1: J Nutr Biochem. 2008 Aug 15. [Epub ahead of print]
Liu TH, Wu CL, Chiang CW, Lo YW, Tseng HF, Chang CK.
No effect of short-term arginine supplementation on nitric oxide production, metabolism and performance in intermittent exercise in athletes.
Arginine supplementation has been shown to alleviate endothelial dysfunction and improve exercise performance through increasing nitric oxide production in patients with cardiopulmonary diseases. In addition, arginine supplementation could decrease accumulations of lactate and ammonia, metabolites involved in development of muscular fatigue. The aim of this study was to investigate the effect of short-term arginine supplementation on performance in intermittent anaerobic exercise and the underlying mechanism in well-trained male athletes. Ten elite male college judo athletes participated with a randomized crossover, placebo-controlled design. The subjects consumed 6 g/day arginine (ARG trial) or placebo (CON trial) for 3 days then performed an intermittent anaerobic exercise test on a cycle ergometer. Blood samples were collected before supplementation, before and during exercise and 0, 3, 6, 10, 30 and 60 min after exercise. ARG trial had significantly higher arginine concentrations than CON trial at the same time point before, during and after exercise. In both trials, nitrate and nitrite concentration was significantly higher during and 6 min after exercise comparing to the basal concentration. The increase in nitrate and nitrite concentration during exercise in both trials was parallel to the increase in plasma citrulline concentrations. There was no significant difference between the 2 trials in plasma nitrate and nitrite, lactate and ammonia concentrations and peak and average power in the exercise. The results of this study suggested that short-term arginine supplementation had no effect on nitric oxide production, lactate and ammonia metabolism and performance in intermittent anaerobic exercise in well-trained male athletes.
Int J Sport Nutr Exerc Metab. 2009 Aug;19(4):355-65.
Bescós R, Gonzalez-Haro C, Pujol P, Drobnic F, Alonso E, Santolaria ML, Ruiz O, Esteve M, Galilea P.
Effects of dietary L-arginine intake on cardiorespiratory and metabolic adaptation in athletes.
To assess the effect of diet enrichment with L-arginine or supplementation at high doses on physiological adaptation during exercise, 9 athletes followed 3 different diets, each over 3 consecutive days, with a wash-out period of 4 d between training sessions: control diet (CD), 5.5 +/- 0.3 g/d of L-arginine; Diet 1 (rich in L-arginine food), 9.0 +/- 1.1 g/d of L-arginine; and Diet 2 (the same as CD but including an oral supplement of 15 g/d), 20.5 +/- 0.3 g/d of L-arginine. Plasma nitrate levels of each participant were determined on the day after each treatment. Participants performed a submaximal treadmill test (initial speed 10-11 km/hr, work increments 1 km/hr every 4 min until 85-90% VO2max, and passive recovery periods of 2 min). Oxygen uptake and heart rate were monitored throughout the test. Blood lactate concentration ([La-]b) was determined at the end of each stage. Repeated-measures ANOVA and paired Student's t tests were used to compare the various physiological parameters between diets. The level of significance was set at p < .05. [La-]b showed a significant effect at the 5-min time point between CD and Diet 2 (CD 3.0 +/- 0.5 mM, Diet 2 2.5 +/- 0.5 mM, p = .03), but this tendency was not found at higher exercise intensities. No significant differences were observed in any of the cardiorespiratory or plasma nitrate levels. In conclusion, dietary L-arginine intake on the days preceding the test does not improve physiological parameters during exercise.
Atherosclerosis. 1995 Dec;118(2):223-31.
Wennmalm A, Edlund A, Granström EF, Wiklund O.
Acute supplementation with the nitric oxide precursor L-arginine does not improve cardiovascular performance in patients with hypercholesterolemia.
