Cardiac Muscle Force-Velocity Relationship

The length-tension relationship examines how changes in preload affect isometric tension development. Generally, however, when a muscle fiber contracts, it also shortens so that external work can be performed. If we were to isolate a piece of cardiac muscle (e.g., papillary muscle) and study the effects of afterload on the velocity of fiber shortening, we would find that the greater the afterload, the slower the velocity of shortening (see Figure 1). This graph illustrates the force-velocity relationship. We all experience this, for example, when we lift heavy versus light objects. The heavier the object that we lift, the slower our muscles contract.  In summary, there is an inverse relationship between shortening velocity and afterload.

The x-intercept in the force-velocity relationship represents the point where the afterload is so great that the muscle fiber cannot shorten, and therefore represents the maximal isometric force. The y-intercept represents an extrapolated value for the maximal velocity (V_max) that would be achieved if there were no afterload. The value is extrapolated because it cannot be measured experimentally. A muscle will not contract in the absence of any load.

It is important to note that a cardiac muscle fiber does not operate on a single force-velocity curve. This relationship is altered by changes in both preload and inotropy. The former shares some similarities with skeletal muscle; the latter, however, is unique to cardiac muscle.

If the preload is increased, a cardiac muscle fiber will have a greater velocity of shortening at a given afterload (figure 2). This occurs because the length-tension relationship dictates that as the preload is increased, there is an increase in active tension development. Once the fiber begins to shorten, the increased tension generating capability at the increased preload results in a greater velocity of shortening. In other words, increasing the preload enables to muscle to contract  faster against a given afterload. Note that increasing preload increases the maximal isometric force, as well as increases the shortening velocity at a given afterload, but does not alter not alter V_max.

Changes in inotropy also alter the force-velocity relationship. If the inotropic state of the cardiac fiber is increased, there is a parallel shift up and to the right in the force-velocity curve such that there is an increase in both V_max and in maximal isometric force (figure 3). The increase in velocity at any given preload results from the increased  inotropy enhancing force generation by the actin and myosin filaments, and increasing the rate of cross bridge turnover. The increase in V_max is particularly noteworthy because V_max represents the intrinsic capability of a muscle fiber to generate force independent of load, and this is one way in which inotropy can be defined. Therefore, V_max is sometimes used in experiments as an index or measure of inotropy for a muscle fiber.

Revised 04/02/2007