ALA bad for Bodybuilding???

[macrophage69alpha]

The whole basis for the increased cellular glucose uptake caused by ALA is due to its pro-oxidant action, this is what you are saying makes rALA so effective:

"alpha-Lipoic acid was recently shown to stimulate glucose uptake into 3T3-L1 adipocytes by increasing intracellular oxidant levels and/or facilitating insulin receptor autophosphorylation presumably by oxidation of critical thiol groups present in the insulin receptor beta-subunit"

This pro-oxidant action is what is causing the decrease in glycogen synthase, as the earlier abstract described.

I definitely wouldn't take it pre or post workout.

re-read what you quoted.. it says no such thing..
once again tire of the sad ala and r-ala bashing.. must be those amazing placebo effects that cause the pumps

btw- before quoting two studies, make sure to read them.. when it says AND/OR (pay attention)... and words like "presumably".. dont mean anything..


nandi- what is with these posts???.. ala does not work.. ala is more effective in adipocytes.. strange..

Why is it that people taking r-ala get leaner?? should'nt they be getting fatter according to your assertions??

why the amazing pumps from ALA and r-ala.. must be the reduced muscle glycogen???


before you leap to conclusion based on loose study findings.. maybe .....

 

[macrophage69alpha]

: Am J Physiol 1997 Jul;273(1 Pt 1):E185-91 Related Articles, Links


Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle.

Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt DL, Tritschler HJ.

Department of Physiology, University of Arizona, Tucson 85721-0093, USA.

The racemic mixture of the antioxidant alpha-lipoic acid (ALA) enhances insulin-stimulated glucose metabolism in insulin-resistant humans and animals. We determined the individual effects of the pure R-(+) and S-(-) enantiomers of ALA on glucose metabolism in skeletal muscle of an animal model of insulin resistance, hyperinsulinemia, and dyslipidemia: the obese Zucker (fa/fa) rat. Obese rats were treated intraperitoneally acutely (100 mg/kg body wt for 1 h) or chronically [10 days with 30 mg/kg of R-(+)-ALA or 50 mg/kg of S-(-)-ALA]. Glucose transport [2-deoxyglucose (2-DG) uptake], glycogen synthesis, and glucose oxidation were determined in the epitrochlearis muscles in the absence or presence of insulin (13.3 nM). Acutely, R-(+)-ALA increased insulin-mediated 2-DG-uptake by 64% (P < 0.05), whereas S-(-)-ALA had no significant effect. Although chronic R-(+)-ALA treatment significantly reduced plasma insulin (17%) and free fatty acids (FFA; 35%) relative to vehicle-treated obese animals, S-(-)-ALA treatment further increased insulin (15%) and had no effect on FFA. Insulin-stimulated 2-DG uptake was increased by 65% by chronic R-(+)-ALA treatment, whereas S-(-)-ALA administration resulted in only a 29% improvement. Chronic R-(+)-ALA treatment elicited a 26% increase in insulin-stimulated glycogen synthesis and a 33% enhancement of insulin-stimulated glucose oxidation. No significant increase in these parameters was observed after S-(-)-ALA treatment. Glucose transporter (GLUT-4) protein was unchanged after chronic R-(+)-ALA treatment but was reduced to 81 +/- 6% of obese control with S-(-)-ALA treatment. Therefore, chronic parenteral treatment with the antioxidant ALA enhances insulin-stimulated glucose transport and non-oxidative and oxidative glucose metabolism in insulin-resistant rat skeletal muscle, with the R-(+) enantiomer being much more effective than the S-(-) enantiomer.

 

[macrophage69alpha]

btw- your second study (helsinki) is a survey that is citing another study.. likely the hebrew one.. though.. even that is not certain..

note- in the system described using what are high molar concentrations.. most anti-ox have pro-oxident effects..

one might venture to guess that with further peer review.. the study will have been found to be flawed..

note2- such an isolated system has no translation to a living breathing, and yes heavily oxidizing organism.. just a small point.. which given the value of the above assertion was not really necessary..

 

[macrophage69alpha]

just and FYI- 2.4millimoles (the amount used in the study) is 2.4 times the concentration at which maximal effect was seen which 1000micromoles... 1000micromoles=1millimole

this in insulin resistant cell lines wherein one might posit a normal cell line (like that of the rat soleus) likely requires a lower dosage to elicit the same effect.

btw- it is somewhat established that at high dosages anti-ox can have pro-ox effects.. so this study really brings nothing new to the table.. and makes conclusions that are not based on a appropriate study model..

 

[MrRTTB]

I know ALa has helped me with musclegains while bulking. Pumps have improved ever since I started taking ALA. Maybe the effect isn't that big, but everyone I know who is taking ALA, not r-ala, seem to get the same pump feeling in the gym.
My experiences with ala are all nice. I get very bloated actually if I do not eat enough carbs while taking ALA. I discovered this one day when I lowered carbs and kept ala dose the same. Next day I woke up all bloated and felt like shit. Next day I did the same and same thing happened. Next day after that I increased carbs very much and no bloat. Seems like muscles really respond to ALa, to little carbs and you get depleted fast looking like you have lost gains and gained fat. So I think one must find a good dose for the carb intake. I therefor see no point overdoing the ALa if you are not eating enough of carbs. Good dose for me seems to be 5-7mg ALA per gram of carbs.

 

[amenselah]

I'm taking ALA 2000mg ED and I'm stronger and getting great pumps...

 

[Ulter]

"...uncoupling of mitochondria."

