Acute and chronic effects of [Beta]-hydroxy-[Beta]-methylbutyrate ([Beta]-HMB) on glucose tolerance, insulin sensitivity and muscle adaptation following chronic resistance training
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Maximizing protein accretion and mitigating protein degradation is a major goal for resistance training regimens and intervention therapies. The branch chain amino acid leucine has historically demonstrated a significant role in the activation of protein synthesis via the activation of the mammalian target of rapamycin complex 1 (mTORC1). A derivative of leucine metabolism, beta-hydroxy-beta-methylbutyrate (HMB) has shown similar effects on mTORC1 with recent literature suggesting adverse effects of HMB on glucose homeostasis and regulation. Herein, we used animal models to test the effects of varying doses of HMB on glucose homeostasis and during a novel chronic resistance whole body training model. These data suggest that HMB effects possess acute modulation to the Akt/mTOR signaling pathway proteins, with minimal contributions to strength gains during chronic resistance whole body exercise. Our novel whole body exercise technique revealed a significant increase in strength gains with no differences in in situ force production in quadriceps and triceps surae muscle groups, but did show increased force per unit mass in both the triceps surae and quadriceps muscle groups. These data suggest an increase in whole body muscular coordination and/or synchronicity in force production that promotes increases in overall total strength. Furthermore, our data suggests that the overload placed on each individual contributing muscle to force output was not significant enough to induce a hypertrophic response. We conclude that HMB ingestion provides minimal benefit during prolonged exercise regimens and the effects of HMB on blood glucose and insulin sensitivity are not adverse. Finally, our whole body resistance model presents a novel paradigm for increasing work output that can be a model of whole body resistance training.