Effect of sustained exercise on concentrations of plasma aromatic and branched-chain amino acids and brain amines

doi:10.1016/0006-291X(86)91188-5

Biochemical and Biophysical Research Communications

Volume 137, Issue 1, 29 May 1986, Pages 149-153

https://doi.org/10.1016/0006-291X(86)91188-5 Get rights and content

Abstract

In both trained and untrained rats, exercise increased the plasma concentration ratio of aromatic amino acids to branched-chain amino acids which might favour entry of the aromatic amino acids into the brain. Exercise in trained rats did not change the brain concentration of 5-hydroxytryptamine but increased that of 5-hydroxyindole acetic acid. Exercise in the untrained rat increased the concentration of brain tryptophan and that of 5-hydroxytryptamine but that of 5-hydroxyindole acetic acid was unchanged. The increased concentration of 5-hydroxytryptamine in untrained rats might be involved in central fatigue.

References (20)

R.J. Wurtman
Lancet
(1983)
G.G. Guidotti et al.
Biochim. Biophys. Acta
(1978)
D.L. Bloxam et al.
Anal. Biochem
(1974)
I.N. Mefford
J. Neurosci. Method
(1981)
J.H. Greist et al.
Comprehensive Psychiatry
(1979)
R.H.T. Edwards
L. Hermansen et al.
Acta Physiol. Scand
(1967)
E.A. Newsholme
E. Asmussen
Med. Sci. Sports
(1979)
B. Bigland-Ritchie

There are more references available in the full text version of this article.

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Effect of sustained exercise on concentrations of plasma aromatic and branched-chain amino acids and brain amines

Abstract

Lancet

Biochim. Biophys. Acta

Anal. Biochem

J. Neurosci. Method

Comprehensive Psychiatry

Acta Physiol. Scand

Med. Sci. Sports