Get a great deal on RPN's "DCP" at the planet!
- Thread starter Trauma1
- Start date
Hank Vangut
Well-known member
Must.........resist..........
Ok, screw it. I'm getting one!
Ok, screw it. I'm getting one!
Trauma1
Legend
Must.........resist..........
Ok, screw it. I'm getting one!
LOL! - For sure my brother.
Trauma1
Legend
ooh nice deal!
Also Trauma did you get my pm i sent the other week?
I'll hit you back here in a few minutes bud.
strategicmove
Legend
Great deal! I did a series of DCP/Shred-XS Hardcore stacks a while ago, when both products were offered as a stack at NutraPlanet. Time to grab some DCP again.
Silver3CSRT8
Well-known member
Any ETA on DCP being back in stock at the planet?
prld2gr8ns
Idiot Savant
And for that matter, what about Zenquality?
dsade
NutraPlanet Fanatic
Material looks to be delivered end of the week, which means we should have stock in around 2 weeks.
Trauma1
Legend
:djparty:
john123131
Well-known member
DCP is amazing!
Silver3CSRT8
Well-known member
I actually purchased DCP at another online store. What are the thoughts on stacking it with ECA + Yohimbime?
dsade
NutraPlanet Fanatic
This is definitely an effective stack.
strategicmove
Legend
Part of the endurance effect comes from Proprionyl-L-Carnitine (PLC). This compound alone rapidly penetrates into heart, endothelial and muscle cells, triggers optimal energy metabolism in the mitochondria, and combats muscle fatigue by enhancing muscle energy stores of glycogen. The other part of the endurance enhancement comes from the synergy between PLC and the other compounds in the matrix.
dsade
NutraPlanet Fanatic
Thanks Strat...good explanation, as always.
As a bonus, the Propionyl ester is eventually cleaved from the Carnitine (after entering Mitochondria) and metabolized into succinate, a very crucial KREBS cycle intermediate and often a bottleneck to energy formation.
This step is energy neutral (does not cost any energy).
It is very much ideal for endurance enhancement, and will be a part of the new endurance formula/MMA formula coming soon.
dsade
NutraPlanet Fanatic
Biochemical profile of propionyl-L-carnitine
Journal Cardiovascular Drugs and Therapy
Biochemical profile of propionyl-L-carnitine
Willem C. Hülsmann1, 2 Contact Information
(1) Department of Biochemistry I, Erasmus Universiteit Rotterdam, The Netherlands
(2) Thorax Centre, Erasmus Universiteit Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
(3) Thorax Centre, Erasmus Universiteit, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
Summary This article briefly discusses biochemical reactions involved in the metabolism of propionate, propionylCoA, and propionyl-L-carnitine in the heart. The aim is to understand the way in which propionyl-L-carnitine can exert a protective effect on the ischemic/reperfused heart. The protection of the plasmalemma by propionyl-L-carnitine during acidosis of the heart is also discussed. One protective mechanism is based on the ability of propionate to replenish mitochondria with dicarboxylic acid intermediates of the citric acid cycle and to increase the cellular content of carnitine, both of which may stimulate the generation of energy in the postischemic reperfusion phase. Another mechanism presumes a stabilizing action of acylcarnitines upon biomembranes.
Journal Cardiovascular Drugs and Therapy
Biochemical profile of propionyl-L-carnitine
Willem C. Hülsmann1, 2 Contact Information
(1) Department of Biochemistry I, Erasmus Universiteit Rotterdam, The Netherlands
(2) Thorax Centre, Erasmus Universiteit Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
(3) Thorax Centre, Erasmus Universiteit, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
Summary This article briefly discusses biochemical reactions involved in the metabolism of propionate, propionylCoA, and propionyl-L-carnitine in the heart. The aim is to understand the way in which propionyl-L-carnitine can exert a protective effect on the ischemic/reperfused heart. The protection of the plasmalemma by propionyl-L-carnitine during acidosis of the heart is also discussed. One protective mechanism is based on the ability of propionate to replenish mitochondria with dicarboxylic acid intermediates of the citric acid cycle and to increase the cellular content of carnitine, both of which may stimulate the generation of energy in the postischemic reperfusion phase. Another mechanism presumes a stabilizing action of acylcarnitines upon biomembranes.
dsade
NutraPlanet Fanatic
1: Cardiovasc Drugs Ther. 1991 Feb;5 Suppl 1:11-5.Links
Propionyl-L-carnitine: biochemical significance and possible role in cardiac metabolism.
