- Jun 25, 2006
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If you’re putting on weight, a diet containing extra BCAAs may help you build up less fat mass. Japanese researchers discovered, when doing experiments with mice, that the liver and muscles play a key role in the fat-mass reducing effect of BCAAs.
Athletes use BCAAs mainly as an anticatabolic supplement. They usually take somewhere between 5 and 25 g before training and notice that this helps them to recover faster.
BCAAs were originally marketed in Japan as clinical nutritional aids. They strengthen liver functioning and also have a positive effect on the insulin and glucose metabolism. Liver disease and diabetes are also possible effects of overweight. Which is why the Japanese wondered whether BCAAs could help to limit the negative health effects of the current obesity epidemic.
The researchers gave their mice feed consisting of 45 or 65 percent fat for six weeks. The mice put on weight fast on these diets. After four weeks the Japanese added BCAAs to the drinking water of half of the lab animals. One ml drinking water contained 20 mg BCAAs.
The BCAA supplementation had no effect on weight gain in the mice that were given feed consisting of 65 percent fat, but it did have an effect on the 45 percent fat group.
The researchers are not able to explain this. The BCAAs didn’t stop the mice from getting fatter, but they did reduce the speed with which the mice built up fat mass, as the figure below shows. What’s more, the BCAA animals had fifty percent less white fat tissue [WAT] than the mice in the control group.
The researchers actually found that the supplementation had the greatest effects in the muscle and liver cells rather than in the fat cells. They found fifty percent less fat [triglycerides] in these cells in the BCAA mice, and much greater activity in the molecules that are involved in fat burning, such as the fat sensor PPAR-alpha, the enzyme COT-1 and the uncoupling proteins 2 and 3. CPT-1 helps the cells to burn fatty acids; uncoupling proteins boost the heat production in cells.
Many athletes who use BCAAs say that they lose noticeable amounts of fat. The Japanese research shows that these athletes may be right.
The effects of branched-chain amino acid granules on the accumulation of tissue triglycerides and uncoupling proteins in diet-induced obese mice.
Arakawa M, Masaki T, Nishimura J, Seike M, Yoshimatsu H.
Source
Department of Internal Medicine1, Faculty of Medicine, Oita University, Japan.
Abstract
It has been demonstrated the involvement of branched-chain amino acids (BCAA) on obesity and related metabolic disorder. We investigated the effects of branched-chain amino acids (BCAA) on obesity and on glucose/fat homeostasis in mice fed on a high-fat (45%) diet. BCAA was dissolved in 0.5% methylcellulose and added to the drinking water (BCAA-treated group). A high-fat diet was provided for 6 weeks and BCAA was given for 2 weeks. The BCAA-treated group gained almost 7% less body weight and had less epididymal adipose tissue (WAT) mass than the control group (p<0.05). BCAA supplementation also reduced the hepatic and skeletal muscle triglyceride (TG) concentrations (p<0.05). The hepatic levels of PPAR-alpha and uncoupling protein (UCP) 2, and the level of PPAR-alpha and UCP3 in the skeletal muscle were greater in the BCAA-treated group than in the control mice (p<0.05). These results demonstrate that the liver and muscle TG concentration are less in BCAA-treated group. BCAA affects PPAR-alpha and UCP expression in muscle and liver tissue.
PMID: 21372430 [PubMed - indexed for MEDLINE]
Can’t train? Keep on using those BCAAs…
Strength athletes who for whatever reason are unable to train for a couple of weeks can reduce their muscle decay by using BCAAs. An animal study that Japanese researchers at Kobe University recently published in Nutrition Research suggests that BCAAs inhibit catabolic processes in inactive muscles.
Inactive muscles wither so quickly that space trips take a heavy toll on cosmonauts, and forced bed rest can cause extra problems for patients who are in recovery. For this reason scientists are keen to find nutritional strategies that doctors can use to prevent muscle decay as a result of inactivity. They have had some success in the past with creatine, leucine and resveratrol.
In many of the studies researchers use rats whose hind legs have been temporarily disabled [HS]. There’s a picture of how these animals look at the top of the page. Rats in a control group were able to use their hind legs normally [Control].
Half of the animals in each group were given 600 mg BCAAs per kg bodyweight daily. The BCAAs were produced by Ajinomoto. The human equivalent of the dose used would be 100 mg BCAA per kg bodyweight. So if you weigh 90 kg that would amount to 9 g per day.
The figure below shows that, while BCAAs couldn’t prevent inactivity from leading to decay of the soleus muscle, administration did mitigate the breakdown. The photos below show that BCAA supplementation did reduce the decrease in the muscle cell size.
The figure above reveals how BCAA supplementation works at molecular level. The amino acids reduced the production of catabolic proteins such as atrogin-1 and MuRF1.
