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BCAA's are a waste of money, providing you eat sufficient protein.
Stimulation of muscle protein synthesis from ingestion of BCAA's post-workout is 50% lower than whey protein.
Although BCAA ingestion does stimulate muscle protein synthesis, the lack of EAA's limits the response.
"Thus, whereas our data clearly show that BCAA ingestion activates cell-signaling pathways that result in increased myofibrillar-MPS, ingestion of BCAAs alone may not be the optimal nutritional regimen to stimulate a maximal MPS response to resistance exercise training."
http://journal.frontiersin.org/article/10.3389/fphys.2017.00390/full
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Stimulation of muscle protein synthesis from ingestion of BCAA's post-workout is 50% lower than whey protein.
Although BCAA ingestion does stimulate muscle protein synthesis, the lack of EAA's limits the response.
"Thus, whereas our data clearly show that BCAA ingestion activates cell-signaling pathways that result in increased myofibrillar-MPS, ingestion of BCAAs alone may not be the optimal nutritional regimen to stimulate a maximal MPS response to resistance exercise training."
http://journal.frontiersin.org/article/10.3389/fphys.2017.00390/full
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STEROIDS AND FAT LOSS
There is no need to run high dose AAS blasts for your fat loss phases.
Here is some research from Bhasin S et al showing no metabolic benefit to dosages upward of 300mg/week of testosterone.
Running your AAS higher than this will result in a greater knock to your health markers, with no additional benefits to your fat loss goals.
I do also stick to this principle for pre-contest clients. 300mg/wk is plenty for 99% of people to retain their LBM deep into prep, and I will typically just throw in a DHT compound for cosmetic effects nearer the show, and possibly some low dosed trenbolone if well tolerated, especially if the individual is also using GH and insulin.
For those of you using AAS on general fat loss phases, 300mg/wk of Testosterone is all you need.
http://m.ajpendo.physiology.org/content/281/6/E1172.long?view=long&pmid=11701431
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There is no need to run high dose AAS blasts for your fat loss phases.
Here is some research from Bhasin S et al showing no metabolic benefit to dosages upward of 300mg/week of testosterone.
Running your AAS higher than this will result in a greater knock to your health markers, with no additional benefits to your fat loss goals.
I do also stick to this principle for pre-contest clients. 300mg/wk is plenty for 99% of people to retain their LBM deep into prep, and I will typically just throw in a DHT compound for cosmetic effects nearer the show, and possibly some low dosed trenbolone if well tolerated, especially if the individual is also using GH and insulin.
For those of you using AAS on general fat loss phases, 300mg/wk of Testosterone is all you need.
http://m.ajpendo.physiology.org/content/281/6/E1172.long?view=long&pmid=11701431
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Another interesting look into the PPAR agonist (like cardarine) & AMPk activator (like metformin) synergy for fat loss purposes.
The short:
They have a strong synergy for increasing endurance, not to mention the secondary effects useful to a physique athlete with each individual compound, most notably with nutrient partitioning. (Such as improving insulin sensitivity with metformin, and increasing muscle cell glucose uptake with GW)
The long:
- AMP-mimetic AICAR can increase endurance in*sedentary mice by genetically reprogramming muscle metabolism
- PPARδ agonists in combination with exercise synergistically induces fatigue-resistant type I fiber specification and mitochondrial biogenesis, ultimately enhancing physical performance.
- The synergy resulted in a unique muscle endurance gene signature.
