the frank-starling mechanism occurs as the result of the length-tension relationship observed in striated muscle, including for example skeletal muscles, arthropod muscle and cardiac (heart) muscle. as a muscle fiber is stretched, active tension is created by altering the overlap of thick and thin filaments. the greatest isometric active tension is developed when a muscle is at its optimal length. in most relaxed skeletal muscle fibers, passive elastic properties maintain the muscle fibers length near optimal, as determined usually by the fixed distance between the attachment points of tendons to the bones (or the exoskeleton of arthropods) at either end of the muscle. in contrast, the relaxed sarcomere length of cardiac muscle cells, in a resting ventricle, is lower than the optimal length for contraction. there is no bone to fix sarcomere length in the heart (of any animal) so sarcomere length is very variable and depends directly upon blood filling and thereby expanding the heart chambers. in the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometers, a length which is rarely exceeded in a normal heart. initial lengths larger or smaller than this optimal value will decrease the force the muscle can achieve. for longer sarcomere lengths, this is the result of there being less overlap of the thin and thick filaments; for shorter sarcomere lengths, the cause is the decreased sensitivity for calcium by the myofilaments. an increase in filling of the ventricle increases the load experienced by each cardiac muscle fiber, stretching the fibers toward their optimal length.