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Join Date: Mar 2005 Age: 24 Posts: 1,406 Rep Power: 51 
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ß-Hydroxy-ß-methylbutyrate (HMB)2 is a common dietary supplement used by many exercise enthusiasts and more recently used in a medically related nutritional product to reduce wasting of muscle tissue in AIDS (Clark et al. 2000 , Nissen et al. 1996a , 1996b and 1997 , Nissen and Abumrad 1997 ). The major benefit of HMB appears to be a reduction in muscle damage and/or reduced protein catabolism, which results in improved gains in muscle size and strength when combined with exercise (Nissen et al. 1996b ). Although several animal studies have shown that HMB consumption does not cause adverse effects (Nissen et al. 1994a and 1994b , Peterson et al. 1999a and 1999b , Van Koevering et al. 1993 and 1994 ), until now there has not been a comprehensive analysis of safety data collected on HMB-fed humans.
HMB is a metabolite of the amino acid leucine and is produced endogenously in both animals and humans. The first step in the metabolism of leucine is transamination to {alpha}-ketoisocaproate (KIC). HMB is then produced from KIC by the cytosolic enzyme KIC-dioxygenase (Sabourin and Bieber 1983 ) and, at least in pigs, is produced exclusively from leucine (Van Koevering and Nissen 1992 ). Plasma concentrations of HMB normally range from 1 to 4 µmol/L, but can increase 5- to 10-fold after leucine is fed (Nissen and Abumrad 1997 ). The cytosolic dioxygenase enzyme has been characterized extensively and differs from the mitochondrial KIC-dehydrogenase enzyme in that the dioxygenase enzyme is a cytosolic enzyme, whereas the dehydrogenase enzyme is found exclusively in the mitochondrion (Sabourin and Bieber 1981 and 1983 ). Recently, the KIC-dioxygenase enzyme was found to be identical to the tyrosine dioxygenase enzyme (Janskiewiez et al. 1996 ). It has been calculated that, under normal conditions, ~5% of leucine oxidation proceeds via this pathway (Van Koevering and Nissen 1992 ).
Numerous biochemical studies have shown that HMB is a precursor of cholesterol (Bloch 1944 , Rabinowitz 1955 , Rudney 1957 , Zabin and Bloch 1951 ). HMB in the cytosol of liver and muscle is first converted to cytosolic ß-hydroxy-ß-methylglutarate-Co-A (HMG-CoA), which can then be used for cholesterol synthesis (Rudney 1957 ). Thus HMB can serve as a precursor for cellular cholesterol synthesis especially in tissues such as muscle that rely on de novo synthesis of cholesterol. The working theory for HMB action is that stressed or damaged muscle cells may not be able to make sufficient HMG-CoA to support adequate cholesterol synthesis for cell functions, including proper functioning of cell membranes. Therefore, supplemental HMB could be a convenient source of HMG-CoA in these cells to maintain adequate cholesterol synthesis and, in turn, plasma membrane function. This contention is supported by the observation that supplementation of HMB can markedly decrease muscle damage as evidenced by leaking of creatine phosphokinase (CPK) out of muscle cells (Cheng et al. 1998 , Nissen et al. 1996b , Nissen and Abumrad 1997 ). Also supporting this concept are several studies showing that inhibition of cholesterol synthesis in muscle with drugs can result in muscle damage (Pierno et al. 1995 ), poor function (Bastiaanse et al. 1997 , Yeagle 1991 ) and even muscle cell death (Mutoh et al. 1999 ).
Supplemental HMB is usually taken by humans at a dosage of ~3 g/d. Therefore, the objective of this study is to report the safety-related data collected on HMB given in a dose of 3 g/d over a series of nine experiments. These experiments encompassed the young, the old, men and women, exercising and nonexercising subjects, and were from 3 to 8 wk in duration. In each of these studies, three batteries of tests were used to determine safety. First, comprehensive blood work was completed at regular intervals during each study. Second, the Circumplex test of emotion (Russell 1980 ) was given periodically during each study; and third, an adverse events questionnaire was filled out at intervals during each study. Together, these measurements should indicate the safety and tolerance of HMB in the general population.
Effect of dietary supplements on lean mass and strength gains with resistance exercise: a meta-analysis
Steven L. Nissen1 and Rick L. Sharp2
The purpose of this study was to quantify which dietary supplements augment lean mass and strength gains during resistance training. Peer-reviewed studies between the years 1967 and 2001 were included in the analysis if they met a predetermined set of experimental criteria, among which were at least 3-wk duration and resistance-training 2 or more times a week. Lean mass and strength were normalized for meta-analysis by conversion to percent change per week and by calculating the effect size for each variable. Of the 250 supplements examined, only 6 had more than 2 studies that met the criteria for inclusion in the meta-analysis. Creatine and beta -hydroxy-beta -methylbutyrate (HMB) were found to significantly increase net lean mass gains of 0.36 and 0.28%/wk and strength gains of 1.09 and 1.40%/wk (P < 0.05), respectively. Chromium, dehydroepiandrosterone, androstenedione, and protein did not significantly affect lean gain or strength. In conclusion, two supplements, creatine and HMB, have data supporting their use to augment lean mass and strength gains with resistance training.
Beta-hydroxy-beta-methylbutyrate ingestion, Part I: effects on strength and fat free mass.
Gallagher PM, Carrithers JA, Godard MP, Schulze KE, Trappe SW.
Human Performance Laboratory, Ball State University, Muncie, IN 47306, USA.
PURPOSE: The purpose of this investigation was 1) to determine whether HMB supplementation results in an increase in strength and FFM during 8 wk of resistance training and 2) determine whether a higher dose of HMB provides additional benefits. METHODS: Thirty-seven, untrained, college-aged men were assigned to one of three groups: 0, 38, or 76 mg x kg(-1) x d(-1) of HMB (approximately equal to 3 and 6 g x d(-1), respectively). Resistance training consisted of 10 different exercises performed 3 d x wk(-1) for 8 wk at 80% of 1-repetition maximum (1RM). The 1RM was reevaluated every 2 wk with workloads adjusted accordingly. RESULTS: No differences were observed in 1RM strength among the groups at any time. However, the 38 mg x kg (-1) x d(-1) group showed a greater increase in peak isometric torque than the 0 or 76 mg.kg(-1) x d(-1) groups (P < 0.05). The 76 mg x kg(-1) x d(-1) group had a greater increase in peak isokinetic torque than the 0 or 38 mg x kg(-1) x d(-1) groups at 2.1, -3.15, and -4.2 rad x s(-1) (P < 0.05). Plasma creatine phosphokinase (CPK) activity was greater for the 0 mg x kg(-1) x d(-1) versus the 38 or 76 mg x kg(-1) x d(-1) groups at 48 h after the initial training bout (P < 0.05). In addition, no differences were observed in body fat between the three groups. However, the 38 mg x kg(-1) x d(-1) group exhibited a greater increase in FFM (P < 0.05). CONCLUSIONS: Although the IRM strength gains were not significantly different, HMB supplementation appears to increase peak isometric and various isokinetic torque values, and increase FFM and decrease plasma CPK activity. Lastly, it appears that higher doses of HMB (i.e., > 38 mg x kg(-1) x d(-1)) do not promote strength or FFM gain |