- GW1516 and AICAR synergistically induced several endurance-related genes
- treatment of animals with AICAR and GW1516 creates a gene signature in skeletal muscle that replicates up to 40% of the genetic effects of combined exercise and GW1516 treatment
- the shared genes between the two profiles are linked to oxidative metabolism, angiogenesis, and glucose sparing pathways that are directly relevant to muscle performance
- synthetic PPARδ activation and AMPK activation alone provides a transcriptional cue that reprograms the skeletal muscle genome and dramatically enhances endurance.
http://www.cell.com/cell/fulltext/S...m/retrieve/pii/S0092867408008386?showall=true
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The short:
They have a strong synergy for increasing endurance, not to mention the secondary effects useful to a physique athlete with each individual compound, most notably with nutrient partitioning. (Such as improving insulin sensitivity with metformin, and increasing muscle cell glucose uptake with GW)
The long:
- AMP-mimetic AICAR can increase endurance in*sedentary mice by genetically reprogramming muscle metabolism
- PPARδ agonists in combination with exercise synergistically induces fatigue-resistant type I fiber specification and mitochondrial biogenesis, ultimately enhancing physical performance.
- The synergy resulted in a unique muscle endurance gene signature.
- GW1516 and AICAR synergistically induced several endurance-related genes
- treatment of animals with AICAR and GW1516 creates a gene signature in skeletal muscle that replicates up to 40% of the genetic effects of combined exercise and GW1516 treatment
- the shared genes between the two profiles are linked to oxidative metabolism, angiogenesis, and glucose sparing pathways that are directly relevant to muscle performance
- synthetic PPARδ activation and AMPK activation alone provides a transcriptional cue that reprograms the skeletal muscle genome and dramatically enhances endurance.
http://www.cell.com/cell/fulltext/S...m/retrieve/pii/S0092867408008386?showall=true
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Here's one piece of research featuring in an upcoming article I am writing on the blast & cruise vs. cycling approach for AAS users.
4,736 men with low testosterone were placed in three groups (levels were correlated with exogenous testosterone use):
1. Low - <212ng/dl
2. Normal - 212-742ng/dl
3. High - >742ng/dl
After 3 years, subjects in the 'normal' testosterone group had decreased incidence rates of cardiac infarction (driven by death) compared to the low group. The high testosterone group also noted this benefit, but with an increase incident rate of stroke.
This suggests anybody cruising long-term should be conservative with their approach, and stick to the 'normal' range as noted above.
https://www.ncbi.nlm.nih.gov/m/pubmed/26772440/
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4,736 men with low testosterone were placed in three groups (levels were correlated with exogenous testosterone use):
1. Low - <212ng/dl
2. Normal - 212-742ng/dl
3. High - >742ng/dl
After 3 years, subjects in the 'normal' testosterone group had decreased incidence rates of cardiac infarction (driven by death) compared to the low group. The high testosterone group also noted this benefit, but with an increase incident rate of stroke.
This suggests anybody cruising long-term should be conservative with their approach, and stick to the 'normal' range as noted above.
https://www.ncbi.nlm.nih.gov/m/pubmed/26772440/
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Rubbish phone pic the Mrs sent me. I dropped my camera and the screen won't come on, but it's nice to be feeling leaner!
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AROMATASE INHIBITORS & INSULIN RESISTANCE
We were just talking about the negatives of AI use in OPD, and this is one that I feel is worth a mention.
The research below from Frasier Gibbs et al shows that AI use reduces insulin sensitivity in healthy men. (via reduced peripheral glucose disposal).
These results echo what we have seen in animal studies showing a correlation between aromatase deficiency and insulin resistance previously.
Insulin resistance really is the enemy of the physique athlete, or anybody interested in health for that matter.
This is one of many reasons I recommend anybody using exogenous AAS in supra-physiological dosages to manage their estrogen via conservative use of aromatising compounds, and use non/low-aromatising compounds as your primary growth anchors in your stack.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4870856/
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We were just talking about the negatives of AI use in OPD, and this is one that I feel is worth a mention.
The research below from Frasier Gibbs et al shows that AI use reduces insulin sensitivity in healthy men. (via reduced peripheral glucose disposal).
These results echo what we have seen in animal studies showing a correlation between aromatase deficiency and insulin resistance previously.
Insulin resistance really is the enemy of the physique athlete, or anybody interested in health for that matter.
