Please Scroll Down to See Forums Below
napsgear
genezapharmateuticals
domestic-supply
puritysourcelabs
Research Chemical SciencesUGFREAKeudomestic
napsgeargenezapharmateuticals domestic-supplypuritysourcelabsResearch Chemical SciencesUGFREAKeudomestic

AF Acetyl-L-Carnitine

Status
Not open for further replies.

Fonz

"Q"
Platinum
Probably one of the best pre-workout energy supplements out there are are not stimulants. Also, great for increasing alertness for exams and the such...just at a lower dosage.
3g(capped) or in a drink and you'll feel it working. Really "feel" it energize you, unlike the old L-Tyrosine.
A good analogy to use is the L-Carnitine vs Acetyl-L-Carnitine one The acetylated version is much more bio-available and a veritable panoply of better effects.

Combie created ALTyr + Green Tea + AlCar +R-ALA and there you have just quite possibly the best non-stimulative combination for energy, fat loss, and improvement of concentration that I have seen so far.

9/10... :)

I had to cap it..it tasted a bit sour......hehe
 
Fonz said:
Probably one of the best pre-workout energy supplements out there are are not stimulants. Also, great for increasing alertness for exams and the such...just at a lower dosage.
3g(capped) or in a drink and you'll feel it working. Really "feel" it energize you, unlike the old L-Tyrosine.
A good analogy to use is the L-Carnitine vs Acetyl-L-Carnitine one The acetylated version is much more bio-available and a veritable panoply of better effects.

Combie created ALTyr + Green Tea + AlCar +R-ALA and there you have just quite possibly the best non-stimulative combination for energy, fat loss, and improvement of concentration that I have seen so far.

9/10... :)

I had to cap it..it tasted a bit sour......hehe

from my position as a pharmacist i do not agree with your statements. the justification for my position is that endogenous L-carnitine only facilitates movement of fatty acids across the mitochondrial membrane, and does not instigate the movement at all. furthermore, endogenous L-carnitine is already in excess, and so adding more L-carnitine will do nothing to affect the number of bound L-carnitine molecules, nor will it change the amount of fatty acid getting across the mitocondrial membrane. supplementation of L-carnitine will only serve to increase teh number of latent, unused L-carnitine molecules within a cell.

i find that this is very much at odds with your assertation that you will "feel" the L-carnitine at rest. it is highly unlikely that anyone will "feel" an increase in the number of excell L-carnitine molecules which are not exerting any physiological effect.

L-carnitine MAY be useful in increasing the ceiling amount of fatty acid getting across the membrane in times of extreme oxidation, such as that experienced by marathon runners or ckd people, but for the most part, supplementation in the normal weight training individual is a costly exercise in frivolity and deception by supplement companies. this is especially true for most weight training individuals, who for the most part produce ATP from anaerobic means (namely the use of carbohydrates), and will be nowhere near their maximum capacity to transport fatty acid molecules across their mitochondrial membrane in any event.

in my capacity as a pharmacist rather than one of the self proclaimed "guru's" or "experts" that one finds in internet forums, i would advise people to use their hard earned money on such useful things as lap-dances (ok ok maybe on protein powder), rather than waste it on hyped up, misconstrued substances such as L-carnitine.

cheers.
 
as an afterthought, perhaps it would be a good idea for people who want to advise others (particularly new, inexperienced members) to buy certain supplements to link their advice to the full text of an unbiased study on the issue. this is particularly relevant in the case of legal supplements such as this amino acid, although may not be feasable in the case of illicit substances for which few studies have been performed.
 
J Lipid Res. 2004 Jan 1 [Epub ahead of print] Related Articles, Links


Acetyl-L-carnitine supplementation restores decreased tissue carnitine levels and impaired lipid metabolisms in aged rats.

Tanaka Y, Sasaki R, Fukui F, Waki H, Kawabata T, Okazaki M, Hasegawa K, Ando S.

