Exercise alters and β-alanine combined with exercise augments histidyl dipeptide levels and scavenges lipid peroxidation products in human skeletal muscle.

Carnosine and anserine are dipeptides synthesized from histidine and β-alanine by carnosine synthase (ATPGD1). These dipeptides, present in high concentration in the skeletal muscle, form conjugates with lipid peroxidation products such as 4-hydroxy trans-2-nonenal (HNE). Although skeletal muscle levels of these dipeptides could be elevated by feeding β-alanine, it is unclear how these dipeptides and their conjugates are affected by exercise training with or without β-alanine supplementation. We recruited twenty physically active men, who were allocated to either β-alanine or placebo-feeding group matched for VO2 peak, lactate threshold, and maximal power (Wmax). Participants completed 2 weeks of conditioning phase followed by 1 week of exercise testing (CPET) and a single session followed by 6 weeks of high intensity interval training (HIIT). Analysis of muscle biopsies showed that the levels of carnosine and ATPGD1 expression were increased after CPET and decreased following a single session and 6 weeks of HIIT. Expression of ATPGD1 and levels of carnosine were increased upon β-alanine-feeding after CPET, while ATPGD1 expression decreased following a single session of HIIT. The expression of fiber type markers myosin heavy chain (MHC) I and IIa remained unchanged after CPET. Levels of carnosine, anserine, carnosine-HNE, carnosine-propanal and carnosine-propanol were further increased after 9 weeks of β-alanine supplementation and exercise training, but remained unchanged in the placebo-fed group. These results suggest that carnosine levels and ATPGD1 expression fluctuates with different phases of training. Enhancing carnosine levels by β-alanine feeding could facilitate the detoxification of lipid peroxidation products in the human skeletal muscle.

RCT Entities:   Population Interventions Outcomes