This is one of many reasons I recommend anybody using exogenous AAS in supra-physiological dosages to manage their estrogen via conservative use of aromatising compounds, and use non/low-aromatising compounds as your primary growth anchors in your stack.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4870856/
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DNP & ANTIOXIDANTS
It seems commonplace to see the recommendation of including antioxidant supplementation when using DNP.
The idea is that as DNP creates high rates of fat oxidisation, mitochondrial stress is increased. Interestingly, DNP in reality does the opposite, and reduces the formation of mitochondrial free radicals. (as shown below)
The real reason you may consider staying on top of your antioxidant intake is because one rare metabolite of DNP has been linked to cataract formation.
There have only been a few VERY rare cases of this in the history of DNP use, but antioxidants can be your 'insurance' as such, if you are one of the 0.1%.
Vitamin C, E, NAC, ubiquinol and pyruvate are all good choices, but DO NOT mega-dose them, as this comes with it's own set of negatives.
https://link.springer.com/article/10.1007/BF00240047
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It seems commonplace to see the recommendation of including antioxidant supplementation when using DNP.
The idea is that as DNP creates high rates of fat oxidisation, mitochondrial stress is increased. Interestingly, DNP in reality does the opposite, and reduces the formation of mitochondrial free radicals. (as shown below)
The real reason you may consider staying on top of your antioxidant intake is because one rare metabolite of DNP has been linked to cataract formation.
There have only been a few VERY rare cases of this in the history of DNP use, but antioxidants can be your 'insurance' as such, if you are one of the 0.1%.
Vitamin C, E, NAC, ubiquinol and pyruvate are all good choices, but DO NOT mega-dose them, as this comes with it's own set of negatives.
https://link.springer.com/article/10.1007/BF00240047
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Some talk on digestive health for physique athletes from myself and Austin Stout!
https://youtu.be/KPNz2ZY9m_Q
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https://youtu.be/KPNz2ZY9m_Q
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An interesting paper looking into the clinical use of trenbolone to combat the catabolic effects of hypogonadism, without the androgenic effects of exogenous testosterone.
Tren has SARM-like properties by having a greater binding affinity to androgen receptors than testosterone. As we all already know, tren has been shown to induce skeletal muscle hypertrophy and reduce adiposity in humans. What is interesting here is that it has also shown reduced growth in androgen-sensitive organs expressing 5-AR enzymes when compared to testosterone.
Therefore, you are avoiding the metabolisation to 'harsher' androgens (estradiol and DHT for example) from testosterone.
It will be interesting to see where the safety/efficacy of this treatment goes with tren and future SARMS.
http://www.sciencedirect.com/science/article/pii/S0039128X1000022X
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Tren has SARM-like properties by having a greater binding affinity to androgen receptors than testosterone. As we all already know, tren has been shown to induce skeletal muscle hypertrophy and reduce adiposity in humans. What is interesting here is that it has also shown reduced growth in androgen-sensitive organs expressing 5-AR enzymes when compared to testosterone.
Therefore, you are avoiding the metabolisation to 'harsher' androgens (estradiol and DHT for example) from testosterone.
It will be interesting to see where the safety/efficacy of this treatment goes with tren and future SARMS.
http://www.sciencedirect.com/science/article/pii/S0039128X1000022X
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JEFF BLACK - BODYBUILDING WITH BRITTLE BONES
Here is some serious motivation for your Thursday afternoon...
Yesterday I had the pleasure to sit and talk with Jeff Black about osteogenesis imperfecta, what it is, how it has affected his life, how it led him into a career in bodybuilding and what he is doing now to help those suffering with OI around the world.
Jeff is unbelievably inspiring, prepare to have a fire lit under your ass after listening to this.
YouTube: https://www.youtube.com/watch?v=86nP6nzwqWg
Audio: https://www.jjphysique.com/podcast/
iTunes: https://itunes.apple.com/gb/podcast/optimal-physique-development/id1265819314
To help support and donate to the OI Angel Tree: https://www.facebook.com/oiangeltree
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Here is some serious motivation for your Thursday afternoon...
