CHAPTER 9 • CARDIOVASCULAR INTEGRATION, ADAPTATION, AND PATHOPHYSIOLOGY
199
TABLE 9-1
SUMMARY OF
CARDIOVASCULAR
CHANGES DURING EXERCISE
T
Cardiac output
• T heart rate (T s ym p a th e tic adrenergic
and i para sym pa th e tic a c tiv ity )
• T stroke volum e (T CVP; T inotropy;
T lusitro p y)
T
Mean arterial pressure and pulse
pressure
• CO increases m ore than SVR
decreases
• T stroke volum e increases pulse
pressure
T
Central venous pressure
• Venous c o n strictio n (T sym p a th etic
adrenergic a c tiv ity )
• Muscle pum p a c tiv ity
• A b d o m in o th o ra cic pum p
i
Systemic vascular resistance
• M etabolic vasodilation in active m uscle
and heart
• C utaneous vasodilation ( i s ym p a th etic
adrenergic a c tiv ity )
• V a s o c o n s tric tio n in spla nch nic,
n o n a c tiv e m uscle, and renal c irc u la -
tio n (T s y m p a th e tic a d re n e rg ic
a c tiv ity )
CVP,
central venous pressure;
CO,
cardiac output;
SVR,
systemic vascular resistance.
activity (e.g., running, bicycling), metabolic
vasodilation (see Chapter 7) in these m us-
cles causes a large fall in system ic vascular
resistance. Ordinarily, this would cause arte-
rial pressure to fall; however, during physical
activity, arterial pressure normally increases
because cardiac output increases at the same
time that system ic vascular resistance begins
to fall. Furthermore, increased sympathetic
activity (see Chapter 6) leads to vasocon-
striction in the gastrointestinal tract, non-
active m uscles, and kidneys, which helps to
lim it the fall in system ic vascular resistance
as w ell as shift blood flow to the active m us-
cles. Venous return to the heart is augmented
by venous constriction and by the skeletal
m uscle and abdominothoracic pumps (see
Chapter 5). Enhanced venous return enables
the cardiac output to increase by preventing
a fall in cardiac preload that would otherwise
occur as heart rate and inotropy increase
(see Chapter 4). Therefore, all the cardio-
vascular changes occurring during physical
activity ensure that active m uscles are sup-
plied with increased blood flow and oxygen
while maintaining normal, or even elevated,
arterial pressures.
Mechanisms Involved in
Cardiovascular Response
to Exercise
Four fundamental mechanisms are responsi-
ble for cardiovascular changes during physical
activity: mechanical, metabolic, autonomic,
and hormonal.
W hen
a person
suddenly
begins to run, cardiac output increases before
metabolic and neurohumoral mechanisms are
activated. This initial increase in cardiac out-
put results primarily from the skeletal mus-
cle pump system, which enhances venous
return and increases cardiac output by the
Frank-Starling mechanism. Within a few sec-
onds of the initiation of m uscle contraction,
metabolic mechanisms
in
the
contracting
muscle dilate resistance vessels and increase
blood flow. At about the same time, changes
begin to occur in the autonomic nervous sys-
tem (Fig. 9.1). Hypothalamic centers coor-
dinate a pattern of increased sympathetic
and decreased parasympathetic (vagal) out-
flow from the medulla (see Chapter 6). This
leads to an increase in heart rate, inotropy,
and lusitropy, which increases cardiac out-
put. Increased sympathetic efferent activity
constricts resistance and capacitance vessels
in the splanchnic circulation and nonactive
muscles to help maintain arterial pressure
and central venous pressure.
In addition,
during strenuous activity, sympathetic nerves
constrict the renal vasculature.
Exercise activates several different hor-
monal system s
that affect cardiovascular
function. Many of the hormonal system s
are activated by the enhanced sym pathetic
activity.
Because
horm onal
changes
take
longer to occur, cardiovascular responses to
these changes lag behind the direct effects
of autonom ic activation on the heart and
circulation.
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