202
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
increase in arterial pulse pressure that accom-
panies the increase in mean arterial pressure.
Stroke volume may decline at very high
workloads because ventricular filling time is
reduced as heart rate increases. Decreased fill-
ing time decreases ventricular filling (decreases
preload), which decreases stroke volume by
the Frank-Starling mechanism. This would
prevent the heart from increasing cardiac out-
put during physical activity if not for several
mechanisms that work together to ensure
that stroke volume is maintained and even
increased as heart rate increases (Table 9-2).
For example, during a physical activity such
as running, enhanced venous return by the
muscle pump and abdominothoracic pump
systems helps to maintain preload despite
the increase in heart rate (see Chapter 5).
Furthermore, increased atrial and ventricular
inotropy enhances ventricular stroke volume
and ejection fraction, and increased lusitropy
helps to augment ventricular filling. When
the heart rate approaches its maximal rate, the
effects of reduced filling time can predomi-
nate over these compensatory mechanisms,
thereby compromising ventricular filling and
reducing stroke volume. The point at which
increased heart rate begins to decrease stroke
volume varies considerably among individu-
als because of age, health, and physical con-
ditioning. Furthermore, this point can vary
TABLE 9-2
MECHANISMS MAINTAINING
STROKE VOLUME AT HIGH
HEART RATES DURING
EXERCISE
• Increased venous return p rom oted by the
a b do m in o th o ra cic and skeletal m uscle
pum ps m aintains central venous pressure
and therefore ven tricu la r preload.
• Venous c o n s trictio n (decreased venous
com pliance) m aintains central venous
pressure.
• Increased atrial in o tro p y augm ents atrial
fillin g o f the ventricles.
• Increased v en tricu la r in o tro p y decreases
end-systolic volum e, w hich increases
stroke volum e and ejection fraction.
• Enhanced rate o f v en tricu la r relaxation
(lu s itro p y ) aids in filling.
within an i ndividual, depending on the type
of exercise and the environmental conditions.
Blood flow to major organs depends upon
the level of physical activity (Fig. 9.2, panel B).
During whole-body exercise (e.g., running),
the blood flow to the working muscles may
increase more than 20-fold (see Chapter 7).
At rest, muscle blood flow is about 20% of car-
diac output; this value may increase to 90%
during strenuous exercise. Coronary blood
flow can increase severalfold as the metabolic
demands of the myocardium increase and
local regulatory mechanisms cause coronary
vasodilation. The need for increased blood
flow to active muscles and the coronary cir-
culation would exceed the reserve capacity of
the heart to increase its output if not for blood
flow being reduced to other organs. During
exercise, blood flow decreases to the splanch-
nic circulation (gastrointestinal, splenic, and
hepatic
circulations)
and
nonactive
skel-
etal muscle as workload increases. This is
brought about primarily by increased sym-
pathetic nerve activity to these organs. With
very strenuous
exercise, renal blood flow
is also decreased by sympathetic-mediated
vasoconstriction.
Skin blood flow increases with increasing
workloads, but it can then decrease at very
high workloads, especially in hot environ-
ments. Increases in cutaneous blood flow are
controlled
by hypothalamic
thermoregula-
tory centers (see Chapter 7). During physical
activity, increased blood temperature is sensed
by thermoreceptors in the hypothalamus. To
enhance heat loss through the skin, the hypo-
thalamus decreases sympathetic nerve activity
to cutaneous blood vessels, which increases
skin blood flow. At the same time, activation
of sympathetic cholinergic nerves to the skin
causes sweating.
W hile cutaneous vasodilation is essential
for thermoregulation during physical activ-
ity, this requirement must be balanced by the
need to maintain arterial pressure. Cutaneous
vasodilation contributes to the fall in systemic
vascular resistance primarily brought about
by vasodilation in active muscles. If increased
cardiac output is unable to maintain arterial
pressure at very high workloads, baroreceptor
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