Cardiovascular Physiology
myocardial contractility, and vascular resistance in the non-
active organs. Such a system permits a fi
ne degree of match-
ing between cardiac pumping and total oxygen and nutrients
required by the exercising muscles. Mechanoreceptors in the
exercising muscles are also stimulated and provide input to the
medullary cardiovascular center.
, the arterial baroreceptors also p
lay a ro
le in
the altered autonomic outfl ow. Knowing that the mean and
pulsatile pressures rise during exercise, you might logically
assume that the arterial baroreceptors will respond to these
elevated pressures and signal for increased parasympathetic and
decreased sympathetic outfl ow, a pattern designed to counter
the rise in arterial pressure. In reality, however, exactly the
opposite occurs; the arterial baroreceptors play an impor-
tant role in
the arterial pressure over that existing
at rest. The reason is that one neural component of the cen-
tral command output goes to the arterial baroreceptors and
“resets” them upward as exercise begins. This resetting causes
the baroreceptors to respond as though arterial pressure had
decreased, and their output (decreased action potential fre-
quency) signals for decreased parasympathetic and increased
sympathetic outfl ow.
Table 12–7
summarizes the changes that occur dur-
ing moderate exercise—that is, exercise (like jogging, swim-
ming, or fast walking) that involves large muscle groups for an
extended period of time.
In closing, let’s return to the other major category of
exercise, which involves maintained high-force, slow short-
ening-velocity contractions, as in weightlifting. Here, too,
cardiac output and arterial blood pressure increase, and the
arterioles in the exercising muscles undergo vasodilation due to
local metabolic factors. However, there is a crucial difference:
During maintained contractions, once the contracting muscles
exceed 10 to 15 percent of their maximal force, the blood fl ow
to the muscle is greatly reduced because the muscles are physi-
cally compressing the blood vessels that run through them. In
other words, the arteriolar vasodilation is completely overcome
by the physical compression of the blood vessels. Thus, the car-
diovascular changes are ineffective in causing increased blood
fl ow to the muscles, and these contractions can be maintained
only briefl y before fatigue sets in. Moreover, because of the
compression of blood vessels, total peripheral resistance may
go up considerably (instead of down, as in endurance exercise),
contributing to a large rise in mean arterial pressure during the
contraction. Frequent exposure of the heart to only this type
of exercise can cause maladaptive changes in the left ventricle,
including wall hypertrophy and diminished chamber volume.
Maximal Oxygen Consumption and Training
As the intensity of any endurance exercise increases, oxygen
consumption also increases in exact proportion until reach-
ing a point when it fails to rise despite a further increment
in workload. This is known as
maximal oxygen consump-
tion (
max has been reached, work can be
increased and sustained only very briefl y by anaerobic metabo-
lism in the exercising muscles.
max could be limited by (1) the cardiac
output, (2) the respiratory system’s ability to deliver oxygen to
the blood, or (3) the exercising muscles’ ability to use oxygen.
In fact, in typical, healthy people (except for a few very highly
Cardiac output
Vasoconstriction in
abdominal organs
and kidneys
Parasympathetic output to heart
Sympathetic output to heart, veins,
and arterioles in abdominal
organs and kidneys
Arterial baroreceptors
Reset upward
“Exercise centers”
Exercising skeletal muscles
Muscle blood flow
in the muscles
Local chemical
in the muscles
in the muscle
Figure 12–63
Control of the cardiovascular system during exercise. The primary outfl ow to the sympathetic and parasympathetic neurons is via pathways
from “exercise centers” in the brain. Afferent input from mechanoreceptors and chemoreceptors in the exercising muscles and from reset arterial
baroreceptors also infl uences the autonomic neurons by way of the medullary cardiovascular center.
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