“In conclusion, BCAA protected against soleus muscle atrophy induced by hindlimb suspension and decreased atrogin-1 and MuRF1 protein levels, suggesting the possibility that BCAA protects against muscle atrophy, at least in part, via the inhibition of the Ub-proteasome pathway”, the researchers write. “Oral BCAA administration appears to have the potential to protect against immobilization or microgravity-induced muscle atrophy.”
Branched-chain amino acids reduce hindlimb suspension-induced muscle atrophy and protein levels of atrogin-1 and MuRF1 in rats.
Maki T, Yamamoto D, Nakanishi S, Iida K, Iguchi G, Takahashi Y, Kaji H, Chihara K, Okimura Y.
Source
Department of Biophysics, Kobe University Graduate School of Health Science, Kobe, Japan.
Abstract
Atrogin-1 and MuRF1, muscle-specific ubiquitin ligases, and autophagy play a role in protein degradation in muscles. We hypothesized that branched-chain amino acids (BCAAs) may decrease atrogin-1, MuRF1, and autophagy, and may have a protective effect on disuse muscle atrophy. To test this hypothesis, we selected hindlimb suspension (HS)-induced muscle atrophy as a model of disuse muscle atrophy because it is an established model to investigate the effects of decreased muscle activity. Sprague-Dawley male rats were assigned to 4 groups: control, HS (14 days), oral BCAA administration (600 mg/[kg day], 22.9% L-isoleucine, 45.8% L-leucine, and 27.6% L-valine), and HS and BCAA administration. After 14 days of the treatment, muscle weights and protein concentrations, cross-sectional area (CSA) of the muscle fibers, atrogin-1 and MuRF1 proteins, and microtubule-associated protein 1 light chain 3 II/I (ratio of LC3 II/I) were measured. Hindlimb suspension significantly reduced soleus muscle weight and CSA of the muscle fibers. Branched-chain amino acid administration partly but significantly reversed the HS-induced decrease in CSA. Hindlimb suspension increased atrogin-1 and MuRF1 proteins, which play a pivotal role in various muscle atrophies. Branched-chain amino acid attenuated the increase in atrogin-1 and MuRF1 in soleus muscles. Hindlimb suspension significantly increased the ratio of LC3 II/I, an indicator of autophagy, whereas BCAA did not attenuate the increase in the ratio of LC3 II/I. These results indicate the possibility that BCAA inhibits HS-induced muscle atrophy, at least in part, via the inhibition of the ubiquitin-proteasome pathway. Oral BCAA administration appears to have the potential to prevent disuse muscle atrophy.
PMID: 23084640 [PubMed - in process]
Athletes use BCAAs mainly as an anticatabolic supplement. They usually take somewhere between 5 and 25 g before training and notice that this helps them to recover faster.
BCAAs were originally marketed in Japan as clinical nutritional aids. They strengthen liver functioning and also have a positive effect on the insulin and glucose metabolism. Liver disease and diabetes are also possible effects of overweight. Which is why the Japanese wondered whether BCAAs could help to limit the negative health effects of the current obesity epidemic.
The researchers gave their mice feed consisting of 45 or 65 percent fat for six weeks. The mice put on weight fast on these diets. After four weeks the Japanese added BCAAs to the drinking water of half of the lab animals. One ml drinking water contained 20 mg BCAAs.
The BCAA supplementation had no effect on weight gain in the mice that were given feed consisting of 65 percent fat, but it did have an effect on the 45 percent fat group.
The researchers are not able to explain this. The BCAAs didn’t stop the mice from getting fatter, but they did reduce the speed with which the mice built up fat mass, as the figure below shows. What’s more, the BCAA animals had fifty percent less white fat tissue [WAT] than the mice in the control group.
The researchers actually found that the supplementation had the greatest effects in the muscle and liver cells rather than in the fat cells. They found fifty percent less fat [triglycerides] in these cells in the BCAA mice, and much greater activity in the molecules that are involved in fat burning, such as the fat sensor PPAR-alpha, the enzyme COT-1 and the uncoupling proteins 2 and 3. CPT-1 helps the cells to burn fatty acids; uncoupling proteins boost the heat production in cells.
Many athletes who use BCAAs say that they lose noticeable amounts of fat. The Japanese research shows that these athletes may be right.
The effects of branched-chain amino acid granules on the accumulation of tissue triglycerides and uncoupling proteins in diet-induced obese mice.
Arakawa M, Masaki T, Nishimura J, Seike M, Yoshimatsu H.
Source
Department of Internal Medicine1, Faculty of Medicine, Oita University, Japan.
