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Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623
It has been proposed that, in skeletal muscle,
the angiogenic response to exercise may be signaled by the increase in
muscle blood flow, via biomechanical changes in the microcirculation (increased shear stress and/or wall tension). To
examine this hypothesis, we compared the change in abundance of
vascular endothelial growth factor (VEGF), basic fibroblast growth
factor (bFGF), and transforming growth
factor-
1
(TGF-1) mRNA in skeletal
muscles of the canine leg after 1 h of pump-controlled high blood flow alone (passive hyperperfusion; protocol
A) and electrical stimulation of the femoral and
sciatic nerves producing muscle contraction (protocol
B). The increase in leg blood flow (5.4- and 5.9-fold change from resting values, respectively) was similar in both groups.
Passive hyperperfusion alone did not increase message abundance for
VEGF (ratio of mRNA to 18S signals after vs. before hyperperfusion,
0.94 ± 0.08) or bFGF (1.08 ± 0.05) but slightly increased that
of TGF-1 (1.14 ± 0.07;
P < 0.03). In contrast, as
previously found in the rat, electrical stimulation provoked more than
a threefold increase in VEGF mRNA abundance (3.40 ± 1.45;
P < 0.02). However, electrical
stimulation produced no significant changes in either bFGF (1.16 ± 0.13) or TGF-1 (1.31 ± 0.27). These results suggest that the increased muscle blood flow of exercise does not account for the increased abundance of these angiogenic growth factor mRNA levels in response to acute
exercise. We speculate that other factors, such as local
hypoxia, metabolite concentration changes, or mechanical effects of
contraction per se, may be responsible for the effects of exercise.
vascular endothelial growth factor; basic fibroblast growth factor; transforming growth factor; Northern analysis
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