Frank–Starling mechanism
Also known as: Starling's law of the heart, heterometric autoregulation, length–tension relationship
The Frank–Starling mechanism is the heart's built-in ability to pump out whatever blood returns to it. When more blood fills the ventricle (higher preload), the muscle fibres are stretched further and contract more strongly, so stroke volume rises.
Overview
Mechanism. When a ventricle fills with more blood, its sarcomeres are stretched toward their optimal length of about 2.0–2.2 µm, where actin and myosin overlap best. More importantly, stretch makes troponin C more sensitive to Ca²⁺ (length-dependent activation). This happens because the filaments move closer together and because of strain on the giant protein titin. The same Ca²⁺ signal therefore produces more force.
Normally the heart works on the rising part of this length–tension curve. Titin and the collagen network stiffen the myocardium enough to stop it being stretched past its optimum.
Why it matters. The Frank–Starling mechanism keeps the outputs of the two ventricles equal beat by beat. If right ventricular output rises briefly, as on inspiration or when lying down, left ventricular filling rises a few beats later, and left ventricular output follows. It also helps cardiac output rise when venous return increases during exercise and changes in posture.
Ventricular function curves. Plotting stroke volume (or stroke work) against end-diastolic pressure gives a ventricular function curve. Positive inotropes and sympathetic stimulation shift the curve upward and to the left. Heart failure shifts it downward and flattens it, so extra filling mainly raises pressure and causes congestion, with little gain in output.
Related mechanisms. The Frank–Starling mechanism is different from the Anrep effect, a gradual increase in contractility after a sudden rise in afterload. It is also different from the Bowditch (treppe) effect, in which force increases with heart rate.
Function
- Matches stroke volume to venous return automatically, without needing nerves.
- Keeps right and left ventricular outputs equal over time.
Clinical significance
Fluid responsiveness
A patient on the steep part of the curve increases stroke volume when given fluid. A passive leg raise, which returns about 300 mL of blood from the legs, tests this without giving any fluid.
Heart failure and diuretics
On the flat part of a failing heart's curve, diuretics lower filling pressure and relieve congestion while reducing stroke volume only slightly. A dilated ventricle has a larger radius, so by Laplace's law its wall tension and oxygen demand are higher.
Test yourself
The Frank–Starling mechanism explains why stroke volume rises when:
- Sympathetic stimulation increases heart rate
- End-diastolic volume (preload) increases
- Aortic pressure (afterload) increases
- Vagal tone increases
Answer: End-diastolic volume (preload) increases
Greater filling stretches the sarcomeres toward their optimal length and increases the Ca²⁺ sensitivity of troponin C. Contraction is therefore stronger. This is intrinsic to the heart and needs no nerves.
Compiled from standard anatomy and physiology references — see the Cardiovascular System sources. For education only; not medical advice.