One evening in the 1980s, I was deep in the archives of a medical library I frequented, excavating a study involving L-carnosine. L-carnosine is similar to its "c" cousins, creatine and L-carnitine, in that it occurs in animal-derived foods and is made in human metabolism. It was being hailed – despite zero human evidence – as a so-called lactic acid extinguisher, capable of extending the runway during exercise for more reps, longer sprints and faster recovery between them.
About 10 years later I had the pleasure of meeting Roger Harris, Ph.D., who led the first human study evaluating supplementation with creatine monohydrate and its impact on muscle creatine.1 Harris and I developed a nice friendship and I had the pleasure of collaborating with him in 2003 (and his then-Ph.D. student, Mark J. Tallon) on the first human study of oral L-carnosine supplementation combined with muscle biopsies (sponsored by Lonza).2
Harris had the notion that beta-alanine, one of the two constituent amino acids of L-carnosine, would be superior to its parent dipeptide (and notably less expensive). Two dozen published clinical trials later, beta-alanine has emerged as a legal, natural, evidence-based, performance-enhancing agent relevant to high intensity exercise.
Unlike creatine monohydrate, beta-alanine does not appear to increase body mass, and the rate of onset of its performance augmentation is markedly slower, similar to that seen very recently with appropriate L-carnitine supplementation.3 Unlike its "c" cousins, beta-alanine elicits a flushing effect experientially similar to that of niacin, although apparently not mediated by prostaglandins, as is the case for niacin. This led Harris (and Natural Alternatives International) to file patents related to a modified-release form of beta-alanine, which led to an increase in the widespread acceptance of this non-protein amino acid.
But the greatest mountain remaining to be ascended is direct demonstration that beta-alanine indeed exerts its performance-enhancing effects through reducing muscle acidification/buffering, as the mechanism remains theoretical. This could be definitively explored in a population of people exhibiting the most common muscle metabolic disease, McArdle's disease,4 wherein lactic acid is not produced during exercise.
Irrespective of how it works, however, beta-alanine is a potent addition to the very small armamentarium of natural, legal, safe and effective performance-enhancing agents.
Anthony L. Almada, MSc, FISSN, was the co-founder/past-president of sports nutrition company EAS, and is the CEO of GENr8, the exclusive marketer of Vitargo in North America and Australia, and the CEO of Fein Innovations.
1. RC Harris, et al. Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation. Clin Sci 1992;83:367-74.
2. Tallon MJ, et al. The effect of L-carnosine supplementation on its content in types I and II muscle fibers. Exp Biol 2005, San Diego, CA. Late Breaking Abstracts.
3. Wall BT, et al. Chronic oral ingestion of L-carnitine and carbohydrate increases muscle carnitine content and alters muscle fuel metabolism during exercise in humans: the dual role of muscle carnitine in exercise metabolism. J Physiol 10.1113/jphysiol.2010.201343.
4. Vissing J, et al. The exercise metaboreflex is maintained in the absence of muscle acidosis: insights from muscle microdialysis in humans with McArdle’s disease. J Physiol 2001;537:641-9.