Frank Staling Law
The Frank–Starling law of the heart (also known as Starling's law or the Frank–Starling mechanism or Maestrini heart's law) states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume). The increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more forcefully (the so-called Frank-Starling mechanisms). The stroke volume may also increase as a result of greater contractility of the cardiac muscle during exercise, independent of the end-diastolic volume. The Frank-Starling mechanism appears to make its greatest contribution to increasing stroke volume at lower work rates, and contractility has its greatest influence at higher work rates.
This allows the cardiac output to be synchronized with the venous return, arterial blood supply and humeral length[1] without depending upon external regulation to make alterations.
As the heart fills with more blood than usual, the force of cardiac muscular contractions increases.[2] This is a result of an increase in the load experienced by each muscle fiber due to the extra blood load entering the heart. The stretching of the muscle fibers augments cardiac muscle contraction by increasing the affinity of troponin C for calcium[citation needed], causing a greater number of actin-myosin cross-bridges to form within the muscle fibers. The force that any single cardiac muscle fiber generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibers is related to the End Diastolic Volume of the left and right ventricles.
In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometers, a length which is rarely exceeded in the normal heart. Initial lengths larger or smaller than this optimal value will decrease the force the muscle can achieve. For larger sarcomere lengths, this is the result of less overlap of the thin
This allows the cardiac output to be synchronized with the venous return, arterial blood supply and humeral length[1] without depending upon external regulation to make alterations.
As the heart fills with more blood than usual, the force of cardiac muscular contractions increases.[2] This is a result of an increase in the load experienced by each muscle fiber due to the extra blood load entering the heart. The stretching of the muscle fibers augments cardiac muscle contraction by increasing the affinity of troponin C for calcium[citation needed], causing a greater number of actin-myosin cross-bridges to form within the muscle fibers. The force that any single cardiac muscle fiber generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibers is related to the End Diastolic Volume of the left and right ventricles.
In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometers, a length which is rarely exceeded in the normal heart. Initial lengths larger or smaller than this optimal value will decrease the force the muscle can achieve. For larger sarcomere lengths, this is the result of less overlap of the thin