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1 Institute of Health and Sport
Sciences, 2 Cardiovascular
Division,
Received 9 August 1996; accepted in final form 27 November 1996.
Maeda, Seiji, Takashi Miyauchi, Michiko Sakane, Makoto
Saito, Shinichi Maki, Katsutoshi Goto, and Mitsuo Matsuda. Does endothelin-1 participate in the exercise-induced changes of blood flow
distribution of muscles in humans? J. Appl.
Physiol. 82(4): 1107-1111, 1997.
one-leg cycle ergometer exercise; working and nonworking muscles ; arteriovenous difference in endothelin-1 concentration; skeletal
muscles; redistribution of blood flow
Endothelin-1
(ET-1) is an endothelium-derived potent vasoconstrictor peptide that
potentiates contractions to norepinephrine in human vessels. We
previously reported that the circulating plasma concentration of ET-1
is significantly increased after exercise (S. Maeda, T. Miyauchi, K. Goto, and M. Matsuda. J. Appl.
Physiol. 77: 1399-1402, 1994). To
study the roles of ET-1 during and after exercise, we investigated
whether endurance exercise affects the production of ET-1 in the
circulation of working muscles and nonworking muscles. Male athletes
performed one-leg cycle ergometer exercise of 30-min duration at
intensity of 110% of their individual ventilatory threshold. Plasma
concentrations of ET-1 in both sides of femoral veins (veins in the
working leg and nonworking leg) and in the femoral artery (artery in
the nonworking leg) were measured before and after
exercise. The plasma ET-1 concentration in the femoral
vein in the nonworking leg was significantly increased after exercise,
whereas that in femoral vein in the working leg was not changed. The
arteriovenous difference in ET-1 concentration was significantly
increased after exercise in the circulation of the nonworking leg but
not of the working leg, which suggests that the production of ET-1 was
increased in the circulation of the nonworking leg by exercise. The
present study also demonstrated that the plasma norepinephrine
concentrations were elevated by exercise in the femoral veins of both
the working and nonworking legs, suggesting that the sympathetic nerve
activity was augmented in both legs during exercise. Therefore, the
present study demonstrates the possibility that the increase in
production of ET-1 in nonworking muscles may cause vasoconstriction and
hence decrease blood flow in nonworking muscles through its direct
vasoconstrictive action or through an indirect effect of ET-1 to
enhance vasoconstrictions to norepinephrine and that these responses
may be helpful in increasing blood flow in working
muscles. We propose that endogenous ET-1 contributes to
the exercise-induced redistribution of blood flow in muscles.
0161-7567/97 $5.00
Copyright © 1997 the American Physiological Society
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