Monday, 22 November 2010

2,4-Dinitrophenol - The anti obesity drug thats been known since 1930

This report makes for a very interesting read and it looks like uncoupling proteins could be the answer for fat loss.

Thursday, 18 November 2010

Sunday, 14 November 2010

Mechanism of amino acid-induced skeletal muscle insulin resistance in humans

"Plasma concentrations of amino acids are frequently elevated in insulin-resistant states, and a protein-enriched diet can impair glucose metabolism"

"In conclusion, plasma amino acid elevation induces skeletal muscle insulin resistance in humans by inhibition of glucose transport/phosphorylation, resulting in marked reduction of glycogen synthesis"

Saturday, 13 November 2010

Surplus dietary tryptophan inhibits stress hormone kinetics and induces insulin resistance in pigs

"In conclusion, long-term feeding of surplus dietary TRP inhibits both baseline adrenocortical and sympathetic nervous system activity, it induces insulin resistance for both glucose and amino acid clearance but it does not affect whole body protein catabolism"

Move support not to over-indulge in the protein.

Low-carbohydrate diet disrupts the association between insulin resistance and weight gain.

"the heavier animals that were fed LFD had impairment in insulin sensitivity, which was not observed in those fed LCD"

"The weight gain in animals fed LCD may be related to their greater caloric intake, lower levels of glucagon-like peptide-1, and higher protein consumption"

"The adoption of LCD promotes a unique metabolic state that prevents insulin resistance, even in guinea pigs that gained more weight."

"The association between weight gain and insulin resistance seems to be dependent on high carbohydrate intake"

Medium-chain fatty acids ameliorate insulin resistance caused by high-fat diets in rats

Good news for coconut oil I guess?

Diet-induced obese mice are leptin insufficient after weight reduction.

This is scary news for people who lose weight by dieting and helps explains why people gain fat mass back.

Get your leptin checked after loosing weight by dieting.

Dietary branched-chain amino acids and protein selection by rats.

"Although BCAA concentrations were high in plasma and brain in all experiments, concentrations of methionine, tyrosine, phenylalanine, tryptophan and histidine were low in brain in experiments in which rats altered their diet or protein selection after BCAA addition."

More evidence against supplementing BCAA?

Monday, 8 November 2010

Protein and Insulin Resistence

Also this excellent thread explains alot

Saturday, 6 November 2010

Diet-induced ketosis increases capillary density without altered blood flow in rat brain.

Also we have

"These data indicate that adaptation to hypoxia did not interfere with ketosis, and that ketosis during hypoxia may lower lactate levels in brain, suggesting decreased glycolysis or increased glucose disposal."

Immediate metabolic availability of dietary fat in combination with carbohydrate.

After reading all the related studies on a pubmed search to this study, it is clear that dietary fat is handled before dietary carbs if combined in the same meal.

Further, it appears that dietary fat is primed for usage as fuel immediately, and that adipocytes promptly actually start taking up FFA from the blood to reform them into trigs.

Preferential uptake of dietary Fatty acids in adipose tissue and muscle in the postprandial period.

"In this study, the most striking findings were the postprandial uptake of fatty acids from the circulating NEFA pool by adipose tissue, the direct confirmation that chylomicrons are the preferred substrate of LPL over VLDL, the preferential channeling of fatty acids derived from LPL-mediated chylomicron hydrolysis into adipose tissue, and the postprandial release of fatty acids across the forearm."

So it looks like it is bad news to combine meals that are both high in fat and carbs. The result will be lots of vLDL particules swimming around in your blood.

Friday, 5 November 2010

The Hexosamine Pathway

Currently there is no wikipedia page for this part of biochemistry and knowledge of it still appears to be developing. It seems to be related to insulin signalling and insulin resistence, and over-expression of the pathway seems to cause IR as suggested by this paper.

This next study was also an interesting find, some AA's are produced in vivo in adipocytes, glutamine being one.

Tuesday, 2 November 2010

Its still working

Still having good success with the below training protocol. After using it for the leg press I suffered severe DOMS for 3 days , 2 of those days i could barely walk.

However, I did feel a good response in hypertrophy. My quads and hamstrings felt noticably bigger, just from 1 session.

Monday, 25 October 2010

Effective training method that defies the science

Started trying a new method of training recently that seems to be getting surprisingly good results. The method is to use a resistence that is about 50% of your 1RM, perform 10 reps at a nice and controlled pace of about 2 seconds up, 2 seconds down, then rest for only about 30 seconds between sets.

Repeat this until you come to failure but adjust the weight if you cant do atleast 5 sets.

Ideally you should come to failure after 5 sets at around 55-65 reps in total. At this point stop, and move onto the next exercise.

This method of training is interesting to me becuase the short rest periods means you keep the intensity and focus on your training high, rather than waiting 3-5 mins between sets and day dreaming. Its also very effecient you can do a whole body workout in a short amount of time and avoids being seen as a machine hogger at the gym. My gym gets so overcrowded all the time so this fast training fits in with it.

