Physiology
The ventricles are the chambers in the heart responsible for pumping blood either to the lungs (right ventricle) or to the rest of the body (left ventricle).
Healthy cardiac hypertrophy (physiologic hypertrophy or "athlete's heart") is the normal response to healthy exercise or pregnancy, which results in an increase in the heart's muscle mass and pumping ability. Trained athletes have hearts that have left ventricular mass up to 60% greater than untrained subjects. Rowers, cyclists, and cross-country skiers tend to have the largest hearts, with an average left ventricular wall thickness of 1.3 centimeters, compared to 1.1 centimeters in average adults. Heart wall thickness can be measured by ultrasound; computed tomography is more accurate, though it is more expensive and has risks of exposure to radiation.
Unhealthy cardiac hypertrophy (pathological hypertrophy) is the response to stress or disease such as hypertension, heart muscle injury (myocardial infarction), heart failure or neurohormones. Valvular heart disease is another cause of pathological hypertrophy. It has also been suggested that the root cause of many heart ailments is cardiac hypertrophy, which in turn is caused by hypoxia due to atmospheric CO, particulate matter, and peroxyl acyl nitrates, which reduces ATP synthesis in cardiac mitochondria. Pathological hypertrophy also leads to an increase in muscle mass, but the muscle does not increase its pumping ability, and instead accumulates myocardial scarring (collagen). In pathological hypertrophy, the heart can increase its mass by up to 150%.
In most situations, described above, the increase in ventricular wall thickness is a slow process. However, in some instances hypertrophy may be "dramatic and rapid." In the Burmese python, consumption of a large meal is associated with an increase in metabolic work by a factor of seven and a 40% increase in ventricular mass within 48 hours, both of which return to normal within 28 days.
Aerobic training results in the heart's being able to pump a larger volume of blood through an increase in the size of the ventricles. Anaerobic training results in the thickening of the myocardial wall to push blood through arteries compressed by muscular contraction. This type of physiologic hypertrophy is reversible and non-pathological, increasing the heart's ability to circulate blood. Chronic hypertension causes pathological ventricular hypertrophy. This response enables the heart to maintain a normal stroke volume despite the increase in afterload. However, over time, pathological changes occur in the heart that lead to a functional degradation and heart failure.
If the precipitating stress is volume overload (as through aerobic exercise, which increases blood return to the heart through the action of the skeletal-muscle pump), the ventricle responds by adding new sarcomeres in-series with existing sarcomeres (i.e., the sarcomeres lengthen rather than thicken). This results in ventricular dilation while maintaining normal sarcomere lengths - the heart can expand to receive a greater volume of blood. The wall thickness normally increases in proportion to the increase in chamber radius. This type of hypertrophy is termed eccentric hypertrophy.
All muscles (including the heart) work more efficiently and safely when they are having an optimal preload. Hence the physiological processes of hypertrophy of aerobic exercise have been the ones that have been optimized by evolution.
In the case of chronic pressure overload (as through anaerobic exercise, which increases resistance to blood flow by compressing arteries), the chamber radius may not change; however, the wall thickness greatly increases as new sarcomeres are added in-parallel to existing sarcomeres. This is termed concentric hypertrophy. This type of ventricle is capable of generating greater forces and higher pressures, while the increased wall thickness maintains normal wall stress. This type of ventricle becomes "stiff" (i.e., compliance is reduced), which can impair filling and lead to diastolic dysfunction.
The axis of the heart shifts toward the hypertrophied ventricle for two reasons: 1. far more muscles exist on the hypertrophied side, which allows excess generation of electrical potentials on this side. 2. more time is required for the depolarization to travel to the hypertrophied ventricle compared with the normal.
Read more about this topic: Ventricular Hypertrophy
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