Effect of Exercise on Blood Pressure

Question: Discuss about the Report for Effect of Exercise on Blood Pressure. Answer: 1. Blood pressure is defined as the force or pressure exerted by blood against the arterial walls as it flows through them (Waugh, 2015). It maintains the essential in-flow and out flow of the blood from the heart to body organs through the blood vessels. The blood pressure should always be kept in normal limits. If blood pressure is raised, it may rupture the blood vessels and if blood pressure is lowered, there will be insufficient tissue and organ perfusion. Both are highly fatal conditions. Usually when the blood flows through the arteries, a pressure is exerted. Systolic blood pressure is the maximum degree of pressure exerted by blood on the blood vessel wall during the ventricular systole when the left ventricle pumps the blood into the aorta (Waugh, 2015, Sembulingam, 2001). It is also called arterial blood pressure. In adults it ranges from 110- 140 mmHg or 16kPa. Diastolic blood pressure is the minimum degree of pressure that is present during cardiac diastole and the heart is in complete resting state following the ejection of blood and just before the left ventricular contraction. In adults it ranges from 60- 80mmHg or 11kPa (Waugh, 2015, Sembulingam, 2001). Pulse pressure is defined as the difference between systolic and diastolic blood pressures (Tortora, 2010). The normal pulse pressure is 40 mmHg (Sembulingam, 2001). A sphygmomanometer is used to check blood pressure. Blood pressure is always written as the diastolic blood pressure below the systolic blood pressure. BP=120/80 mmHg or 16/11kPa ((Waugh, 2015, Lewis, 2004). Generally, the arteries transport blood from the heart and perfuse the tissues and internal organs. The arteries have three layers as outer, middle and inner layer. A pressure wave is generated in the elastic tissues of middle layer (tunica media) when the heart contracts causing stretching of the wall (Tortora, 2010, VanPutte, 2012). Arterioles pose resistance to blood flow called resistance vessels to determine the systemic blood pressure. When the left ventricle contracts, blood is pumped into the aorta and so the aorta expands and recoils to push blood for tissue perfusion. Expansion and recoiling is noted through the entire arterial system. The diastolic pressure is maintained by the elastic recoil of the arteries. Mean arterial pressure is defined as the average pressure present in the arteries (Marieb, (2012). This is measured by adding one third of pulse pressure and the diastolic pressure. As the diastolic time is longer than the systolic time, it helps to determine the diastolic pressure. The normal value of mean arterial pressure is 93 mm Hg (Smelter, 2002). 2. Table 1 Frequency and the Class Average Percentage Changes of blood pressure during exercise Category Pulse pressure (mm Hg) Pulse pressure Frequency N Class average percentage P Optimal (no pressure change) 3 7 Mild (1- 20) 23 52 Moderate (21- 40) 11 25 Severe (above 40) 4 9 Decreased (below 0) 3 7 Table 1 show that exercise affects the pulse pressure apparantly. It is noted that the majority (52 %) of the people had mild changes in pulse pressure. Most of the people (25 %) showed moderate increase and 9% showed severely increased pulse pressure. 7 % remained optimal with no pressure change. In contrast, 7% showed a decrease in pulse pressure. Therefore it is evident that the difference in blood pressure during exercise is apparent. 3. Regulation and control of blood pressure while resting Blood pressure often changes due to the regulatory mechanisms in the body. There are four regulatory systems as short term (nervous) regulatory system, long term (renal) regulatory system, hormonal and local regulation. 1. Short term regulation- It is a rapid mechanism. It causes vasoconstriction or vasodilatation to regulate the blood pressure. The cardiovascular centre located in the pons and medulla oblongata controls the blood pressure. The baroreceptors, chemoreceptors and higher centers in the brain send impulses to the cardiovascular centre that integrates and coordinates the impulses (Tate, 2012). This centre sends sympathetic and parasympathetic nerves (autonomic nerves) to the heart and smooth muscles in the middle layer. It causes vasodilatation or vasoconstriction causing an increase or decrease in the heart rate and thereby controls the blood pressure. They control the volume of blood in the vessels by changing the diameter of the blood vessel lumen. There are no innervations of parasympathetic nerves in most of the blood vessel and so the degree of sympathetic nerve activity determines the diameter of the blood vessel (Jenkins, 2010). The constriction of the smooth muscle occurs due to the vasoconstricting action of sympathetic nerves that increases the pressure in the blood vessels. The relaxation of smooth muscle occurs due to the decreased sympathetic nerve stimulation causing vasodilatation (Sembulingam, 2001, Antonio, 2014). Chopra in 2011 reported that the autonomic nervous system controls the local and global blood flow by causing changes in cardiac output and blo od pressure. Baroreceptors (pressure receptors): They are situated in the aortic and carotid sinuses. These are highly sensitive to changes in pressure within the blood vessel. This is the main regulatory mechanism of our body. The increased blood pressure stimulates the baroreceptors which increases their impulses to the cardiovascular centre. This increases parasympathetic nerve activity to the heart that decreases heart rate, cardiac output and ultimately blood pressure. At the same time, blood pressure is decreased by inhibiting the sympathetic activity to the blood vessels causing vasodilatation. If there is decreased blood pressure, baroreceptors are inactivated and it acts vice versa (Waugh, 2015, Antonio, 2014). Chemoreceptor: These are nerve endings situated in the carotid and aortic bodies and are primarily involved