010. Sleep Apnea and Heart Disease [Online]. Available: http://sleepfoundation.org/sleep-news/sleep-apnea-and-heart-disease [Accessed October 21st 2014]. FRANZEN, P. L., GIANAROS, P. J., MARSLAND, A. L., HALL, M. H., SIEGLE, G. J., DAHL, R. E. & BUYSSE, D. J. 2011. Cardiovascular reactivity to acute psychological stress following sleep deprivation. Psychosomatic medicine, 73, 679-682. LATINA, J. M., ESTES, N. A. M. & GARLITSKI, A. C. 2013. The Relationship between Obstructive Sleep Apnea and Atrial Fibrillation: A Complex Interplay. Pulmonary Medicine, 2013, 621736. QUAN, S. F. 2009. Sleep Disturbances and their Relationship to Cardiovascular Disease. American journal of lifestyle medicine, 3, 55s-59s. REDWINE, L., HAUGER, R. L., GILLIN, J. C. & IRWIN, M. 2000. Effects of Sleep and Sleep Deprivation on Interleukin-6, Growth Hormone, Cortisol, and Melatonin Levels in Humans. The Journal of Clinical Endocrinology & Metabolism, 85, 3597-3603. LEPROULT, R. & VAN CAUTER, E. 2010. Role of Sleep and Sleep Loss in Hormonal Release and Metabolism. Endocrine development, 17, 11-21. RUSSEL J. REITER, D.-X. T., AHMET KORKMAZ, AND SHURAN MA 2012. Obesity and metabolic syndrome: Association with chronodisruption, sleep deprivation, and melatonin suppression. Anuals of Medicine 44, 564-577. MAUROVICH-HORVAT E., P. T., ŠONKA K. 2008. The Effects of Sleep and Sleep Deprivation on Metabolic, Endocrine and Immune Parameters. Prague Medical Report, 109, 275-285. MORSELLI, L., LEPROULT, R., BALBO, M. & SPIEGEL, K. 2010. Role of sleep duration in the regulation of glucose metabolism and appetite. Best practice & research. Clinical endocrinology & metabolism, 24, 687-702. SHAHRAD TAHERI, L. L., DIANE AUSTIN, TERRY YOUNG, EMMANUEL MIGNOT 2004. Short Sleep Duration Is Associated with Reduced Leptin, Elevated Ghrelin, and Increased Body Mass Index. PLOS Medicine, 100.SPIEGEL, K., LEPROULT, R. & VAN CAUTER, E. 1999. Impact of sleep debt on metabolic and endocrine function. The Lancet, 354, 1435-1439.
Figures Figure 1: Bartha, T 2014, Lecture Slides- Physiology of the Heart. Slide 77: Neural Factors Influencing Heart Rate. Viewed 21st October 2014 Figure 2: Bartha, T 2014, Lecture Slides- Endocrinology. Slide 132: Episodic Release of GH. Viewed 29st October 2014 Figure 3: WIKIPEDIA. 2014. The Corticotropin Axis [Online]. Available: http://en.wikipedia.org/wiki/Hypothalamic%E2%80%93pituitary%E2%80%93adrenal_axis [Accessed 21st October 2014].