Endothelial dysfunction based on lack of nitric oxide (NO) may contribute to several settings of cardiovascular disorder. Chronic oral supplementation with the NO precursor L-arginine counteracts the development of aortic atherosclerosis in cholesterol-fed rabbits, and i.v. infusion of L-arginine may acutely improve endothelium-dependent coronary epicardial vasodilation in patients with hypercholesterolemia (HC). To clarify whether excess NO precursor may also improve general cardiovascular performance in HC, we measured working capacity indices of myocardial ischemia, and basal and post-occlusive forearm and skin blood flow in nine patients with elevated plasma cholesterol (9.1 +/- 0.2 mumol/l) following random double-blinded administration of L-arginine (16 g i.v.) or placebo. Infusion of L-arginine raised the plasma concentration of this amino acid from 85 +/- 12 to 2460 +/- 230 mumol/l but did not change the plasma level of the major NO metabolite nitrate. Maximal working capacity, indices of myocardial ischemia, and basal and post-occlusive blood flow in the skin or forearm did not differ between the treatments. The lack of positive effect of L-arginine compared to placebo indicates that excess NO precursor did not improve microvascular endothelial function in the patients, or alternatively, that the indices measured in the present study were not dependent on endothelial microvessel function. Thus, in patients with HC, deficiency of precursor for NO formation does not seem to impair either maximal exercise capacity myocardial perfusion during maximal exercise, or maximal vasodilator capacity in skeletal muscle or skin.
Circulation. 2007 Jul 10;116(2):188-95. Epub 2007 Jun 25.
Wilson AM, Harada R, Nair N, Balasubramanian N, Cooke JP.
L-arginine supplementation in peripheral arterial disease: no benefit and possible harm.
BACKGROUND: L-arginine is the precursor of endothelium-derived nitric oxide, an endogenous vasodilator. L-arginine supplementation improves vascular reactivity and functional capacity in peripheral arterial disease (PAD) in small, short-term studies. We aimed to determine the effects of long-term administration of L-arginine on vascular reactivity and functional capacity in patients with PAD. METHODS AND RESULTS: The Nitric Oxide in Peripheral Arterial Insufficiency (NO-PAIN) study was a randomized clinical trial of oral L-arginine (3 g/d) versus placebo for 6 months in 133 subjects with intermittent claudication due to PAD in a single-center setting. The primary end point was the change at 6 months in the absolute claudication distance as assessed by the Skinner-Gardner treadmill protocol. L-arginine supplementation significantly increased plasma L-arginine levels. However, measures of nitric oxide availability (including flow-mediated vasodilation, vascular compliance, plasma and urinary nitrogen oxides, and plasma citrulline formation) were reduced or not improved compared with placebo. Although absolute claudication distance improved in both L-arginine- and placebo-treated patients, the improvement in the L-arginine-treated group was significantly less than that in the placebo group (28.3% versus 11.5%; P=0.024). CONCLUSIONS: In patients with PAD, long-term administration of L-arginine does not increase nitric oxide synthesis or improve vascular reactivity. Furthermore, the expected placebo effect observed in studies of functional capacity was attenuated in the L-arginine-treated group. As opposed to its short-term administration, long-term administration of L-arginine is not useful in patients with intermittent claudication and PAD.
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04-25-2010, 05:45 AM #1
Arginine fails to elicit enhance NO production, and has no place in NO products
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Wherever progression lacks.... regress can be found in abundance.
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04-25-2010, 05:48 AM #2
SYNAPSE:
If you want [significantly enhanced NO production/vasodilation, the efficacy of nitrates is overwhelming in the clinical field, and is becoming more obvious in the exercise/bodybuilding community.
J Appl Physiol. 2009 Oct;107(4):1144-55. Epub 2009 Aug 6.
Bailey SJ, Winyard P, Vanhatalo A, Blackwell JR, Dimenna FJ, Wilkerson DP, Tarr J, Benjamin N, Jones AM.
Dietary nitrate supplementation reduces the O2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans.