Siliprandi N, Di Lisa F, Menabò R.
Dipartimento di Chimica Biologica, Università di Padova, Italy.
Propionyl-CoA is formed principally during amino acid catabolism. It is then converted chiefly to succinate in a described three-step sequence. Free propionate is formed from propionyl-CoA to a very limited extent, but this anion can participate in a futile cycle of activation and hydrolysis, which can significantly deplete mitochondrial ATP. Free CoA and propionyl-CoA cannot enter or leave mitochondria, but propionyl groups are transferred between separate CoA pools by prior conversion to propionyl-L-carnitine. This reaction requires carnitine and carnitine acetyl transferase, an enzyme abundant in heart tissue. Propionyl-L-carnitine traverses both mitochondrial and cell membranes. Within the cell, this mobility helps to maintain the mitochondrial acyl-CoA/CoA ratio. When this ratio is increased, as in carnitine deficiency states, deleterious consequences ensue, which include deficient metabolism of fatty acids and urea synthesis. From outside the cell (in blood plasma), propionyl-L-carnitine can either be excreted in the urine or redistributed by entering other tissues. This process apparently occurs-without prior hydrolysis and reformation. It is suggested that heart tissue utilizes such exogenous propionyl-L-carnitine to stimulate the tricarboxylic acid cycle (via succinate synthesis) and that this may explain its known protective effect against ischemia.
Propionyl-L-carnitine: biochemical significance and possible role in cardiac metabolism.
Siliprandi N, Di Lisa F, Menabò R.
Dipartimento di Chimica Biologica, Università di Padova, Italy.
Propionyl-CoA is formed principally during amino acid catabolism. It is then converted chiefly to succinate in a described three-step sequence. Free propionate is formed from propionyl-CoA to a very limited extent, but this anion can participate in a futile cycle of activation and hydrolysis, which can significantly deplete mitochondrial ATP. Free CoA and propionyl-CoA cannot enter or leave mitochondria, but propionyl groups are transferred between separate CoA pools by prior conversion to propionyl-L-carnitine. This reaction requires carnitine and carnitine acetyl transferase, an enzyme abundant in heart tissue. Propionyl-L-carnitine traverses both mitochondrial and cell membranes. Within the cell, this mobility helps to maintain the mitochondrial acyl-CoA/CoA ratio. When this ratio is increased, as in carnitine deficiency states, deleterious consequences ensue, which include deficient metabolism of fatty acids and urea synthesis. From outside the cell (in blood plasma), propionyl-L-carnitine can either be excreted in the urine or redistributed by entering other tissues. This process apparently occurs-without prior hydrolysis and reformation. It is suggested that heart tissue utilizes such exogenous propionyl-L-carnitine to stimulate the tricarboxylic acid cycle (via succinate synthesis) and that this may explain its known protective effect against ischemia.
dsade
NutraPlanet Fanatic
and a fantastic summary of why PLCAR is, indeed, the ****.
