Final answer:
Filling of the ventricles affects the myocardium by altering the overlap of actin and myosin, which adjusts the force of contraction in response to changes in blood volume. Known as the Frank-Starling mechanism, it enhances the force of systolic contractions within optimal limits to prevent overstretched myocardium.
Step-by-step explanation:
The filling of the ventricles primarily affects the myocardium by altering the overlap of actin and myosin within the cardiac muscle cells, which influences the force of contraction during systole. It is part of the intrinsic mechanism by which the heart adjusts its pumping capacity to match the incoming blood volume, a relationship described by the Frank-Starling law.
During ventricular filling, the ventricles experience an increase in end-diastolic volume (EDV) also known as preload. The increased EDV results in greater stretching of the ventricular myocardium, which in turn increases the length of the sarcomeres—the fundamental units of muscle contraction within the cardiac muscle cells—towards their optimal range. This optimal sarcomere length allows for a more effective interaction between actin and myosin filaments, enhancing the ability of myosin heads to form cross-bridges with actin and thus increases the strength of contraction and consequently the stroke volume (SV).
It is important to note that this effect is limited by the physical dimensions of the heart, preventing overstretching of the myocardium. Nevertheless, the heart has a significant range within which it can modulate its contractile strength in response to changes in venous return and ventricular filling.