PLCAR - Bulk Powder

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    PLCAR - Bulk Powder


    I ordered an extra 25 kilograms of PLCAR, in 100 gram containers.

    I won't mark them up much to go to Nutra, but looking at around $25 per 100 grams.

    Interest?

    /FYI, standard preworkout dose is 1-2 grams - so about 50-75 days' worth.
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    Yeah, I'd def bite on that.
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    HELL YEAH! Been waiting for PLCAR to come back in bulk for months man.
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    in.
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    Sounds good to me
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    I'm in. I've been waiting for this forever.
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    Great move.
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    Quote Originally Posted by strategicmove View Post
    Great move.
    true that
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    NICE~!

    (Quick question for dosing. How much teaspoon-wise is 1 gram? Thanks)
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    I'm hard

    err I mean.. yes.. yes im interested!
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    haha dammmm, put away 2-3 tubs for me...

    any benefits from mega dosing or stick to 2-3g?
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    PLCAR doesn’t stop after it’s created the perfect anabolic environment for Androsterone
    and 11-Alpha. PLCAR is a powerful anti-oxidant that is clinically proven to enhance the
    shuttling of fatty acids into muscle cellular mitochondria to be burned as a fuel source for
    greater energy production in skeletal, cardiac, and smooth muscles during exercise.
    This action alone prolongs an athlete’s energy levels and delays muscle fatigue onset for
    superior result-generating workouts(2). PLCAR has also shown the ability to combat the
    destructive effects on muscle tissue that low levels of oxygen induce when fatigue sets
    in(15). Finally, Carnitines such as PLCAR have even proven to have promising, positive
    effects on the human cardiovascular system!
    .
    .
    .

    Can anyone else tell me a little bit more feedback about what it is, and why it's so great since everyone seems to want it? just trying to learn a little
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    how many weeks out are we looking?
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    i want.
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    Quote Originally Posted by Ev52 View Post
    how many weeks out are we looking?
    My containers arrive Tuesday...everything else is ready to go.
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    Hmm... if it arrives at NP next week, this could take some finagling - I'm moving next week and won't have a shipping address for 5 days!
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    Depending on what time they arrive here, Nutra will have stock by Next Friday.

    Then again, they still haven't really accepted the product, so I am just assuming they will.
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    I was looking to buy some PLCAR
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    WHERE THE HELL DID YOU GET THIS STUFF????
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    Dsade sourcing Pclar 55 gallon drums! Awesome man I wanna pick up 2 or 3. Hoping I can time this order where I can get Pclar, A-yohombine, and strange ecstasy before they all sell out.
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    testofen,PLCAR and alpha Y!!
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    Finally came to your senses!


    Yeah, I'd hit that!.
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    any news?
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    Going out today...should be there Friday.
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    ETA thread worthy
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    So wait, what makes this so great???
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    Quote Originally Posted by TexasTitan View Post
    So wait, what makes this so great???
    PLCAR is a special esterified carnitine with a high affinity for cardiac and skeletal muscle tissue. It transports fatty acids directly into thes mitochondria to be used as fuel. The propionate ester is cleaved upon entry and coverted, without enrgy cost, into succinate which is a rate limiting KREBs intermediate - further enhancing energy production.

    It has profound effects on the body.
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    Here come some of the studies.

    After VB-12, looking at a Coq10 strip as well. Looks like the Krillipid Balance will have some awesome synergy here:

    1: Biofactors. 2008;32(1-4):135-44.Click here to read Links
    Positive inotropic effect of coenzyme Q10, omega-3 fatty acids and propionyl-L-carnitine on papillary muscle force-frequency responses of BIO TO-2 cardiomyopathic Syrian hamsters.
    Vargiu R, Littarru GP, Faa G, Mancinelli R.

    Dipartimento di Scienze Applicate ai Biosistemi, Sezione di Fisiologia e Nutrizione Umana, Università di Cagliari, Cagliari, Italy.

