trained athletes), cardiac output is the factor that determines
max. With increasing workload (
), heart rate
increases progressively until it reaches a maximum. Stroke vol-
ume increases much less and tends to level off at 75 percent of
max (it actually starts to go back down in elderly people).
The major factors responsible for limiting the rise in stroke
volume and, thus, cardiac output are (1) the very rapid heart
rate, which decreases diastolic ﬁ lling time, and (2) inability of
the peripheral factors favoring venous return (skeletal muscle
pump, respiratory pump, venous vasoconstriction, arteriolar
vasodilation) to increase ventricular ﬁ lling further during the
very short time available.
max is not ﬁ xed at any given value but can
be altered by his or her habitual level of physical activity. For
example, prolonged bed rest may decrease
max by 15 to
25 percent, whereas intense, long-term physical training may
increase it by a similar amount. To be effective, the training
must be endurance-type exercise and must reach certain mini-
mal levels of duration, frequency, and intensity. For example,
jogging 20 to 30 min three times weekly at 5 to 8 mi/h deﬁ -
nitely produces a signiﬁ cant training effect in most people.
At rest, compared to values prior to training, the trained
individual has an increased stroke volume and decreased heart
rate with no change in cardiac output (see Figure 12–64). At
max, cardiac output is increased compared to pretrain-
ing values; this is due entirely to an increased maximal stroke
volume since training does not alter maximal heart rate (see
Figure 12–64). The increase in stroke volume is due to a com-
bination of (1) effects on the heart (remodeling of the ventric-
ular walls produces moderate hypertrophy and an increase in
chamber size), and (2) peripheral effects, including increased
blood volume and increases in the number of blood vessels in
skeletal muscle, which permit increased muscle blood ﬂ ow and
Training also increases the concentrations of oxidative
enzymes and mitochondria in the exercised muscles. These
changes increase the speed and efﬁ ciency of metabolic reac-
tions in the muscles and permit 200 to 300 percent increases
in exercise endurance, but they do not increase
they were not limiting it in the untrained individuals.
Aging is associated with signiﬁ cant changes in the heart’s
performance during exercise. Most striking is a decrease in the
Cardiovascular Changes During Moderate Exercise
Heart rate and stroke volume both increase, the former to a much greater extent.
Sympathetic nerve activity to the SA node increases, and parasympathetic nerve activity
Contractility increases due to increased sympathetic nerve activity to the ventricular
myocardium; increased ventricular end-diastolic volume also contributes to increased
stroke volume by the Frank-Starling mechanism.
Total peripheral resistance
Resistance in heart and skeletal muscles decreases more than resistance in other vascular
Mean arterial pressure
Cardiac output increases more than total peripheral resistance decreases.
Stroke volume and velocity of ejection of the stroke volume increase.
Filling time is decreased by the high heart rate, but the factors favoring venous return—
venoconstriction, skeletal muscle pump, and increased inspiratory movements—more
than compensate for it.
Blood ﬂ ow to heart and
Active hyperemia occurs in both vascular beds, mediated by local metabolic factors.
Blood ﬂ ow to skin
Sympathetic nerves to skin vessels are inhibited reﬂ exly by the increase in body
Blood ﬂ ow to viscera
Sympathetic nerves to the blood vessels in the abdominal organs and kidneys are
Blood ﬂ ow to brain
Autoregulation of brain arterioles maintains constant ﬂ ow despite the increased mean