For exercise to be sustained, it is essential that adequate blood flow
be provided to skeletal muscle. The local vascular control mechanisms
involved in regulating muscle perfusion during exercise include metab
olic control, endothelium-mediated control, propagated responses, myog
enic control, and the muscle pump. The primary determinant of muscle p
erfusion during sustained exercise is the metabolic rate of the muscle
. Metabolites from contracting muscle diffuse to resistance arterioles
and act directly to induce vasodilation, or indirectly to inhibit nor
adrenaline release from sympathetic nerve endings and oppose alpha-adr
enorecepror-mediated vasoconstriction. The vascular endothelium also r
eleases vasodilator substances (e.g., prostacyclin and nitric oxide) t
hat are prominent in establishing basal vascular tone, but these subst
ances do not appear to contribute to the exercise hyperemia in muscle.
Endothelial and smooth muscle cells may also be involved in propagati
ng vasodilator signals along arterioles to parent and daughter Vessels
. Myogenic autoregulation does not appear to be involved in the exerci
se hyperemia in muscle, but the rhythmic propulsion of blood from skel
etal muscle veins facilitates venous return to the heart and muscle pe
rfusion. It appears that the primary determinants of sustained exercis
e hyperemia in skeletal muscle are metabolic vasodilation and increase
d Vascular conductance via the muscle pump. Additionally, sympathetic
neural control is important in regulating muscle blood flow during exe
rcise.