    The inability of heart muscle to generate ventricular pressure to adequately propel blood through the cardiovascular system is a primary defect associated with congestive heart failure (CHF). Force-frequency relationship (FFR) is one of the main cardiac defects associated with congestive heart failure. Thus FFR is a convenient methodological tool for evaluating the severity of muscle contractile dysfunction and the effectiveness of therapeutic agents. Papillary muscle isolated from BIO TO-2 cardiomyopathic Syrian hamsters (CMSHs), show a depressed FFR and represents an animal model of human idiopathic dilated cardiomyopathy. In the present study we investigated the effect of CoQ10, omega-3 fatty acids, propionyl-L-carnitine (PLC) and a combination of these 3 agents (formulation HS12607) on FFR in 8 month old BIO TO-2 CMSHs. Papillary muscles isolated from the anesthetized animals were placed in an incubation bath and attached to an isometric force transducer. A digital computer with an analog/digital interface allowed control of both muscle developed force and electrical stimulus parameters. Force-frequency response was evaluated, at Lmax, with increasing frequencies: 0.06, 0.12, 0.25, 0.5, 1, 2 and 4 Hz. HS12607-treatment produced a positive inotropic effect resulting in a significant enhancement (p < 0.05) of the peak force at the highest frequencies (1-4 Hz). In the range of frequency of 1-4 Hz also CoQ10 and omega-3 significantly (p < 0.05) attenuated the fractional decline in developed force. The significant improvement (p < 0.05) of the timing parameter peak rate of tension rise (+ T') and peak rate of tension fall (-T') indicating a faster rate of muscle contraction and relaxation respectively, found in CoQ10, omega-3 and PLC-treated CMSHs, may be due to the positive effects of these substances on sarcoplasmic reticulum functions. These findings suggest that naturally occurring CoQ10, omega-3 and PLC, particularly when administered together in a coformulation, might be a valid adjuvant to conventional therapy in dilated cardiomyopathy especially when considering that they are natural substances, devoid of side effects.
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    1: Drugs R D. 2008;9(2):83-91.Links
    ATP production and TCA activity are stimulated by propionyl-L-carnitine in the diabetic rat heart.
    Broderick TL.

    Department of Physiology, Midwestern University, Glendale, AZ 85308, USA. tbrode@midwestern.edu

    BACKGROUND AND OBJECTIVE: The beneficial effect of propionyl-L-carnitine (PLC) on cardiac function in diabetes mellitus is well documented. This study was designed to determine whether the improvement in cardiac function mediated by PLC in the diabetic rat heart is associated with an increase in ATP production and tricarboxylic acid (TCA) cycle activity. METHODS: Diabetes was induced by an intravenous injection of streptozotocin (60 mg/kg). Following diagnosis of diabetes, treatment was initiated by supplementing the drinking water with PLC at a concentration of 1 g/L for a period of 6 weeks. ATP production and TCA cycle activity were determined from oxidative rates of glucose and palmitate measured in isolated working hearts from control and diabetic animals. RESULTS: The effect of diabetes was associated with a decrease in heart function, expressed as rate-pressure product (RPP), and in rates of myocardial glucose oxidation. Rates of palmitate oxidation in diabetic hearts were similar to those of control hearts. In PLC-treated diabetic hearts, rates of both glucose and palmitate oxidation were increased and a significant improvement in RPP was observed. As a result, overall ATP production and TCA cycle activity from glucose and palmitate oxidation were increased in diabetic hearts. CONCLUSION: Our results indicate that the depression in RPP in the diabetic rat heart can be prevented with chronic PLC treatment. Increases in glucose and palmitate utilization with resultant increases in ATP production and TCA cycle activity may explain the benefit of PLC on diabetic rat heart function.
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    Combined with NOxidant -

    Free Radic Res. 2007 Aug;41(8):884-91.Click here to read Links
    l-carnitine and its propionate: improvement of endothelial function in SHR through superoxide dismutase-dependent mechanisms.
    de Sotomayor MA, Mingorance C, Rodriguez-Rodriguez R, Marhuenda E, Herrera MD.

