Strength athletes who are unable to train for a while lose less muscle mass and strength if they take the leucine metabolite HMB, according to an animal study published by researchers at West Virginia University in the American Journal of Physiology – Regulatory Integrative and Comparative Physiology.
HMB is a supplement that is attracting widespread interest outside strength sports circles. And it’s not surprising. At a dose of 3 g per day, HMB enhances the effect of a slimming diet according to a Taiwanese study, and it also boosts the results of the over-seventies who start weight training according to a 2001 human study. Researchers at Iowa State discovered that HMB slows down muscle breakdown in endurance athletes, and scientists at the Hebrew University of Jerusalem recently published the results of a study in which HMB supplementation made volleyball players stronger and more muscular.
HMB may also be interesting for sick or elderly people who are losing muscle mass, for example through forced inactivity. Sarcopaenia researchers at West Virginia University tested this theory in an experiment involving old lab rats aged 34 months. The researchers disabled the hind foot of one group of animals for 14 days [HS], after which they let the rats use the leg for the following 14 days [R]. In a control group nothing was done to the animals’ hind leg [CC].
The researchers measured the amount of strength the rats could develop with their hind leg before HS, after HS and after R. The figure below shows that inactivity weakened the muscles, but that HMB supplementation reduced the strength loss. The researchers used a dose of 340 mg HMB per kg bodyweight per day. The human equivalent of this dose would be 4-7 g HMB per day.
The figures below show what happened to the plantaris muscle. You can see that HMB supplementation reduced the decrease in muscle mass in the experimental group.
Under the microscope the researchers saw more dead muscle cells [the apoptotic index was higher] in the muscles of the HS rats, but they also saw that HMB supplementation reduced muscle cell death. In the muscle cells of the HS rats, HMB inhibited the production of the suicide protein caspase-9.
“HMB should be further evaluated and considered as part of a potential therapeutic strategy along with more moderate muscle loading to prevent muscle loss in aging and perhaps other conditions of muscle wasting”, the researchers write.
The study was funded by Abbott Laboratories, which manufactures, among other things, supplements and sports nutrition products. Abbot has a patent on the use of HMB in products “for the prevention and treatment of chronic inflammatory diseases, cancer, and involuntary weight loss”. [United States Patent 8217077]
?-Hydroxy-?-methylbutyrate reduces myonuclear apoptosis during recovery from hind limb suspension-induced muscle fiber atrophy in aged rats.
?-Hydroxy-?-methylbutyrate (HMB) is a leucine metabolite shown to reduce protein catabolism in disease states and promote skeletal muscle hypertrophy in response to loading exercise. In this study, we evaluated the efficacy of HMB to reduce muscle wasting and promote muscle recovery following disuse in aged animals. Fisher 344×Brown Norway rats, 34 mo of age, were randomly assigned to receive either Ca-HMB (340 mg/kg body wt) or the water vehicle by gavage (n = 32/group). The animals received either 14 days of hindlimb suspension (HS, n = 8/diet group) or 14 days of unloading followed by 14 days of reloading (R; n = 8/diet group). Nonsuspended control animals were compared with suspended animals after 14 days of HS (n = 8) or after R (n = 8). HMB treatment prevented the decline in maximal in vivo isometric force output after 2 wk of recovery from hindlimb unloading. The HMB-treated animals had significantly greater plantaris and soleus fiber cross-sectional area compared with the vehicle-treated animals. HMB decreased the amount of TUNEL-positive nuclei in reloaded plantaris muscles (5.1% vs. 1.6%, P < 0.05) and soleus muscles (3.9% vs. 1.8%, P < 0.05). Although HMB did not significantly alter Bcl-2 protein abundance compared with vehicle treatment, HMB decreased Bax protein abundance following R, by 40% and 14% (P < 0.05) in plantaris and soleus muscles, respectively. Cleaved caspase-3 was reduced by 12% and 9% (P < 0.05) in HMB-treated reloaded plantaris and soleus muscles, compared with vehicle-treated animals. HMB reduced cleaved caspase-9 by 14% and 30% (P < 0.05) in reloaded plantaris and soleus muscles, respectively, compared with vehicle-treated animals. Although, HMB was unable to prevent unloading-induced atrophy, it attenuated the decrease in fiber area in fast and slow muscles after HS and R. HMB's ability to protect against muscle loss may be due in part to putative inhibition of myonuclear apoptosis via regulation of mitochondrial-associated caspase signaling. PMID: 21697520 [PubMed - indexed for MEDLINE] PMCID: PMC3174754 Source: http://www.ncbi.nlm.nih.gov/pubmed/21697520