Simultaneous Changes In Muscle Carnosine and Taurine During and Following Supplementation with b-alanine

Abstract

Carnosine in muscle (M-Carn) contributes significantly to pH control through physio-chemical buffering of H+. Its synthesis in muscle is limited by the availability of b-Alanine (b-Ala). b-Ala is synthesised in the liver from the degradation of uracil and is available also from carnosine, anserine and balanine with ingestion of red meat, fish and poultry. Direct supplementation of the diet with b-Ala for up to 10 weeks has been shown to increase the muscle carnosine content by 80% and this is paralleled by an increase in anaerobic exercise capacity. The transport of b-Ala into muscle is mediated by the same transporter involved with Taurine (Tau) transport into muscle. Previous studies have pointed to a reciprocal relationship between muscle Tau (M-Tau) and M-Carn. PURPOSE: To test if the reciprocal relationship between M-Tau and M-Carn is maintained when b-Ala supplementation results in an increase in M-Carn. METHOD: Seven males received 2x800mg b-Ala controlled release tablets, twice daily for 4w. The study was explained to each of the subjects before their prior informed consent was obtained. Controlled release tablets (CarnoSyn®) were supplied by Collegiate Sport Nutrition, USA. A muscle biopsy from the vastus lateralis was taken at 0 and 4w, and, 3 and 6w post supplementation and analysed by HPLC. No control group was included as previous studies have demonstrated no change in M-Carn or M-Tau in the absence of b-Ala supplementation. RESULTS: Pre and post supplementation M-Carn was 25.9 ± 4.3 and 41.3 ± 5.5 mmol.kg-1dry muscle and M-Tau 28.1 ± 7.1 and 22.6 ± 7.0 mmol.kg-1dry muscle. Despite the 20% fall in M-Tau, values of M-Tau remained within the normal physiological range. Before supplementation M-Tau was negatively correlated with M-Carn, evidenced by subjects with the highest M-Carn having the lowest M-Tau, expressing a similar relationship to that reported earlier. The same negative relationship was preserved after b-Ala supplementation and during the 6 weeks recovery from supplementation (overall data: [M-Tau] = -0.634 · [M-Carn] + 46.6; r = 0.72; p<0.001; n = 28). CONCLUSION: The decrease in M-Tau, occurring with M-Carn increase, are consistent with a role of M-Tau in osmoregulation in which M-Tau compensates for changes in M-Carn. Financial support was provided by UK Sport, London, UK and NAI, San Marcos, Ca, USA.