Pharmacological sodium nitrate supplementation has been reported to reduce the O2 cost of submaximal exercise in humans. In this study, we hypothesized that dietary supplementation with inorganic nitrate in the form of beetroot juice (BR) would reduce the O2 cost of submaximal exercise and enhance the tolerance to high-intensity exercise. In a double-blind, placebo (PL)-controlled, crossover study, eight men (aged 19-38 yr) consumed 500 ml/day of either BR (containing 11.2 +/- 0.6 mM of nitrate) or blackcurrant cordial (as a PL, with negligible nitrate content) for 6 consecutive days and completed a series of "step" moderate-intensity and severe-intensity exercise tests on the last 3 days. On days 4-6, plasma nitrite concentration was significantly greater following dietary nitrate supplementation compared with PL (BR: 273 +/- 44 vs. PL: 140 +/- 50 nM; P < 0.05), and systolic blood pressure was significantly reduced (BR: 124 +/- 2 vs. PL: 132 +/- 5 mmHg; P < 0.01). During moderate exercise, nitrate supplementation reduced muscle fractional O2 extraction (as estimated using near-infrared spectroscopy). The gain of the increase in pulmonary O2 uptake following the onset of moderate exercise was reduced by 19% in the BR condition (BR: 8.6 +/- 0.7 vs. PL: 10.8 +/- 1.6 ml.min(-1).W(-1); P < 0.05). During severe exercise, the O2 uptake slow component was reduced (BR: 0.57 +/- 0.20 vs. PL: 0.74 +/- 0.24 l/min; P < 0.05), and the time-to-exhaustion was extended (BR: 675 +/- 203 vs. PL: 583 +/- 145 s; P < 0.05). The reduced O2 cost of exercise following increased dietary nitrate intake has important implications for our understanding of the factors that regulate mitochondrial respiration and muscle contractile energetics in humans.
Acta Physiol (Oxf). 2007 Sep;191(1):59-66. Epub 2007 Jul 17.
Larsen FJ, Weitzberg E, Lundberg JO, Ekblom B.
Effects of dietary nitrate on oxygen cost during exercise.
AIM: Nitric oxide (NO), synthesized from l-arginine by NO synthases, plays a role in adaptation to physical exercise by modulating blood flow, muscular contraction and glucose uptake and in the control of cellular respiration. Recent studies show that NO can be formed in vivo also from the reduction of inorganic nitrate (NO(3) (-)) and nitrite (NO(2) (-)). The diet constitutes a major source of nitrate, and vegetables are particularly rich in this anion. The aim of this study was to investigate if dietary nitrate had any effect on metabolic and circulatory parameters during exercise. METHOD: In a randomized double-blind placebo-controlled crossover study, we tested the effect of dietary nitrate on physiological and metabolic parameters during exercise. Nine healthy young well-trained men performed submaximal and maximal work tests on a cycle ergometer after two separate 3-day periods of dietary supplementation with sodium nitrate (0.1 mmol kg(-1) day-1) or an equal amount of sodium chloride (placebo). RESULTS: The oxygen cost at submaximal exercise was reduced after nitrate supplementation compared with placebo. On an average Vo(2) decreased from 2.98 +/- 0.57 during CON to 2.82 +/- 0.58 L min(-1) during NIT (P < 0.02) over the four lowest submaximal work rates. Gross efficiency increased from 19.7 +/- 1.6 during CON to 21.1 +/- 1.3% during NIT (P < 0.01) over the four lowest work rates. There was no difference in heart rate, lactate [Hla], ventilation (VE), VE/Vo(2) or respiratory exchange ratio between nitrate and placebo during any of the submaximal work rates. CONCLUSION: We conclude that dietary nitrate supplementation, in an amount achievable through a diet rich in vegetables, results in a lower oxygen demand during submaximal work. This highly surprising effect occurred without an accompanying increase in lactate concentration, indicating that the energy production had become more efficient. The mechanism of action needs to be clarified but a likely first step is the in vivo reduction of dietary nitrate into bioactive nitrogen oxides including nitrite and NO.~
Wherever progression lacks.... regress can be found in abundance.
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04-25-2010, 06:00 AM #3
Since exogenous nitrates have been clinically demonstrated to significantly enhance NO distribution/vasodilation, an increase in exercise-mediated glucose transport seems to be an plausible hypothesis.
Am J Physiol. 1997 Jul;273(1 Pt 1):E220-5.
Roberts CK, Barnard RJ, Scheck SH, Balon TW.
Exercise-stimulated glucose transport in skeletal muscle is nitric oxide dependent.
