Effects of essential amino acids supplementation on muscle damage following a heavy-load eccentric training session

Abstract

Summary Aim Unaccustomed physical exercise, particularly repeated eccentric muscle contractions, induces muscle soreness and alterations on muscle cellular structure. An increase in myofibrillar protein accretion can occur in the early post-exercise period and be potentiated by essential amino acid ingestion. We hypothesized that essential amino acid supplementation could reduce the efflux of indirect markers of muscle damage and delay the onset of muscular soreness in the week following a heavy-load eccentric training session. Methods Twenty-three randomly assigned young males performed a bench press exercise under eccentric condition. They were subdivided into a placebo group (n = 11) and an essential amino acids group (n = 12). The effect of the training session was assessed by analysing two indirect markers of muscle damage, namely plasma concentrations of creatine kinase and myoglobin measured before, immediately after, and post-workout day 1, 2, 3, 4 and 7. Muscle soreness was evaluated by a visual analogy scale at the same time point as the markers of muscle damage. Results The training session induced a significant increase in muscle soreness in both placebo and essential amino acids groups. Plasma creatine kinase release increased significantly at D+3 and D+4 while myoglobin efflux rose at D+3 in placebo group only. No statistical differences were observed between groups for the two indirect markers of muscle damage. Gaussian distribution was found to be the best-fit model for the plasma myoglobine and creatine kinase concentration curves. F-test support that individual curves were statistically distinguishable as comparing to the best-fit values of the three parameters (area, SD and mean) between placebo and essential amino acids group data sets (P  Conclusion These data indicate that essential amino acids supplementation do have minor effects on the overall plasma release of indirect markers of muscle damage during the recovery period without impact on delayed-onset muscular soreness.