What is the Frank-Starling mechanism?

• A. A larger end-diastolic stretch leads to a weaker contraction
• B. A larger end-diastolic stretch has no effect on contraction
• C. A larger end-diastolic stretch leads to a stronger contraction but lower stroke volume
• D. A larger end-diastolic stretch leads to a stronger contraction and higher stroke volume

Answer: (D)

The main idea being tested is how the heart’s force of contraction changes as the ventricle is filled more during diastole. When venous return increases, the ventricles stretch to a greater end-diastolic length. Cardiac muscle shows a length–tension relationship: at this longer length, the overlap of actin and myosin allows more cross-bridge interactions, so the contraction becomes stronger. That stronger contraction pumps more blood out, reducing end-systolic volume and increasing stroke volume. This intrinsic mechanism, which helps match cardiac output to venous return, is the Frank–Starling mechanism.

So a larger end-diastolic stretch leads to a stronger contraction and higher stroke volume. The other statements don’t fit because increasing preload does not weaken contraction, nor is there no effect; and a stronger contraction would not produce a lower stroke volume under normal physiology.