Titre du document / Document title
Therapeutic effects of L-carnitine and propionyl-L-carnitine on cardiovascular diseases: A review
Auteur(s) / Author(s)
FERRARI Roberto ; MERLI E. ; CICCHITELLI G. ; MELE D. ; FUCILI A. ; CECONI C. ;
Résumé / Abstract
Several experimental studies have shown that levocarnitine reduces myocardial injury after ischemia and reperfusion by counteracting the toxic effect of high levels of free fatty acids, which occur in ischemia, and by improving carbohydrate metabolism. In addition to increasing the rate of fatty acid transport into mitochondria, levocarnitine reduces the intramitochondrial ratio of acetyl-CoA to free CoA, thus stimulating the activity of pyruvate dehydrogenase and increasing the oxidation of pyruvate. Supplementation of the myocardium with levocarnitine results in an increased tissue carnitine content, a prevention of the loss of high-energy phosphate stores, ischemic injury, and improved heart recovery on reperfusion. Clinically, levocarnitine has been shown to have anti-ischemic properties. In small short-term studies, levocarnitine acts as an antianginal agent that reduces ST segment depression and left ventricular end-diastolic pressure. These short-term studies also show that levocarnitine releases the lactate of coronary artery disease patients subjected to either exercise testing or atrial pacing. These cardioprotective effects have been confirmed during aortocoronary bypass grafting and acute myocardial infarction. In a randomized multicenter trial performed on 472 patients, levocarnitine treatment (9 g/day by intravenous infusion for 5 initial days and 6 g/day orally for the next 12 months), when initiated early after acute myocardial infarction, attenuated left ventricular dilatation and prevented ventricular remodeling. In treated patients, there was a trend towards a reduction in the combined incidence of death and CHF alter discharge. Levocarnitine could improve ischemia and reperfusion by (1) preventing the accumulation of long-chain acyl-CoA, which facilitates the production of free radicals by damaged mitochondria; (2) improving repair mechanisms for oxidative-induced damage to membrane phospholipids; (3) inhibiting malignancy arrhythmias because of accumulation within the myocardium of long-chain acyl-CoA; and (4) reducing the ischemia-induced apoptosis and the consequent remodeling of the left ventricle. Propionyl-L-camitine is a carnitine derivative that has a high affinity for muscular carnitine transferase, and it increases cellular carnitine content, thereby allowing free fatty acid transport into the mitochondria. Moreover, propionyl-L-carnitine stimulates a better efficiency of the Krebs cycle during hypoxia by providing it with a very easily usable substrate, propionate, which is rapidly transformed into succinate without energy consumption (anaplerotic pathway). Alone, propionate cannot be administered to patients in view of its toxicity. The results of phase-2 studies in chronic heart failure patients showed that long-term oral treatment with proplonyl-L-carnitine improves maximum exercise duration and maximum oxygen consumption over placebo and indicated a specific propionyl-L-carnitine effect on peripheral muscle metabolism. A multicenter trial on 537 patients showed that propionyl-L-carnitine improves exercise capacity in patients with heart failure, but preserved cardiac function.
Titre du document / Document title
Therapeutic effects of L-carnitine and propionyl-L-carnitine on cardiovascular diseases: A review
Auteur(s) / Author(s)
FERRARI Roberto ; MERLI E. ; CICCHITELLI G. ; MELE D. ; FUCILI A. ; CECONI C. ;
Résumé / Abstract
Several experimental studies have shown that levocarnitine reduces myocardial injury after ischemia and reperfusion by counteracting the toxic effect of high levels of free fatty acids, which occur in ischemia, and by improving carbohydrate metabolism. In addition to increasing the rate of fatty acid transport into mitochondria, levocarnitine reduces the intramitochondrial ratio of acetyl-CoA to free CoA, thus stimulating the activity of pyruvate dehydrogenase and increasing the oxidation of pyruvate. Supplementation of the myocardium with levocarnitine results in an increased tissue carnitine content, a prevention of the loss of high-energy phosphate stores, ischemic injury, and improved heart recovery on reperfusion. Clinically, levocarnitine has been shown to have anti-ischemic properties. In small short-term studies, levocarnitine acts as an antianginal agent that reduces ST segment depression and left ventricular end-diastolic pressure. These short-term studies also show that levocarnitine releases the lactate of coronary artery disease patients subjected to either exercise testing or atrial pacing. These cardioprotective effects have been confirmed during aortocoronary bypass grafting and acute myocardial infarction. In a randomized multicenter trial performed on 472 patients, levocarnitine treatment (9 g/day by intravenous infusion for 5 initial days and 6 g/day orally for the next 12 months), when initiated early after acute myocardial infarction, attenuated left ventricular dilatation and prevented ventricular remodeling. In treated patients, there was a trend towards a reduction in the combined incidence of death and CHF alter discharge. Levocarnitine could improve ischemia and reperfusion by (1) preventing the accumulation of long-chain acyl-CoA, which facilitates the production of free radicals by damaged mitochondria; (2) improving repair mechanisms for oxidative-induced damage to membrane phospholipids; (3) inhibiting malignancy arrhythmias because of accumulation within the myocardium of long-chain acyl-CoA; and (4) reducing the ischemia-induced apoptosis and the consequent remodeling of the left ventricle. Propionyl-L-camitine is a carnitine derivative that has a high affinity for muscular carnitine transferase, and it increases cellular carnitine content, thereby allowing free fatty acid transport into the mitochondria. Moreover, propionyl-L-carnitine stimulates a better efficiency of the Krebs cycle during hypoxia by providing it with a very easily usable substrate, propionate, which is rapidly transformed into succinate without energy consumption (anaplerotic pathway). Alone, propionate cannot be administered to patients in view of its toxicity. The results of phase-2 studies in chronic heart failure patients showed that long-term oral treatment with proplonyl-L-carnitine improves maximum exercise duration and maximum oxygen consumption over placebo and indicated a specific propionyl-L-carnitine effect on peripheral muscle metabolism. A multicenter trial on 537 patients showed that propionyl-L-carnitine improves exercise capacity in patients with heart failure, but preserved cardiac function.
