Final answer:
Stretching of the myocardium affects cardiac function primarily by altering stroke volume. The Frank-Starling mechanism explains that greater ventricular stretch leads to more forceful contractions, thereby increasing stroke volume. This is due to optimal sarcomere length allowing for maximum cross-bridge formation between myosin and actin filaments.
Step-by-step explanation:
The question relates to how stretching of the myocardium affects cardiac function. Specifically, it involves the Frank-Starling mechanism, which describes the relationship between ventricular stretch and contraction. This principle states that, within physiological limits, the force of heart contraction is directly proportional to the initial length of the muscle fiber. Therefore, the greater the stretch of the ventricular muscle (within limits), the more powerful the contraction. This increased power of contraction means that more of the myosin heads can bind to the actin filaments, resulting in an increased formation of cross bridges during systole, which enhances the strength of contraction and increases the stroke volume (SV).
It is important to note that while excessive stretch could potentially decrease the force of contraction, the physical constraints of the heart's location within the body prevent this from becoming a concern in most physiological scenarios. Therefore, the primary effect of the myocardium's stretching on cardiac function is an alteration in stroke volume, not filling time or heart rate directly.