Assessment of Blood Flow and Vascular Function - Assignment Example

Lab Report: Assessment of Blood Flow and Vascular Function The cardiovascular system is essentially comprised of blood vessels and of the heart. The purpose of blood vessels is to transport blood into and out of the heart. The two major types of blood vessels are arteries and veins. It is the responsibility of arteries to carry oxygenated blood away from the heart and to the body’s organs, under relatively high pressure, as compared to the pressure under which the veins opperate. The pulmonary artery is the only artery that does not actually transport oxygenated blood away from the heart. Arteries are composed of narrow lumens and elastic muscle tissue. It is the sympathetic nervous system which sends out signals to arteries instructing the smooth muscle, arterial wall to contract and relax. Veins are the other type of major blood vessel and are responsible for carrying blood towards and into the heart, in order to become oxygenated. Veins operate under lower pressure than arteries and do not possess the same elasticity that arteries do. Veins transport unoxygenated blood as opposed to arteries which carry oxygenated blood. Veins, like arteries, have lumens, but they are comparably wider than the lumens of arteries. Veins are composed of venules, which are tiny blood vessels that pull blood from capillaries into the actual vein. Veins are actually composed of three tissue layers but are less elastic than the walls of arteries. The regulation of blood flow during exercise is governed by the demands of the muscle tissue being used. Certainly, when an individual is exercising, the heart rate increasing as a response to the body’s immediate need for larger amounts of oxygenated blood. The body’s blood flow rate can increase during exercise by as much as 20 times more than what it is at rest. During periods of exercise, all of the body’s capillaries are opened and in use versus the mere ¼ of the body’s capillaries which are used at rest. During periods of exercise, the body experiences what is called low oxygen tension. This is a result of the use of multiple muscular groups during periods of heavy activity. In addition, vasodilators are released as the demand for oxygenated blood throughout the body increases, “Low oxygen tensions resulting from greatly increased muscular activity or the release of vasodilator substances such as lactic acid, carbon dioxide, and potassium ions causes dilation of precapillary sphincters. Increased sympathetic stimulation and epinephrine released from the adrenal medulla cause some vasoconstriction in the blood vessels of the skin and viscera and some vasodilatation of blood vessels in skeletal muscles” (www.mhhe.com). During vasoconstriction, which occurs as a response to the increased demand placed on skeletal muscles during exercise, blood volume entering into the heart is increased. Ultimately, what is happening is that the skeletal muscles are placing a demand for oxygenated blood on the cardiovascular system, which responds cyclically by providing the blood in greater volume. It is relevant to discuss what is known as arterial stiffness as it is pertinent to the cardiovascular system and exercise. Arterial stiffness is often part of the aging process or a result of an unhealthy lifestyle. Atherosclerosis is also responsible for causing arteries to stiffen. Individuals who have stiffening arteries are often prime candidates for cardiac events such as myocardial infarction (blood clot or thrombosis in the heart) and stroke. When pressure within the arteries in compromised, coronary perfusion and cardiac function are altered. It is structural and cellular components which when changed, alter the walls of blood vessels. These alterations translate to arterial stiffening. Factors which can contribute to arterial stiffening, from a physiological standpoint, are homodynamic issues (blood related), hormone regulation, sodium regulation and glucose regulation. Diseases such as diabetes and high blood pressure (hypertension) are also responsible for causing arterial stiffness. There are two components which are crucial to retaining arterial elasticity and health. These two components are proteins called collagen and elastin, “The stability, resilience, and compliance of the vascular wall are dependent on the relative contribution of its 2 prominent scaffolding proteins: collagen and elastin” (Zieman et al, 2005). Inflammatory responses will offset the balance between these two proteins over time and result in an overproduction of collagen and an underproduction of elastin. The result is arteries which are rigid or stiff due to a deficit in elastin, which provides the elasticity to arteries. An increase in blood pressure or luminal pressure will also cause collagen to overproduce and elastin to under produce. This too results in arterial stiffening. During periods of exercise, the heart places a demand on the arteries which forces them to comply and essentially function as they are supposed to, “Aerobic exercise increases the compliance of our arteries, providing a way to improve and maintain heart health. Compliant arteries are flexible and dilated, allowing for more blood, oxygen, and other nutrients to flow easily to the vital organs and skeletal muscle” (Borell et al, 2006). In individuals with arterial stiffness, the pressure wave that is normally sent through the blood vessels at a certain rate, is sent more rapidly. This means that the arterial