strategicmove
Legend
A propionyl carnitine ester plus glycine?
dsade
NutraPlanet Fanatic
No...I find the GPLC to be inferior to straight PLCAR.
nunes
Well-known member
SM do you agree with this claims made by AX :
Propionyl L-Carnitine (PLCAR) is an esterified Carnitine that has demonstrated a unique ability to dramatically increase the number of androgen receptors on the muscle cell surface, and to keep androgen receptors up-regulated while on cycle. The more androgen receptors you have, the more muscle mass you can ultimately signal to grow!
Is there any study that prove this claims?
why?
dsade
NutraPlanet Fanatic
There are studies done on various carnitine esters, which seem to have similar MOA - though the study cited used L-Carnitine-L-Tartarate, IIRC, I do believe the same holds for PLCAR - especially given its affinity for skeletal muscle.
One reason:
1: Int J Sport Nutr Exerc Metab. 2008 Feb;18(1):19-36.Links
Effect of glycine propionyl-L-carnitine on aerobic and anaerobic exercise performance.
Smith WA, Fry AC, Tschume LC, Bloomer RJ.
Dept. of Health and Sport Sciences, University of Memphis, Memphis, TN 38152, USA.
The purpose of this study was to evaluate the effect of glycine propionyl-L-carnitine (GPLC) supplementation and endurance training for 8 wk on aerobic- and anaerobic-exercise performance in healthy men and women (age 18-44 yr). Participants were randomly assigned to 1 of 3 groups: placebo (n=9), 1 g/d GPLC (n=11), or 3 g/d GPLC (n=12), in a double-blind fashion. Muscle carnitine (vastus lateralis), VO(2peak), exercise time to fatigue, anaerobic threshold, anaerobic power, and total work were measured at baseline and after an 8-wk aerobic-training program. There were no statistical differences (p> .05) between or within the 3 groups for any performance-related variable or muscle carnitine concentrations after 8 wk of supplementation and training. These results suggest that up to 3 g/d GPLC for 8 wk in conjunction with aerobic-exercise training is ineffective for increasing muscle carnitine content and has no significant effects on aerobic- or anaerobic-exercise performance.
nunes
Well-known member
interesting, but I think that gplc is not a useless sup:
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dsade
NutraPlanet Fanatic
Oh, don't get me wrong - I don't think it is useless at all. Just in an endurance capacity and compared to PLCAR, I find PLCAR to be superior.
Silver3CSRT8
Well-known member
Man, you guys have completely lost me.:wtf: All I want to know is will this help me lose these last stubborn belly fat. I work out with heavy weights and cardio for 30 minutes at least 4 times a week. Is this going to give me what I need to encourage the final lbs to melt off?
Trauma1
Legend
I think it's an excellent foundation for a stack that can achieve that for certain.
I would encourage a 3-4 tablet dosing 45 minutes prior to your cardio workout. This will encourage a higher degree of fatty acid oxidized energy providing for more endurance while getting rid of that stubborn last few pounds.
Silver3CSRT8
Well-known member
Thx for the feedback. Just kidding about the technical discussion. Now I know how my wife feels when I start talking computers with people.
strategicmove
Legend
I know this is a benefit usually associated with L-Carnitine-L-Tartrate supplementation. I do not know if PLCAR can elicit this effect.
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