Which mechanism explains how preload increases stroke volume?

• A. Frank-Starling mechanism.
• B. Windkessel effect.
• C. Venous reservoir expansion.
• D. Beta-adrenergic blockade.

Answer: (A)

The main idea is that the heart’s pumping strength increases when the muscle fibers are stretched more at the start of contraction. When preload (end-diastolic volume) rises, the ventricular fibers are stretched closer to their optimal length. At this length, the overlap of actin and myosin allows more cross-bridge cycling during systole, so the ventricle contracts more forcefully and ejects a larger portion of the filled blood. This length-dependent increase in force of contraction is the Frank-Starling mechanism, which makes stroke volume rise in response to greater filling, up to a physiological limit.

The other options don’t explain this length–tension link. The Windkessel effect concerns arterial compliance and smooths pressure/flow, not how muscle fiber length boosts contractile force. Venous reservoir expansion can raise preload by increasing venous return, but it doesn’t describe the mechanism by which the day-to-day change in stretch translates into a stronger contraction. Beta-adrenergic blockade reduces contractility, which would blunt the preload-to-stroke-volume relationship rather than explain it.