Let's see
I know you are pretty much refering to a study such as this one in red just below
To study the fate of enterally delivered nonessential amino acids, glutamine and glutamate, 14 healthy adults were infused in the postabsorptive state with [2-15N]glutamine and [15N]glutamate for 7 h by intravenous (iv) and nasogastric (ng) tube routes. The amount of enterally delivered tracer that was sequestered by the splanchnic bed on the first pass was 54 +/- 4 and 88 +/- 2% for the [2-15N]glutamine and [15N]glutamate tracers, respectively. Only 46 and 12% of the ng glutamine and glutamate tracers entered systemic blood, respectively. The relative amount of 15N transferred from glutamate to glutamine, the transaminating amino acids leucine, isoleucine, valine, and alanine, and to proline was significantly higher when the [15N]glutamate was infused by the ng vs. iv route. The same was also true for [2-15N]glutamine, which presumably transferred 15N after it was converted to glutamate. Thus we conclude that the splanchnic bed sequesters over one-half of the glutamine and almost all of the glutamate delivered to it in the postabsorptive state. There is production of transaminating amino acids in the splanchnic bed, and the splanchnic bed produces simultaneously both glutamine from glutamate and glutamate from glutamine.
The above study does state that only half of Glutamine makes it through the splanchic bed. Which is essentially the liver/ gut mechanism, and never makes it to the actual blood stream for delivery to skeletal muscle. So what you saying is not wrong.
However, it's dependant on what you argument really is. Is it one of "Is glutamine fully absorbed and utilized to a great degree 'directly' by the barrier beyond this splanchic bed, i.e. blood stream/muscle cells" There are in fact studies that suggest that enteral glutamine extraction is for oxidation and that only a minor portion is used for gluconeogenesis. Which gluconeogenesis (essentially the biosynthesis of glucose from non carb sources) is the effect that bodybuilders desire.
If this is in fact your arguement then you have a valid point. However there is always two sides to a story. It seems that the anabolic/anti-catabolic benefits doesn't come from Glutamine in a simple singular pathway of consuming it
it following a direct single pathway and thus breaking down into smaller sub-structures for use by the skeletal tissue. If it was there could be no debate. But there is a two way street here. When the intestines is in a state of need it will utilize the skeletal muscle stores of glutamine under normal conditions. I would have to guess it's the easiest route for the intestine to take since it's sitting there probably ready to be 'turned over' anyway. However this is IMO dependant on other factors. Mostly relating to nitrogen levels from factors outside of present glutamine.
So if Glutamine is ingested via the oral route, during the process of it attempting to pass through this liver/gut barrier, It is being utilized by the gut which does infact make great use of the glutamine. Which I think you will agree with. This in turn leaves Skeletal tissue free to hold more easily it's stores of Glutamine. Which saturates the muscle 'fibers' giving users this fuller look and feel that it realized with supplementation not due to the direct biosynthesis but by the sparing effect. It's a point that is hard to argue and one that if looked at on simplier one way street terms would seem easy to argue. But thats not the action taking place here at all. This excerpt below in blue backs this up.
Supplemental L-glutamine's possible immunomodulatory role may be accounted for in a number of ways. L-glutamine appears to play a major role in protecting the integrity of the gastrointestinal tract and, in particular, the large intestine. During catabolic states, the integrity of the intestinal mucosa may be compromised with consequent increased intestinal permeability and translocation of Gram-negative bacteria from the large intestine into the body. The demand for L-glutamine by the intestine, as well as by cells such as lymphocytes, appears to be much greater than that supplied by skeletal muscle, the major storage tissue for L-glutamine. L-glutamine is the preferred respiratory fuel for enterocytes, colonocytes and lymphocytes. Therefore, supplying supplemental L-glutamine under these conditions may do a number of things. For one, it may reverse the catabolic state by sparing skeletal muscle L-glutamine. It also may inhibit translocation of Gram-negative bacteria from the large intestine. L-glutamine helps maintain secretory IgA, which functions primarily by preventing the attachment of bacteria to mucosal cells.
You would be correct to say that the "glut isn't getting past the gut" According to the above theory says it doesn't have too. It is taking the task of what the skeletal muscle would have to take on if supplemental forms of glutamine either via oral, tube feed or IV. There is obviously stores of glutamine being stored beyond this barrier that you claim can't be passed through with oral glutamine. And the reason that glutamine is typically used via IV is because the body can use it via this route easier. But it can also use it via the oral route but only by sparing the gluatmine already hanging out on the systemic blood/skeletal muscle.
I can post study references if you want. But all of the above pretty much says it doesn't really matter. That is if we are talking about "Does glutamine really have anabolic/anti-catabloic properties in an orally ingested form" Which I think is all us muscle heads really care about.... But it we are going to touch on the point that glut doesn't easily pass through the gut then I abate my point. Because it's irrelevent to our primary cause, since it's not the mecahnism that makes glut effective for us.
Sup
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