The Frank-Starling law: more filling, stronger beat

Same heart, stronger beat

In the video at 0:00

When more blood fills the heart, the very next beat is stronger. Nothing else has to change: no signal from a nerve or a hormone is needed. The heart muscle itself responds to how far it is stretched, and that is the Frank-Starling law.

Ventricles and stroke volume

In the video at 0:21

The two big lower chambers of the heart, the ventricles, fill with blood and then squeeze it out. The amount pushed out by one squeeze is the stroke volume (SV).

The exam words for the two amounts are end-diastolic volume (EDV), the blood in the ventricle at the end of filling, and end-systolic volume (ESV), the blood left after the squeeze. So SV = EDV − ESV. A typical resting stroke volume is about 70 mL (normal range 55–100 mL).

Preload

In the video at 0:36

Preload is the stretch on the ventricles just before they contract. It is another way of expressing EDV: the more blood fills the ventricle, the greater the preload.

What raises it: more venous return (blood coming back to the heart through the veins) and a longer filling time. Most filling happens while the whole heart is relaxed, and the atrial kick, the contraction of the atria, adds the last 20–30 percent. A very fast heart rate shortens filling time, so preload can fall.

Why stretch makes a stronger squeeze

In the video at 0:45

Heart muscle is built from repeating units called sarcomeres. Inside each one, myosin heads (the hooks in the video) bind to the actin of the thin filaments, forming cross-bridges, and pull.

At rest there is little stretch and the sarcomeres stay short, so only some myosin heads can bind. As filling stretches the muscle, the sarcomeres get longer, and as they reach their best (optimal) length, more myosin heads can bind at once, so the contraction is stronger and the stroke volume rises.

Stretched past the optimal length, the force would fall again. In a healthy heart this overstretch is not a concern, because the heart's position in the chest limits how far it can stretch.

The Frank-Starling law

In the video at 1:20

Within physiological limits, the force of heart contraction is directly proportional to the initial length of the muscle fiber. More preload, a stronger squeeze, a bigger stroke volume. Less filling works the other way: less stretch, fewer cross-bridges, a weaker squeeze.

It is named for Otto Frank (1865–1944), a German physiologist, and Ernest Starling (1866–1927), an English physiologist, who worked largely independently and reached similar conclusions.

Contractility and afterload: the other two factors

Stroke volume depends on three factors. Preload is the one this lesson follows. Contractility is the force of the contraction itself at a given stretch: a stronger contraction gives a bigger SV and a smaller ESV. Things that raise contractility are called positive inotropes (sympathetic stimulation, epinephrine and norepinephrine, thyroid hormone); things that lower it are negative inotropes (parasympathetic stimulation). Textbooks also list some heart drugs in each group; this page gives no medical advice.

Afterload is the tension the ventricles must build to push blood out against the resistance in the blood vessels. Higher resistance, or a stiff narrowed valve, raises afterload.

Back to the question

In the video at 1:55

A heart squeezes harder when more blood fills it because the filling stretches the muscle, and a stretched sarcomere, up to its best length, lets more myosin heads grab at once. More filling, more stretch, more cross-bridges, a stronger squeeze.

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