The cardiovascular system is a network of blood vessels of which blood travels to reach the vast distances of the body in regulation of tissues and other important functions as exchange of nutrient, waste elimination etc. Exercise can be seen to have an involvement in the reduction of the risk of cardiovascular diseases which include hypertension, stroke and Myocardial infarction. This reduction includes mechanisms in which exercise can reduces the risks of CVD by involvement of inflammation factors or EPCs in the bloodstream.
The organisation of the cardiovascular system consists of where the body's blood flows through a network of blood vessels which extend between the heart in the thoracic cavity and the peripheral tissues throughout the body. These blood vessels can be divided into a pulmonary circuit, which carries blood to and from the gas exchange surfaces in the lungs, and the systemic circuit, which transports blood to and from the rest of the body (fig.1) (Martini, 2006).
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Each circuit begins and ends at the heart and blood travels through these circuits in sequence so blood returning to the heart from the systemic circuit must complete the pulmonary circuit before re-entering the systemic circuit. The blood is carried away from the heart by arteries which have to withstand more pressure and are thicker than veins (Opie, 2004). The blood returns by veins and the small thin-walled capillaries interconnect the smallest arteries and veins and act as exchange vessels, exchanging nutrients, dissolved gases, and waste products between blood and surrounding tissues (Martini, 2006).
The heart has four muscular chambers of which two are associated with each circuit. The right atrium receives blood from the systemic circuit and passes it to the right ventricle which pumps blood into the pulmonary circuit. The right atrium collects oxygenated blood from the pulmonary circuit and pumps it into the left ventricle and this is pumped into the systemic circuit. The heat beat indicates the contraction of the atria and then the ventricles and the ventricles contract at the same time (Martini, 2006).
The Definition of Exercise
The modern association of exercise and CVD when Morris and colleagues in 1949 began to understand how vocational and leisure time physical activity relate to fitness and risk of Coronary heart disease. By studying London transient workers and other civil servants and found that bus conductors were at lower risk than the bus drivers (Paffenbarger, 2000).
In describing the specific terms and concepts, there is a difference between physical activity and exercise and physical fitness. Physical activity is the description of any bodily movement produced by contraction of the skeletal muscles that result in the released energy beyond the resting type released amount of energy. The term of exercise can be described as a subset physical activity that is planned, structured, repetitive, and purposeful in the sense that improvement or maintenance of physical fitness is an objective. There are numerous effects of exercise that contribute to the reduction of vascular events in physically active woman and men. Exercise is associated with favourable changes to the body fat percentage, lipoprotein profile, carbohydrate tolerance and insulin sensitivity, neuro-hormonal release and blood pressure (Niebauer & Cooke, 1996).
The Positive Effects of Exercise
The endothelium produces a number of paracrine hormones that include the nitric oxide (NO), which are anti-atherogenic. Dysfunction of the endothelium can precede and predict the development of atherosclerotic disease and initially occurs at coronary branch points, as do atherosclerotic plaques. Interventions of known cardiovascular benefit improve endothelial function and coronary and peripheral endothelial dysfunction predicts cardiovascular events and improvement in endothelial function improves prognosis. Endothelial dysfunction can be considered an early and integral manifestation of vascular disease and improvement in endothelial function should impact CV risk (Green et al., 2008).
An important pharmacological stimulus to endothelial-mediated vasodilatation is shear stress. Removal of endothelium abolishes flow and pharmacological NO-mediated arterial dilation and no-dependent flow-mediated vasodilatation normalises endothelial shear. Exercise training of the small and large muscle groups is associated with improvement in NO-vasodilator function and since CVD risk factors are associated with impaired endothelial function, exercise training improves endothelial function by the good value of its impact on the risk factors. (Green et al., 2008).
Exercise Training Effect on the Vascular Wall and Function
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In the autopsy and angiographic studies, there is a suggestion that vascular structure physical conditioning increases arterial cross-section area and athletes' exhibit enlarged skeletal muscle conduit and resistance arteries compared with controls (Green et al., 2008). In a study by Hambrecht and colleagues on the impact of 4 week cycle exercise on the internal mammary artery of CAD patients which showed that training significantly increased endothelial-dependent dilating and that exercise increases NO-synthase protein expression and phosphrylation, which are effects consistent with a shear-stress mechanism for enhanced NO bioactivity (Green et al., 2008).
Another mechanism may relate to the impact of exercise on oxidative stress. Repeated NO production as a result of exercise may reduce its degradation by free radicals, directly decrease free radical production, or increase the expression of antioxidant enzymes. After moderate exercise, improvement in endothelial function can be observed, as they did not alter oxidative stress (Green et al., 2008).
