518 SECTION VICardiovascular Physiology
INTEGRATED CONTROL
OF CARDIAC OUTPUT
The mechanisms listed above operate in an integrated way to
maintain cardiac output. For example, during muscular exer-
cise, there is increased sympathetic discharge, so that myocar-
dial contractility is increased and the heart rate rises. The
increase in heart rate is particularly prominent in normal in-
dividuals, and there is only a modest increase in stroke volume
(see Table 31–4 and Clinical Box 31–3). However, patients
with transplanted hearts are able to increase their cardiac out-
put during exercise in the absence of cardiac innervation
through the operation of the Frank–Starling mechanism (Figure
31–9). Circulating catecholamines also contribute. If venous
return increases and there is no change in sympathetic tone,
venous pressure rises, diastolic inflow is greater, ventricular
end-diastolic pressure increases, and the heart muscle con-
tracts more forcefully. During muscular exercise, venous re-
turn is increased by the pumping action of the muscles and the
increase in respiration (see Chapter 33). In addition, because
of vasodilation in the contracting muscles, peripheral resis-
tance and, consequently, afterload are decreased. The endCLINICAL BOX 31–3
Circulatory Changes during Exercise
The blood flow of resting skeletal muscle is low (2–4 mL/100 g/
min). When a muscle contracts, it compresses the vessels in it if
it develops more than 10% of its maximal tension; when it de-
velops more than 70% of its maximal tension, blood flow is
completely stopped. Between contractions, however, flow is so
greatly increased that blood flow per unit of time in a rhythmi-
cally contracting muscle is increased as much as 30-fold. Local
mechanisms maintaining a high blood flow in exercising mus-
cle include a fall in tissue PO 2 , a rise in tissue PCO 2 , and accumu-
lation of K+ and other vasodilator metabolites. The tempera-
ture rises in active muscle, and this further dilates the vessels.
Dilation of the arterioles and precapillary sphincters causes a
10- to 100-fold increase in the number of open capillaries. The
average distance between the blood and the active cells—and
the distance O 2 and metabolic products must diffuse—is thus
greatly decreased. The dilation increases the cross-sectional
area of the vascular bed, and the velocity of flow therefore
decreases.
The systemic cardiovascular response to exercise that pro-
vides for the additional blood flow to contracting muscle de-
pends on whether the muscle contractions are primarily iso-
metric or primarily isotonic with the performance of external
work. With the start of an isometric muscle contraction, the
heart rate rises, probably as a result of psychic stimuli acting on
the medulla oblongata. The increase is largely due to de-
creased vagal tone, although increased discharge of the car-
diac sympathetic nerves plays some role. Within a few seconds
of the onset of an isometric muscle contraction, systolic and
diastolic blood pressures rise sharply. Stroke volume changes
relatively little, and blood flow to the steadily contracting mus-
cles is reduced as a result of compression of their blood vessels.
The response to exercise involving isotonic muscle contraction
is similar in that there is a prompt increase in heart rate, but dif-
ferent in that a marked increase in stroke volume occurs. In ad-
dition, there is a net fall in total peripheral resistance due to
vasodilation in exercising muscles. Consequently, systolic
blood pressure rises only moderately, whereas diastolic pres-
sure usually remains unchanged or falls.The difference in response to isometric and isotonic exer-
cise is explained in part by the fact that the active muscles
are tonically contracted during isometric exercise and conse-
quently contribute to increased total peripheral resistance.
Cardiac output is increased during isotonic exercise to values
that may exceed 35 L/min, the amount being proportionate
to the increase in O 2 consumption. The maximal heart rate
achieved during exercise decreases with age. In children, it
rises to 200 or more beats/min; in adults it rarely exceeds 195
beats/min, and in elderly individuals the rise is even smaller.
Both at rest and at any given level of exercise, trained ath-
letes have a larger stroke volume and lower heart rate than
untrained individuals and they tend to have larger hearts.
Training increases the maximal oxygen consumption
(VO2max) that can be produced by exercise in an individual.
VO2max averages about 38 mL/kg/min in active healthy men
and about 29 mL/kg/min in active healthy women. It is lower
in sedentary individuals. VO2max is the product of maximal
cardiac output and maximal O 2 extraction by the tissues, and
both increase with training.
A great increase in venous return also takes place with ex-
ercise, although the increase in venous return is not the pri-
mary cause of the increase in cardiac output. Venous return is
increased by the activity of the muscle and thoracic pumps;
by mobilization of blood from the viscera; by increased pres-
sure transmitted through the dilated arterioles to the veins;
and by noradrenergically mediated venoconstriction, which
decreases the volume of blood in the veins. Blood mobilized
from the splanchnic area and other reservoirs may increase
the amount of blood in the arterial portion of the circulation
by as much as 30% during strenuous exercise. After exercise,
the blood pressure may transiently drop to subnormal levels,
presumably because accumulated metabolites keep the mus-
cle vessels dilated for a short period. However, the blood
pressure soon returns to the pre-exercise level. The heart rate
returns to normal more slowly.