Hypertrophy is derived from the Greek hyper, meaning over, and trophy, meaning abnormal enlargement of a part of organ or excessive growth. Hypertrophy is widely believed to be an adaptive response to increased workload or excessive training. By undergoing hypertrophy, ventricular wall stress remains constant at higher intraventricular pressures.
The primary molecular cause of enlargement of the heart is hypertrophy of myocytes (i.e., enlargement of existing cells, without an increase in the number of cells).
At a molecular level, it has been shown to be a dynamic process during the progression of long-standing hypertrophy to eventual heart failure.
First type, eccentric hypertrophy, in which the precipitating stress is volume overload, is characterized by increased heart-wall thickness and ventricular dilation but addition of sarcomere in series. It is more commonly associated with endurance exercise training (e.g., swimming, cycling, and running) pregnancy, and volume overload.
Second one, concentric hypertrophy, in which the imposed stress is pressure overload, is characterized by an increase in wall thickness with the deposition of new sarcomeres, but the chamber radius may not change. It is most often the result of chronic pressure overload, but is possible to a minor degree with isometric physical training such as weight training, weight and hammer throwing, wrestling and bodybuilding.
Cardiac Hypertrophy
Note: Sarcomere is the basic contractile unit of muscle fiber. Each sarcomere is composed of two main protein filaments—actin and myosin
