Athlete’s heart is a non-pathological condition in which the heart enlarges and thickens due to prolonged intensive endurance training such as cycling, swimming, or jogging. Intensive endurance exercises and workouts enlarge the heart due to thickening of its muscular walls and blood vessels. The enlargement of the organ is necessitated by structural changes of the chambers to increase the volume of blood pumped per heartbeat. Athletic heart syndrome is common sportsmen who devote more than an hour of training or exercise on a daily basis, or for better days of the week. Although medics know athlete’s heart syndrome to be benign, it is confused with other severe medical conditions. Athlete’s heart syndrome manifests in three major cardiac conditions: cardiac hypertrophy, cardiomegaly, and bradycardia.
Symptoms of Bradycardia
Research conducted by Ellison, Waring, Vicinanza, and Torella revealed that 80% of the adult participants with athlete’s heart have a very low resting heart rate: less than sixty (60) beats per minutes (BPM). The condition in which the heart rate falls below 60 BPM is described as bradycardia (bradyarrhythmia). Highly trained sportsmen and athletes have very low heart rates at rest due to structural modifications of the heart to overcome oxygen debt occasioned by strenuous physical exercise. Students who actively participate in athletics are predisposed to ventricular bradycardia, atrial bradycardia and atrioventricular nodal bradycardia.
Atrial bradycardia is a common cause of low heart rate experienced in young athletes. It is also called sinus bradycardia. Atrial bradycardia manifests in increased heart rate during inhalation; and low heart rate during exhalation. Consequently, an individual experiences some variation in vagal tone during breathing. The changes in the inhalation and exhalation patterns culminate in irregular and difficult breathing by the affected individual. Atrial bradycardia is caused by physiological conditioning of the heart muscle to pump higher volume of blood in a single stroke. Therefore, the heart muscles of conditioned athletes pump the same volume of blood in fewer but more powerful contractions. In addition to irregular breathing, 23% of conditioned athletes do lack nervous impulse from sinus nodes of their hearts.
Atrioventricular nodal bradycardia is the cardiac disorder caused in athletes when their sinus nodes fail to generate electrical impulses. It results in dysrhythmia- a condition in which the rate of atrioventricular node exceeds that of depolarization at the sinoatrial node. It occurs when electrical impulses generated at the sinoatrial nodes is blocked from reaching the atrioventricular node. Subsequently, the heartbeat is delayed.
The absence of stimuli or electrical impulses from the atrium, the condition is referred to as ventricular bradycardia. Considering that the powerful ventricular muscles generate much pressure during the contraction of the heart, the compromised stroking power of the ventricles significantly reduces heart rates in sportsmen to a range of twenty beats per minute (20 bpm) to forty beats per minute (40 bpm). Ventricular bradycardia is associated with atrioventricular block, sinus arrest and sinus bradycardia in sportsmen with athletes heart. Most people with various forms of bradycardia are stable and do not show any symptoms. However, clinical intervention is required in few cases where the individuals are not stable.
Treatment of Bradycardia
The line of treatment of bradycardia involves administration of intravenous atropine. In the event that the affected individual does not respond to intravenous atropine, transcutaneous pacing and infusion of intravenous inotrope are recommended. A combination of epinephrine and dopamine can also be used in place of Inotrope. During the clinical treatment, the affected athlete is advised to take a break from the physical exercise to enable the heart regain its original muscle tone.
Cardiomegaly refers to the enlargement of an athlete’s heart as a result of his/her involvement in strenuous training exercises. Once the pumping organ is overworked due to intensified physical exercise, the contracting myogenic fibres get elongated. A gradual increase in the size of the myogenic fibers is brought about a reduction in the overlapping of protein filaments (myosin and actin) within the bundles of muscle fibre. The muscle fibers of the pumping organ then become more inelastic thus, the sliding movement of the heart. The impaired contraction and shortening of the cardiac muscles significantly reduces the efficiency of the heart to pump blood rich in oxygen to the body tissues.
The advanced forms of cardiomegaly precipitate a serious medical condition called congestive heart failure because an enlarged heart ineffectively pumps blood to all body tissues. Cardiomegaly has been identified to be the leading cause of sudden cardiac death in athletes and other groups of sportsmen. Medical experts have observed that an enlarged heart can regain its normal size over a period when an athlete stops training. Nonetheless, proper medication is required when the affected person is unstable.
Symptoms of Cardiomegaly
Cardiomegaly, in its advanced stages, is symptomatic since the heart fails to pump oxygenated blood to underlying body tissues away from the heart. Common symptoms of acromegaly are difficulty in breathing and weak irregular heart beat. Other symptoms include fainting, chest pain, swollen legs, fatigue, weight gain, and increase in abdominal belt. Heart murmurs and disruption of the heart beat (heart failure) are the general warning signs of cardiomegaly.
Athletes with symptomatic cardiomegaly can be given oral beta blockers to reduce their blood pressure. The oral treatment will improve the ability of cardiac muscles to effectively pump blood to other body tissues. Additionally, a combination of anti-arrhythmics and digoxin could also be administered to restore normal rhythmic heartbeat. Heart valve surgery can be performed as a remedy of the last resort if the first line oral medication fails. It involves surgical insertion of artificial valves to prevent leakages and backflow of blood between the ventricles and atrium. Assistive devices of the heart such as implantable mechanical pumps could also be fixed to resolve the problem of low blood circulation around the body posed weak cardiac muscles.
Cardiac hypertrophy is a condition in which walls of the lower heart chambers (ventricles) are thickened as a result of synthesis of more sarcomeres. The left ventricle then becomes stiff. The rigidity of the ventricles reduces cardiac systolic stroke to effectively pump the required volume of blood to the lungs and other body tissues. A study conducted by Olson Hill reveals that the ventricular mass of trained athletes is 60% thicker than the ventricular mass of the non-athletes. Furthermore, the study also established that all athletes have enlarged ventricle mass; and that the degree of thickening is proportional to the duration and intensity of training.
Ventricular hypertrophy is asymptomatic and does not pose any health risk. Athletes with ventricular hypertrophy will regain the original shape of their heart after quitting intensive training.
All sportsmen who train for more than five hours in a week have one or more than cardiac conditions: cardiac hypertrophy, cardiomegaly, and bradycardia. Athlete’s heart is the non-pathological condition in which the heart enlarges and thickens due to prolonged intensive endurance training. Apart from athletes, cyclists, swimmers, footballers, basketball players develop ventricular hypertrophy, cardiomegaly, and bradycardia. The structural modification of the cardiac muscles is necessitated by the increased demand for oxygen in the body tissues. It is the modification which causes cardiac abnormalities.