What does the Frank-Starling mechanism describe about preload and stroke volume?

• A. Preload has no effect on stroke volume.
• B. Greater end-diastolic stretch optimizes actin–myosin overlap, increasing contraction and stroke volume within physiological limits.
• C. Stroke volume equals heart rate times preload.
• D. Stroke volume decreases as preload increases.

Answer: (B)

Preload, the end-diastolic stretch of the heart muscle, sets the initial length of the sarcomeres. As preload increases within the physiological range, the sarcomeres lengthen toward their optimal length for actin–myosin cross-bridge formation, producing a stronger contraction and therefore a greater stroke volume. This length–tension relationship is the essence of the Frank-Starling mechanism and helps the heart match its output to venous return. Beyond very high filling, the overlap becomes suboptimal and the contractile force no longer increases (and can decline). The other statements don’t fit because preload does affect stroke volume, stroke volume is not simply heart rate times preload, and stroke volume does not decrease with increased preload in the normal range.