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BeastCook
06-03-09, 6:24 pm
hey arginine is for more vascularity right? and better pumps?

mfl5027
06-03-09, 7:37 pm
That's what supplement companies say but the science isn't conclusive and seems to be pointing more and more toward arginine being ineffective.

Here's a meta-study for reference:
http://tinyurl.com/oosb8d

On Letting Go
06-04-09, 7:08 am
Arginine is a conditionally-essential amino acid. Among other things, its said to be a pre-cursor to the synthesis of Nitric Oxide, which is a vaso-dilator.

As stated above, i dont think it's been scientifically proven to be effective.

TheDarkHalf
06-04-09, 1:53 pm
L-Arginine and L-Lysine taken together help stimulate and release of GH, but only when taken together. If you took about 2g of each together 3x a day, you'd see some good results.

Here is a study....

Acute effect of amino acid ingestion and resistance exercise on plasma growth hormone concentration in young men.

Suminski RR, Robertson RJ, Goss FL, Arslanian S, Kang J, DaSilva S, Utter AC, Metz KF.

Human Performance Laboratory, University of Houston, TX 77204, USA.

Sixteen men completed four trials at random as follows: (Trial A) performance of a single bout of resistance exercise preceded by placebo ingestion (vitamin C); (Trial B) ingestion of 1,500 mg L-arginine and 1,500 mg L-lysine , immediately followed by exercise as in Trial A; (Trial C) ingestion of amino acids as in Trial B and no exercise; (Trial D) placebo ingestion and no exercise. Growth hormone (GH) concentrations were higher at 30, 60, and 90 min during the exercise trials (A and B) compared with the resting trials (C and D) (p < .05). No differences were noted in [GH] between the exercise trials. [GH] was significantly elevated during resting conditions 60 min after amino acid ingestion compared with the placebo trial. It was concluded that ingestion of 1,500 mg arginine and 1,500 mg lysine immediately before resistance exercise does not alter exercise-induced changes in [GH] in young men. However, when the same amino acid mixture is ingested under basal conditions, the acute secretion of GH is increased.

Current Medical Research & Opinion

Vol. 7, No. 7, 1981

A. Isidori M.D. A. Lo Monaco, M.D.& M. Cappa, M.D.
Medical Clinic V. University of Rome, Rome, Italy. Received: 13th March 1981

Summary

A study was carried out in 15 male volunteers to evaluate qualitatively the secretion of growth factors following stimulation by oral amino acids. the results showed that oral administration of a combination of two amino acids (1200 mg l-lysine plus 1200 mg l-arginine pyroglutanate) provoked a release of pituitary somatotrophin & insulin. This phenomenon was reproducible & the growth hormone secreted in response to this stimulation had biological activity (as demonstrated by radiorecepter assay & somatomedin induction). The effect appeared to be specific to the combination of the two amino acids; neither of the amino acids demonstrated appreciable stimulating activity when administered alone, even at the same doses.


There is also another intersting study in whic ARG blunted the inhibitory effect of IGF-1 on GH release

Arginine counteracts the inhibitory effect of recombinant human insulin-like growth factor I on the somatotroph responsiveness to growth hormone-releasing hormone in humans.

Gianotti L, Maccario M, Lanfranco F, Ramunni J, Di Vito L, Grottoli S, Muller EE, Ghigo E, Arvat E.

Department of Internal Medicine, University of Turin, Italy.

Insulin-like growth factor I (IGF-I) exerts a negative feedback effect on GH secretion via either direct actions at the pituitary level or indirect ones at the hypothalamic level, through stimulation of somatostatin (SS) and/or inhibition of GHRH release. In fact, recombinant human IGF-I (rhIGF-I) in humans inhibits spontaneous GH secretion as well as the GH response to GHRH and even more to GH/GH-releasing peptides, whose main action is on the hypothalamus, antagonizing SS and enhancing GHRH activity. The aim of the present study was to further clarify in humans the mechanisms underlying IGF-I-induced inhibition of somatotroph secretion. In six normal young volunteers (all women; mean +/- SEM: age, 28.3+/-1.2 yr; body mass index, 21.3+/-1.2 kg/m2) we studied the GH response to GHRH (1 microg/kg, iv, at 0 min), both alone and combined with arginine (ARG; 0.5 g/kg, iv, from 0-30 min), which probably acts via inhibition of hypothalamic SS release, after pretreatment with rhIGF-I (20 microg/kg, sc, at -180 min) or placebo. rhIGF-I increased circulating IGF-I levels (peak at -60 vs. -180 min: 54.9+/-3.9 vs. 35.9+/-3.3 mmol/L; P < 0.05) to a reproducible extent, and these levels remained stable and within the normal range until 90 min. The mean GH concentration over 3 h (from -180 to 0 min) before ARG and/or GHRH was not modified by placebo or rhIGF-I. After placebo, the GH response to GHRH (peak, 23.6+/-2.9 microg/L) was strikingly enhanced (P < 0.05) by ARG coadministration (69.6+/-9.9 microg/L). rhIGF-I blunted the GH response to GHRH (13.1+/-4.5 microg/L; P < 0.05), whereas that to GHRH plus ARG was not modified (59.5+/-8.9 microg/L), although it occurred with some delay. Mean glucose and insulin concentrations were not modified by either placebo or rhIGF-I. In conclusion, ARG counteracts the inhibitory effect of rhIGF-I on somatotroph responsiveness to GHRH in humans. These findings suggest that the acute inhibitory effect of rhIGF-I on the GH response to GHRH takes place on the hypothalamus, possibly via enhancement of SS release, and that ARG overrides this action.