    Departamento de Farmacologia, Facultad de Farmacia, Universidad de Sevilla, Seville, Spain. aldesoto@us.es

    To clarify the mechanism underlying the antioxidant properties of l-carnitine (LC) and propionyl-l-carnitine (PLC) on spontaneously hypertensive (SHR) and normotensive WKY, animals were treated with either PLC or LC (200 mg kg(- 1)). Aorta was dissected and contraction to (R)-( - )-phenylephrine (Phe) and relaxation to carbachol (CCh) were assessed in the presence or not of the NO synthase (NOS) inhibitor, l-NAME. [image omitted] production was evaluated by lucigenin-enhanced chemiluminescence and its participation on relaxation was observed after incubation with superoxide dismutase (SOD) plus catalase. Protein expressions of eNOS, Cu/Zn-SOD and Mn-SOD were studied by western blot. Both LC and PLC treatments improved endothelial function of SHR through increasing NO participation and decreasing [image omitted] probably involving higher Cu/Zn-SOD expression. PLC treatment augmented eNOS expression in SHR. Surprisingly, LC increased [image omitted] produced by aorta from WKY and thus diminished NO and damaged endothelial function. Conversely, PLC did not affect CCh-induced relaxation in WKY. These results demonstrate that LC and PLC prevent endothelial dysfunction in SHR through an antioxidant effect.
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    Not going to elaborate at this time (another product coming down the road) but add in the VB-12 to this stack:

    1: Haematologica. 2005 Dec;90(12 Suppl):ECR45.Click here to read Links
    Two newborns with nutritional vitamin B12 deficiency: challenges in newborn screening for vitamin B12 deficiency.
    Campbell CD, Ganesh J, Ficicioglu C.

    The Children's Hospital of Philadelphia, Section of Metabolism, PA 19104, USA.

    Vitamin B12 deficiency causes decreased Methionine Synthase and L-Methylmalonyl-CoA Mutase activity and results in accumulation of Homocysteine, Methylmalonic acid and Propionylcarnitine. Propionylcarnitine is included in tandem mass spectrometry-based newborn screening programs for detection of certain inborn errors of metabolism. We report two asymptomatic newborns with Vitamin B12 deficiency due to maternal deficiencies. One was detected incidentally at 3 weeks of age; the second on supplemental newborn screening based on elevated Propionylcarnitine at 2 days of age. This illustrates the potential for false negative results for Vitamin B12 deficiency screening by acylcarnitine profiling in newborn screening. Homocysteine and Methylmalonic acid may be better markers of Vitamin B12 deficiency. In conclusion, we suggest measuring Methylmalonic acid, Propionylcarnitine and Homocysteine levels in blood spots in expanded newborn screening in order to detect asymptomatic newborns with Vitamin B12 deficiency. Further studies are needed to establish the sensitivity of these three markers in screening for Vitamin B12 deficiency.
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    1: Ann N Y Acad Sci. 2004 Nov;1033:79-91.Click here to read Links
    Therapeutic effects of L-carnitine and propionyl-L-carnitine on cardiovascular diseases: a review.
    Ferrari R, Merli E, Cicchitelli G, Mele D, Fucili A, Ceconi C.

    Chair of Cardiology, University Hospital of Ferrara, Gussago (Brescia), Italy. fri@dns.unife.it

    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 after 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-carnitine 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 propionyl-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.
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    highly intriguing:

    1: Curr Med Res Opin. 2004 Sep;20(9):1377-84.Click here to read Links
    Preliminary observations on the use of propionyl-L-carnitine in combination with sildenafil in patients with erectile dysfunction and diabetes.
    Gentile V, Vicini P, Prigiotti G, Koverech A, Di Silverio F.

