Β-alanine is one of the most popular sports supplements used by strength / power athletes today. The popularity of β-alanine derives its buffering capacity at the intracellular level as a buffer agent in skeletal muscle, with the consequent delay of fatigue during high intensity exercise.
This supplement is a non-protein amino acid that does not seem to have any ergogenic potential on its own. Although once ingested, it is combined with histidine in a reaction catalyzed by the enzyme carnosine synthase, where the pKa of the imidazole ring of the histidine residue allows it to act as a highly effective intracellular pH buffer within the skeletal muscle and other organs.
Found abundantly in excitable tissues, such as skeletal muscle, the heart and in some regions of the brain, although the highest concentrations in humans are found in muscle (with a higher prevalence in type II fibers).
Beta alanine is produced endogenously in the liver from the degradation of uracil together with an alternative synthesis in the intestine and the kidney. Although the researchers suggest that the endogenous synthesis is quite low even adding the intake of dietary origin (higher prevalence in foods of animal origin, needing quantities impractical for day to day).
So if we look for certain benefits perhaps beta alanine supplementation is the only way or the easiest way to raise carnosine levels. Since this (beta alanine) is considered as the limiting step in the synthesis speed of this. Thus the objective of its supplementation is to increase the carnosine content in the skeletal muscle, which improves the capacity of intracellular buffering and other functions of which we will speak from the prism of the clinical field where there is much to investigate.
Several physiological functions have been attributed to carnosine in skeletal muscle, including antioxidant activity and protection against protein glycosylation and carbonylation. The antioxidant properties of carnosine have been demonstrated through its ability to eliminate reactive oxygen species (ROS). This capacity as an antioxidant is mainly due to its histidine component, whereas β-alanine has been shown to be ineffective as an antioxidant in itself.
High intensity exercise causes a significant response to oxidative stress, causing inflammation and muscle damage. Being the attenuation of oxidative stress beneficial for later recovery. However, carnosine as an antioxidant in vivo has been limited to animal models, where it has been shown to have different physiological functions. Therefore, the effectiveness of carnosine as an antioxidant in humans remains to be explored and investigated.
In vitro studies with human and animal muscle fibers have also attributed other functions to carnosine, including calcium sensitization, transient calcium regulation (ie, increased calcium release and reuptake by the sarcoplasmic reticulum) and amelioration of arousal -muscle contraction.
However, a recent human study did not support the hypothesis of increased carnosine to increase calcium, its sensitivity and release, but it did support the finding that carnosine can improve calcium reuptake. Clearly, more studies are still required to investigate these problems to clarify the physiological roles of carnosine. Despite some controversies, an indisputable function of carnosine is regulation as an intracellular buffer since its side chain (ie, that of the imidazole ring) has a pKa of 6.83, which makes carnosine a mandatory physicochemical buffer.
Also, as a point of interest, it has been shown that carnosine acts as an ion chelating agent such as copper and excessive zinc accumulation that can lead to lipid peroxidation and cell damage. In addition, it has been shown to act as a protective agent against the formation of final lipoxidation and advanced glycosylation products, delaying the aging process and possible prevention of various diseases.
Another novelty in the studies of recent years, is the use of beta alanine supplementation and its important role as an antioxidant in the brain. One of the initial studies that examined β-alanine supplementation and brain function was performed by Murakami and Furuse (2010) where they enriched the β-alanine feed for about 5 weeks in mice and observed a significant increase in carnosine content in the cerebral cortex and the hypothalamus. These increases were associated with an increase in the brain-derived neurotrophic factor (BDNF) exerting a neuroprotective effect and a decrease in the concentration of 5-hydroxyindoleacetic acid, a metabolite of serotonin, despite the exposure of rodents to stressful conditions (anxiolytic compounds).
The mechanism associated with high brain carnosine and maintenance of the expression of BDNF in hippocampus is not well understood but is probably related to the role of carnosine as neural protector through its action as an antioxidant. It has been suggested that oxidative stress and inflammation in the brain are part of the aftermath of physiological events that contribute to PTSD but can also contribute to cognitive neurodegeneration and associated mild traumatic brain injury (mTBI).
A recent study by Hoffman et al. (2017) investigated the benefit of β-alanine supplementation in cognitive and behavioral responses related to mTBI. In addition, the effects of the ingestion of β-alanine on the expression of the inflammatory protein, neurotrophin and tau in the hippocampus were also examined.
The results indicated that 30 days of intake of β-alanine in rats were effective in reducing the incidence of similar MTBI where also appeared to have a reduced inflammatory response (attenuation of glial fibrillary acidic protein) and increased expression phenotype of BDNF in specific regions of the hippocampus compared to rats exposed to trauma and fed a normal diet. The results of this study provided initial evidence that 30 days of β-alanine supplementation may increase resistance to mTBI-like responses in exposed animals and may provide additional support for a possible antioxidant role of elevated carnosine levels.
