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declare that they have no competing interests. Authors’ contributions LYB was the primary author of the manuscript. TP was involved in subject recruitment, data collection and helped to draft the manuscript. DM was involved in data collection and editing the manuscript. YPP conceived of the study, participated in its design and coordination and helped to draft the manuscript. All authors read

and approved the final manuscript.”
“Introduction Skeletal muscle damage is a phenomenon that can occur due to several factors, such as rupture and/or cell necrosis, representing about 10-55% of total muscular injuries [1]. The main feature of skeletal muscle damage without cell necrosis is the disruption of muscle fibers, specifically the sheath of basal Thymidine kinase lamina [1]. Regarding mechanical stimuli, specifically resistance exercise (RE), it is known that it can promote microdamage in muscle fibers imposed by contractions and/or overload and, according to the intensity, length, and volume the severity and degree of damage and discomfort may be compounded over time and persist chronically [2]. As functional consequence, muscle damage is manifested by a temporary decrease in strength, increased muscle passive tension, delayed onset muscle soreness (DOMS), and edema [2]. In this context, some prophylactic interventions have been proposed in order to attenuate the negative effects associated with RE-induced muscle damage. Among the nutritional strategies, supplementation with branched-chain amino acids (BCAA – leucine, isoleucine, and valine) has been considered a potential intervention [3, 4].