Research Paper on Physiology of Stress

5 pages
1228 words
Boston College
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Research paper
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Stress is an unavoidable aspect of life. Understanding the biochemical mechanisms of stress at cellular level necessitates the definition of stress. Stress is a common physiological problem that affects the normal functioning of the body. Therefore, under stressful conditions, the bodys homeostatic function is adjusted to respond changes in stimuli. It is the bodys response mechanism to environmental stressors. When the body perceives stress, there is a balance between stimuli and response. Identifying the cause of stress is an important way of dealing with physical and emotional stressors being the most common causes. Often, stress is caused by fear of threatening situations in benign forms, overwork and fatigue, and internal worry. Folkman, (2013) points out that stress is what happens when the body does not respond in an appropriate manner to threats.

Stress impacts negatively on the health of an individual owing to the effects of stress hormones on multiple body systems. Stress can reach a harmful and chronic level leading to deleterious consequences such as paralysis, depression, and suffocation. However, can be beneficial where it exerts pressure as an incentive to motivation and improving performance.

The stress response entails a complex signaling pathway among somatic cells and neurons. Environmental stimuli such as grief, anxiety, and depression which induce stress to stimulate the production of corticotropin-releasing hormone (CRH) and arginine-vasopressin (AVP). These two hormones play an important role in activating the hypothalamic-pituitary-adrenal (HPA) axis (Arnsten, et al., 2015). The hypothalamic-pituitary-adrenal axis consists of the adrenal glands, the hypothalamus, and the pituitary gland.

Corticotropin-releasing hormone is then transported from the hypothalamus to the anterior pituitary where it triggers the production of corticotropin which in turn stimulates the production of corticosteroids such as cortisol, the primary hormone that mediates the stress response. Conversely, vasopressin production from the posterior pituitary where transported through the bloodstream to the kidneys and increases water reabsorption in the cortical collecting ducts resulting in oliguria and increased blood pressure.

Cortisol is also plays a role in the inhibitory feedback mechanism. It inhibits the secretion of the corticotropin-releasing hormone that prevents the interactions of the hypothalamic-pituitary-adrenal axis central to secretion of glucocorticoid. Chronic stress can disrupt the feedback balance, causing a failure of inhibition feedback for the continued cortisol release.

Homeostasis preserves a constant internal environment that ensures the proper functioning of the body especially when there is a perceived change in the external environment. Homeostasis is challenged by external or internal adverse effects called stressors. Under stressful conditions, hypothalamic neurons are stimulated to secrete corticotropin-releasing hormone which increases the production of corticosteroid, cortisol. Cortisol which is regulated via the hypothalamic-pituitary-adrenal axis directly impacts the bodys response to stress (Doom & Gunnar, 2013). Its levels are high in the morning and functions to restore homeostasis in stress. The effects of this hormone are felt in almost all organ systems where it exerts a metabolic effect. Moreover, cortisol also affects memory, immune response, and ion transport.

Cortisol stimulates gluconeogenesis and encourages the synthesis of blood sugar from oxaloacetate. The secretion of cortisol activates the expression of metabolic enzymes responsible for gluconeogenesis. This leads to increased levels of glucose in the blood. Increased blood glucose gives an individual strength and energy (Quiros, Mottis & Auwerx, 2016). Conversely, cortisol secretion stimulates the synthesis of glycogen in the liver with a net effect of decreasing blood sugar. Therefore, cortisol regulates blood glucose. Cortisol ensures that blood glucose levels are steady especially during fasting when glucose is depleted. Cortisol also plays in ion regulation, particularly regarding potassium and sodium (Tsigos et al., 2016). Cortisol ensures that cells do not lose sodium and increases excretion of potassium. This is important in the regulation of body pH that is destabilized by the effects of stress.

Stress compromises the immunity of a person based on the physiological effect exerted by cortisol. Cortisol exerts its effects on the immune response where it blocks proliferation of T-cell lymphocytes, a component of the cell-mediated immunity via the signaling pathway. In this regard, T-cells are not able to recognize interleukin signals. Therefore, this weakens the immune systems rendering individuals suffering from stress particularly vulnerable to infection and prolongs healing time. Additionally, high levels of cortisol overwhelm the hippocampus that contains cortisol receptors causing atrophy. This leads to significant memory loss.

Stress has multiple and severe effects on the sense of well-being, mood, and the overall health of a person. Long-term exposure to cortisol due to chronic stress produce symptoms such as decreased function of thyroid function, impairment of cognitive function, and fat accumulation which as cardiovascular effects such as hypertension. Similarly, constriction of blood vessels due to high levels of cortisol increases blood pressure that my precipitate the build- up of plaque resulting in heart attacks (Driskell & Salas, 2013). High levels of cortisol above normal levels can lead to Cushings syndrome. This condition is characterized by hypercalcemia and hyperhidrosis.

The major implications of stress whether acute or chronic include its effects on the musculoskeletal system. Muscles are usually tensed up in stressful conditions that result in a state of guardedness when they are tensed. This triggers a migraine and tension-type headaches associated with muscle tension.

Stress elevates the level of cortisol in the body. This leads to mobilization of triglycerides resulting in the storage of visceral fat. Weight gain that results from fat storage is due to cellular biochemical processes that are responsible for converting cortisone into cortisol. Cortisol also causes weight gain through blood sugar. High blood sugar levels coupled with suppression of insulin leads to starvation of cells from glucose. Unused glucose in the brain is stored as body fat that causes obesity.

The respiratory system is also affected because stress induces faster breathing that can lead to panic attacks in individuals with asthma and emphysema. Moreover, the effects of stress are also observed in the cardiovascular system due to the release of adrenaline. Long-term hypertension, dilatation of the blood vessels, and inflammation of the circulatory system are noticeable effects in chronic stress. Indeed, there is an elevation of heart rate which can predispose an individual to episodic heart attacks when stress hormones are elevated above the normal physiological levels. Stress also results in constipation due to decreased digestion, decreased secretion and gut motility in the gastrointestinal system. Stress causes sensations in the stomach, vomiting, nausea, and even ulcers in severe chronic stress. Chronic stress and abnormally high levels of cortisol have also been linked with chronic fatigue, insomnia, and depression. Fertility problems can also set in due to prolonged stress. Some of the symptoms of fertility problems include erectile dysfunction and abnormal ovulation in women. Stressful circumstances whether acute or chronic can precipitate poor health and therefore exposure to stress needs to be minimized.



Arnsten, A. F., Raskind, M. A., Taylor, F. B., & Connor, D. F. (2015). The effects of stress exposure on prefrontal cortex: Translating basic research into successful treatments for post-traumatic stress disorder. Neurobiology of stress, 1, 89-99.

Doom, J. R., & Gunnar, M. R. (2013). Stress physiology and developmental psychopathology: past, present, and future. Development and psychopathology, 25(4pt2), 1359-1373.

Driskell, J. E., & Salas, E. (Eds.). (2013). Stress and human performance. Psychology Press.

Folkman, S. (2013). Stress: appraisal and coping (pp. 1913-1915). Springer New York.

Quiros, P. M., Mottis, A., & Auwerx, J. (2016). Mitonuclear communication in homeostasis and stress. Nature Reviews Molecular Cell Biology, 17(4), 213-226.

Tsigos, C., Kyrou, I., Kassi, E., & Chrousos, G. (2016). Stress, endocrine physiology and pathophysiology.


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