in control of respiration. The chemical constituents of blood sensitize chemoreceptors. Chemoreceptors are stimulated by increased PCO2 and hydrogen ions and decreased PO2 (Tate, 2012). This activates cardiovascular centre that increases sympathetic activity to the heart and blood vessels and causes vasoconstriction. This increases stroke volume, heart rate and ultimately increases BP. Conversely, in case of decreased hydrogen ions, and PCO2 and increased PO2, it acts vice versa and decreases BP. (Garrett, 2013). Chemoreceptors are activated only when there is severe respiratory disruption and blood pressure below 80mm Hg. Higher centers in the brain: The blood pressure is increased at times of emotional states such as pain, fear, and anger that stimulate the cardiovascular centre by increasing vasomotor tone. Vasodilatation is caused by stimulation of anterior hypothalamus that decreases blood pressure while vasoconstriction is caused by stimulation of posterior hypothalamus that increases blood pressure. Long term blood pressure regulation: It is exerted by kidneys. They regulate blood pressure in two ways as (a). Regulation of extracellular fluid volume: when the blood volume is increased, there is an increase in the extracellular fluid volume that increases blood pressure. At the time of increased pressure, more amounts of fluid and sodium are excreted that decreases blood pressure by reducing extracellular fluid volume (Sembulingam, 2001). (b). Renin- angiotension mechanism: When there is decreased blood pressure, renin is secreted by juxtaglomerular apparatus which acts on angiotensinogen and converts it into angiotension I. By the action of converting enzyme secreted from lungs angiotension I is converted into angiotension II (Waugh, 2015). Angiotension II causes vasoconstriction that increases peripheral resistance and blood pressure. Angiotension II also stimulates adrenal cortex to secrete aldosterone which increases sodium resorption from renal tubules thereby increasing blood pressure (Tate, 2012). Hormonal regulation: Many hormones have an effect on blood pressure. Secretion of few hormones like adrenaline, noradrenaline, vasopressin,aldosterone, angiotension, thyroxine, and serotonin increases blood pressure whereas bradykinin, prostaglandins, histamine, acetylcholine, atrial natriuretic peptide decreases blood pressure (Sembulingam, 2001). Local regulation: The local vasoconstrictor substances originate from the endothelium known as endothelin. These substances activate phospholipase which again activates prostacyclin and thromboxane A2 causing stretching of the blood vessels. This causes vasoconstriction that increases blood pressure. The blood pressure is decreased by some local vasodilators that are metabolic and endothelial origin. 4. Effects of exercise on blood pressure and its regulation Exercise increases metabolic needs of the cells, tissues and muscles and is of two types as dynamic and static exercise (Douglas, 2012). When the exercise involves the isotonic muscular contraction with external work, it is termed as dynamic exercise. In this type, the heart rate, contractile force of heart, cardiac output and systolic blood pressure increases. As the peripheral resistance remains unaltered or decreased in dynamic exercise, the diastolic blood pressure remains unaltered or reduced as supported by a study conducted by Kelley in 2000. When the exercise involves isometric muscular contraction without external work, it is called as static exercise. In this, the heart rate, contractile force of heart, cardiac output and systolic blood pressure increases and even diastolic blood pressure increases due to increase in peripheral resistance. Blood pressure varies based on the severity of exercise. In severe exercise, blood pressure increases whereas there is no change in blood pressure during moderate and mild exercise. The blood pressure depends on the cardiac output (CO) and peripheral vascular resistance (R). It is expressed as BP= CO X R. (Smelter, 2002). Cardiac output is the amount of blood pumped from each ventricle (Marieb, 2012). During exercise, cardiac output increases which in turn increases blood pressure. During exercise the heart rate increases. Even the thought of exercise or preparation for it increases heart rate. The heart rate is increased to 180 beats /min in case of moderate exercise and reaches 240-260 beats/min in severe exercise. It thereby increases the stroke volume and blood pressure. Stroke volume is defined as the amount of blood pumped from each ventricle during each contraction. The normal stroke volume ranges from 60 to 80 ml (Marieb, 2012). The exercise increases venous return that increases ventricular filling, cardiac output. This ultimately increases systolic and diastolic pressure and thereby pulse pressure and mean arterial pressure increases. This is evident from the given study that exercise has increased the systolic pressure to 22 mmHg, diastolic pressure to 16 mmHg, pulse pressure to 17 mmHg and mean arterial pressure to 10 mmHg. It was found that exercise has increased both systolic and diastolic blood pressure in females whereas it has increased only the systolic pressure apparently but decreased the diastolic pressure in most of the males. It was noted that few subjects have no change in their blood pressure after exercise. It was evident from table 1 that exercise has increased pulse pressure apparently except in few males. During exercise, large amount of metabolic end products are produced (Douglas, 2012). The accumulation of these products occurs mostly in skeletal muscles that causes vasodilatation. Therefore the blood pressure slightly decreases after the exercise. But the BP returns to normal quickly. Hypoxia may occur at the time of strenuous exercise. This stimulates chemoreceptors that activates cardiovascular centre which in turn increases sympathetic activity to the heart and blood vessels. 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