Starling’s Law — also known as the Frank–Starling law of the heart — describes how the heart automatically adjusts its pumping force in response to changes in the volume of blood returning to it. 
 
The law states that: 
 
“Stroke volume (of the heart) increases in response to an increase in the volume of blood (in the ventricles) before contraction (the end-diastolic volume, ‘preload’), when all other factors remain constant.” 
 
In simpler terms: 
 
The more the cardiac muscle (fibre) is stretched during filling (diastole), 
The greater the force of contraction during systole, 
The more blood can be ejected with each heartbeat, 
*Up to a physiological limit. 
 
Mechanism 
 
When more blood returns to the heart → the ventricular walls stretch. 
This stretching optimally aligns the actin and myosin filaments in cardiac muscle cells. 
The result is a stronger contraction → greater stroke volume (amount of blood pumped out). 
Note: Cardiac Output = Heart rate x Stroke Volume 
 
Graphical Representation 
 
The relationship between end-diastolic volume (preload) and stroke volume (and therefore, over time, cardiac output) forms the Frank–Starling curve. 
Initially, the curve rises steeply (increased filling → increased output). 
Beyond a certain point, excessive stretching reduces efficiency (the curve flattens). 
 
 
 
Physiological Importance 
 
Balances output between the two ventricles — prevents blood from pooling in either systemic (left heart) or pulmonary (right heart) circulation. 
Adapts cardiac output to venous return — maintains equilibrium (ins and outs) in circulation. 
Important in exercise and posture (orthostatic) changes — helps match cardiac output to body needs in healthy individuals. 
 
Clinical Relevance (examples) 
 
Heart failure: The curve flattens — thus increasing filling (preload) no longer increases output effectively. 
Fluid overload: Excessive filling, in a poor heart, can worsen pulmonary congestion. 
Hypovolemia: Low filling causes low stroke volume (in health individuals heart rate increases in an attempt to compensate to try to maintain cardiac output; this compensatory mechanism is less effective in heart failure meaning that patients with heart failure tolerate shifts in fluid status less well than healthy individuals).