Beta-hydroxy-beta-methylbutyrate HMB supplement health benefit
Beta-hydroxy beta-methylbutyrate, is a metabolite of the essential amino acid leucine and is synthesized in the human body. This compound plays a part in protein synthesis and was discovered by Dr. Steve Nissen. Claims are made that Beta-hydroxy-beta-methylbutyrate HMB increases muscle mass and decreases muscle breakdown.
Exercise-Induced Muscle Damage Is Not Attenuated by
beta-Hydroxy-beta-Methylbutyrate and alpha-Ketoisocaproic Acid Supplementation.
J Strength Cond Res. 2010; Nunan D, Howatson G. School of Life Sciences, Kingston University, Kingston-upon-Thames, United Kingdom; School of Psychology and Sport Sciences, Northumbria University, Newcastle-upon-Tyne, United Kingdom; and 3English Institute of Sport, Bisham Abbey, United Kingdom.
The purpose of this study was to examine the effects of combined oral beta-hydroxy-beta-methylbutyrate (HMB) and alpha-ketoisocaproic acid (KIC) supplementation on indices of exercise-induced muscle damage (EIMD) after an acute bout of eccentric-biased exercise. Fourteen male subjects were allocated to 2 groups: a placebo group (3 g.d corn flour) or an HMB + KIC group (3 g.d HMB and 0.3 g.d KIC). Supplementation commenced 11 days before a 40-minute bout of downhill running and continued for 3 days post-exercise. Delayed-onset muscle soreness, mid-thigh girth, knee extensor range of motion, serum creatine kinase (CK) activity, and isometric and concentric torque were assessed pre-exercise and at 24, 48, and 72 hours post-exercise. Delayed-onset muscle soreness, CK activity, and isometric and concentric torque all changed over the 72-hour period; however, HMB + KIC had no significant effect on any of the indices of muscle damage. Although 14 days HMB and KIC supplementation did not attenuate indices of EIMD after an acute bout of unaccustomed eccentric-biased exercise, there was a trend for a more rapid rate of recovery in isometric and isokinetic muscle function. beta-hydroxy-beta-methylbutyrate and KIC may therefore provide limited benefit in the recovery of muscle function after EIMD in untrained subjects or after unaccustomed exercise.
Benefit of Beta-hydroxy-beta-methylbutyrate HMB
Beta-hydroxy-beta-methylbutyrate supplementation in critically ill trauma patients.
J Trauma. 2007. Kuhls DA, Rathmacher JA, Musngi MD, Frisch DA, Nielson J, Barber A, MacIntyre AD, Coates JE, Fildes JJ.
Department of Surgery, University of Nevada School of Medicine, Las Vegas, Nevada, USA.
Negative nitrogen balance and skeletal muscle loss are common in critically injured patients and may contribute to morbidity, mortality and resource utilization. Juven, an enteral supplement which is a combination of beta-hydroxy-beta-methylbutyrate (HMB), arginine (ARG), and glutamine (GLN) has been shown to restore muscle in cachetic acquired immunodeficiency syndrome (AIDS) and cancer patients. More recently HMB has been shown to attenuate cancer-induced muscle loss by decreasing muscle proteolysis. The purpose of this study was to analyze whether Beta-hydroxy-beta-methylbutyrate alone or in combination with ARG and GLN would have a similar effect on critically injured trauma patients. We hypothesized that nitrogen balance would be improved and muscle proteolysis decreased with HMB and HMB/ARG/GLN supplementation. There were 100 adult trauma patients with Injury Severity Score (ISS) >18 were enrolled in this prospective, randomized, blinded study. All patients received standard tube feeds and one of three iso-nitrogenous supplements; Beta-hydroxy-beta-methylbutyrate, HMB/ARG/ GLN, or placebo for 28 days. Change in nitrogen balance from the first 7 days to the last 7 days was -4.3 for the Beta-hydroxy-beta-methylbutyrate and -5.6 g/d HMB/ARG/GLN groups compared with -8.9 g/d for the placebo group. These data suggest that supplementation with Beta-hydroxy-beta-methylbutyrate alone may improve nitrogen balance in critically injured adult patients and that this effect is not a result of lowered muscle protein turnover as originally hypothesized.
Mechanism of attenuation by beta-hydroxy-beta-methylbutyrate
of muscle protein degradation induced by lipopolysaccharide.
Mol Cell Biochem. 2009. Russell ST, Tisdale MJ. Nutritional Biomedicine, School of Life and Health Sciences, Aston University, Birmingham, UK.
The mechanism of the effect of beta-hydroxy-beta-methylbutyrate (HMB) on protein degradation induced by lipopolysaccharide (LPS) has been evaluated in murine myotubes. HMB completely attenuated total protein degradation induced by LPS (1-100 ng/ml), formation of reactive oxygen species (ROS) and activation of caspase-3/-8. Specific inhibitors of caspase-3/-8 completely attenuated ROS production, total protein degradation and the LPS-induced autophosphorylation of dsRNA-dependent protein kinase (PKR). Protein degradation in response to LPS or ROS production was not seen in myotubes transfected with mutant PKRDelta6, suggesting that PKR was involved in ROS production, which was essential for total protein degradation. This was confirmed using the antioxidant butylated hydroxytoluene (BHT) which completely attenuated protein degradation in response to LPS. The link between PKR activation and ROS production was mediated through p38 mitogen-activated protein kinase (MAPK), which was activated by LPS in myotubes transfected with wild-type PKR, but not PKRDelta6. LPS induces protein degradation through a signalling cascade involving activation of caspase-3/-8, activation of PKR and production of ROS through p38MAPK, and that this process is attenuated by beta-hydroxy-beta-methylbutyrate.