E-14L FREE COMMUNICATION POSTER/CREATINE
Carnosine contributes to physico-chemical buffering of H+ in muscle by virtue of its histidine residue which exhibits a pKa of 6.83. Carnosine (β-alanylhistidine) is synthesised in muscle from its 2 constituent amino acids of which β-alanine (β-Ala) appears to be limiting. β-Ala is normally obtained from ex-muscle synthesis or meat ingestion.
To investigate if β-Ala supplementation increases the capacity to undertake intense exercise normally associated with lactate accumulation.
28 healthy male subjects (24–30 years; 65–95kg), active in one or more sport, were supplemented with (a) (4 × 800 mg).d−1 β-Ala for 5w with (4 × 5g).d−1 creatine monohydrate (CrM) during the 5th week (n = 10); (b) (4 × 800mg).d−1 placebo for 5w with (4 × 5g).d−1 CrM over the 5th week (n = 9); (c) (4 × 800mg).d−1 matching placebo for 5w with an additional (4 × 5g).d−1 placebo replacing the CrM during the 5th week (n = 9). Treatments were allocated randomly and the study conducted double blind. Isometric endurance at 50% MVC and power output during a 4 min all-out maximal ergometer exercise (PO4max) were assessed before and at the end of the 5th week.
The mean endurance at 50% MVC and the product of force × time showed a small and equal increase in (a) and (b) relative to (c) though this was not significant. PO4max was increased in (a) >(b) >(c) (38.2, 8.7 and −1.6W, respectively). The contrast of (a) with (b) or (c) was significant (P < 0.05) but not (b) with (c). Most of the gain in PO in (a) occurred during the 1 minute of exercise.
Supplementation with β-Ala increases maximal PO during the first minute of maximal dynamic exercise before full cardiovascular adjustment occurs, probably as a result of an increase in H+ buffering by muscle carnosine.