When muscles contract during exercise,
blood flow can increase more than 20-fold.
If muscle contraction is occurring during
whole-body exercise (e.g., running), more
than 80% of cardiac output can be directed to
the contracting muscles. Therefore, skeletal
muscle has a very large flow reserve (or capac-
ity) relative to its blood flow at rest, indicat-
ing that the vasculature in resting muscle has
a high degree of tone (see Table 7-1). This
resting tone is brought about by the interplay
between vasoconstrictor
(e.g., sympathetic
adrenergic and myogenic influences) and vas-
odilator influences (e.g., nitric oxide produc-
tion, and tissue metabolites). In the resting
state, the vasoconstrictor influences domi-
during muscle
vasodilator influences dominate to increase
oxygen delivery to the contracting muscle fib-
ers and remove metabolic waste products that
accumulate. Vasodilation of resistance vessels,
particularly the small terminal arterioles, not
only increases muscle blood flow, but also
increases the number of flowing capillaries. In
the past, some have hypothesized that muscle
capillary recruitment results from relaxation
of precapillary sphincters; however, there is
little or no direct evidence for their existence.
Instead, capillary recruitment appears to be a
consequence of altered distribution of micro-
vascular pressures brought about by arteriolar
The blood flow response to skeletal muscle
contraction depends on the type of contrac-
tion. With rhythmic or phasic contraction of
muscle (Fig. 7.14, top panel), as occurs during
normal locomotory activity, mean blood flow
increases during the period of muscle activity.
However, if blood flow is measured without
filtering or averaging the flow signal, the flow
is found to be phasic— flow decreases dur-
ing contraction and increases during relaxa-
tion phases of the muscle activity because of
mechanical compression of the vessels. In
contrast, a sustained muscle contraction (e.g.,
lifting and holding a heavy weight) decreases
mean blood flow during the period of contrac-
tion, followed by a postcontraction hyperemic
response when the contraction ceases (see
Fig. 7.14, bottom panel).
The precise mechanisms responsible for dilat-
ing skeletal muscle vasculature during contrac-
tion are not clearly understood, although many
potential vasodilator candidates have been
identified. These include increases in intersti-
tial K+ during muscle contraction, formation of
adenosine (particularly during ischemic con-
tractions), increased H+ production, endothe-
lial and skeletal muscle-derived nitric oxide
and prostaglandins, and ATP release from red
blood cells. Other candidates, although less
likely, are CO2, increased interstitial and blood
osmolarity, and inorganic phosphate. It is very
likely that multiple factors play a role and at
different times during the flow response to
muscle contraction. A nonchemical mecha-
nism that is very important in facilitating
blood flow during coordinated contractions
of groups of muscles (as occurs during nor-
mal physical activity such as running) is the
skeletal muscle pump (see Chapter 5). Regard-
less of the mechanisms involved in producing
active hyperemia, the outcome is that there
is a close correlation between the increase in
oxygen consumption and the increase in blood
flow during muscle contraction.
Skeletal muscle vasculature is innervated
ers. The norepinephrine released by these
fibers binds to a-adrenoceptors and causes
vasoconstriction. Under resting conditions,
a significant portion of the vascular tone is
generated by sympathetic activity, so that if
a resting muscle is suddenly denervated or
are blocked pharma-
cologically by a drug such as phentolamine,
blood flow will transiently increase two- to
threefold until local regulatory mechanisms
reestablish a new steady-state flow. Activation
of the sympathetic adrenergic nervous sys-
tem (e.g., baroreceptor reflex in response to
hypovolemia) can dramatically reduce blood
flow in resting muscle. When this reduction
in blood flow occurs, the muscle extracts
more oxygen
(the arterial-venous oxygen
difference increases) and activates anaerobic
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