Human Physiology, 14th edition (2016)

Cardiac Output, Blood Flow, and Blood Pressure 453

As discussed in chapter 12, stretch can also increase the con-

traction strength of skeletal muscles (see fig. 12.21). The resting

length of skeletal muscles, however, is close to ideal, so that sig-

nificant stretching decreases contraction strength. This is not true

of the heart. Prior to filling with blood during diastole, the sarco-

mere lengths of myocardial cells are only about 1.5  m m. At this

length, the actin filaments from each side overlap in the middle of

the sarcomeres, and the cells can contract only weakly ( fig. 14.3 ).

The proportion of the end-diastolic volume that is ejected
against a given afterload depends on the strength of ventricular
contraction. Normally, contraction strength is sufficient to eject
70 to 80 ml of blood out of a total end-diastolic volume of 110
to 130 ml. The ejection fraction is thus about 60%. The ejection
fraction remains relatively constant over a range of end-diastolic
volumes, so that the amount ejected per beat (stroke volume)
increases as the end-diastolic volume increases. In order for this
to be true, the strength of ventricular contraction must increase
as the end-diastolic volume increases.

Frank-Starling Law of the Heart

Two physiologists, Otto Frank and Ernest Starling, demonstrated
that the strength of ventricular contraction varies directly with
the end-diastolic volume ( fig. 14.2 ). Even in experiments where
the heart is removed from the body (and is thus not subject to
neural or hormonal regulation) and where the still-beating heart
is filled with blood flowing from a reservoir, an increase in EDV
within the physiological range results in increased contraction
strength and, therefore, in increased stroke volume. This rela-
tionship between EDV, contraction strength, and stroke volume
is thus a built-in, or intrinsic, property of heart muscle, and is
known as the Frank-Starling law of the heart.

Intrinsic Control of Contraction Strength

The intrinsic control of contraction strength and stroke volume
is due to variations in the degree to which the myocardium
is stretched by the end-diastolic volume. As the EDV rises
within the physiological range, the myocardium is increasingly
stretched and, as a result, contracts more forcefully.

Figure 14.2 The frank-starling law and sympathetic

nerve effects. The graphs demonstrate the Frank-Starling law:

As the end-diastolic volume is increased, the stroke volume is

increased. The graphs also demonstrate, by comparing the three

curves, that the stroke volume is higher at any given end-diastolic

volume when the ventricle is stimulated by sympathetic nerves.

This is shown by the steeper curves to the left (see the red arrow).

Stroke volume (ml)

Frank-Starling law

Ventricular end-diastolic volume (ml)

Increased contractility

caused by sympathetic

nerve stimulation

Figure 14.3 The Frank-Starling

law of the heart. When the heart muscle is

subjected to an increasing degree of stretch

( a through d ), it contracts more forcefully. The

contraction strength is indicated on the y -axis

as the tension. Notice that the time required to

reach maximum contraction remains constant,

regardless of the degree of stretch.

(d)

(d)

A

H

2.4 μm

II

(c)

(c)

(b)

(b)

(a)

(a)

0 500

msec

Tension (g)

Time

1000

Resting sarcomere lengths

Stretch

2.2 μm

ZZ

Actin

Myosin

2.0 μm

1.5 μm