Yesterday I had the pleasure to sit and talk with Jeff Black about osteogenesis imperfecta, what it is, how it has affected his life, how it led him into a career in bodybuilding and what he is doing now to help those suffering with OI around the world.
Jeff is unbelievably inspiring, prepare to have a fire lit under your ass after listening to this.
YouTube: https://www.youtube.com/watch?v=86nP6nzwqWg
Audio: https://www.jjphysique.com/podcast/
iTunes: https://itunes.apple.com/gb/podcast/optimal-physique-development/id1265819314
To help support and donate to the OI Angel Tree: https://www.facebook.com/oiangeltree
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With dieting and DNP, my pump has unfortunately done a runner these past couple of months. Today, for the first time in a long time, I had a pretty decent pump. Nothing skin splitting, but a mile ahead of what I've been used to.
Now, the only variable I have changed this week has been to increase my electrolyte intake to 7g sodium and 7g potassium per day, so I'm chalking it up to that unless it was just a good day. I suppose the sessions to follow will give me a greater amount of evidence to base this conclusion on.
In any case, keeping a tight control on your daily electrolyte intake is essential for a physique athlete for optimal health, performance and look. This does require a great deal of experimentation, and is highly individual, and is thus very difficult to advise specific intakes on. One recommendation would be to start with a 1:1 ratio of K to Na and adjust based on your own bio-feedback.
Anyway, it's now time to refeed with the Mrs and catch up on Hannibal. Have a great Friday night!
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Now, the only variable I have changed this week has been to increase my electrolyte intake to 7g sodium and 7g potassium per day, so I'm chalking it up to that unless it was just a good day. I suppose the sessions to follow will give me a greater amount of evidence to base this conclusion on.
In any case, keeping a tight control on your daily electrolyte intake is essential for a physique athlete for optimal health, performance and look. This does require a great deal of experimentation, and is highly individual, and is thus very difficult to advise specific intakes on. One recommendation would be to start with a 1:1 ratio of K to Na and adjust based on your own bio-feedback.
Anyway, it's now time to refeed with the Mrs and catch up on Hannibal. Have a great Friday night!
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Here is the reason I recommend anybody using curcumin to opt for the BCM-95 version.
Curcumin itself has poor bio-availability. You often see it paired with piperine for this reason, but this research demonstrated BCM-95 having just under 7x greater bio-availability than curcumin + piperine. Not to mention, long-term use of piperine having its own issues.
If you aren't taking a curcumin supplement, you should be! The list of benefits are extremely long... anti-inflammatory, anti-cancer, protective against neurological dysfunction, and most notably for the case of AAS and GH users, heart remodelling effects protective against LVH and cardiomyopathy.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2792534/
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Curcumin itself has poor bio-availability. You often see it paired with piperine for this reason, but this research demonstrated BCM-95 having just under 7x greater bio-availability than curcumin + piperine. Not to mention, long-term use of piperine having its own issues.
If you aren't taking a curcumin supplement, you should be! The list of benefits are extremely long... anti-inflammatory, anti-cancer, protective against neurological dysfunction, and most notably for the case of AAS and GH users, heart remodelling effects protective against LVH and cardiomyopathy.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2792534/
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You know you're a bodybuilder when you shoot GH in the gym car park, right?
In all seriousness, I have another instalment of my mini-cut vlog series coming out this evening, featuring a tonne of useful rambles, including GH + insulin timing peri-workout, and utilising both sub-q and IM shots to your advantage. (Along with tonnes of other bits).
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In all seriousness, I have another instalment of my mini-cut vlog series coming out this evening, featuring a tonne of useful rambles, including GH + insulin timing peri-workout, and utilising both sub-q and IM shots to your advantage. (Along with tonnes of other bits).
