|Jmol-3D images||Image 1|
|Molar mass||89.09 g mol−1|
|Appearance||white bipyramidal crystals|
|Density||1.437 g/cm3 (19 °C)|
207 °C, 480 K, 405 °F (decomposes)
|Solubility in water||54.5 g/100 mL|
|Solubility||soluble in methanol. diethyl ether, acetone|
|LD50||1000 mg/kg (rat, oral)|
| (what is: / ?) |
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
β-Alanine (or beta-alanine) is a naturally occurring beta amino acid, which is an amino acid in which the amino group is at the β-position from the carboxylate group (i.e., two atoms away, see Figure 1). The IUPAC name for β-alanine is 3-aminopropanoic acid. Unlike its counterpart α-alanine, β-alanine has no stereocenter.
β-Alanine is not used in the biosynthesis of any major proteins or enzymes. It is formed in vivo by the degradation of dihydrouracil and carnosine. It is a component of the naturally occurring peptides carnosine and anserine and also of pantothenic acid (vitamin B5), which itself is a component of coenzyme A. Under normal conditions, β-alanine is metabolized into acetic acid.
β-Alanine is the rate-limiting precursor of carnosine, which is to say carnosine levels are limited by the amount of available β-alanine. Supplementation with β-alanine has been shown to increase the concentration of carnosine in muscles, decrease fatigue in athletes and increase total muscular work done.
Typically, studies have used supplementing strategies of multiple doses of 400 mg or 800 mg, administered at regular intervals for up to eight hours, over periods ranging from 4 to 10 weeks. After a 10-week supplementing strategy, the reported increase in intramuscular carnosine content was an average of 80.1% (range 18 to 205%).
A study conducted at Adams State College, Alamosa, Colorado, compared the effects of β-alanine to a placebo group in two sports: wrestling and American football. The subjects taking β-alanine achieved more desirable results on all tests compared to placebo. The wrestlers, both placebo and supplement lost weight; however, the supplement group increased lean mass by 1.1 lb., while the placebo group lost lean mass (-0.98 lb). Both American football groups gained weight; however, the supplement group gained an average 2.1 lb lean mass compared to 1.1 lb for placebo.
L-Histidine, with a pKa of 6.1 is a relatively weak buffer over the physiological intramuscular pH range. However, when bound to other amino acids, this increases nearer to 6.8-7.0. In particular, when bound to β-alanine, the pKa value is 6.83, making this a very efficient intramuscular buffer. Furthermore, because of the position of the beta amino group, β-alanine dipeptides are not incorporated proteins and thus can be stored at relatively high concentrations (millimolar). Occurring at 17-25 mmol/kg (dry muscle), carnosine (β-alanyl-L-histidine) is an important intramuscular buffer, constituting 10-20% of the total buffering capacity in type I and II muscle fibres.
β-Alanine, provided in solution or as powder in gelatine capsules, however, causes paraesthesia when ingested in amounts above 10 mg per kg body weight (bwt). This is variable between individuals. Symptoms may be experienced by some individuals as mild even at 10 mg per kg bwt, in a majority as significant at 20 mg per kg bwt, and severe at 40 mg per kg bwt. However, an equivalent amount (equimolar) to 40 mg per kg bwt, ingested in the form of histidine containing dipeptides in chicken broth extract, did not cause paraesthesia.
It is probable that the paraesthesia, a form of neuropathic pain, results from high peak blood-plasma concentrations of β-alanine, since greater quantities, ingested in the form of the β-alanine/histidine (or methylhistidine)-containing dipeptides (i.e., carnosine and anserine) in meat, do not cause the same symptoms. In this case the β-alanine absorption profile is flattened but sustained for a longer period of time, whereas the β-alanine samples in the studies were administered as gelatine capsules containing powder. This resulted in the rapid rise of plasma concentrations, peaking within 30 to 45 minutes, and being eliminated after 90 to 120 minutes. The paraesthesia caused is no indication of efficacy, since the published studies undertaken so far have utilised doses of 400 mg or 800 mg at a time to avoid the paraesthesia. Furthermore, excretion of β-alanine in urine accounted for 0.60%(+/-0.09), 1.50%(+/-0.40), or 3.64%(+/-0.47) of the administered doses of 10, 20, or 40 mg per kg body weight, indicating greater losses occurring with increasing dosage.
Even though much weaker than glycine (and, thus, with a debated role as a physiological transmitter), β-alanine is an agonist next in activity to the cognate ligand glycine itself, for strychnine-sensitive inhibitory glycine receptors (GlyRs) (the agonist order: glycine >> β-alanine > taurine >> alanine, L-serine > proline).
- KEGG map of β-alanine metabolism
- International Society of Sports Nutrition Conference Proceedings