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Occlusive Coronary artery disease or in other words atheroschlerotic coronary artery disease or commonly called as CAD remains to be among the main reasons for deaths all over the world. More than 1.5 million natives of the USA die of CAD which accounts for myocardial infarction. CAD results in more than 500,000 deaths per year. Since the last decade, there have been a significant number of studies that have been carried out in this direction that have significantly reduced the mortality rate related to CAD. These studies have been both in the medical and surgical management of the disease and also in the direction of finding and modifying the various risk factors involved in the causation of the disease, these risk factors being alcohol, smoking and hypertension. In the recent past a lot of studies have been directed to find the relationship between physical exercise and development of CAD. All the studies carried out in this course have lead to one general assumption, that being that physical activity does remarkably decrease the chances of CAD. A study carried out by Powell in the year 1995 (exercise and heart disease) in 121 subjects had the conclusions that stated that physically active individuals had almost half the incidence of CAD and that among the active individuals there existed an inverse relationship between the activity and development of CAD. With the numerous studies carried out in this way it can be postulated that physical activity does bring around positive alterations and changes in the physical and physiological functioning of the heart that reduces the chances of developing CAD and its various isoforms like MI or hypertension. The heart or the cardiac tissue undergoes certain changes and alterations both in the physical and physiological aspects whenever a load or stress is placed on it. One of these changes is Cardiac hypertrophy. Cardiac hypertrophy is a response of a living human heart to any stimuli either external or internal placed on it causing a biomechanical stress on the heart. Cardiac hypertrophy is a necessary evil as even though it helps in easing the pressure on the cardiac wall it can progress to CAD or even heart failure. Cardiac hypertrophy is of two types, one of them being pathologic which is a result of hypertension and the other being physiological which is caused due to regular exercise loads. Hypertension, termed as a sustained and prolonged abnormal increase in blood pressure is the diseased state of the heart caused, due to an increase in blood pressure to abnormally high levels.
Hypertension is one of these stimuli and also is physical exercise. Both of these stimuli bring about cardiac hypertrophy but in different forms and cause changes in the heart wall myocardium both physically and physiologically.
Hypertension causes a number of alterations in physical and functional aspects of the heart. These changes include a reduction in the left ventricular cardiac functions, changes in myocardial structure, the conduction system of the heart and also the coronary vasculature. All these changes brought about by hypertension progress to pathologic cardiac hypertrophy and eventually result in the development of left ventricular failure or left ventricular hypertrophy. The other manifestations of hypertension are MI, angina, valvular disorders and finally congestive heart failure. Left ventricular hypertrophy is termed as an enlargement in the anatomical dimensions of the left ventricular region of the heart or an expansion of its walls. These changes are the result of the responses of cardiac myocytes to the various stimuli that accompany hypertension. Hypertension is accompanied by several mechanical and neuro-hormonal stimuli that produce myocardial cell growth, altered gene expression and stimulation of the renin angiotensin system which indirectly leads to abnormal growth of the interstitium and cell matrix components, an increase in apoptosis( ) and a reduction in cardiac tissues (article 2a). "Hypertension and eventually left ventricular hypertrophy are characterized by an abnormal imbalance between the cardiac myocytes and the interstitium of the cardiac muscle" (Kokkinos PF, Papademetriou V. Exercise and hypertension. Coron Artery Dis. Mar 2000; 11(2):99-102). A number of changes is seen even in the left atrium. The changes in the left atrium are seen as a result of an elevated pressure or load at the end of diastole also termed as "end diastolic pressure". The rise in the pressure at the termination of diastole is due to a higher amount of blood left in the left atrium which indirectly is the result of an increased blood pressure. This increase in the end-diastolic pressure and an increase in the after load damages a few areas of the heart specifically the left atrial wall, appendages and a thickening and widening of the atrial chamber on the left side of the heart. Hypertrophy of the left ventricular wall causes notable changes in cardiac morphology as in a dilation of both the left atrial and ventricular chambers of the heart. It quite frequently also leads to an increase in the dimensions of both the cardiac chambers on the right side and, is accompanied by varying degrees of pulmonary edema. Prolonged hypertension also causes valvular abnormalities like aortic and mitral insufficiency and aortic sclerosis (Drayer et al, Weber et al, DeYoung et al, 1983). Exercise training is supposed to act as a curative factor in the cure for a person suffering from elevated blood pressure or hypertension. The other beneficial effect of exercises and regular fitness schedules is that it builds up human endurance that in turn helps in bringing about physiologic hypertrophy which is beneficial for patients. This physiological hypertrophy is brought about in response to the elevated mechanical stress on the heart that is caused by the repeated bouts of exercise and work outs. Regular exercises are not only curative in nature but are also preventive in nature as a person who exercises regularly and maintains a healthy lifestyle would generally have a physiologically hypertrophied heart which would in turn protect him from many cardiac disorders like heart failure, hypertension and congestive heart disorders (young I lee et al,2007).
In a study carried out in the year 2006 by Young et al and his colleagues they tried to look into the association existing between genes, apoptosis, exercise training and cardiac disorders. They found that elevated levels of blood lipids could cause hypertension. They postulated that people who are devoid of regular exercises and work outs have higher levels of blood lipids in comparison to people who exercise regularly thus emphasizing on the fact that exercise does play a role in causing physiologic hypertrophy and preventive cardiac disorders. They found that spontaneously hypertensive rats exhibited abnormal and irregular insulin action and lipid metabolism and this was quite similar to the humans suffering with hypertension or who had the human hypertensive syndrome.
