protein + creatin + vanadyl

[jimmy.klitschi]

hi leute!

ich wollte fragen wie man das am besten einnimmt:

also ich nehme 2x vanadyl tabs am morgen + creatin mit wasser...

nun möchte ich dazu aber auch noch protein nehmen... nur wann darf man es verwenden da ja das creatin sich nicht mit milch verträgt..

bitte helft mir!

Danke im Vorraus

mfg Kevin

Die Milch sollte hinsichtlich Crea sowieso kein Problem sein, zumindest wenn du entrahmte, fettarme Milch oder eben statt Milch ganz simpel Wasser nimmst.

Das mit dem Vanadyl würde ich mir an deiner Stelle noch mal überlegen. Es wirkt insulinähnlich auf Kohlenhydrate, Fett (was wir nicht unbedingt wollen) und evtl. auch auf Creatin.
Aber: Es wird diskutiert, dass es auf Aminosäuren eher gegenteilige Wirkung (Verminderung der Einschleusung!) ausübt.
Warum bleibst du nicht bei dem altbewährten PostWorkoutShake mit Molkeprotein/kurzkettigen KH/Creatin?

Gruß

Kopiere im Folgenden mal noch was rein, was rantanplan vor einiger Zeit zum Thema "Vanadyl" geschrieben hat:

-->

Zitat:
Und warum soll es nicht wie Insulin eine Verbesserung der Proteinsynthese zur Folge haben?

Weil Vanadyl nur bezüglich des Kohlehydrat- und Fettstoffwechsels eine insulinähnliche Wirkung hat. Im Proteinstoffwechsel wirkt Vanadyl anders als Insulin, folglich hat es auch keine positive Wirkung auf die Proteinsynthese (im Gegenteil: wie schon gesagt, scheint Vanadyl Sulfat wahrscheinlich sogar eine negative Wirkung auf die Proteinsynthese auszuüben).

Bsp.:


Zitat:
Biochem J. 1985 Nov 15;232(1):273-6.

Selectivity of the insulin-like actions of vanadate on glucose and protein metabolism in skeletal muscle.

Clark AS, Fagan JM, Mitch WE.

To determine if vanadate has insulin-like actions in skeletal muscle, we measured its effects on glucose and protein metabolism in epitrochlearis muscles of rats. Compared with insulin, vanadate increased glucose uptake, glycogen synthesis and glycolysis to a lesser degree, but caused a greater stimulation of lactate and glucose oxidation. Unlike insulin, vanadate did not change either protein synthesis or degradation. These different metabolic responses could be related to the different pattern of insulin-receptor phosphorylation caused by insulin and vanadate.




Zitat:
Am J Physiol. 1997 Jan;272(1 Pt 1):C156-62.

Insulin-mimetic agents vanadate and pervanadate stimulate glucose but inhibit amino acid uptake.

Tsiani E, Abdullah N, Fantus IG.

Department of Medicine, Mount Sinai Hospital, Toronto, Ontario, Canada.

The protein tyrosine phosphatase (PTP) inhibitors vanadate and pervanadate (pV) exert insulin-like biologic effects. In cultured differentiated rat L6 skeletal muscle cells, vanadate and pV stimulated 2-deoxy-D-[3H]glucose uptake in a dose- and time-dependent manner. There was no increase in maximum stimulation by additional insulin. In contrast, whereas insulin stimulated [14C]methylaminoisobutyric acid (MeAIB) uptake, basal uptake was inhibited by vanadate and pV. Insulin-stimulated MeAIB uptake was also inhibited in a dose-dependent manner and completely abolished by 5 mM vanadate or 0.1 mM pV. The inhibitory effect on basal MeAIB uptake was associated with a decrease in transporter affinity and a small decrease in maximum transport capacity, whereas the insulin-stimulated increase in maximum transport capacity was completely inhibited. Inhibition of MeAIB uptake by vanadate and pV was not blocked by cycloheximide, and oubain did not inhibit uptake. Vanadate also inhibited amino acid deprivation-stimulated MeAIB uptake. Insulin-stimulated MeAIB uptake was also inhibited in rat hepatoma cells. Thus vanadate and pV mimic insulin to stimulate glucose uptake but inhibit system A amino acid uptake. The relative inhibitory concentrations of vanadate and pV suggest that the mechanism may involve PTP inhibition.



Zitat:
Eur J Biochem. 2001 Apr;268(8):2308-14.

Growth factor-stimulated protein synthesis is inhibited by sodium orthovanadate.

Vinals F, McKenzie FR, Pouyssegur J.

Institute of Signaling, Developmental Biology and Cancer Research, Nice, France. fvinals@bell.ub.es

The study of intracellular signaling pathways has been aided by the use of sodium orthovanadate, a cell-permeable inhibitor of tyrosine phosphatases. However, long-term addition of sodium orthovanadate is often cytotoxic. In this study we demonstrate that the growth factor-mediated increase in the rate of protein synthesis was inhibited by sodium orthovanadate. This effect of sodium orthovanadate was dose-dependent, with an IC50 of 40 microM and maximal inhibition obtained at 100 microM. As a consequence, the fetal bovine serum-mediated induction of the immediate-early genes, c-Fos and MKP-1, at the protein level was inhibited by orthovanadate. Orthovanadate's ability to attenuate protein synthesis was partially reversible, and was no longer evident when the agent was added 6 h after addition of growth factor to cells. Analysis of several elements of signaling pathways which are known to regulate protein synthesis in a positive manner (p42/p44 MAPK, AKT and p70 S6K stimulation, and hyperphosphorylation of PHAS-I) were not inhibited but rather were stimulated by orthovanadate. Thus, sodium orthovanadate is a potent inhibitor of growth factor-stimulated protein synthesis independent of p42/p44 MAPK or PI3K-p70 S6K activation.