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METABOLIC SYNDROME & BODYBUILDING
Metabolic syndrome is a cluster of at least three of these medical conditions: elevated fasted BG, elevated blood pressure, abdominal obesity, high serum triglycerides and low HDL levels.
(Insulin resistance and metabolic syndrome are very closely related).
These are ALL things that we see in off-season physique athletes all the time. Pushing calorie intake, pushing GH doses etc can all result in IR/metabolic syndrome.
So, what can we do if you/somebody you know/a client is showing any of the above signs?
The easiest changes you can make right away are dietary:
- reduce saturated fat intake
- reduce total carbohydrate intake
- consume your daily carbohydrate intake around periods of high activity, so resistance training for our population. Intra, and post-workout.
Here's some more reading for you guys on an evidenced based approach to treating metabolic syndrome/insulin resistance with diet: https://www.ncbi.nlm.nih.gov/pubmed/10889805
Some other modalities include:
- use a glucose disposal agent with carbohydrate based meals to improve nutrient partitioning, such as Slin from EnhancedAthlete
- use metformin around carbohydrate based meals (more on that here: https://www.youtube.com/watch?v=QK-khHKY8XQ&t=36s)
- depending on the severity of your elevated BG, implementing a basal insulin such as Lantus may be a good initial move before you are able to drop your BG via other means
- resistance training
- HIIT and LISS/MISS cardio
- Keeping your nutrient intake to protein + fat only around periods of low activity, to keep insulin as dormant as possible
For you guys that want to listen to me ramble about improving insulin sensitivity for 20 minutes a little more in-depth, then follow this link: https://www.youtube.com/watch?v=2DAkInEjiSo&t=25s
EVERYBODY should be regularly monitoring their BG, keeping body fat in check and watching how hard they are pushing their condition before having to 'clean up', as any period of time being insulin resistant will detract both from your physique goals, and more importantly your health.
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Metabolic syndrome is a cluster of at least three of these medical conditions: elevated fasted BG, elevated blood pressure, abdominal obesity, high serum triglycerides and low HDL levels.
(Insulin resistance and metabolic syndrome are very closely related).
These are ALL things that we see in off-season physique athletes all the time. Pushing calorie intake, pushing GH doses etc can all result in IR/metabolic syndrome.
So, what can we do if you/somebody you know/a client is showing any of the above signs?
The easiest changes you can make right away are dietary:
- reduce saturated fat intake
- reduce total carbohydrate intake
- consume your daily carbohydrate intake around periods of high activity, so resistance training for our population. Intra, and post-workout.
Here's some more reading for you guys on an evidenced based approach to treating metabolic syndrome/insulin resistance with diet: https://www.ncbi.nlm.nih.gov/pubmed/10889805
Some other modalities include:
- use a glucose disposal agent with carbohydrate based meals to improve nutrient partitioning, such as Slin from EnhancedAthlete
- use metformin around carbohydrate based meals (more on that here: https://www.youtube.com/watch?v=QK-khHKY8XQ&t=36s)
- depending on the severity of your elevated BG, implementing a basal insulin such as Lantus may be a good initial move before you are able to drop your BG via other means
- resistance training
- HIIT and LISS/MISS cardio
- Keeping your nutrient intake to protein + fat only around periods of low activity, to keep insulin as dormant as possible
For you guys that want to listen to me ramble about improving insulin sensitivity for 20 minutes a little more in-depth, then follow this link: https://www.youtube.com/watch?v=2DAkInEjiSo&t=25s
EVERYBODY should be regularly monitoring their BG, keeping body fat in check and watching how hard they are pushing their condition before having to 'clean up', as any period of time being insulin resistant will detract both from your physique goals, and more importantly your health.
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How our weekly refeeds are currently looking - pizza and cake!
Our refeeds are specifically high carb/low fat in nature, so we make our own.
Here we have home made pizzas made with a shop bought base, tomato and garlic sauce, BBQ chicken and BBQ sauce.
