HMB prevents the loss of lean body mass
- 09-22-2013, 10:53 AM
HMB prevents the loss of lean body mass
Effect of β-hydroxy-β-methylbutyrate () on lean body mass during 10 days of bed rest in older adults
Loss of due to prolonged bed rest decreases functional capacity and increases hospital morbidity and mortality in older adults.
To determine if , a metabolite, is capable of attenuating muscle decline in healthy older adults during complete bed rest.
A randomized, controlled, double-blinded, parallel-group design study was carried out in 24 healthy (SPPB ≥ 9) older adult subjects (20 women, 4 men), confined to complete bed rest for ten days, followed by resistance training rehabilitation for eight weeks. Subjects in the experimental group were treated with HMB (calcium salt, 1.5 g twice daily – total 3 g/day). Control subjects were treated with an inactive placebo powder. Treatments were provided starting 5 days prior to bed rest till the end rehabilitation phase. DXA was used to measure body composition.
Nineteen eligible older adults (BMI: 21–33; age: 60–76 year) were evaluable at the end of the bed rest period (Control n = 8; Ca-HMB n = 11). Bed rest caused a significant decrease in total lean body mass (LBM) (2.05 ± 0.66 kg; p = 0.02, paired t-test) in the Control group. With the exclusion of one subject, treatment with HMB prevented the decline in LBM over bed rest −0.17 ± 0.19 kg; p = 0.23, paired t-test). There was a statistically significant difference between treatment groups for change in LBM over bed rest (p = 0.02, ANOVA). Sub-analysis on female subjects (Control = 7, HMB = 8) also revealed a significant difference in change in LBM over bed rest between treatment groups (p = 0.04, ANOVA). However, differences in function parameters could not be observed, probably due to the sample size of the study.
In healthy older adults, HMB supplementation preserves muscle mass during 10 days of bed rest. These results need to be confirmed in a larger trial.PESCIENCE.COM
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- 09-23-2013, 03:34 AM
09-23-2013, 03:49 AM
Yeah a big thing to be aware of here is their dietary leucine intake. If I remember correctly, in another recent study on hmb the participants received all of their dietary protein via a very low leucine protein source.
Obviously this is necessary to determine the function of HMB, however further study comparing HMB to leucine or a complete protein source is necessary before there can be a justification of paying any sort of premium for HMB.
SNS Representative - DeeB@seriousnutritionsolutions .com
05-27-2014, 12:35 PM
Leucine and HMB differentially modulate proteasome system in skeletal muscle under different sarcopenic conditions.
AuthorsBaptista IL, et al. Show all Journal
PLoS One. 2013 Oct 4;8(10):e76752. doi: 10.1371/journal.pone.0076752.
In the present study we have compared the effects of leucine supplementation and its metabolite β-hydroxy-β-methyl butyrate (HMB) on the ubiquitin-proteasome system and the PI3K/Akt pathway during two distinct atrophic conditions, hindlimb immobilization and dexamethasone treatment. Leucine supplementation was able to minimize the reduction in rat soleus mass driven by immobilization. On the other hand, leucine supplementation was unable to provide protection against soleus mass loss in dexamethasone treated rats. Interestingly, HMB supplementation was unable to provide protection against mass loss in all treatments. While solely fiber type I cross sectional area (CSA) was protected in immobilized soleus of leucine-supplemented rats, none of the fiber types were protected by leucine supplementation in rats under dexamethasone treatment. In addition and in line with muscle mass results, HMB treatment did not attenuate CSA decrease in all fiber types against either immobilization or dexamethasone treatment. While leucine supplementation was able to minimize increased expression of both Mafbx/Atrogin and MuRF1 in immobilized rats, leucine was only able to minimize Mafbx/Atrogin in dexamethasone treated rats. In contrast, HMB was unable to restrain the increase in those atrogenes in immobilized rats, but in dexamethasone treated rats, HMB minimized increased expression of Mafbx/Atrogin. The amount of ubiquitinated proteins, as expected, was increased in immobilized and dexamethasone treated rats and only leucine was able to block this increase in immobilized rats but not in dexamethasone treated rats. Leucine supplementation maintained soleus tetanic peak force in immobilized rats at normal level. On the other hand, HMB treatment failed to maintain tetanic peak force regardless of treatment. The present data suggested that the anti-atrophic effects of leucine are not mediated by its metabolite HMB.
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