The Frank-Starling law is a postulate that indicates that the heart has the ability to vary its force of contraction - and consequently, its volume of contraction - in response to changes in the volume of blood inflow (venous return).
Frank-Starling's law can be described simply: the more the heart is stretched (increased blood volume), the greater the force of the posterior ventricular contraction.
Consequently, the greater the amount of blood expelled through the aortic and pulmonary valves.
Origin of the law
The name of this law refers to two great pioneering physiologists in the study of the heart.
A German scientist named Frank and an English scientist named Starling, each on their own, studied the hearts of different animals.
Each observed that a healthy heart does not expel every last drop of blood from the ventricles when they contract, but rather a remnant of blood remains in the ventricles, which is known as end-stroke volume.
They noted that the increase in diastolic volume, or preload, results in an increase in stroke volume and the expulsion of more blood from the heart with each heart beat.
Over time this theory became popular in cardiac physiology and is now known as the Frank-Starling cardiac law.
Cardiac output
The volume of blood pumped by the heart per minute is known as cardiac output and it is a factor that varies depending on the demands of the body.
Cardiac output can be calculated by multiplying the number of beats per minute (the heart rate) by the volume of blood leaving the heart with each beat (the stroke volume).
Cardiac output is a variable that makes it possible to measure the cardiac adjustment in relation to the physical and emotional demands that the body suffers.
Regulation of preload and stroke volume
There are some factors that influence the amount of blood pumped during each heartbeat, which is known as stroke volume.
During the resting phase of the heart, known as diastole, the ventricles of the heart fill with blood passively.
Later, at the end of diastole, the atria contract, filling the ventricles even more.
The volume of blood in the ventricles at the end of diastole is called the end diastolic volume.
An increase in end diastolic volume then results in more stretching of the ventricles because there is more blood there.
When the ventricle stretches further, it contracts more forcefully, just like a rubber band.
A good way to think of end diastolic volume is to think of it as the amount of blood “loaded” into the ventricles before contraction. For this reason, the final diastolic volume is called the preload.
Afterload
Another important influence of the end stroke volume is the pressure in the arteries exiting the heart.
If there is high pressure in the arteries, the heart will have a hard time pumping blood.
This blood pressure that represents the resistance that the ventricle has to overcome to expel blood is called afterload.
References
- Hale, T. (2004) Exercise Physiology: A Thematic Approach (1st ed.). Wiley.
- Iaizzo, P. (2005). Handbook of Cardiac Anatomy, Physiology and Devices (1st ed.). Humana Press.
- Shiels, HA, & White, E. (2008). The Frank-Starling mechanism in vertebrate cardiac myocytes. Journal of Experimental Biology, 211 (13), 2005–2013.
- Stouffer, G., Klein, J. & McLaughlin, D. (2017). Cardiovascular Hemodynamics for the Clinician (2nd ed.). Wiley-Blackwell.
- Tortora, G. & Derrickson, B. (2012). Principles of Anatomy and Physiology (13th ed.). John Wiley & Sons Inc.