Abstract
It has been demonstrated the involvement of branched-chain amino acids (BCAA) on obesity and related metabolic disorder. We investigated the effects of branched-chain amino acids (BCAA) on obesity and on glucose/fat homeostasis in mice fed on a high-fat (45%) diet. BCAA was dissolved in 0.5% methylcellulose and added to the drinking water (BCAA-treated group). A high-fat diet was provided for 6 weeks and BCAA was given for 2 weeks. The BCAA-treated group gained almost 7% less body weight and had less epididymal adipose tissue (WAT) mass than the control group (p<0.05). BCAA supplementation also reduced the hepatic and skeletal muscle triglyceride (TG) concentrations (p<0.05). The hepatic levels of PPAR-alpha and uncoupling protein (UCP) 2, and the level of PPAR-alpha and UCP3 in the skeletal muscle were greater in the BCAA-treated group than in the control mice (p<0.05). These results demonstrate that the liver and muscle TG concentration are less in BCAA-treated group. BCAA affects PPAR-alpha and UCP expression in muscle and liver tissue.
PMID: 21372430 [PubMed - indexed for MEDLINE]
Can’t train? Keep on using those BCAAs…
Strength athletes who for whatever reason are unable to train for a couple of weeks can reduce their muscle decay by using BCAAs. An animal study that Japanese researchers at Kobe University recently published in Nutrition Research suggests that BCAAs inhibit catabolic processes in inactive muscles.
Inactive muscles wither so quickly that space trips take a heavy toll on cosmonauts, and forced bed rest can cause extra problems for patients who are in recovery. For this reason scientists are keen to find nutritional strategies that doctors can use to prevent muscle decay as a result of inactivity. They have had some success in the past with creatine, leucine and resveratrol.
In many of the studies researchers use rats whose hind legs have been temporarily disabled [HS]. There’s a picture of how these animals look at the top of the page. Rats in a control group were able to use their hind legs normally [Control].
Half of the animals in each group were given 600 mg BCAAs per kg bodyweight daily. The BCAAs were produced by Ajinomoto. The human equivalent of the dose used would be 100 mg BCAA per kg bodyweight. So if you weigh 90 kg that would amount to 9 g per day.
The figure below shows that, while BCAAs couldn’t prevent inactivity from leading to decay of the soleus muscle, administration did mitigate the breakdown. The photos below show that BCAA supplementation did reduce the decrease in the muscle cell size.
The figure above reveals how BCAA supplementation works at molecular level. The amino acids reduced the production of catabolic proteins such as atrogin-1 and MuRF1.
“In conclusion, BCAA protected against soleus muscle atrophy induced by hindlimb suspension and decreased atrogin-1 and MuRF1 protein levels, suggesting the possibility that BCAA protects against muscle atrophy, at least in part, via the inhibition of the Ub-proteasome pathway”, the researchers write. “Oral BCAA administration appears to have the potential to protect against immobilization or microgravity-induced muscle atrophy.”
Branched-chain amino acids reduce hindlimb suspension-induced muscle atrophy and protein levels of atrogin-1 and MuRF1 in rats.
Maki T, Yamamoto D, Nakanishi S, Iida K, Iguchi G, Takahashi Y, Kaji H, Chihara K, Okimura Y.
Source
Department of Biophysics, Kobe University Graduate School of Health Science, Kobe, Japan.
Abstract
Atrogin-1 and MuRF1, muscle-specific ubiquitin ligases, and autophagy play a role in protein degradation in muscles. We hypothesized that branched-chain amino acids (BCAAs) may decrease atrogin-1, MuRF1, and autophagy, and may have a protective effect on disuse muscle atrophy. To test this hypothesis, we selected hindlimb suspension (HS)-induced muscle atrophy as a model of disuse muscle atrophy because it is an established model to investigate the effects of decreased muscle activity. Sprague-Dawley male rats were assigned to 4 groups: control, HS (14 days), oral BCAA administration (600 mg/[kg day], 22.9% L-isoleucine, 45.8% L-leucine, and 27.6% L-valine), and HS and BCAA administration. After 14 days of the treatment, muscle weights and protein concentrations, cross-sectional area (CSA) of the muscle fibers, atrogin-1 and MuRF1 proteins, and microtubule-associated protein 1 light chain 3 II/I (ratio of LC3 II/I) were measured. Hindlimb suspension significantly reduced soleus muscle weight and CSA of the muscle fibers. Branched-chain amino acid administration partly but significantly reversed the HS-induced decrease in CSA. Hindlimb suspension increased atrogin-1 and MuRF1 proteins, which play a pivotal role in various muscle atrophies. Branched-chain amino acid attenuated the increase in atrogin-1 and MuRF1 in soleus muscles. Hindlimb suspension significantly increased the ratio of LC3 II/I, an indicator of autophagy, whereas BCAA did not attenuate the increase in the ratio of LC3 II/I. These results indicate the possibility that BCAA inhibits HS-induced muscle atrophy, at least in part, via the inhibition of the ubiquitin-proteasome pathway. Oral BCAA administration appears to have the potential to prevent disuse muscle atrophy.
PMID: 23084640 [PubMed - in process]