"The only time I have seen it work was when used by IV
route in hospitals.
It gets destroyed by the stomach acids. "
That's news to me. Admittedley a large proportion of it gets taken up by gut endothelium, but the rest of it certainly does get absorbed in 'normal' folks:
Nutrition 2002 May;18(5):367-70
Impact of oral L-glutamine on glutathione, glutamine, and glutamate blood levels in volunteers.
OBJECTIVE: We investigated the effect of glutamine supplementation on plasma glutamine (Gln), glutamate (Glu), and whole-blood
glutathione (GSH) concentrations in human volunteers. METHODS: Subjects first adapted to a standard diet with known intakes of
protein, total GSH, cysteine, methionine, and total Glu (Glu values include Glu and Gln) for 3 d. Plasma Gln, Glu, and whole-blood
GSH levels were then measured at 4-h intervals over 24 h. Supplemental oral Gln (0.3 g x kg(-1) x d(-1)) was ingested for 10 d and
then 24-h plasma levels of Gln, Glu, and whole-blood GSH were measured. RESULTS: The plasma concentrations of Glu (116%; P
= 0.006) and Gln (20%; P = 0.046) were significantly higher, whereas concentrations of GSH were significantly lower (37%; P =
0.00091) after oral Gln supplementation. CONCLUSION: Oral Gln increases Glu and Gln levels in plasma of healthy subjects but
does not increase GSH red cell (whole-blood) levels. Thus, GSH biosynthesis and preservation of GHS stores in red blood cells may
involve rate-limiting substrates other than Gln.
Nutrition 2002 Mar;18(3):222-4
Glutamine: an anaplerotic precursor.
There is an up to four-fold increase in the concentration of the tricarboxylic acid (TCA) cycle intermediates at the start of exercise. The
rate of TCA cycle flux and, hence, oxidative metabolism may be limited by the concentration of the intermediates in the cycle. The
dramatic decline in intramuscular glutamate at the start of exercise, in tandem with increased intramuscular alanine, suggests that
glutamate is an important anaplerotic precursor. We hypothesized that oral glutamine might enhance the exercise-induced TCA cycle
intermediate pool expansion. Indeed, a greater increase in the sum of muscle citrate, malate, fumarate, and succinate concentrations
(approximately 85% total TCA intermediate pool) occurred at the start of exercise after ingestion of glutamine rather than of placebo
or ornithine alpha-ketoglutarate.
And etc..........
However, this appears to have little impact on muscle growth or recovery unless there is a deficiency of glutamine to begin with, and frankly, most bodybuilders eat soooo much protein anyway that it's a non-issue IMHO (thus the lack of results on the anabolic board). Severe dieting with heavy training and cardio is a different matter.
For instance:
Br J Sports Med 1998 Mar;32(1):25-32;
Contrasting plasma free amino acid patterns in elite athletes: association with fatigue and infection.
AIM: There is little information on the plasma free amino acid patterns of elite athletes against which fatigue and nutrition can be
considered. Therefore the aim was to include analysis of this pattern in the medical screening of elite athletes during both especially
intense and light training periods. METHODS: Plasma amino acid analysis was undertaken in three situations. (1) A medical screening
service was offered to elite athletes during an intense training period before the 1992 Olympics. Screening included a blood
haematological/biochemical profile and a microbial screen in athletes who presented with infection. The athletes were divided into three
groups who differed in training fatigue and were considered separately. Group A (21 track and field athletes) had no lasting fatigue;
group B (12 judo competitors) reported heavy fatigue at night but recovered overnight to continue training; group C (18 track and field
athletes, one rower) had chronic fatigue and had been unable to train normally for at least several weeks. (2) Athletes from each group
were further screened during a post-Olympic light training period. (3) Athletes who still had low amino acid levels during the light
training period were reanalysed after three weeks of additional protein intake. RESULTS: (1) The pre-Olympics amino acid patterns
were as follows. Group A had a normal amino acid pattern (glutamine 554 (25.2) micromol/l, histidine 79 (6.1) micromol/l, total amino
acids 2839 (92.1) micromol/l); all results are means (SEM). By comparison, both groups B and C had decreased plasma glutamine
(average 33%; p<0.001) with, especially in group B, decreased histidine, glucogenic, ketogenic, and branched chain amino acids
(p<0.05 to p<0.001). None in group A, one in group B, but ten athletes in group C presented with infection: all 11 athletes had plasma
glutamine levels of less than 450 micromol/l. No intergroup differences in haematological or other blood biochemical parameters, apart
from a lower plasma creatine kinase activity in group C than in group B (p<0.05) and a low neutrophil to lymphocyte ratio in the
athletes with viral infections (1.2 (0.17)), were found. (2) During post-Olympic light training, group A showed no significant amino acid
changes. In contrast, group B recovered normal amino acid levels (glutamine 528 (41.4) micromol/l, histidine 76 (5.3) micromol/l, and
total amino acids 2772 (165) micromol/l) (p<0.05 to p<0.001) to give a pattern comparable with that of group A, whereas, in group
C, valine and threonine had increased (p<0.05), but glutamine (441 (24.5) micromol/l) and histidine (58 (5.3) micromol/l) remained
low. Thus none in group A, two in group B, but ten (53%) in group C still had plasma glutamine levels below 450 micromol/l, including
eight of the 11 athletes who had presented with infection. (3) With the additional protein intake, virtually all persisting low glutamine
levels increased to above 500 micromol/l. Plasma glutamine rose to 592 (35.1) micromol/l and histidine to 86 (6.0) micromol/l. Total
amino acids increased to 2761 (128) micromol/l (p<0.05 to p<0.001) and the amino acid pattern normalised. Six of the ten athletes on
this protein intake returned to increased training within the three weeks. CONCLUSION: Analysis of these results provided
contrasting plasma amino acid patterns: (a) a normal pattern in those without lasting fatigue; (b) marked but temporary changes in those
with acute fatigue; (c) a persistent decrease in plasma amino acids, mainly glutamine, in those with chronic fatigue and infection, for
which an inadequate protein intake appeared to be a factor.
Also, would it be better to take the glutamine all at once or split it in half during the day or doesn't it matter?
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