Infinite One Series: Acetyl-L-Carnitine

Acetyl-L-carnitine is the acetylated ester of the amino acid L-carnitine. Acetyl-L-carnitine is reported to be better absorbed and to cross the blood-brain barrier more efficiently compared to carnitine. Acetyl-L-carnitine enhances energy production in every cell of the body. Acetyl-L-carnitine is produced through endogenous biosynthesis of lysine and methionine, primarily in the brain, liver, and kidneys, and can also be consumed through foods and supplementation Acetyl-L-carnitine has been considered a “mitochondrial nutrient”, that reverses both aging-related mitochondrial dysfunction and the reaction of elderly mitochondria to challenge. Acetyl-L-carnitine may support youthful memory function, improve mitochondrial structure and function, inhibit age-related oxidative damage, and restore the activity of key enzymes.

Acetyl-L-Carnitine (ALCAR) is an acetylated form of L-carnitine that may assist in cardiovascular function, energy metabolism and weight management.*

Several reports showed that treatment with Acetyl-L-carnitine may have an impact on mitochondrial biogenesis. Mitochondrial biogenesis is the creation of new mitochondria. Chronic oral supplementation with Acetyl-L-carnitine in rats reverses the age-related decline in carnitine content in the brain, plasma, skeletal muscle, and heart. A plethora of published studies on acetyl-L-carnitine has heightened our awareness of the multi-faceted benefits of this amino acid. Published research shows acetyl-L-carnitine is critical to youthful cellular function in the brain, heart, liver, peripheral nerve and immune system.

Rosca MG, Lemieux H, Hoppel CL. Mitochondria in the elderly: Is
acetylcarnitine a rejuvenator? Adv Drug Deliv Rev. 2009 Nov 30;61(14):1332-42.

Shen W, Liu K, Tian C, Yang L, Li X, Ren J, Packer L, Head E, Sharman E, Liu J. Protective effects of R-alpha-lipoic acid and acetyl-L-carnitine in MIN6 and isolated rat islet cells chronically exposed to oleic acid. J. Cell. Biochem. 2008;104:1232–1243.

Liu J, Ames BN. Reducing mitochondrial decay with mitochondrial nutrients to delay and treat cognitive dysfunction, Alzheimer’s disease, and Parkinson’s disease. Nutr. Neurosci. 2005;8:67–89.

Moriggi M, Cassano P, Vasso M, Capitanio D, Fania C, Musicco C, Pesce V, Gadaleta MN, Gelfi C. A DIGE approach for the assessment of rat soleus muscle changes during unloading: effect of acetyl-L-carnitine supplementation. Proteomics. 2008;8:3588–3604.

Gadaleta MN, Petruzzella V, Renis M, Fracasso F, Cantatore P. Reduced transcription of mitochondrial DNA in the senescent rat. Tissue dependence and effect of L-carnitine. Eur. J. Biochem. 1990;187:501–506.

Rebouche CJ. Carnitine function and requirements during the life cycle. Faseb J. 1992;6:3379–3386.

Liu J, Ames BN. Reducing mitochondrial decay with mitochondrial nutrients to delay and treat cognitive dysfunction, Alzheimer’s disease, and Parkinson’s disease. Nutr. Neurosci. 2005;8:67–89.

Bigford GE, Del Rossi G. Supplemental substances derived from foods as
adjunctive therapeutic agents for treatment of neurodegenerative diseases and
disorders. Adv Nutr. 2014 Jul 14;5(4):394-403.

Carter AL, Lennon DL, Stratman FW. Increased acetyl carnitine in rat skeletal
muscle as a result of high-intensity short-duration exercise. Implications in the control of pyruvate dehydrogenase activity. FEBS Lett. 1981 Apr 6;126(1):21-4.

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