CHAPTER 9 • CARDIOVASCULAR INTEGRATION, ADAPTATION, AND PATHOPHYSIOLOGY
201
resulting from increased plasma osmolarity.
Although these hormonal changes promote
renal retention of sodium and water, espe-
cially after prolonged periods of exercise,
blood volume often decreases during exercise
(particularly in hot environments) because
of water loss through sweating and increased
respiratory exchange.
Two mechanisms operate to activate the
autonomic nervous system during exercise.
One mechanism is referred to as “central
command.” W hen physical activity is antici-
pated or already under way, higher brain
centers (e.g., the cortex) relay information
to hypothalamic centers to coordinate auto-
nomic outflow to the cardiovascular system.
By this central command mechanism, antici-
pation of exercise can lead to autonomic
changes
that increase
cardiac output and
arterial pressure before exercise begins. This
serves to prime the cardiovascular system
for exercise. A second mechanism involves
muscle mechanoreceptors and chemorecep-
tors.
Once
physical
activity is
underway,
these muscle receptors respond to changes in
muscle mechanical activity and tissue chemi-
cal environment (e.g., increased lactic acid),
and then relay that information to the central
nervous system via afferent fibers. This infor-
mation is processed by the hypothalamus
A
and medullary autonomic control regions to
enhance the sympathetic outflow to the heart
and systemic vasculature.
Arterial baroreceptor function is altered
during physical activity. Exercise normally is
associated with a rise in both arterial pressure
and heart rate. If arterial baroreceptor func-
tion were not modified, the increase in arterial
pressure would result in a reflex bradycardia.
Instead, the baroreceptor reflex is modified
(reset to a higher control point) by the central
nervous system (see Chapter 6).
Steady-State Changes in
Cardiovascular Function
during Exercise
Changes
in
cardiovascular
function
dur-
ing physical activity depend upon the level
of physical exertion. If the level of physical
exertion is expressed as workload, heart rate,
cardiac output, and arterial pressure increase
in nearly direct proportion to the increase
in workload (Fig. 9.2, panel A). In contrast,
systemic vascular resistance falls as workload
increases because of vasodilation in the active
muscles. Ventricular stroke volume increases
at low-to-moderate workloads and then pla-
teaus. Although not shown in Figure 9.2, the
increase in stroke volume is responsible for an
B
Rest
Moderate
Heavy
Rest
Moderate
Heavy
■ FIGURE 9.2 Systemic hemodynamic and organ blood flow responses at different levels of exercise
intensity. Panel A shows systemic hemodynamic changes. Systemic vascular resistance
(SVR)
decreases
because of vasodilation in active muscles; mean arterial pressure
(MAP)
increases because cardiac output
(CO) increases more than SVR decreases. CO and heart rate
(HR)
increase almost proportionately to the
increase in workload. Stroke volume
(SV)
plateaus at high heart rates. Panel B shows organ blood flow
changes. Muscle blood flow increases to very high levels because of active hyperemia; skin blood flow
increases because of the need to remove excess heat from the body. Sym pathetic-m ediated vasoconstric-
tion decreases gastrointestinal
(GI)
blood flow and renal blood flow. Brain blood flow changes very little.
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