Their study was done in order to find the effects of endurance exercises on cardiac morphology in terms of left ventricular wall thickness, levels of lipids and fats and other changes in cardiac anatomy and alterations in physiologic functions of the heart like heart rate and blood pressure. Through the results obtained from this study it was seen that the body weight of the exercised SHR rats was comparable to the sedentary WKY rats but was lower than the non exercised SHR rats. Exercise training was also found to cause a lowering of the heart to body weight ratio. RHR (heart rate at rest) comparisons made in between the exercised SHR and WKY rats showed that it was elevated in the exercised SHR than in the WKY rats. In agreement with these above mentioned results were the results that showed that exercise even led to reduction in the systolic and diastolic blood pressures as seen in case of exercise trained SHR's while the WKY rats had higher blood pressure readings. In short the results of the above mentioned study by young et al in 2006 showed that regular exercise training caused a reduction in heart rates, blood pressure and body weights and also caused a reduction in the thickness of the interior wall of the left ventricular chamber of the heart. The thickness associated with the wall of the left ventricle was found to be more among the non exercised SHR's and WKY rats in comparison to the exercised SHR's. These results emphasize on the hypothesis that exercise does reduce blood pressures and heart rates and cause a considerable thickening of the interior wall of the left ventricle which is less in comparison to what a pathologic cardiac hypertrophy due to hypertension would cause (Young I lee et al, 2006). Moreover the levels of blood plasma and blood lipids were also found to be decreased in exercised rats. With the help of many such studies it has been found that regular exercise training brings about a number of alterations in the cardiovascular systems of both the hypertensive animals as well as humans. Regular exercise routines bring about a decrease in cardiac output, increase in the capillary supply and decrease in sympathetic activity (nelson et al, 1986, grassi et al, 1994, versa-silva et al, 1997, gute et al, 1996). However, the magnitude of the changes both physical and functional seen in the heart as a result of exercise also depend on the type of exercise carried out. Resistance exercises and endurance exercises have their own physical and functional distinct, effects on the cardiovascular system (haykowski et al, 1998). Activities consisting of endurance exercises bring about the most notable increase in the LV size and wall thickness whereas, on the other hand, resistance exercise training causes an irregular thickening of the walls of the left ventricle in relation to the size of the left ventricular cavity dimensions. In a study carried out in female athletes it was found that resistance training done for an extended period of time did not reveal any increase or changes in the left ventricular dimensions including its mass, size of its cavity or the thickness of its walls. The same studies carried out in males also led to the same results leading to the notion that resistance training irrespective of male or female athletes is not an efficient cause of LV hypertrophy. A study was carried out by Haykowski et al focusing on making comparisons among the non exercised controls and the resistance exercise trained female athletes based on the changes seen in the left ventricular mass, wall thickness both of the posterior wall and the septal wall, and internal cavity dimensions and the results emphasized on the fact that there were no notable differences found among the two groups. Similar studies were obtained from other studies looking into effects of RT based on sex and consistent results were obtained leading to the confirmation of the hypothesis that resistance training (RT) is not a suitable precursor for causing hypertrophy of the left ventricle. With many studies done at the same time it was seen that endurance training had the maximum effect on cardiac morphology (article 2H, Left ventricular morphology in elite female resistance trained athletes, Haykowski et al, 1998). "Endurance exercises cause a significant and sustained increase in venous return resulting in an increase in the volume of blood in the left ventricle at the end of the diastolic phase and to accommodate this increased volume a rise in the left ventricular cavity dimensions in terms of its internal diameter. The increased left ventricular volume also leads to a thickening of the walls of the left ventricle in order to counter the increased wall stress" (whyte et al, 2003, article 5H). Endurance training leads to an elevation in the readings of the end diastolic volume or also termed as preload. This increase in preload according to the Frank Starling law causes a stretch that is mechanical in nature leading to the thickening of the walls of the left ventricular compartment that finally helps meeting the increased wall stresses. Endurance exercise training also causes an elevation in the levels of the after load which is the force that the left ventricle needs to exert during systole to overcome the aortic pressure and ultimately open the aortic valve or the systolic BP. The elevation in the levels of the after load from endurance training depends upon the different modes of exercise training used. Adding to all these effects of endurance exercises is another effect that is that endurance training leads to an elevation in the readings of the end diastolic volume or also termed as preload. This increase in preload according to the Frank Starling law (this law states that there is a direct relation between diastolic filling or preload and amount of blood pumped) causes a stretch that is mechanical in nature leading to the thickening of the walls of the left ventricular compartment that finally helps meeting the increased wall stresses. Comparing the effects of different types of exercises like rowing and cycling emphasizes the differences caused in volumes of preload and after load (systolic blood pressures). Rowing causes a slow and steady increase in the after load to peaks of 200mm/hg while, on the other hand, cycling has been recorded to cause a significantly higher and sustained elevation of the after load. Cycling causes a significantly higher increase in after load due to its nature of causing an increased isometric stress due to its involving both the lower and upper limbs. Thus, this shows that the slow, steady and sustained increases in both the pre and after loads as a result of endurance training bring about the distinction in changes in cardiac morphology as compared to resistance training.
An adaptation to endurance training is observed as an increase in Stroke volume (SV). This increase in SV brings about a subsequent increase in the size of the left ventricle and a thickened wall of the left ventricle but is not accompanied by any changes in EF (Ejection fraction) which is a clinically reliable and useful measure of the LV function. This information collected from various studies carried out by Whyte et al shows that the increase in LV mass and a thickening of the walls of the left ventricular walls is and all other changes seen in the cardiac morphology seen as a result of endurance training are physiologic in nature and are not pathologic and do not indicate a diseased state of the heart and in turn indicate towards a healthy exercised heart (ARTICLE 5H).
The term that signifies the wholesome effects of repetitive exercise on the morphology and function of the heart is Athletes heart. Many studies using electrocardiography have looked into the various changes brought in the cardiac structure and function as a result of regular and repetitive exercise training. Continue from article 4h.