There are a number of factors that change the force developed by heart muscle cells. In a manner similar to that seen in skeletal muscle, there is a relationship between the muscle length and the isometric force developed. As the muscle length is increased, the active force developed reaches a maximum and then decreases. This maximum point is the length at which the heart normally functions. As with skeletal muscle, changes in length alter the active force by varying the degree of overlap of the thick myosin and thin actin filaments. The force developed by heart muscle also depends on the frequency at which the muscle is stimulated. As the stimulus frequency is increased, the force is increased until the maximum is reached, at which point it begins to decrease. An increase in the level of circulating epinephrine and norepinephrine from the sympathetic nervous system also increases the force of contraction. All of these factors can combine to allow the heart to develop more force when required. At any given length the velocity of contraction is a function of the load lifted, with the velocity decreasing as the load is increased. The force–velocity relationship is similar to that of skeletal muscle and takes the shape of a rectangular hyperbola. When force–velocity curves are measured at different lengths, there is a change in maximum force while the maximum velocity of shortening (Vmax) remains unchanged. Under conditions where there is an increase in inotropic performance of the muscle (frequency, epinephrine or norepinephrine) there is a shiftin both the maximum velocity and maximum force developed.