TL;DR: Proton MRS can be used to noninvasively quantify human muscle Carnosine content and muscle carnosine is increased by oral beta-alanine supplementation in sprint-trained athletes; carnosinesine loading slightly but significantly attenuated fatigue in repeated bouts of exhaustive dynamic contractions; and the increase in muscle Carnival did not improve isometric endurance or 400-m race time.
Abstract: Carnosine (β-alanyl-l-histidine) is present in high concentrations in human skeletal muscle. The ingestion of β-alanine, the rate-limiting precursor of carnosine, has been shown to elevate the musc...
TL;DR: Of concern should be findings of hepatic enlargement and increases in ammonia and glutamine and of decrease in branched-chain amino acids in blood plasma indicating that HIS supplementation is inappropriate in patients with liver disease.
Abstract: L-histidine (HIS) is an essential amino acid with unique roles in proton buffering, metal ion chelation, scavenging of reactive oxygen and nitrogen species, erythropoiesis, and the histaminergic system. Several HIS-rich proteins (e.g., haemoproteins, HIS-rich glycoproteins, histatins, HIS-rich calcium-binding protein, and filaggrin), HIS-containing dipeptides (particularly carnosine), and methyl- and sulphur-containing derivatives of HIS (3-methylhistidine, 1-methylhistidine, and ergothioneine) have specific functions. The unique chemical properties and physiological functions are the basis of the theoretical rationale to suggest HIS supplementation in a wide range of conditions. Several decades of experience have confirmed the effectiveness of HIS as a component of solutions used for organ preservation and myocardial protection in cardiac surgery. Further studies are needed to elucidate the effects of HIS supplementation on neurological disorders, atopic dermatitis, metabolic syndrome, diabetes, uraemic anaemia, ulcers, inflammatory bowel diseases, malignancies, and muscle performance during strenuous exercise. Signs of toxicity, mutagenic activity, and allergic reactions or peptic ulcers have not been reported, although HIS is a histamine precursor. Of concern should be findings of hepatic enlargement and increases in ammonia and glutamine and of decrease in branched-chain amino acids (valine, leucine, and isoleucine) in blood plasma indicating that HIS supplementation is inappropriate in patients with liver disease.
TL;DR: This paper reviews the available evidence relating to the effects of β-alanine supplementation on muscle carnosine synthesis and the subsequent effects on exercise performance and proposes a method of increasing intracellular buffering capacity during exercise, which could provide a means of increasing high-intensity exercise capacity and performance.
Abstract: High-intensity exercise results in reduced substrate levels and accumulation of metabolites in the skeletal muscle. The accumulation of these metabolites (e.g. ADP, Pi and H+) can have deleterious effects on skeletal muscle function and force generation, thus contributing to fatigue. Clearly this is a challenge to sport and exercise performance and, as such, any intervention capable of reducing the negative impact of these metabolites would be of use. Carnosine (β-alanyl-l-histidine) is a cytoplasmic dipeptide found in high concentrations in the skeletal muscle of both vertebrates and non-vertebrates and is formed by bonding histidine and β-alanine in a reaction catalysed by carnosine synthase. Due to the pKa of its imidazole ring (6.83) and its location within skeletal muscle, carnosine has a key role to play in intracellular pH buffering over the physiological pH range, although other physiological roles for carnosine have also been suggested. The concentration of histidine in muscle and plasma is high relative to its Km with muscle carnosine synthase, whereas β-alanine exists in low concentration in muscle and has a higher Km with muscle carnosine synthase, which indicates that it is the availability of β-alanine that is limiting to the synthesis of carnosine in skeletal muscle. Thus, the elevation of muscle carnosine concentrations through the dietary intake of carnosine, or chemically related dipeptides that release β-alanine on absorption, or supplementation with β-alanine directly could provide a method of increasing intracellular buffering capacity during exercise, which could provide a means of increasing high-intensity exercise capacity and performance. This paper reviews the available evidence relating to the effects of β-alanine supplementation on muscle carnosine synthesis and the subsequent effects on exercise performance. In addition, the effects of training, with or without β-alanine supplementation, on muscle carnosine concentrations are also reviewed.
TL;DR: It can be concluded that carnosine is a stable compound in human skeletal muscle, confirming the absence of carnosinase in myocytes, and shows that washout periods for crossover designs in supplementation studies for muscle metabolites may sometimes require months rather than weeks.
Abstract: Carnosine (β-alanyl-l-histidine) is present in high concentrations in human skeletal muscles. The oral ingestion of β-alanine, the rate-limiting precursor in carnosine synthesis, has been shown to ...
TL;DR: It can be concluded that the positive correlation between baseline muscle carnosine levels and rowing performance and thepositive correlation between changes in muscle Carnosine and performance improvement suggest that muscle carnOSine is a new determinant of roowing performance.
Abstract: The role of the presence of carnosine (β-alanyl-l-histidine) in millimolar concentrations in human skeletal muscle is poorly understood. Chronic oral β-alanine supplementation is shown to elevate m...