There has been a surge in research interest about r-Alpha-Lipoic acid (r-ALA 200), it is without a doubt an intriguing supplement.
Due to r-ALA’s multifaceted benefits, this article will update you on the latest findings and clarify how to use this supplement to build a premium body.
ALA, exercise and insulin
There’s a research history showing ALAs positive impact on insulin action and muscle glucose transport, where insulin function is ineffective [1–7]. Collectively, in vitro (cell culture) results indicate that although a portion of ALA action enhances muscle insulin sensitivity (via the insulin signal transduction pathway), the majority of the benefits of ALA on skeletal muscle glucose transport is insulin-independent.
With strong research indicating ALA enhances insulin activity and may also work independently of insulin to transport nutrients into muscle makes r-ALA 200 one exciting supplement for bodybuilders and athletes.
Scientists at The University of Arizona College of Medicine, Tucson, Arizona were the first to demonstrate that exercise training and ALA interacted in an additive fashion to improve insulin action .
Whereas the previously mentioned studies focused on obesity models, a more recent study assessed the interactions of exercise and ALA on insulin action and oxidative stress in non-obese rodents. Although six weeks of exercise training and ALA supplementation (30 mgs/body wt/day) caused reductions in soleus protein carbonyls (an index of oxidative stress), ALA supplementation failed to improve insulin action or glucose transport in these healthy, lean animals .
The effects of ALA as an insulin “mimicker” appears only to be strong in models where insulin metabolism is defective. The only study to investigate ALA’s effects on healthy insulin management did not show this compound to be effective at enhancing insulin action any further, nor did ALA improve glucose disposal within muscle .
While these findings may seem a little disappointing, ALAs benefits to bodybuilders go far beyond its glucose disposal potential.
ALA enhances brain function
The loss of memory and mental capacity associated with aging seems to be caused in good part by oxidative mitochondrial decay in brain nerve cells (neurons). In the case of age-related neurodegenerative diseases, such as Alzheimer’s disease, this damage proves debilitating and fatal. Recent research has demonstrated that feeding ALA to old rats improved performance on memory tasks, reduced brain mitochondrial structure decay, and reduced oxidative damage in the brain .
This research was a continuation of work by Stoll and co-workers several years ago that showed that ALA supplementation improved long-term memory in aged female mice. Therefore, there is strong evidence to suggest that ALA supplementation may prevent mitochondrial decay in neurons and delay brain aging as well as other age-associated neurodegenerative diseases .
Doesn’t matter how big your biceps are, without the ol’ grey matter in tip-top condition, you’ve nothing but a hairy bag of chemical soup. ALA appears to have a key role in preserving cognitive function. However, ALA supplementation will provide a number of other subtle yet vital roles in building a lean, mean body.
ALA is an essential co-factor in many mitochondrial dehydrogenase reactions, which means ALA is intimately involved in the proper metabolism of all carbohydrates and fats. However, probably ALA’s most powerful virtue as a supplement for bodybuilders lay in its unique capability as a muscle mass-stimulating antioxidant.
ALA: The bodybuilder’s antioxidant
ALA and particularly the r-isomer (r-ALA) is considered a premium antioxidant that serves to increase lean muscle mass [1, 13].
While this aspect alone warrants r-ALA to be an essential supplement to anyone interested in a healthy, disease free body, r-ALA appears to be an antioxidant that is biologically tailor-made for bodybuilders.
Firstly, r-ALA works specifically to protect cells from the barrage of free radicals generated by intense, regular exercise training . r-ALA is unique in that it quenches all reactive oxygen species such as superoxide radicals, hydroxyl radicals, hypochlorous acid, peroxyl radicals, and singlet oxygen species. It also protects cell membranes by interacting with glutathione, which in turn recycles vitamins C and E . If you’re interested in building lean mass, this is important.
Second, in muscle cells, r-ALA is shown to actually harness the metabolic power of the cell to continuously regenerate its own active dithiol form, maintaining a continuous supply of cysteine within cells to boost glutathione levels. 
Over the years, I’ve extensively documented the importance of increasing and maintaining cysteine and glutathione levels for building lean muscle mass. Increasing and maintaining circulating cysteine and glutathione levels correlates directly to gains in lean mass. Low cysteine/glutathione levels correlate directly with losing lean muscle mass. If you’ve been training diligently for months or years with little to show for your efforts, I guarantee that you’re suffering from low levels of circulating cysteine.
In research, when a cysteine-rich supplement is introduced, lean muscle mass increases.  The biochemistry on this is complex, but the clear facts are all there — unlike the bogus, transparent supplements that are flooding the bodybuilding market today.
Due to r-ALA’s unique ability to work synergistically within cells to continuously regenerate its own active form, r-ALA 200 appears to be the most potent cysteine supplement available today. Do not forget, there is some rather compelling research that demonstrates cysteine levels govern how much muscle you gain from weight training. If you want a healthy, lean, muscular body for life, base your nutritional supplementation program around research-proven-compounds like r-ALA 200.
1. Henriksen, EJ. In: Antioxidants in Diabetes Management, edited by Packer L, Rosen P, Tritschler HJ, King GL, and Azzi A.New York: Dekker, 303–318, 2000.
2. Haugaard, N, and Haugaard E. Biochim Biophys Acta 222: 583–586, 1970.
3. Singh, HPP, and Bowman RH. Biochem Biophys Res Commun 41: 555–561, 1970.
4. Strödter, D, Lehmann E, Lehmann U, Tritschler HJ, Bretzel RG, and Federlin K. Diabetes Res Clin Pract 29: 19–26, 1995.
5. Estrada, DE, Ewart HS, Tsakiridis T, Volchuk A, Ramlal T, Tritschler H, and Klip A. Diabetes 45: 1798–1804, 1996.
6. Maddux, BA, See W, Lawrence JC, Jr, Goldfine AL, Goldfine ID, and Evans JL. Diabetes 50: 404–410, 2001.
7. Henriksen, EJ, Jacob S, Streeper RS, Fogt DL, Hokama JY, and Tritschler HJ. Life Sci 61: 805–812, 1997
8. Saengsirisuwan, V, Kinnick TR, Schmit MB, and Henriksen EJ. J Appl Physiol 91: 145–153, 2001.
9. Saengsirisuwan V, FR. Perez, TR. Kinnick, and EJ. Henriksen. J Appl Physiol 92: 50–58, 2002.
10. Jiankang L. Head E, Gharib AM, Yuan W, Ingersoll RT, Hagen§ TM, Cotman CW, and Ames BN. Proc. Natl. Acad. Sci. USA. 99 4 2356–2361, 2002.
11. Khanna S et al. J.Appl.Physiol. 86(4):1191–1196, 1999.
12. Packer L, Roy S,Sen CK. Adv Pharmacol 38: 79–101, 1997.
13. Packer, L, Witt EH, and Tritschler HJ. Free Radic Biol Med 19: 227–250, 1995.
14. Cribb PJ, Hayes. Curr Opin Clin Nutr Metab Care. 2008 Jan;11(1):40-4. Review.