    Department of Urology U Bracci, University La Sapienza, Rome, Italy.

    PURPOSE: To investigate the efficacy and tolerability of oral propionyl-L-carnitine (PLC) plus sildenafil in men with erectile dysfunction (ED) and diabetes unresponsive to sildenafil monotherapy. MATERIALS AND METHODS: Patients with medically documented ED of organic or mixed aetiology and diabetes (type 1 and 2) were randomised to receive oral PLC (2 g/day) plus sildenafil (50 mg twice weekly) (20 patients, Group 1) or sildenafil alone (20 patients, Group 2), in a double-blind, fixed-dose study. All patients had been previously treated unsuccessfully with a minimum of eight administrations of sildenafil. Efficacy was evaluated using the International Index of Erectile Function (IIEF) questionnaire: total score, subscores for questions 3 (Q3; achieving an erection) and 4 (Q4; maintaining an erection) and global efficacy question (GEQ: 'Has treatment improved your erections?'). Patients Event Logs were also used. RESULTS: After 24 weeks of treatment, mean scores for IIEF Q3 and Q4 had improved significantly in patients of Group 1 (4.25 +/- 0.63 and 3.95 +/- 1.0) compared with Group 2 (2.9 +/- 0.71 and 2.7 +/- 0.96) (p < 0.01). Moreover, the percentage of patients with improved erections (GEQ 68% vs. 23%) and successful intercourse attempts (76% vs. 34%) was significantly increased in Group 1 compared with Group 2 (p < 0.01). Fourteen (70%) patients in Group 1 and four (20%) in Group 2 reported an increase in mean IIEF EF domain score of > or = 4 (p < 0.01). Treatments were well tolerated and no patient discontinued study medication. Two patients in Group 1 reported mild gastric pain.CONCLUSIONS: Salvage therapy with PLC plus sildenafil was more effective than sildenafil in the treatment of ED in patients with diabetes refractory to sildenafil monotherapy.
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    with Alpha-Burn anyone?

    Coron Artery Dis. 2004 Feb;15(1):65-71.Click here to read Links
    Improvement of cardiac function and beta-adrenergic signal transduction by propionyl L-carnitine in congestive heart failure due to myocardial infarction.
    Sethi R, Wang X, Ferrari R, Dhalla NS.

    Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre and Department of Physiology, University of Manitoba, Winnipeg, Canada.

    OBJECTIVES: Earlier studies have revealed beneficial effects of metabolic therapy in animals with congestive heart failure (CHF) due to myocardial infarction. Because heart failure is also associated with attenuated response to catecholamines, we examined the effects of propionyl L-carnitine (PLC) (a carnitine derivative) therapy on the beta-adrenoceptor (beta-AR) signal transduction in the failing heart. METHODS: Heart failure in rats was induced by occluding the coronary artery and 3 weeks later the animals were treated with or without 100 mg/kg (intraperitoneally, daily) PLC for 5 weeks. The animals were assessed for their left ventricular function and inotropic responses to isoproterenol. Crude membranes were isolated from the remote, nonischemic (viable) left ventricle and examined for changes in beta-AR and adenylyl cyclase (AC) activity. RESULTS: Animals with heart failure exhibited depressions in ventricular function, positive inotropic response to isoproterenol, beta-AR receptor density and basal AC activity; these changes were also attenuated by PLC treatment. The stimulation of AC activities with isoproterenol, 5'-guanyl imidodiphosphate, forskolin and sodium fluoride was decreased in the failing hearts and these changes were also prevented by PLC treatment. CONCLUSION: The results indicate that metabolic therapy with PLC not only attenuates the defects in heart function but also prevents changes in the beta-AR signal transduction in CHF due to myocardial infarction. Copyright 2004 Lippincott Williams & Wilkins
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    Dsade, on it as usual
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