The Anti-Inflammatory Effect of Regular Exercise and Reduced Risk of CVD
One way that exercise may modify CVD risk is by the reduction of inflammation. Yet there is a paradox of which inflammation can also trigger mechanisms to restore vascular wall. Following acute exercise, there is a transient increase in circulating levels of anti-inflammatory cytokines and the inducement of the expression of antioxidants and anti-inflammatory mediators in the vascular wall that might inhibit the development of atherosclerosis. The atherosclerotic CVD was formally characterised as an accumulation of lipids in the artery wall but now is recognised as a chronic inflammatory disorder that results from interactions between modified lipoproteins and various components of the immune system, including monocyte-derived macrophages, T-lymphocytes and a variety of cytokines secreted by these and other cells in the artery wall (Wilund, 2007).
Factors can contribute to the development of atherosclerosis but the oxidation of protein and lipid components of LDL (low-density lipoprotein) is among the most important initiating events (Wilund, 2007).
Arterial wall injury triggers an inflammatory response to restore arterial wall integrity. However persistent risk-factor mediated arterial wall injury leads to endothelial dysfunction, atheromatous plaque formation, plaque rupture and thrombotic complications. Simultaneously, inflammation also starts a process of repair through 3 main defence mechanisms and these include endothelial repair by progenitor cells, plaque neovascularisation, and reverse cholesterol transport (fig.2) (Moreno et al., 2009).
Fig.2 - Defence mechanisms for maintaining endothelial and vessel wall homeostasis (Moreno et al., 2009).
Endothelial Repair by Progenitor Cells
Endothelial dysfunction finally leads to endothelial cell death, lipid entry, invasion of inflammatory cells, and vascular smooth muscle cell proliferation turning into structural damage. Regeneration can occur as bone-marrow derived circulating endothelial progenitor cells (EPCs) from the bloodstream have a regenerative potential. They have a role in predicting CVD in patients with risk factors (Moreno et al., 2009). The number of circulating and colony-forming units of EPCs is associated with a lower risk score in men without history of CVD as a competent bone marrow can translate injury into productive EPC consumption and recruitment and this restores the endothelial function yet a high risk factor profile perpetuates injury, the bone marrow becomes incompetent and so the EPCs number in the process of repair. The number of circulating EPCs is also associated with reduced risk of cardiac death and other coronary events suggesting decreased levels of EPCs are seen in patients with coronary risk factors (Moreno et al., 2009).
Enhancement of EPCs can be considered as a promising therapeutic alternative for cardiovascular disease as mobilization of EPCs and regeneration can be achieved by exercise by increasing nitric oxide bioavailability (Moreno et al., 2009).
Reverse Cholesterol Transport
This defence mechanism is involved in the preserving of the blood vessel wall integrity and describes a process by which extraheptatic (peripheral) cholesterol returns to the liver for excretion in the bile and faeces. Free unesterfied cholesterol is toxic to cells and atherosclerosis can result from an imbalance between deposition and removal of arterial cholesterol after endothelial injury. There is an inverse relationship between high-density lipoprotein cholesterol (HDL-C) and cardiovascular disease as increasing HDL-C level may reduce the risk of cardiovascular disease. This is consistent with the concept of a beneficial role of HDL-C, which is based on free cholesterol efflux from macrophages out of vessel wall. This efflux occurs either by passive diffusion or by interaction with the SR-BI receptor or the ABCA1 transporter (Moreno et al., 2009). The ABCA1 transporter system is the most efficient, responsible for over 50% of cholesterol efflux from macrophages to poorly lipidated ApoA-1 and this protein is converted to mature Î±-HDL after esterfication. The mature HDL-C also transfers esterified cholesterol to other lipoproteins by the enzyme cholesterol ester transporter protein (CETP), increasing the efficiency of the system. HDL-C also improves re-endothelialisation through EPC activation and proliferation (Moreno et al., 2009).
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In the future alternatives for RCT and plaque regression Two potential pathways are being actively investigated for clinical implementation and these are the ABCA1 transporter and ApoA-I system. Experimental over expression of ABCA1 transporter protein is related with a major regression of atherosclerosis in mice and both ABCA1 and ABCG1 are regulated by liver x receptor (LXR) and synthetic agonists of this nuclear receptor can promote reverse cholesterol transport in vivo and reduce atherosclerosis in mice (Moreno et al, 2009). Another potential pathway is the repeated infusion/over expression of ApoA-I with regression of atherosclerosis in animal and human models as currently studied concept of ApoA-I mimetic peptides, which mimic the anti-atherosclerotic and anti-inflammatory properties of full-length ApoA-I but must be administered parenterally (Moreno et al, 2009).
Exercise in combination with weight reduction can decrease low density lipoprotein-C (LDL-C) concentrations and limit the reduction in HDL-C. There is also evidence that HDL-C also reduces LDL-C oxidation and endothelial cell adhesion expression (Thompson et al., 2003). The oxidizability of LDL is enhanced in exercisers compared with sedentary controls, due to exercisers containing increased amounts of preformed lipid peroxides, which account for the increased oxidizability (Shern-Brewer et al., 1998).