It has been suggested that there are separate insulin-stimulated and contraction-stimulated glucose transport pathways in skeletal muscle. This study examined the effects of nitric oxide on glucose transport in rat skeletal muscle by use of an isolated sarcolemmal membrane preparation and the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME), administered in the drinking water (1 mg/ml). Female Sprague-Dawley rats were divided into five groups: control, acute exercise, acute exercise+L-NAME, insulin stimulated, and insulin stimulated+L-NAME. Exercise (45 min of exhaustive treadmill running) increased glucose transport (37 +/- 2 to 76 +/- 5 pmol.mg-1.15 s-1) and this increase was completely inhibited by L-NAME (40 +/- 4 pmol.mg-1.15 s-1). A maximum dose of insulin increased glucose transport (87 +/- 10 pmol.mg-1.15 s-1), and adding L-NAME had no effect (87 +/- 11 pmol.mg-1.15 s-1). In addition, exercise, but not exercise+L-NAME, increased sarcolemma GLUT-4 content. This study confirms that there are separate pathways for contraction- and insulin-stimulated glucose transport. More importantly, although exercise and insulin both significantly increased glucose transport, L-NAME had no effect on insulin-stimulated glucose transport but blocked the exercise-stimulated transport. We conclude that nitric oxide is involved in the signal transduction mechanism to increase glucose transport during exercise.Last edited by NO HYPE; 04-25-2010 at 06:51 AM.
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Wherever progression lacks.... regress can be found in abundance.
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04-25-2010, 01:11 PM #4
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04-25-2010, 01:37 PM #5
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so really, arginine can enhance bloodflow through vasodilation but has no effect on NO levels?
this is what i needed to hear to settle this debate, thank you.Sci-Fit Representative
www.scifitauthentic.com
forum.scifitauthentic.com
Any views or opinions presented are those of the author and do not represent the company. Representatives of Scifit are required not to make defamatory statements and not to infringe. The company will not accept any liability in respect of such communication, and the reps responsible will be personally liable for any damages or other liability arising.-
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04-26-2010, 09:46 AM #6
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04-26-2010, 11:25 AM #7
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04-26-2010, 01:24 PM #8
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04-26-2010, 05:20 PM #9
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sorry : /
elevated levels of arginine have been proven to cause herpes outbreaks. the reason for this is that it causes vasodialation and allows the virus to be more active.
you say vasodialation is not possible because arginine does not elicit an NO increase, and i say you are wrong. respectfully of course.ZachSmash is a *******
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04-26-2010, 06:06 PM #10
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04-26-2010, 10:00 PM #11
- Join Date: Jul 2007
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you guys have seriously never heard of the arginine/n.o. pathway?!?! its a main regulatory function in the body for muscle cells, hypertension control, bp control...
your body has "no synthase", its sole purpose is to use arginine to create no.
http://journals.lww.com/cardiovascul...Pathway.2.aspx
http://www.ncbi.nlm.nih.gov/pmc/arti...01038-0308.pdf
http://content.nejm.org/cgi/content/short/329/27/2002
VVVVV
"The discovery that mammalian cells generate nitric oxide, a gas previously considered to be merely an atmospheric pollutant, is providing important information about many biologic processes. Nitric oxide is synthesized from the amino acid L-arginine by a family of enzymes, the nitric oxide synthases, through a hitherto unrecognized metabolic route -- namely, the L-arginine-nitric oxide pathway1,2,3,4,5,6,7,8. "
this is an entire book on the subject:
http://books.google.com/books?id=-G5...athway&f=falseZachSmash is a *******
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04-26-2010, 10:39 PM #12
- Join Date: Feb 2008
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Yes, I am aware of the role of arginine in nitric oxide synthesis.
http://forum.bodybuilding.com/showpo...1&postcount=13
That said, oral L-arginine supplementation has failed to augment nitric oxide production in clinical trials.Nutrition and Supp Science FAQ:
http://forum.bodybuilding.com/showthread.php?t=139153843&p=849049173&viewfull=1#post849049173
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04-27-2010, 07:38 AM #13
Agreed. Herpes viral replication occurs when the ratio of arginine to lysine, favors arginine.
Without coming across as argumentative, do you by chance have any literature that would support that notion. From what I understand, the aforementioned HSV-1 outbreaks are due to the viral growth-promoting action of arginine itself and/or to the considerably higher demand of [endogenous] arginine for L glycoproteins. I'm not so sure this is merely attributed to arginine being a precursor to nitric oxide, thereby generating excessive iNOS.
Please understand my stance. In healthy adults without a NOS dysfunction, [exogenous] arginine has no physiological impact on NOS, and thereby has no impact on vasodilation [as observed in the research]. The reason is that healthy adults have a more-than-sufficient arginine substrate pool.~
Wherever progression lacks.... regress can be found in abundance.