The aim of this study was to evaluate the effect of long-term carnitine supplementation on age-related changes in tissue carnitine levels and in lipid metabolism. The total carnitine levels in heart, skeletal muscle, cerebral cortex and hippocampus were about 20 % less in aged rats than in young rats. On the contrary, serum carnitine levels were not affected by aging. Young and aged rats were given acetyl-L-carnitine (ALCAR, 100 mg/kg BW/day) for 3 months and sacrificed at ages of 6 and 22 months. This treatment significantly increased the tissue carnitine levels in aged rats, but had little effect on the tissue carnitine levels in young rats. Serum triacylglycerol, cholesterol and phospholipid levels were higher in aged rats than in young rats. Lipoprotein analyses revealed that triacylglycerol levels in very low density lipoprotein (VLDL), and cholesterol levels in low density lipoprotein (LDL) and in high density lipoprotein (HDL) were all significantly higher in aged rats than in young rats. Supplementation of ALCAR decreased all lipoprotein fractions and consequently the levels of triacylglycerol and cholesterol. The reduction in serum cholesterol contents in aged rats when treated with ALCAR was mainly due to a decrease of cholesteryl esters than to a decrease of free cholesterol. Another remarkable effect of ALCAR was that it decreased the cholesterol content and cholesterol/phospholipid ratio in the brain tissues of aged rats. These results indicate that chronic ALCAR supplementation reverses the age-associated changes in lipid metabolism.
 
J Neurol Sci. 2004 Mar 15;218(1-2):103-8. Related Articles, Links


Comparison of the effects of acetyl L-carnitine and amantadine for the treatment of fatigue in multiple sclerosis: results of a pilot, randomised, double-blind, crossover trial.

Tomassini V, Pozzilli C, Onesti E, Pasqualetti P, Marinelli F, Pisani A, Fieschi C.

Department of Neurological Sciences, University of Rome "La Sapienza", viale dell' Universita 30, Rome 00185, Italy.

Treatment with acetyl L-carnitine (ALCAR) has been shown to improve fatigue in patients with chronic fatigue syndrome, but there have been no trials on the effect of ALCAR for treating fatigue in multiple sclerosis (MS). To compare the efficacy of ALCAR with that of amantadine, one of the drugs most widely used to treat MS-related fatigue, 36 MS patients presenting fatigue were enrolled in a randomised, double-blind, crossover study. Patients were treated for 3 months with either amantadine (100 mg twice daily) or ALCAR (1 g twice daily). After a 3-month washout period, they crossed over to the alternative treatment for 3 months. Patients were rated at baseline and every 3 months according to the Fatigue Severity Scale (FSS), the primary endpoint of the study. Secondary outcome variables were: Fatigue Impact Scale (FIS), Beck Depression Inventory (BDI) and Social Experience Checklist (SEC). Six patients withdrew from the study because of adverse reactions (five on amantadine and one on ALCAR). Statistical analysis showed significant effects of ALCAR compared with amantadine for the Fatigue Severity Scale (p = 0.039). There were no significant effects for any of the secondary outcome variables. The results of this study show that ALCAR is better tolerated and more effective than amantadine for the treatment of MS-related fatigue
 
enhanced neural metabolism

Brain Res. 2002 Oct 4;951(2):330-5. Related Articles, Links


Effects of acetyl-L-carnitine on regional cerebral glucose metabolism in awake rats.

Ori C, Freo U, Pizzolato G, Dam M.

Department of Anesthesiology, University of Padua, Padua, Italy.