For dessert we have our homemade banana cake, made with crushed bananas, flour, sugar, egg whites, cinammon and baking powder. I mix this with fat-free frozen yoghurt and coco pops.
As you can see, all very low fat! Low fat can be fun
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Our refeeds are specifically high carb/low fat in nature, so we make our own.
Here we have home made pizzas made with a shop bought base, tomato and garlic sauce, BBQ chicken and BBQ sauce.
For dessert we have our homemade banana cake, made with crushed bananas, flour, sugar, egg whites, cinammon and baking powder. I mix this with fat-free frozen yoghurt and coco pops.
As you can see, all very low fat! Low fat can be fun
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MYTH-BUSTING
'High protein diets cause bone loss'.
How many times have you heard this? I saw this tagline on one of my Mum's magazines and this reminded me of this old gem.
To put it bluntly, this is a load of rubbish.
From a very recent review linked below: 'Current evidence shows no adverse effects of higher protein intakes.'
http://ajcn.nutrition.org/content/early/2017/04/17/ajcn.116.145110.abstract
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'High protein diets cause bone loss'.
How many times have you heard this? I saw this tagline on one of my Mum's magazines and this reminded me of this old gem.
To put it bluntly, this is a load of rubbish.
From a very recent review linked below: 'Current evidence shows no adverse effects of higher protein intakes.'
http://ajcn.nutrition.org/content/early/2017/04/17/ajcn.116.145110.abstract
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The.Shadow
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A quick progress photo upon waking this morning for my check in with my coach.
Today marks 16 weeks into this fat loss phase. Watery and flat as hell from GH, DNP and yohimbine, but things are still progressing nicely!
I have ran my AAS no higher than TRT for this whole phase, so I thought it may provide some value to share my current anecdote for this approach vs. previous fat loss phases running supra-physiological amounts of AAS.
Positives:
- Reduced hunger
- Lower overall systemic stress, which will ultimately result in greater net fat loss
- Long period spent with improved health markers
- Massively improved sleep. I have previously struggled to sleep when dieting, but this phase it has been easy
- Extended 'off' period allowing AR's to completely resensitise, so when you get into that 'golden spot' to add tissue, you are ready to blast
Negatives:
- reduced transient cosmetic effects that come with supra-physiological AAS use, specifically non-aromatising and DHT based drugs.
That's honestly about it, and with my own trials with myself and clients this year running fat loss phases (outside of contest preps), I am very confident that the benefits strongly outweigh the negatives of sticking to TRT-like dosages.
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Today marks 16 weeks into this fat loss phase. Watery and flat as hell from GH, DNP and yohimbine, but things are still progressing nicely!
I have ran my AAS no higher than TRT for this whole phase, so I thought it may provide some value to share my current anecdote for this approach vs. previous fat loss phases running supra-physiological amounts of AAS.
Positives:
- Reduced hunger
- Lower overall systemic stress, which will ultimately result in greater net fat loss
- Long period spent with improved health markers
- Massively improved sleep. I have previously struggled to sleep when dieting, but this phase it has been easy
- Extended 'off' period allowing AR's to completely resensitise, so when you get into that 'golden spot' to add tissue, you are ready to blast
Negatives:
- reduced transient cosmetic effects that come with supra-physiological AAS use, specifically non-aromatising and DHT based drugs.
That's honestly about it, and with my own trials with myself and clients this year running fat loss phases (outside of contest preps), I am very confident that the benefits strongly outweigh the negatives of sticking to TRT-like dosages.
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The.Shadow
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Check out this research, where melatonin, reservatrol and letrozole were added into breast adipose tissue in vitro.
As we know, aromatisation of testosterone to estrogen can occur at the aromatase enzyme in fat cells.
Both melatonin and reservatrol were found to act as aromatase inhibitors in this co-culture model, however, melatonin was 1000x more potent than reservatrol.