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04-27-2010, 07:53 AM #14
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04-27-2010, 07:57 AM #15
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04-27-2010, 09:51 AM #16
- Join Date: Jul 2007
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i was mistaken with the MOA for the arginine and herpes relationship.... my mistake!!!! that led me to assume things (stupid!)
i am going to diligently look for more specific sources. i misunderstood wha toyu were actually saying with your op an dnow i feel like an ******* (embaressed)!
so the body only utilizes the arginine that it makes on its own then? from the study you posted it looks like citruline actually causes no2?ZachSmash is a *******
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04-27-2010, 09:59 AM #17
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Those 3 studies from above though had the subjects supplementing days leading up to exercise, but not immediately prior. Are there studies that have looked at ingesting arginine as a pre-WO product, say 30 mins before testing? I think one of those studies even said they did a wash out period of several days before testing.
Back in action.
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04-27-2010, 10:30 AM #18
For nitric oxide production at least.
Originally Posted by zrenigerLast edited by NO HYPE; 04-27-2010 at 12:36 PM.
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Wherever progression lacks.... regress can be found in abundance.
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04-27-2010, 10:31 AM #19
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04-30-2010, 05:02 AM #20
So what exactly is the Arginine (I assume you mean AAKG) in No2 supps doing if not increasing No2 levels? Seems many feel it is worthless but it seems to "work" and please do not tell me it is placebo.
I think the major confusion we have here is with what No2 products are supposed to do and whether or not they do it. There is absolutely ZERO placebo effect IMHO when it comes to No2 products, this stuff gives sick pumps and at least in me, an increase in weight/reps for any given exercise. I am currently uising n02 with no stims or additives so I know its the n02. The pump is so fun that it is an extra motivation to get your ass in the gym and maybe even do more while there. Whether or not this pump and whatever else No2 products does to the end user will result in an increase in LBM is something up for debate and I can't argue one way or another with it.
One of my buddies saw me the other day at the end of my workout, I was noticeably pumped up from the workout and his said "hey I though you said you weren't going to take "anything" until next winter". By anything I think you know what he means, he also has no idea I am taking No2 so this stuff works unless placebo effects are airborne now and other guys in the gym who get a whiff of the placebo that flys in the air will imagine they are seeing things that are really not there in the physiques of others.
I can't prove it causes increases in LBM but if it gives me a better workout or what not then what is wrong with it? It is like saying pre workout supps are also a waste.Keto Legend
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04-30-2010, 07:01 AM #21
Nothing to do with enhanced NO distribution [as studies have demonstrated].
Originally Posted by J Nutr Biochem. 2008 Aug 15.
Considering the majority of pre-workout NO supplements combine an ass-load of alternative compounds, I'm not at all surprised that users "feel" something, but unless they are measuring plasma and/or serum nitrate/nitrite concentrations, VO2max/02 cost, ect., how exactly do you know [by feel] when NO distribution is enhanced via a supplement? Pumps come naturally, and in no way compare to the clinical methods used to evaluate NO distribution.~
Wherever progression lacks.... regress can be found in abundance.
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04-30-2010, 07:38 AM #22
If you read what I wrote again I was saying that many people feel it is worthless as the studies you posted back up. As far as no2 supps, I get insane pumps and stronger in various lifts on just basic no2 with no extras, I am talking about cheap ol $19.95 Body Fortress n02 from Walmart.
As per what you posted "The results of this study suggested that short-term arginine supplementation had no effect on nitric oxide "
At the end of the day I can't argue whether or not n02 supps (even just plain aakg like I take) will result in gains in LBM but I can tell you that it does effect me in the gym so if aakg has no effect on nitric oxide it still does something with regard to blood flow for sure and in some strength increases. Again I am talking about basic cheap AAKG.Keto Legend
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04-30-2010, 12:09 PM #23
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05-01-2010, 01:34 PM #24
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05-02-2010, 11:45 AM #25
Along with sufficient endogenous arginine substrate pools, I forgot to mention the arginase-mediated degradation issue.
Sufficient [endogenous] arginine substrate pools:
Proc. Natl. Acad. Sci. USA
Vol. 90, pp. 7749-7753, August 1993. Applied Biological Sciences
LETICIA CASTILLO et al.
