Length-Tension Relationship for Cardiac Muscle (Effects of Preload)
When the mechanical properties of isolated cardiac muscle are studied in the laboratory, we find that if the muscle is stimulated to contract at low resting lengths (low preloads
) under isometric conditions, the amount of active tension developed (total tension minus the resting tension) is relatively small. If the same experiment is repeated with the muscle at a longer preload length, the active tension that is developed is greatly increased. If this experiment is done at several different preload lengths, and the active tension is plotted as a function of preload, we find the relationship shown in Figure 1. This plot is called the length-tension diagram
. In summary, increases in preload lead to an increase in active tension. Furthermore, not only is the magnitude of active tension increased, but also the rate of active tension development.
The changes in active tension caused by changes in preload are related to changes in the number of actin and myosin cross bridges formed, which depends on the sarcomere length. Changes in preload also affect active tension by altering the sensitivity of troponin C to calcium. This is referred to as length-dependent activation of the muscle fiber.
The length-tension diagram shows that as preload increases, there is an increase in active tension up to a maximal limit. The maximal active tension corresponds in cardiac muscle to a sarcomere length of 2.2 microns. Cardiac muscle, unlike skeletal muscle, does not display a descending limb on the active tension curved because the greater stiffness of cardiac muscle normally prevents its sarcomeres from being stretched beyond 2.2 microns.
There is no single, unique active tension curve in the length-tension relationship. The active tension curve depends upon the inotropic state
of the muscle. If, for example, inotropy is increased by applying norepinephrine
, the total tension curve shifts up and to the left as shown in Figure 2. This results in an increase in active tension development at any given preload length. The opposite occurs when inotropic state is reduced. Therefore, effects of preload on active tension development depends on the inotropic state of the contracting muscle.
The above discussion describes how changes in preload (and inotropy) affect the force generated by cardiac muscle fibers during isometric contractions (i.e., with no change in length). Cardiac muscle fibers, however, also undergo shortening when they contract (i.e., isotonic contractions). Changes in preload also affect the degree of shortening and the velocity of fiber shortening.