Exercise and Hypertension
Hypertension is one of the most common medical disorders and is a condition in which the blood pressure is chronically elevated above the normal level. It is associated with an increased incidence of all-cause and CVD mortality (Pescatello et al., 2004). Although it often produces no symptoms, over time the elevated pressure is associated with irreversible damage to the blood vessels and certain vital organs, particularly the heart and kidneys. As a result, people with uncontrolled hypertension can often become the victims of stroke, kidney failure, and MIs or heart failure (Dubbert, 1987).
There are numerous proposed mechanisms for the salutary effects of exercise on blood pressure including eurohormonal, vascular, and structural adaptation. Decreases in catecholamine's, total peripheral resistance (TPR) and body weight and fat stores and alterations in vasodilators and vasoconstrictors are suggested to explain the antihypertensive effects on exercise (Pescatello et al., 2004).
Treatment of hypertension has greatly reduced the morbidity and mortality associated with CVD, and most of the advances are due to development of effective pharmacological therapy. Yet the antihypertensive medication could cause problems in some patients as many medications are known to produce short-term negative side effects including impotence and depression. As concerns have grown about the risks of drug treatments, this has resulted in increased interest in lifestyle modification intervention of exercising, a method which could control blood pressure for some hypertensive people (Dubbert et al., 1987). Angiotensin converting enzyme (ACE) inhibitors (or Angiotensis II receptor blockers in case of ACE inhibitor intolerance) and calcium channel blockers are currently the drug of choice for recreational exercisers and athletes with hypertension (Pescatello et al., 2004).
Physical Activity for Preventing Stroke and After Stroke
Stroke is the most common life threatening neurological disorder and accounts for 10% of all deaths worldwide (Batty & Lee, 2002). It is also the leading cause of disability and the treatment consists of prolonged hospitalisation with increasing financial difficulties so its prevention is therefore economical and health importance (Batty & Lee, 2002). Epidemiological studies have identified modifiable risk factors for stroke such as blood pressure, obesity, glucose intolerance, smoking, and alcohol abuse and ischaemic stroke and ischaemic heart disease share similar pathophysiological traits and points out to that a sedentary lifestyle is a possible risk factor in the occurrence of stroke (Batty & Lee, 2002).
According to McDonnell (2010), the amount of physical activity practiced by stroke victims remains low, despite increased efforts to increase the practice and intensity of rehabilitation. Recommendations to increase the amount of practice in stroke victims have not been effectively implemented. Reduced physical activity levels after stroke can lead to disuse atrophy, cardiovascular deconditioning and combined social isolation and psychological factors, stroke victims can be at greater risk for secondary cardiac complications and recurrent stroke. Exercise can improve tolerance and reduce risk of cardiovascular disease (McDonnell, 2010).
The cardiac response to acute exercise in individuals who had a stroke has been seen in small number of studies showing the patients achieving significant lower maximal workloads and heart rate and blood pressure responses than control subjects during progression exercise testing to voluntary fatigue. Oxygen uptake at a given sub maximal workload un stroke patients is greater than in healthy subjects, possibly due to reduced mechanical efficiency, the effects of spasticity or both (Gordon et al., 2004).
Risks of Physical Activity
In the recommendation of physical activity and exercise training, there are risk factors that have to be considered for the general population and for individuals with cardiovascular disease and the most common risk of exercise in adults is musculoskeletal injury and risk of injury increases with obesity, volume of exercise and involvement in vigorous exercise such as competitive sport (Thompson et al., 2003).
Vigorous physical activity acutely increases the risk of sudden cardiac failure and myocardial infarction in individuals with both diagnosed and occult heart disease. There are a variety of congenital and acquired conditions such as hypertrophic cardiomyopathy, coronary artery anomalies, aortic stenosis, and cardiomyopathies associated with sudden death during vigorous activity in children and young adults. Atherosclerotic coronary artery disease (CAD) is the majority cause of exercise related death in adults with an incidence of 1 exertion-related death per year for every 15000-18000 healthy men. Exercise also transiently increases the risk of acute myocardial infarction. The relative risk of both exercise-related MI and sudden death is greatest in individuals who are the least physically active and are performing impracticable vigorous activity (Thompson et al., 2003).
The mechanisms of exercise on the reduction of risk of CVD are numerous. Dysfunction of the endothelium can predict the development of atherosclerotic diseases and is seen as an early manifestation of vascular disease and NO synthase increase during exercise by shear stress mechanism can enhance NO bioavailability for endothelial repair. Anti-inflammatory effect on the CVD risk by exercise also can restore vascular wall and its factors can also oxidise the LDL-C and increase the HDL-C formation. Repair of the endothelium by progenitor cells is initiated by exercise by increased circulation of EPCs in the bloodstream which helps reduce the risk of CVD and coronary risk factors. Also reverse cholesterol transport can help HDL-C improve re-endothelialisation with EPC activation and proliferation. The effect of exercise on some CVDs like hypertension and stroke can help reduce their risk of CVD while treatment. There are risk factors of exercise and in the effect of excessiveness or vigorous there can be inducement of cardiac failure and skeletal injuries. Future investigation should include further studies in the effect of exercise in CVD sufferers and a more promotion of basic exercise for children and young adults to limit or reduce the risks of CVD.