Athletic heart syndrome Paper
Athletic heart syndrome is a series of conditions steming from a physiologically enlarged heart that is noticed in athletes. Athletic heart syndrome basically as a result of an hypertrophied heart. The resting heart rate, including that measured during exercise, is low when compared with that of other normal persons (both the basal rate and the working rate) (Kenneth et al, 1973).
Muscle contraction is the primary physiological event that occurs during exercising. This is one of the processes in the body that consumes much energy. The cardiovascular system is a conduit for the transport of this energy all round the body. At the same time, the cells are detoxified of all waste products of metabolism.
Exercise puts a whole lot of stress on the cardiovascular system. Athletes are constantly involved in exercising. They frequently strain the cardiovascular system through the demand of the muscle cells (myocytes) for more perfusion. This constant strain on the heart in particular, leads to a physiological hypertrophy of the cardiac muscle cells. The left ventricle of the heart is most affected because it is a high pressure pump that supplies blood to the Aorta, the largest artery in the body. The aorta transmits the blood to other parts of the body including the brain, limbs and all other organs of the body (Kumar et al, 2004) A hypertrophy of the heart is most evident by the thickening of the left ventricle, although, other chambers of the heart are affected. This effect is a sort of physiological conditioning for the heart to be able to cope with the increased load and at the same time, does not feel stressed up. By so doing, athletes can persist in the vigorous activity for a longer time than other individuals without overworking the cardiovascular system. (Microsoft Encarta, 2008)
Oxygen consumption of like-sized active athletes and normal individuals will be roughly the same at rest or at a given level of exercise. However, the fit individual (the athlete) will be able to achieve greater maximal oxygen consumption, even at a lower heart rate, due to the training effect that takes place with regular exercise. As the athlete engages in regular aerobic exercise, the heart, lungs, and muscles all become more efficient at utilizing oxygen. The heart pumps more blood with cardiac output, the lung capacity of each inhalation increases, and the muscle fibers (myocytes) extract more oxygen from the blood. The training effect on the heart is quite evident when heart rates are compared between long-distance runners and sedentary individuals. The athlete will have a lower heart rate at rest (perhaps as low as 50 beats per minute) and during light jogging, for example, than the non-athlete (who might have a resting rate of 80). During light jogging, the untrained person will experience a large increase in heart rate, while the athlete’s heart rate will not rise nearly as much.
The heart has an intrinsic property of being able to generate electrical impulses that excite the myocytes. The Sinoatrial, Atrioventricular, Bundle of His and the Purkinje fibers all make up the electrical conduction system of the heart. Besides this intrinsic control, the heart is control by autonomic nerves that form part of the autonomic nervous system. The sympathetic part of the ANS causes a stimulation of the heart – the rate and force of contraction are increased. The parasympathetic system on the other hand causes a decrease in the rate and force of contraction of the heart. In times of need, for instance, when an individual is exercising, the heart rate is increased so as to increase the cardiac output of the heart. In athletes, however, the heart rate is not increased in spite of the dramatic increase in the cardiac output of the heart. This is because of the physiological hypertrophy of the myocytes and also the basal firing of Vagal impulses to the heart. The Vagus nerve supplies the parasympathetic innervation to the heart.(Ganong, 2001)
Athletic heart syndrome is asymptomatic. The syndrome cannot be detected unless series or medical tests are carried out. A chest x-ray will show an enlarged heart – this is possible by checking the cardiothoracic ratio and determining if it is normal or not. Other medical tests include stress tests. During stress tests, the athlete is asked to go on a Treadmill and exercise. Assessment of a person’s physical fitness includes measurement of aerobic capacity in the form of maximum oxygen consumption during aerobic exercise. At regular intervals, the pulse rate and the blood pressure are measured; this would give an indication of the rate at which these parameters are changing with the progression of exercise. Also, on electrocardiography, increased activity is noticed in the region of the left ventricle, evidenced by a large QRS complex. The complex is tall and peaked, showing an increase in time that that the ventricular muscle fibers have to depolarize and repolarize. Systolic murmurs, slow heart rates, arrhythmias and alterations in S-T segments and T-waves are all features of the athletic heart syndrome (Kenneth et al, 1973)
MORTALITY AND MORBIDITY
Athletic Heart Syndrome is asymptomatic therefore, it is a potentially morbid condition. Athletes with this condition are prone to s number of heart diseases. Cardiomyopathy, which is damage to the weakened heart, is likely to occur in some athletes – Heart failure is the ultimate. Also, in some athletes, heart failure has caused sudden death. This is because they were no prior diagnosis of any heart disease.
After a period of relative inactivity by the athlete, the myriad of modifications to the cardiovascular system normalize. The cardiomegaly subsides. This is important as it distinguishes this syndrome from other cardiomyopathies. Rich (2007).
W. F. Ganong (2001). Review of Medical Physiology. 20th ed. McGraw Hill Companies. pp 275 – 290
V. Kumar, A. K. Abbas, N. Fausto (2004) Robins and Cotran Pathologic Basis of Disease, 7th ed. Saunders – Elsevier. pp 460 -466
Microsoft Encarta (2008). The Human Heart. Microsoft Inc.
Microsoft Encarta (2008). Exercise. Microsoft Inc.
B. Kenneth, A. Benchimol, J. Schumacher (1973). External Pulse and Vectocardiographic Abnormalities in the Athletic Heart Syndrome. “Ches. American College Of Physicians. Pp 289-295
B. E. Rich (2007). The athletic heart syndrome. Current Sports Medicine Reports. Current Medicine Group LLC