An Overview on Beta-Hydroxy-Beta-Methylbutyrate Supplementation in Skeletal Muscle Function and Sports Performance

Amino acids such as leucine and its metabolite alpha-ketoisocaproate (KIC) are returning to the focus of several studies. It was observed that these compounds, or even a subproduct of their metabolism, could inhibit proteolysis and promote muscle hypertrophy in mice, leading to a reduction of urinary nitrogen loss and protein catabolism (Hider et al., 1969; Nissen and Abumrad, 1997). KIC or other metabolite of leucine inhibits protein degradation in vitro because the use of inhibitors of leucine transamination to KIC prevented this effect (Tischler et al., 1982). It is noteworthy that other branched chain amino acids, isoleucine or valine as well as their metabolites, did not promote these effects, reinforcing the possibility that some metabolite of leucine may act as a key element in triggering this anticatabolic effect (Holecek et al., 2009). Nissen et al. (1996) suggested that beta-hydroxy-beta-methylbutyrate (HMB) be the metabolite responsible for these effects. In fact, direct effects of HMB were reported, with decreased proteolysis (∼80%) and increased protein synthesis (∼20%) in skeletal muscle of rats and chickens incubated with various concentrations of HMB (Nissen and Abumrad, 1997).