x_muscle said:
BC.
do u know anything about prostaglandin E1 (PGE1), i heard it effects the skeletal muscle. there is a research company that sells it. do you how it will effect the body?
Dunno the brand I have, its not lutalyse, couldn't find that. Think its called prostine or something. I have yet to receive it, so we will see. Its intended for human use though. If you know more, feel free to let me know.
On PGE1 and skeletal muscle, not much, its mostly a vascular factor. Did find this though :
Klin Wochenschr. 1990 Apr 2;68(7):380-3.
[Effect of prostaglandin E1 on amino acid metabolism of human skeletal muscle]
Stiegler H, Wicklmayr M, Rett K, Mehnert H.
III. Medizinische Abteilung des Stadtischen Krankenhauses Munchen Schwabing.
The influence of an intraarterial infusion of PGE1 on the amino acid metabolism of human skeletal muscle was examined in healthy volunteers using the forearm technique. A continuous increase of perfusion from 2.9 +/- 0.1 ml/100 g x min to 5.4 +/- 1.5 after 60 min could be observed. Muscular amino acid balances were not changed after 30 min but significantly after 60 min of PGE1 infusion. Muscular release of most of the amino acids was reduced or shifted to an uptake. The accumulated balance of the amino acids showed a significant increase from -21.9 to +33.2 nmol/100 g x min after 60 min. Thus the infusion of PGE1 led to an inhibition of muscular proteolysis and/or to a stimulation of proteosynthesis. In view of the fact that kinines are released during exercise and are partially effective via prostaglandine liberation, the protein-anabolic effect of exercise might be explained by action of prostaglandins.
Vasa Suppl. 1989;28:14-8.
Metabolic effects of prostaglandin E1 on human skeletal muscle with special regard to the amino acid metabolism.
Stiegler H, Rett K, Wicklmayr M, Mehnert H.
The influence of intra-arterial (i.a.) prostaglandin E1 (PGE1) on the metabolism of amino acids, glucose and free fatty acids in healthy volunteers was determined by means of the forearm technique. The continuous increase of perfusion from baseline 2.9 +/- 0.1 ml/100 g x min to 5.4 +/- 1.5 after 60 minutes of PGE1 infusion, indicates an increase of basal glucose utilisation from 0.51 +/- 0.11 to 2.5 +/- 0.36 mumol/100 g x min via and additional raised glucose extraction rate. Furthermore, PGE1 resulted in a cessation of the basal muscular glycerol production and led to a change from a basal production of free fatty acids to a net absorption into the muscle. This change from an oxidation of free fatty acids to glucose results in an improved energetic gain of 0.72 mol ATP/mol 02. Baseline values showed a release of most amino acids which, after PGE1 decreased significantly or even changed to an intake. The overall balance of all amino acids changed from baseline -27.9 (i.e. release) to +33.2 nmol/100 x min (i.e. intake). This indicates an inhibition of muscular proteolyses and/or a stimulation of protein synthesis under i.a. PGE1. This additional metabolic effect of PGE1 might be an explanation as to why agents with purely vasodilating actions did not prove therapeutically effective in the treatment of peripheral arterial disease in the past.
Possibly mediated by its vascular effects, but it appears PGE1 does have minor anti-catabolic activity.