The time-course and relation to dose of regional metabolic rates for glucose (rCMRglc) were measured in awake adult Fischer-344 rats after administration of acetyl-L-carnitine (ALCAR), an agent that modulates neuronal energy processes and neurotransmitter synthesis. rCMRglc were determined with the quantitative [(14)C]2-deoxy-D-glucose technique in 50 brain regions at 10, 30 and 60 min after i.v. administration of ALCAR 500 mg/kg and at 30 min after ALCAR 250 and 700 mg/kg or coadministration of acetate (500 mg/kg) and carnitine (500 mg/kg). ALCAR resulted in significant rCMRglc increases that were maximal by 30 min; by that time, ALCAR 250 produced small, non-significant increase in rCMRglc (no region affected, mean increase 13%) and ALCAR 500 and 750 similar, larger increases in rCMRglc (eight and 11 brain regions affected, mean increases 21 and 22%, respectively). In contrast with ALCAR, carnitine plus acetate did not alter significantly rCMRglc in any brain regions, suggesting that acetate metabolism and carrier are not involved in ALCAR pharmacological activities. ALCAR increased rCMRglc more markedly in subcortical cholinergic (i.e. diagonal band, preoptic magnocellular area) and non-cholinergic (i.e. locus coeruleus, median raphe) nuclei and, to a lesser degree, in limbic and sensorimotor cortical areas. The topographic distribution of rCMRglc increases induced by ALCAR differs from those produced by cholinergic muscarinic agonists and suggest a preferential activation of nicotinic receptors.
 
perhaps more topic appropriate and "exciting"

J Nutr. 2002 Apr;132(4):636-42. Related Articles, Links


Acetyl-L-carnitine supplementation differently influences nutrient partitioning, serum leptin concentration and skeletal muscle mitochondrial respiration in young and old rats.

Iossa S, Mollica MP, Lionetti L, Crescenzo R, Botta M, Barletta A, Liverini G.

Department of General and Environmental Physiology, University of Naples Federico II, Italy I-80134.

Variations in energy balance, body composition, and nutrient partitioning induced by acetyl-L-carnitine (ALCAR) supplementation were studied in young (2 mo) and old (24 mo) Wistar rats. Changes in skeletal muscle metabolism as well as in serum free triiodothyronine and leptin levels were also evaluated. Rats were administered 0 (control) or 15 g/L ALCAR in their drinking water for 1 mo. ALCAR treatment significantly decreased body lipid percentage in young rats and significantly increased body protein percentage in old rats. The percentage of metabolizable energy (ME) intake stored as lipid was lower in ALCAR-treated young rats, whereas the percentage of ME intake stored as protein was greater in ALCAR-treated old rats compared with their age-matched controls. In addition, ALCAR supplementation significantly decreased serum leptin levels in old rats. Elevated skeletal muscle respiration was found in old rats treated with ALCAR, due to an increase in mitochondrial protein mass. In conclusion, ALCAR supplementation decreases efficiency of lipid deposition in young rats and increases efficiency of protein deposition in old rats. In addition, ALCAR supplementation partly reduces the leptin resistance that occurs in old rats, and improves ATP production in skeletal muscle mitochondria through an increase in mitochondrial protein content.
 
study 1: age related, applicability of data corresponds to age. usefulness to the athlete- questionable
study 2: multiple sclerosis dependent, useful for people with multiple sclerosis. usefulness to the athlete-poor
study 3: administration of 500mg/kg meaning an 80 kilo guy would need virtually the whole tub, usefulness for the athlete- poor
study 4: interesting, but human data would be more appropriate
 
Score one for Macro!

GoldenD, at least macro had some studies, you are discounting them with ancidotal comments, but no evidence. In fact, you never post evidence, except for your 1 DNP study from the 1930's. I have no problem with you, but you seem dead set on attacking everything that Fonz posts and I do have a problem with that. If you have PROOF, then fine post it, but with your personal vendetta against Fonz, what is really happening, is that your credibility is going down fast.

Please stop the attacking. You may think that your position as pharmacist would lend you credence and it would and did at frist, but you throw it around like we are supposed to swoon over it. News Flash - its not all that impressive anymore. You act like you are so educated, but one thing that most people also learn as the grow up is tact. You seem to have missed this lesson.

You want everyone to treat you like you are an MD - which you are not. But the think about these boards is that you dont have to be an MD to help out. We all learn from each others experience. There is no question that Fonz has gained a great deal more experience than you in this regard. And sometimes that is the most useful info that we can get.
 
Status
Not open for further replies.
Top Bottom