Plasma arginine and citrulline kinetics in adults given adequate and arginine-free diets
The conversion of plasma citruiline to arginine approximated 5.5 ,umol*kg'l-hr-1 for the various groups and also was unaffected by arginine intake. Thus, endogenous arginine synthesis is not markedly responsive to acute alterations in arginine intake in healthy adults. We propose that arginine homeostasis is achieved largely via modulating arginine intake and/or the net rate of arginine degradation. http://www.pnas.org/content/90/16/7749.full.pdf
Am J Physiol. 1993 Dec;265(6 Pt 2):H1965-71.
Wu G, Meininger CJ.
Regulation of L-arginine synthesis from L-citrulline by L-glutamine in endothelial cells.
These results suggest that L-glutamine decreased L-arginine synthesis from extracellular L-citrulline by interfering with its transport. Inasmuch as nitric oxide (NO) and L-citrulline are constantly generated from L-arginine, with L-citrulline being actively converted into L-arginine in venular, microvascular, and aortic EC, our data indicate a functioning intracellular arginine-citrulline cycle in these cells. This cycle may function to efficiently scavenge the carbon and alpha-amino group of L-arginine and to maintain a sufficient cellular concentration of L-arginine during prolonged synthesis of NO in EC. http://www.ncbi.nlm.nih.gov/pubmed/8285235
American Society for Nutrition J. Nutr. 137:1602S-1609S, June 2007
Arginine Metabolism: Boundaries of Our Knowledge
Sidney M. Morris, Jr.*
In addition to the known cellular and subcellular localization of arginine within specific physical compartments, evidence has recently been obtained for at least ]2 kinetically distinct subcellular compartments/pools of arginine substrate for NOS in macro****e and endothelial cells (45,46). One pool can be depleted by exchange with extracellular lysine, but the other cannot. http://metacyc.org/META/new-image?ty...=ARGASEDEG-PWY
Arginine is subjected to extensive degradation via arginase-1, thereby diminishing the bioavailability and terminal half-life:
Br J Clin Pharmacol. 1999 March; 47(3): 261–266.
Oranee Tangphao et al.
Pharmacokinetics of intravenous and oral l-arginine in normal volunteers
Studies in humans have also demonstrated that total body arginine homeostasis is related to the rate of degradation by hepatic arginase [22]. The activity of this enzyme is directly related to the concentration of arginine substrate [23]. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014227/
MetaCyc Pathway: arginine degradation I (arginase pathway)
Arginase-mediated L-arginine degradation is widely distributed in the biosphere, and is found in all primary kingdoms [Jenkinson96]. The first step in this process, catalyzed by the enzyme arginase, is the hydrolysis of L-arginine to form L-ornithine and urea.
There are many variations of the arginase pathway, since the fate of the products of the arginase reaction may be different in different organisms. Variants of arginase-based L-arginine-degradation pathways include arginine degradation I (arginase pathway), arginine degradation VI (arginase 2 pathway), and arginine degradation VII (arginase 3 pathway). http://metacyc.org/META/new-image?ty...=ARGASEDEG-PWY~
Wherever progression lacks.... regress can be found in abundance.
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05-02-2010, 03:34 PM #26
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05-02-2010, 04:01 PM #27
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05-02-2010, 04:43 PM #28
In terms of blood flow, as I won't even get into arginine and increased LBM, the only logical hypothesis in my own opinion, is that high doses of arginine [may] be eliciting an increase in serum glucose concentrations, thereby inducing an insulin-mediated stimulation of blood flow. Either way as for myself, I took arginine and AAKG back in the day, and I never noticed any physiological benefits whatsoever. When it comes down to significantly enhanced NO distribution, nothing touches nitrates in my opinion however, I do give credit to GPLC.
If it ain't broke.... don't fix it right?~
Wherever progression lacks.... regress can be found in abundance.
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05-03-2010, 02:17 AM #29
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05-03-2010, 05:39 AM #30
I think it is good to include aakg into pre workout supps, I have no problem saying it does not increase no2 or what not, it does have some nice effects in the gym though and so does pre workout stims, neither increase LBM as far as I can see so I don't think AAKG is worthless, may be worthless for what the products claim it is supposed to do.
GlyoCarn I like, as far as nitrates I have only seen them in VPX Power Shock (bcaa's) which I have yet to purchase.Keto Legend
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