system is not able to absorb pulsations from the heart. In addition, reflective waves are returned early from the periphery. These events cause an overall increase in systolic blood pressure. When the blood pressure is elevated, the heart places a greater demand for oxygen, on the vascular system. All of these factors increase one’s risk for cardiac events such as myocardial infarctions and stroke. It is frequent exercise however, that decreases lipids within the blood as well as overall blood pressure. This ultimately prevents and even reverses the stiffening of the arteries. Endothelial function is directly impacted by arterial stiffening. Exercise is a proactive way to improve endothelial function and cardiovascular health without the use of medication. The inner layer of the vascular system is essentially comprised of the endothelium. It is the layer of vasculature between the blood and organs, “In contrast to previous concepts the endothelium is not just a passive interior lining of the blood vessels but a vital dynamic tissue involved in many other active functions, such as secretion and modification of vasoactive substances or participation in the process of contraction and relaxation of vascular smooth muscle”(Walther et al, 2004). The purpose of this experiment is to examine and observe the effects of exercise on blood flow and vascular function, specifically of the non working muscles. This will be done using non invasive techniques. These techniques will include venous occlusion plethysmography and pulse wave velocity. There are three specific purposes for this experiment. These purposes include examining the effects of exercise on blood flow of the non-working muscles, assessing the effects of isometric exercise on vasodilatory capacity and assessing the effects of rhythmic handgrip exercise on arterial stiffness. Hypothesis: It is believed that when conducting the following experiments, that an increase in heart rate will be recorded during times of exercise and skeletal muscle use. It is also believed that though blood pressure may increase slightly with exercise, it will decrease during times of rest after exercise is completed. Overall, it is expected to see an increase in blood flow during periods of exertion and a recorded decrease in blood pressure after those periods of exertion. Methods: Experiment 1, Group 1: The first subject used in this experiment was a 26 year old male. He was measured as follows: height: 179 cm, weight: 88 kg. The equipment used was a blood pressure cuff, a handgrip dynamometer (biopac), venous occlusion plethysmography and strain gauges (Hokanson). The software used included an Acq 373, in order to perform data acquisition. The Acq 373 was used in conjunction with the biopic in order to collect and record force. The first procedure which was performed was the obtaining of anthropometric measurements which included subject’s height and weight. This was established to be 179 cm and 88 kg. The next step was to properly calibrate the hand grip dynamometer. At this time, the subject was instructed to assume a supine position and perform 3 MVCs using their right hand. MVC was then determined after the execution of 3 trials as the highest score. At this time, 30% of this value was calculated. The widest circumference of the forearm was then measured in centimeters. A strain gauge, 2-3 centimeters smaller than the circumference of the forearm being used was then selected and placed around the subject’s forearm. A blood pressure cuff in a children’s size was also placed around the subject’s wrist. At this time, it was necessary to have the subject rest for ten minutes. This was due to the fact that a resting blood pressure (BP) measurement needed to be obtained and recorded. This was done with the use of a stethoscope and a sphygmomanometer. It was also necessary to obtain a measurement reflecting the subject’s resting blood flow or FBF (forearm blood flow) in the non exercising forearm. Approximately one minute before this measurement was to be taken however, the children’s size blood pressure cuff around the subject’s wrist was inflated to 50 mm Hg above SBP. In addition, the rapid cuff inflator was preset to 50 mm Hg. It was then necessary to take 6-8 FBF measurements using the NIVP3 software. The resting forearm FBF could then be measured Once the FBF in the resting forearm was determined, the wrist cuff was deflated. At this point in the experiment, the subject was instructed to rest for five minutes and then perform isometric handgrip exercises at 30% MVC for a time period of three minutes. Thirty seconds after initiation of exercise, the children’s size cuff around the wrist was inflated to 100 mm Hg above SBP. One minute after the cuff inflation, FBF measurements were obtained. Experiment 2, Group 2: This particular experiment dealt specifically with vasodilatory capacity. The subject used was a 23 year old male whose measurements were as follows: height: 165.2 cm, weight: 105 kg. The equipment necessary for this experiment was the same as used in experiment 1, group 1. The software used was also the same. The first measurement obtained and recorded was the subject’s height and weight. The following steps were identical to the steps taken in experiment 1, up through the determining the average score of three trials and then taking 30% of that value. At this point, the widest circumference of the left forearm was measured and recorded in centimeters. A strain gauge was then selected and fitted to the