The Frank-Starling law of the heart explains the factors which
control stroke volume and the heart's ability to respond to
changes in demand for cardiac output. The ability of the heart
muscle to generate force is dependent on the 
initial
length or
stretch of the muscle cells prior to contraction. The degree
of
stretch (also called preload) of the cardiac muscle cells before
they contract determines stroke volume. The amount of blood
returning to the chambers and distending the ventricles is an
important factor in stretching the cardiac muscle cells. The
greater the end diastolic volume the more the muscle fibers are
stretched leading to a greater stroke volume.
There are two mechanisms which may explain this phenomenon.
First, the stretching of muscle fibers beyond their normal
physiological limits results in a greater length-tension
relationship. Resting cardiac muscle cells are 
normally
shorter
than their optimal length, thus, any increase in the length
of
cardiac muscle cells from stretching results in a dramatic
increase in contractile force.
Secondly, the stretching of muscle fibers increases the
number of 
active cross bridges between the actin and myosin
filaments. When contraction occurs these increased numbers of
cross bridges yield a greater force of contraction.