Does endogenous endothelin-1 participate in the exercise-induced
changes in distribution of blood flow of muscles in humans ?.
Maeda, Seiji, Takashi Miyauchi, Michiko Sakane, Makoto Saito, Shinichi
Maki, Katsutoshi Goto, and Mitsuo Matsuda.
Institute of Health and Sport Sciences (Se.M., Ma.S., M.M.),
Cardiovascular Division, Department of Internal Medicine, Institute
of Clinical Medicine (T.M., Mi.S., Sh.M.) and Department of
Pharmacology, Institute of Basic Medical Sciences (K.G.), University
of Tsukuba, Tsukuba, Ibaraki 305, Japan
APStracts 3:0573A, 1996.
Endothelin-1 (ET-1) is an endothelium-derived potent vasoconstrictor
peptide, which potentiates contractions to norepinephrine in human
vessels. We previously reported that the circulating plasma
concentration of ET-1 is significantly increased after exercise. To
study 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 non-working 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 non-working leg) and the femoral artery were measured
before and after exercise. The plasma ET-1 concentration in femoral
vein in the non-working leg was significantly increased after
exercise, while 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 non
-working leg but not working leg, suggesting that the production of
ET-1 was increased in the circulation of the non-working leg by
exercise. The present study also demonstrated that the plasma
norepinephrine concentrations were elevated by exercise in the
femoral veins of both working and non-working legs, suggesting that
the sympathetic nerve activity was augmented in both legs during
exercise. Therefore, the present study provides a possibility that
the increase in production of ET-1 in non-working muscles may cause
vasoconstriction and hence decrease blood flow in non-working muscles
through its direct vasoconstrictive action or an indirect effect of
ET-1 to enhance vasoconstrictions to norepinephrine, and that these
responses may be helpful in increase in blood flow in working
muscles. We propose that endogenous ET-1 contributes to the exercise
-induced redistribution of blood flow in muscles.
Received 9 August 1996; accepted in final form 27 November 1996.
APS Manuscript Number A765-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996