416
Chapter 12
in these three beds, arteriolar vasoconstriction—manifested
as decreased blood fl ow in Figure 12–61—is occurring in the
kidneys and gastrointestinal organs, secondary to increased
activity of the sympathetic neurons supplying them.
Vasodilation of arterioles in skeletal muscle, cardiac mus-
cle, and skin causes a decrease in total peripheral resistance to
blood fl ow. This decrease is partially offset by vasoconstric-
tion of arterioles in other organs. Such resistance “juggling,”
however, is quite incapable of compensating for the huge dila-
tion of the muscle arterioles, and the net result is a decrease in
total peripheral resistance.
What happens to arterial blood pressure during exercise?
As always, the mean arterial pressure is simply the arithme-
tic product of cardiac output and total peripheral resistance.
During most forms of exercise (
Figure 12–62
illustrates the
case for mild exercise), the cardiac output tends to increase
somewhat more than the total peripheral resistance decreases,
so that mean arterial pressure usually increases a small amount.
Pulse pressure, in contrast, signifi cantly increases because of
an increase in both stroke volume and the speed at which the
stroke volume is ejected. It should be noted that by “exercise,”
we are referring to cyclic contraction and relaxation of muscles
occurring over a period of time, like jogging. A single, intense
isometric contraction of muscles has a very different effect on
blood pressure, and will be described shortly.
The increase in cardiac output during exercise is due to
a large increase in heart rate and a small increase in stroke vol-
ume. The increase in heart rate is caused by a combination
of decreased parasympathetic activity to the SA node and
increased sympathetic activity. The increased stroke volume
is due mainly to an increased ventricular contractility, mani-
fested by an increased ejection fraction and mediated by the
sympathetic nerves to the ventricular myocardium.
Note, however, in Figure 12–62 that there is a small
increase (about 10 percent) in end-diastolic ventricular vol-
ume. Because of this increased fi lling, the Frank-Starling
mechanism also contributes to the increased stroke volume,
although not to the same degree as the increased contractility
does. The increased contractility also accounts for the greater
speed at which the stroke volume is ejected, as noted in the
previous discussion of pulse pressure.
We have focused our attention on factors that act directly
upon the heart to alter cardiac output during exercise. By them-
selves, however, these factors are insuffi cient to account for the
elevated cardiac output. The fact is that cardiac output can be
increased to high levels only if the peripheral processes favor-
ing venous return to the heart are simultaneously activated to
the same degree. Otherwise, the shortened fi lling time result-
ing from the high heart rate would lower end-diastolic volume,
and thus stroke volume, by the Frank-Starling mechanism.
Factors promoting venous return during exercise are:
(1) increased activity of the skeletal muscle pump, (2) increased
depth and frequency of inspiration (the respiratory pump),
(3) sympathetically mediated increase in venous tone, and
(4) greater ease of blood fl
ow from arteries to veins through
the dilated skeletal muscle arterioles.
What control mechanisms elicit the cardiovascular changes
in exercise? As described previously, vasodilation of arterioles in
skeletal and cardiac muscle once exercise is underway represents
active hyperemia as a result of local metabolic factors within
the muscle. But what drives the enhanced sympathetic out-
fl ow to most other arterioles, the heart, and the veins, and the
decreased parasympathetic outfl ow to the heart? The control
of this autonomic outfl
ow during exercise offers an excellent
example of what we earlier referred to as a preprogrammed
pattern, modifi
ed by continuous afferent input. One or more
discrete control centers in the brain are activated during
exercise by output from the cerebral cortex, and descending
pathways from these centers to the appropriate autonomic pre-
ganglionic neurons elicit the fi ring pattern typical of exercise.
These centers become active, and changes to cardiac and vas-
cular function occur even before exercise begins. Thus, this
constitutes a feedforward system.
Once exercise is underway, local chemical changes in
the muscle can develop, particularly during intense exercise,
because of imperfect matching between blood fl ow and meta-
bolic demands. These changes activate chemoreceptors in
the muscle. Afferent input from these receptors goes to the
medullary cardiovascular center and facilitates the output
reaching the autonomic neurons from higher brain centers
(
Figure 12–63
). The result is a further increase in heart rate,
Figure 12–62
Summary of cardiovascular changes during mild upright exercise
like jogging. The person was sitting quietly prior to the exercise.
Total peripheral resistance was calculated from mean arterial
pressure and cardiac output.
Time
3000
1030
93
120
80
5
72
70
135
18.6
113
180
10.3
11
80
130
85
148
Skeletal muscle blood flow
(ml/min)
Mean arterial pressure (mmHg)
Systolic arterial pressure (mmHg)
Diastolic arterial pressure
(mmHg)
Total peripheral resistance
(mmHg • min/L)
Cardiac output (L/min)
Heart rate (beats/min)
Stroke volume (ml/beat)
End-diastolic ventricular volume
(ml)
Exercise
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