Given the ergogenic properties of β-alanyl-
L-histidine (
carnosine) in skeletal muscle, it can be hypothesized that elevated levels of circulating
carnosine could equally be advantageous for high-intensity exercises. Serum
carnosinase (CN1), the
enzyme hydrolyzing the
dipeptide, is highly active in the human circulation. Consequently, dietary intake of
carnosine usually results in rapid degradation upon absorption, yet this is less pronounced in subjects with low CN1 activity. Therefore, acute
carnosine supplementation before high-intensity exercise could be ergogenic in these subjects. In a cross-sectional study, we determined plasma CN1 activity and content in 235 subjects, including 154 untrained controls and 45
explosive and 36 middle- to long-distance elite athletes. In a subsequent double-blind, placebo-controlled, crossover study, 12 men performed a cycling capacity test at 110% maximal power output (CCT 110%) following acute
carnosine (20 mg/kg body wt) or placebo supplementation. Blood samples were collected to measure CN1 content,
carnosine, and acid-base balance. Both male and female
explosive athletes had significantly lower CN1 activity (14% and 21% lower, respectively) and content (30% and 33% lower, respectively) than controls. Acute
carnosine supplementation resulted only in three subjects in
carnosinemia. The CCT 110% performance was not improved after
carnosine supplementation, even when accounting for low/high CN1 content. No differences were found in acid-base balance, except for elevated resting
bicarbonate following
carnosine supplementation and in low CN1 subjects. In conclusion,
explosive athletes have lower serum CN1 activity and content compared with untrained controls, possibly resulting from genetic selection. Acute
carnosine supplementation does not improve high-intensity performance.