forearm, which was 2-3 cm smaller than the forearm itself. Once again, the children’s cuff was placed on the wrist. The subject was then asked to rest for a period of ten minutes. At this time, the resting BP (blood pressure) was measured. At this time, reactive hyperemia responses were obtained in the left arm. In order to obtain the and record hyperemia responses, the large cuff was placed over the Hokanson cuff. The Hokanson cuff was inflated to a pressure equal to 100 mm Hg above resting SBP. The inflation pressure was maintained for five minutes. One minute prior to the release occlusive pressure, wrist cuff was inflated to 50 mm Hg above SBP. Immediately after the release of occlusive cuff, the Hokanson’s automatic readings of forearm blood flow were initiated. At this time, FBF readings were performed for 3 minutes. The subject was then told to rest for a period of five minutes. After a period of five minutes at rest, the subject performed isometric handgrip exercises at 10% MVC for 3 minutes with the left hand. Immediately after the isometric exercise was performed, the reactive hyperemia measurements were taken. At this point, variables were recorded, both BP and FBF. Experiment 3, Group 3 - Exercise and Arterial Stiffness The equipment used for this procedure included the blood pressure cuff, the handgrip (Biopac) and the Complior system for measuring pulse and wave velocity. The subject of this experiment was a 28 year old males. He was measured at 175 cm (height) and weighing 72 kg (weight). The procedure for this experiment was identical to the previous two through the process of measuring the subject and having the subject assume a supine position. At this time, the subject was asked to perform 3 MVC’s using their right hand. The greatest score of the 3 trials was then used as MVC and 50% of this was calculated. The subject was then asked to rest for a period of ten minutes, after the MVC was determined. It was then necessary to acquire resting HR and BP. The measurement for BP was taken using a stethoscope and a sphygmomanometer. The HR (heart rate) was measured using a heart monitor. The following arteries were then located: carotid, radial, femoral, dorsalis and peids (dorsal artery in the foot). The distance between carotid to radial artery was then measured using a measuring tape and measuring in centimeters. Other distances between arteries were then measured, including the carotid to femora land the carotid to dorsalis pedis . These measurements were then recorded and entered into the Complior software. At this time, pulse wave sensors were placed above the previously mentioned arteries, and baseline pulse wave velocity was then obtained. The subject then performed rhythmic handgrip exercises at 50% MVC for a period of 3 minutes (2 second contractions - 2 seconds to relax). Heart rate and blood pressure measurements were obtained during exercise. Immediately after the exercise was performed, pulse wave velocity (PWV) measurements were obtained. Results Refer to Graph Discussion The main limitations of the series of experiments conducted, was that there were only three subjects and they were all male. The data cannot apply to humans in general when only male humans were tested. Certainly, it can be said however, that exercise has a direct and positive impact on overall blood pressure and long term arterial and vascular health. Chronic and moderate exercise can reduce the onset of arterial stiffening with age as well as prevent health related arterial stiffening. Regular exercise is imparative in maintaining the necessary elasticity in arterial walls and endothelial tissue, Regular physical activity makes your heart stronger. A stronger heart can pump more blood with less effort. And the less your heart has to work, the less force, or pressure, thats exerted on your arteries”(Mayo Clinic, 2008). Ultimately, it was apparent that blood flow and heart rate did in fact increase with periods of isometric muscle contraction and exertion. It was also discovered that blood pressure was positively effected by periods of exertion and therefore confirms the original hypothesis of this study. Ultimately, the knowledge that can be derived from this study is that exercise is crucial to cardiovascular health. Works Cited: High blood pressure and exercise: Why activity is key, (2008) retrieved April 18, 2008 from Mayo Clinic website:http://www.mayoclinic.com/health/high-blood-pressure/HI00024 Health and the Human Body (2008) retrieved April 16, 2008 from: http://www.ivy- rose.co.uk/Topics/Blood_Vessels.htm Blood Flow Through Tissues During Exercise (2008) retrieved April 16, 2008 from: http://www.mhhe.com/biosci/ap/seeleyap/cardio/reading4.mhtml Borell, Alyssa L. Davis, Cristen. (2006). The Effect of an Acute Bout of Aerobic Exercise on Arterial Stiffness and Wave Reflection in Patients with Coronary Artery Disease retrieved April 16, 2008 from Inquiry Journal web site: http://www.unh.edu/inquiryjournal/06/articles/borell_davis.html Walther, Claudia. Geilan, Stephen. Hambrecht, Rainer. (October 14, 2004). The Effect of Exercise Training on Endothelial Function in Cardiovascular Disease in Humans retrieved April 16, 2008 from Medscape Today website: http://www.medscape.com/viewarticle/490847 Zieman, Susan J. Melenovsky, Vojtech. Kass, David. (2005). Mechanisms, Pathophysiology and Therapy of Arterial Stiffness retrieved April 16, 2008 from the American Heart Association web site: http://atvb.ahajournals.org/cgi/content/abstract/25/5/932 Read More