One: Blood vessel structure and function
Arteries have a thick wall and a relatively small and regular lumen. Arteries have a thick smooth muscle layer than veins. The smooth muscle layer – also tunica media – is has a circular and a longitudinal layer. The adventitia of elastic arteries like the aorta mainly contains elastin fibers while that of non-elastic arteries mainly contains collagen fibers (Young 2006). The structure of the artery allows it to withstand pressure and also to control blood pressure (Barett et al. 2012).
The walls of veins have three layers just like the arteries. However, the veins have a thinner tunica media and a thinner adventitial layer. Moreover, the adventitial layer of the vein mainly comprises of tough collagen fibers with little elastin (Young 2006). The collagen is good for support. This structure of veins allows them to play a capacitance role and to generate enough vasomotor tone to enhance venous return.
The capillaries are the smallest blood vessels. They lack muscle and adventitial layers. They are comprised of a single layer of endothelial cells on a thin basement membrane which contains a special type of collagen and elastin (Kumar et al. 2013). The single cell thickness of the capillary allows for easy exchange of materials between the capillary and the interstitial fluid. The endothelial cells of the capillaries in a capillary bed have pores between them – this pores facilitate the exchange of materials between the plasma and interstitial fluid (Hall 2016). The diagram below shows a capillary bed.
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Two: Structure of the Heart
The heart has three structural layers. The outermost layer is called the pericardium (Drake et al. 2010). The pericardium has a parietal layer which is inseparable from the fibrous layer above it. The fibrous layer is tough and protects the heart. The visceral layer forms part of the epicardium – it is strongly adherent to the heart and has secretory cells which produce a lubricant for the heart. Below the pericardium is the myocardium. It consists of specialized cardiomyocytes which can contract rhythmically, autonomously, and strongly enough to facilitate the continuous pumping action of the heart. The most inner layer of the heart is called the endocardium (Drake et al. 2010). It consists of a single layer of endothelial cells and extends over the valve leaflets and into the tunica intima of blood vessels.
Blood flows through the heart systemically. The heart has four chambers – two atria and the two ventricles. The atria are the receiving chambers. The right atrium receives blood directly from the inferior vena cava, the superior vena cava, and the sinus venosus. The left atrium receives blood from the four pulmonary veins. During diastole, blood flows from the atria into the ventricles via the tricuspid valve on the right and the mitral valve on the left (Hall 2016). The ventricles then pump blood into the arterial system during systole; on the right, blood flows into the pulmonary trunk via the pulmonary valve while on the left blood flows into the ascending aorta via the aortic valve.
The nerve supply of the heart comes directly from the cardioregulatory center of the medulla oblongata. This center consists of an upper cardioacceleratory or pressor center and a lower cardioinhibitory or depressor center. The sympathetic nerves from the pressor center of the medulla pass to the heart via the superior, middle, and inferior cervical ganglia and onto the second, third, and fourth thoracic nerves (Drake et al. 2010). These sympathetic nerves have a sensory component and a motor component which speeds up the process of depolarization hence heart rate. Parasympathetic nerves to the heart emerge from the depressor center and access the heart via the vagus nerve – they slow the rate of depolarization in the sino-atrial node (SAN) hence slowing heart rate (Drake et al. 2010). They also have potential to block transmission at the atrioventricular node (AVN). Sympathetic nerves only act on the SAN.
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Three: Cardiac cycle
The cardiac cycle comprises of two main parts –systole and diastole. Although the atria and the ventricles contract differently, systole denotes contraction of the ventricles while diastole denotes relaxation of the ventricles. Ventricular systole occurs immediately after atrial systole. Electrical signals travel from the SAN via the AVN and into the Purkinje fibers thus causing ventricular cardiomyocytes to contract in synchrony (Sembulingam & Sembulingam 2013). Meanwhile, the atrioventricular valves close immediately after atrial systole. Thus, contraction of the ventricular walls forces blood into the major arteries via the aortic and pulmonary valves. Immediately afterward, the pulmonary and aortic valves close to prevent backflow of blood. The ventricular walls also relax thus causing the atrioventricular walls to relax. Relaxation of the atrioventricular walls allows blood to flow rapidly from the atria and the returning veins on either side and into the ventricles. In the meantime, the SAN generates a new signal which causes the atrial walls to contract and push the residual blood into the ventricles – this is called atrial systole. It is followed immediately by ventricular systole and the cycle repeats itself.
One cardiac cycle takes approximately 0.8 seconds. The number of cycles occurring in a single minute for an individual is their heart rate. The average heart rate is thus about 75 beats per minute. The heart rate is a factor of the metabolic requirements of the tissues. Blood from the heart delivers oxygen and nutrients to tissues and takes metabolic waste away from the tissues. Thus, situations that increase the metabolic requirements of tissues such as exercise usually increase the heart rate. During exercise, the muscles exhaust all their energy reserves and thus require more glucose and more oxygen to carter for faster respiration (Widmaier et al. 2016). Other situations cause accumulation of metabolic wastes in tissues hence triggering an increase in heart rate to drain these wastes from the tissues.
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Four: Impact of Exercise on Heart Rate
During exercise, muscles spend most of their reserve glucose and glycogen. Active muscles also spend most of their reserve myoglobin. These two expenditures cause a deficit hence the muscles require more glucose and more oxygen. The muscles need more glucose to provide energy while they require the oxygen for the process of respiration that produces the energy. Moreover, the rapid rate of respiration in the muscles causes a build-up of metabolic wastes. It is the role of blood to carry away these wastes. Therefore, during exercise, the muscles require more blood and at a faster flow rate hence the increase in cardiac output during exercise (Hall 2016). Cardiac output is the cumulative amount of blood that the heart can pump in a single minute. Cardiac output is a product of the heart rate and the amount of blood that the left ventricle can pump with every systole – stroke volume.
The depletion of glucose and the accumulation of metabolic waste products during exercise induce the production of various hormones including catecholamines from the adrenal medulla. Apart from their role in energy resource mobilization, these hormones have vasoconstrictive effects of veins hence enhancing venous return. Increased venous return increases cardiomyocyte contractility via the Frank-Starling mechanism (Hall 2016). Increased myocardial contractility increases stroke volume. These hormones also cause direct sympathetic effects on the SAN hence increasing the heart rate.
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Bibliography
Barrett, K. E., & Ganong, W. F. (2012). Ganong’s review of medical physiology. New York, McGraw-Hill Medical.
Drake, R. L., Vogl, W., Mitchell, A. W. M., Gray, H., & Gray, H. (2010). Gray’s anatomy for students. Philadelphia, PA, Churchill Livingstone/Elsevier.
Hall, J. E. (2016). Guyton and Hall textbook of medical physiology. https://www.clinicalkey.com/dura/browse/bookChapter/3-s2.0-C20120065131.
Kumar, V., Abbas, A. K., Aster, J. C., & Robbins, S. L. (2013). Robbins basic pathology. Philadelphia, PA, Elsevier/Saunders.
Sembulingam, K., & Sembulingam, P. (2013). Essentials of medical physiology. New Delhi, Jaypee Brothers Medical Publishers.
Snell, R. S. (2008). Clinical anatomy by regions. Philadelphia, Lippincott Williams & Wilkins.
Widmaier, E. P., Raff, H., & Strang, K. T. (2016). Vander’s human physiology: the mechanisms of body function. New York, McGraw-Hill Education
Young, B. (2006). Wheater’s functional histology: a text and colour atlas. [Edinburgh?], Churchill Livingstone/Elsevier. http://www.clinicalkey.com/dura/browse/bookChapter/3-s2.0-B9780443068508X50015.
