ALA bad for Bodybuilding???

[Iron Gamer]

I just read an article in the January MD that says ALA decreases the rate at which muscle and liver tissue make new glycogen and decreases the efficiency of cellular energy systems.
I know ALA is supposed to be good for the liver during a cycle. Does anyone have any thoughts on this? Do the benefits out way the negatives? This is the first negative I've heard about ALA.

 

[prophet]

i started a thread a while back where i swore ala made my mucles fail much quicker while i was lifting. i never made any strenth gains when i was on ala....i have never tried r-ala but i am guessing its that same story

 

[wilson6]

We got into the r-ALA topic pretty deep over on the women's board. Discussed some of those studies (glycogen and protein synthesis). Might want to do a search.

W6

 

[mrt]

Hmmm, that's a interesting claim. I'd really like to hear what experts say about this.

 

[Fonz]

I just read an article in the January MD that says ALA decreases the rate at which muscle and liver tissue make new glycogen and decreases the efficiency of cellular energy systems.
I know ALA is supposed to be good for the liver during a cycle. Does anyone have any thoughts on this? Do the benefits out way the negatives? This is the first negative I've heard about ALA.

Thats in respect to RACEMIC ALA not r-ala.

Fonz

 

[Iron Gamer]

BUMP for more replies

 

[Nelson Montana]

I've resisted recommending ALA for liver protection due to the fact that it lowers blood sugar levels and instigates symptoms of hypoglycemia and even anxiety. I never made the muscle connection before but it makes sense. Decreased glycogen equals flat muscles and lessened energy levels.

 

[Ulter]

Like Fonz said that is ONLY ALA not r-ALA.

 

[Jguns]

Studies show ALA inhibits glycogen repletion. Post workout, you have a short window to optimally replenish wasted glycogen stores. ALA will sabotage this..


Alpha-lipoic acid inhibits glycogen synthesis in rat soleus muscle via its oxidative activity and the uncoupling of mitochondria.

Dicter N, Madar Z, Tirosh O.

Institute of Biochemistry, Food Science and Nutrition, Faculty of Agricultural, Food and Environmental Quality Sciences, The Hebrew University of Jerusalem, Rehovot 76100, Israel.

alpha-Lipoic acid (LA) is currently being investigated as a glucose-lowering agent for diabetes control; it is also considered a powerful dietary antioxidant. The objective of this study was to investigate the fate of glucose in isolated rat muscles incubated with LA and determine its effects on intramuscular redox status. Rat soleus muscles were incubated for up to 60 min with 2.4 mmol/L LA in the presence or absence of insulin. Intramuscular concentrations of LA were evaluated (uptake and reduction), and glycogen synthesis, glucose oxidation, intramuscular reactive oxygen species (ROS) production and mitochondrial membrane potential investigated. Insulin enhanced glycogen synthesis, whereas LA decreased rates by >50%. LA elevated ROS production and in combination with t-butylhydroperoxide, an oxidant, additively inhibited glycogen synthesis rates by 80%. Insulin acted as an antioxidant and attenuated ROS production by 30%. LA uncoupled the mitochondria and accelerated glucose oxidation 1.5-fold relative to the control. The glycogen synthesis pathway was found to be dependent on mitochondrial function because treatment with mitochondrial inhibitors eliminated the majority of glycogen synthesis. These data show that in this model, LA acts as a mild prooxidant, causing mitochondrial uncoupling and inhibition of glycogen synthesis. It appears that LA regulates glucose metabolism in the muscle differently than insulin.

It is the same way for rALA.

http://www.ncbi.nlm.nih.gov/entrez/...6&dopt=Abstract

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.

 

[nandi12]

I couldn't get that last link to work so I will post the abstract in its entirety. The salient point is this has nothing to do with isomers of ALA. It is the basic prooxidant property of ALA that is responsible for its enhancement of glucose uptake in diabetic individuals, as well as its negative effects on glycogen synthase:

Toxicol Appl Pharmacol 2002 Jul 1;182(1):84-90 Related Articles, Links


Antioxidant and prooxidant activities of alpha-lipoic acid and dihydrolipoic acid.

Moini H, Packer L, Saris NE.

Department of Applied Chemistry and Microbiology, PB 56 Viikki Biocenter, FIN-00014, University of Helsinki, Helsinki, Finland. [email protected]

Reactive oxygen (ROS) and nitrogen oxide (RNOS) species are produced as by-products of oxidative metabolism. A major function for ROS and RNOS is immunological host defense. Recent evidence indicate that ROS and RNOS may also function as signaling molecules. However, high levels of ROS and RNOS have been considered to potentially damage cellular macromolecules and have been implicated in the pathogenesis and progression of various chronic diseases. alpha-Lipoic acid and dihydrolipoic acid exhibit direct free radical scavenging properties and as a redox couple, with a low redox potential of -0.32 V, is a strong reductant. Several studies provided evidence that alpha-lipoic acid supplementation decreases oxidative stress and restores reduced levels of other antioxidants in vivo. However, there is also evidence indicating that alpha-lipoic acid and dihydrolipoic acid may exert prooxidant properties in vitro. alpha-Lipoic acid and dihydrolipoic acid were shown to promote the mitochondrial permeability transition in permeabilized hepatocytes and isolated rat liver mitochondria. Dihydrolipoic acid also stimulated superoxide anion production in rat liver mitochondria and submitochondrial particles. 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. Whether alpha-lipoic acid and/or dihydrolipoic acid-induced oxidative protein modifications contribute to their versatile effects observed in vivo warrants further investigation.


Likewise, in the previous abstract posted by JGUNS.

"These data show that in this model, LA acts as a mild prooxidant, causing mitochondrial uncoupling and inhibition of glycogen synthesis."


So you ALA advocates can't have your cake and eat it too. If you accept that ALA enhances glucose transport, then the evidence points to the same mechanism being responsible for inhibition of glycogen synthase.

As Ulter knows, I have been cautioning people against ALA from day one. I have no vested interest in any competing product. This is not about having a financial stake in a product as far as I am concerned. It is about providing the most up to date information possible about supplements.