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), the amount of active tension
developed 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.
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.
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.
RK Revised 04/02/2007