The most surprising finding here was that melatonin was equally as potent as letrozole!
http://www.sciencedirect.com/science/article/pii/S0887233314001040?via=ihub
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As we know, aromatisation of testosterone to estrogen can occur at the aromatase enzyme in fat cells.
Both melatonin and reservatrol were found to act as aromatase inhibitors in this co-culture model, however, melatonin was 1000x more potent than reservatrol.
The most surprising finding here was that melatonin was equally as potent as letrozole!
http://www.sciencedirect.com/science/article/pii/S0887233314001040?via=ihub
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Rest day nutrition is super simple right now, generally because my rest days at the moment are spent travelling and working away.
I start with a fast, so today I had my first meal at 5pm. This is because 1) my intake is very low at the moment, and I never get hungry when fasting. Fitting my daily intake into a smaller window is a much more satiating situation. I'm definitely a fan of the benefits of fasting too. 2) It allows me to take advantage of a longer window of accelerated FFA mobilisation when using yohimbine and GH upon waking.
Current rest day macros are at 300p/40c/50f and electrolytes at 10g potassium/8g sodium. My day consists of 500g spinach, 500g 95% lean beef, 700g courgette, 740g chicken breast, 8g coconut oil, 15g sea salt, 6g losalt and I split this into 4/5 meals.
Have a great Saturday everybody
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I start with a fast, so today I had my first meal at 5pm. This is because 1) my intake is very low at the moment, and I never get hungry when fasting. Fitting my daily intake into a smaller window is a much more satiating situation. I'm definitely a fan of the benefits of fasting too. 2) It allows me to take advantage of a longer window of accelerated FFA mobilisation when using yohimbine and GH upon waking.
Current rest day macros are at 300p/40c/50f and electrolytes at 10g potassium/8g sodium. My day consists of 500g spinach, 500g 95% lean beef, 700g courgette, 740g chicken breast, 8g coconut oil, 15g sea salt, 6g losalt and I split this into 4/5 meals.
Have a great Saturday everybody
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As you age, the threshold to maximally stimulate muscle protein synthesis in one sitting increases, and thus the anabolic response to protein intake is reduced.
This research took 66 malnourished elderly individuals, and controlled their nutrition for 6 weeks.
One group were given four meals in which protein intake was spread evenly. (pulse feeding)
In the other group, the majority of their protein intake was consumed in one meal (spread feeding)
At the end of the 6 weeks, the pulse feeding group showed a beneficial outcome when compared to the spread feeding group, with the subjects showing significantly greater lean body mass increases.
To keep this in context, although I feel there is absolutely merit in ensuring you are maximally stimulating muscle protein synthesis throughout the day for hypertrophy goals in physique athletes, this research was done on an elderly population with zero resistance training. Therefore, we cannot realistically base any conclusions from this research on our population.
I am sharing this for a few people (including my Mum!) who specialise in elderly rehabilitation that follow this page.
Enjoy Mum, lol
http://www.clinicalnutritionjournal.com/article/S0261-5614(12)00182-3/fulltext
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This research took 66 malnourished elderly individuals, and controlled their nutrition for 6 weeks.
One group were given four meals in which protein intake was spread evenly. (pulse feeding)
In the other group, the majority of their protein intake was consumed in one meal (spread feeding)
At the end of the 6 weeks, the pulse feeding group showed a beneficial outcome when compared to the spread feeding group, with the subjects showing significantly greater lean body mass increases.
To keep this in context, although I feel there is absolutely merit in ensuring you are maximally stimulating muscle protein synthesis throughout the day for hypertrophy goals in physique athletes, this research was done on an elderly population with zero resistance training. Therefore, we cannot realistically base any conclusions from this research on our population.
I am sharing this for a few people (including my Mum!) who specialise in elderly rehabilitation that follow this page.
Enjoy Mum, lol
http://www.clinicalnutritionjournal.com/article/S0261-5614(12)00182-3/fulltext
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