Abstract
Prolonged periods of muscle disuse cause a rapid loss of muscle mass and force output. Aging exacerbates muscle loss and reduces muscle recovery after reloading in part, as a result of accelerated apoptosis and reduced satellite cell proliferation. Beta-hydroxy-beta-methylbutyrate (HMB) is a leucine metabolite that has been studied extensively as an ergogenic aid specifically with regard to decreasing protein catabolism and thus promoting skeletal muscle hypertrophy. Therefore, HMB may prove to be an effective countermeasure to unloading induced atrophy and muscle recovery following disuse. PURPOSE: To investigate the efficacy of HMB to promote muscle recovery following disuse in aged animals. METHODS: 64 aged (34 mo) FBN x 344 rats were randomly assigned to receive either Ca-HMB (340 mg/kg body weight), or water by gavage. Eight rats in each group were sacrificed following 1 week of treatment and the remaining 16 animals had Brdu pellets implanted subcutaneously and were subsequently suspended for 14 days. One half of each group was either immediately sacrificed following hindlimb suspension to induce muscle atrophy, or allowed to recover for 2 weeks prior to sacrifice. The soleus, plantaris and gastrocnemius muscles were dissected, weighed and snap frozen for further analysis. The effects of HMB on fiber type shifts, satellite cell proliferation and myonuclear apoptosis were evaluated by immunohistochemistry, TUNEL staining and immunoblotting. RESULTS: HMB treatment had no effect on muscle atrophy, or in vivo force output following 14 days of hindlimb unloading. However, there was a tendency for HMB to improve body weight, muscle mass and maximal in vivo isometric force output after 2 weeks of recovery from hindlimb unloading. Furthermore, there was a tendency for HMB to increase the percentage of type II fibers, satellite cell activation, and BrdU, MyoD, and Pax7 expression in plantaris muscles. Additionally, HMB decreased the amount of TUNEL positive nuclei and pro-apoptotic proteins in reloaded soleus muscles. CONCLUSION: Although, HMB was unable to protect against unloading-induced atrophy, HMB may have the potential to reduce myonuclear apoptosis and promote satellite cell proliferation during recovery from disuse in aged rodents.
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