This is not what r-ALA does. It is what ALA does to a certain extent. If they would have used r-ALA they would have seen that it doesn't affect PDC in the mitochondria and s-ALA does.

 

[jboldman]

Macro, the study you posted was with respect to insulin resistant muscle cells. There is recent research demonstrating that the same procedures when used with insulin sensitive subjects had no effect. i am not trying to jump onto the ala bashing here, simply providing the research that I have found. Note that both of these studies were done with r-ala. The most recent study is posted first and the previous study with the insulin resistant rats posted last.
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J Appl Physiol 2002 Jan;92(1):50-8 Related Articles, Links


Effects of exercise training and antioxidant R-ALA on glucose transport in insulin-sensitive rat skeletal muscle.

Saengsirisuwan V, Perez FR, Kinnick TR, Henriksen EJ.

Muscle Metabolism Laboratory, Department of Physiology, University of Arizona, College of Medicine, Tucson, Arizona 85721-0093, USA.

We have recently demonstrated (Saengsirisuwan V, Kinnick TR, Schmit MB, and Henriksen EJ, J Appl Physiol 91: 145-153, 2001) that exercise training (ET) and the antioxidant R-(+)-alpha-lipoic acid (R-ALA) interact in an additive fashion to improve insulin action in insulin-resistant obese Zucker (fa/fa) rats. The purpose of the present study was to assess the interactions of ET and R-ALA on insulin action and oxidative stress in a model of normal insulin sensitivity, the lean Zucker (fa/-) rat. For 6 wk, animals either remained sedentary, received R-ALA (30 mg. kg body wt(-1). day(-1)), performed ET (treadmill running), or underwent both R-ALA treatment and ET. ET alone or in combination with R-ALA significantly increased (P < 0.05) peak oxygen consumption (28-31%) and maximum run time (52-63%). During an oral glucose tolerance test, ET alone or in combination with R-ALA resulted in a significant lowering of the glucose response (17-36%) at 15 min relative to R-ALA alone and of the insulin response (19-36%) at 15 min compared with sedentary controls. Insulin-mediated glucose transport activity was increased by ET alone in isolated epitrochlearis (30%) and soleus (50%) muscles, and this was associated with increased GLUT-4 protein levels. Insulin action was not improved by R-ALA alone, and ET-associated improvements in these variables were not further enhanced with combined ET and R-ALA. Although ET and R-ALA caused reductions in soleus protein carbonyls (an index of oxidative stress), these alterations were not significantly correlated with insulin-mediated soleus glucose transport. These results indicate that the beneficial interactive effects of ET and R-ALA on skeletal muscle insulin action observed previously in insulin-resistant obese Zucker rats are not apparent in insulin-sensitive lean Zucker rats.
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J Appl Physiol 2001 Jul;91(1):145-53 Related Articles, Links


Interactions of exercise training and lipoic acid on skeletal muscle glucose transport in obese Zucker rats.

Saengsirisuwan V, Kinnick TR, Schmit MB, Henriksen EJ.

Muscle Metabolism Laboratory, Department of Physiology, University of Arizona College of Medicine, Tucson, Arizona 85721-0093, USA.

Exercise training (ET) or the antioxidant R(+)-alpha-lipoic acid (R-ALA) individually increases insulin action in the insulin-resistant obese Zucker rat. The purpose of the present study was to determine the interactions of ET and R-ALA on insulin action and oxidative stress in skeletal muscle of the obese Zucker rat. Animals either remained sedentary, received R-ALA (30 mg x kg body wt(-1) x day(-1)), performed ET (treadmill running), or underwent both R-ALA treatment and ET for 6 wk. During an oral glucose tolerance test, ET alone or in combination with R-ALA resulted in a significant lowering of the glucose (26-32%) and insulin (29-30%) responses compared with sedentary controls. R-ALA alone decreased (19%) the glucose-insulin index (indicative of increased insulin sensitivity), and this parameter was reduced (48-52%) to the greatest extent in the ET and combined treatment groups. ET or R-ALA individually increased insulin-mediated glucose transport activity in isolated epitrochlearis (44-48%) and soleus (37-57%) muscles. The greatest increases in insulin action in these muscles (80 and 99%, respectively) were observed in the combined treatment group. Whereas the improvement in insulin-mediated glucose transport in soleus due to R-ALA was associated with decreased protein carbonyl levels (an index of oxidative stress), improvement because of ET was associated with decreased protein carbonyls as well as enhanced GLUT-4 protein. However, there was no interactive effect of ET and R-ALA on GLUT-4 protein or protein carbonyl levels. These results indicate that ET and R-ALA interact in an additive fashion to improve insulin action in insulin-resistant skeletal muscle. Because the further improvement in muscle glucose transport in the combined group was not associated with additional upregulation of GLUT-4 protein or a further reduction in oxidative stress, the mechanism for this interaction must be due to additional, as yet unidentified, factors.

 

[GinNJuice]

You know, I hate to say this....... BUT

It seems that the only people that defend, or get mad about r-ALA bashing, are the ones who have monitary interest in selling R-ala.

I just don't know if I should take these statements with a grain of salt or not.

I don't know about ulter and macro......... but Fonz is not really the model of integrity..... I hope that's not true for the others.

Ever notice that macro bumps the yohimburn threads with no info but just the p) symbol?

 

[Tony104104]

I like ALA....Works very well for me and i don't see any loss in strength....I can lose weight fast when taking it or bulk with it...What else can you ask for?

Ive been thinking about trying r ALA, but i figured since Regular ALA works so well for me,why go with something else.....

If it aint broke don't fix it...