Its difficult to say why this method of training is so effective when trying to explain it from the known science of muscle anatomy and hypertrophy. Using a weight of only about 50% means you hit most of the fibres quite hard, and going to failure means you hit all the different motor neuron sizes.

Further, in reps 30-50 you keep the muscle in a pro-longed state of high acidosis. The total time here is the time it takes to complete reps 30-40, plus 30 seconds rest, plus 40-50 reps, plus 30 seconds, then another 5 reps or so to failure, then it will take about 2-3 minutes for the muscle to recover from the acidosis.

In comparison to just doing 3 sets of 20 reps with 3 mins rest, there are gaps in the state of acidosis here.

Monday, 20 September 2010

Exercise to help relieve insomnia

Insomnia is one of the worst things that can happen to you, having suffered it myself quite severely but for only 3 weeks, the change in my mood was outrageous. It completely ruins your life faster than other kind of sickness.

Body Clock and blood glucose

A possible link between diabetes and the body clock, whats interesting is we also found out before that ghrelin is also regulated by the body clock.

Saturday, 18 September 2010

Nitric Oxide and AMPK upregulate Mitchondrial Biogenesis

AMPK is upregulated in endurance style exercises like HIIT.

Nitric Oxide can come from arginine supplementation of beetroot juice or leafy green veg's through Nitrates.

Friday, 17 September 2010

Afternoon Melatonin to advance sleep at night

I took 3mg of melatonin at about 3:30pm yesterday, I felt drowsy afterwards for the rest of the day but avoided napping or lying down, at 9:45pm I got to sleep and slept soundly throughout the night until 7:20am when I had to wake for work.

People with insomnia may just have severely delayed circadian rythm's, and taking melatonin in the afternoon may be alot more beneficial than taking it at bedtime to shift the body clock forward.

Beware though taking melatonin in the afternoon will make you feel drowsy for the rest of the day.

Wednesday, 15 September 2010

Stretching induces hypoxia

This study offers some prediction that strecthing actually induces hypoxia, contrary to what I believed.

If this really is the case then actually I would expect stretching to be somewhat beneficial before exercise and deterimental after exercise. After exercise, we what to give muscles as much oxygen as possible to maximise thier growth.

Monday, 13 September 2010

Are modern bodybuilding methods flawed?

Consider the barbell curl. You start with the muscle in a stretched position, This puts the actin and myosin configuration in thier weakest arrangement, but the relative force exerted by the weight on the muscle in this position is also modulated by the torque it exerts on your forearm.

The force exerted by the weight is always acting in the same direction, downwards towards to floor, this means that as you move the weight through the motion, the stress exerted on your muscle from the torque in your forearm varies exactly as the Sin function.

The force and torque is maximal when perpendicular to your forearm, thus half way through the motion when your forearm is parallel to the floor is the only time during the entire motion that your really lifting the amount of weight on the barbell.

However, at 90degrees, the actin and myosin fibres are approx half way through thier ratcheting system, and this is also the configuration at which they are at thier strongest.

As you move up past 90 dgerees, the torque and therefore tension exerted once again diminishes as sin 90 -> sin 180, meanwhile the relative strength of the actin and myosin also decreases again as the maximum contracted position is reached.

One way around this is to move your torso as you curl your arms, always keeping your forearms parallel to the floor thus always keeping the maximum torque on your muscles. This way, each configuration of the actin and myosin arrangment is exposed to the same degree of tension, which is pretty much the maxmium.

This machine is an excellent example for the pec fly.

In this machine, the force is pretty much always perpendicular to your forearm, thus maximising the actin/moysin multiplied by tension stimulus.

Compared to the traditional pec fly laying down with dumbells, the maximal force in only exerted in the starting position. As you move your arms up, the force decreases as the sin function once again.

I would predict that keeping the tension constant throughout the range of motion to be superior for mass gains.

Saturday, 11 September 2010

Aromatase Steals your Testosterone!

Aromatase is a unwelcome enzyme that converts your T into estradiol.

Insulin is a driver of aromatase, just another reason to keep your diet ketogenic on non-training days.

CLA is actually an inhibitor of aromatase. This could be where the fat loss effectiveness of CLA comes from.

Friday, 10 September 2010

Supplements for Sleep - My Experiences

Being a shift worker makes me a good candidate to evaluate the potential effects of sleep aids.

Valerian - Produces a slight relaxing sensation but does not help with sleep in any shape or form

ZMA - Helps a bit if your already tired and with morning wood sometimes

L-Theanine - To be tested, some on order

Taurine - To be tested, will order some

Melatonin - quite effective, but the dose needs to be quite high like 3mg, may have potential bad side effects in longterm use by your pineal gland down-regulating its own production like steroids and testosterone

Zopiclone - Very effective, but potentially very addictive.

Thursday, 9 September 2010

Nitric Oxide, Niacin Flush, Antartica and Monsters

More wild speculation here, but here goes....

Sealife in the antartic ocean is generally much larger than thier equivalent species found elsewhere in the world. They are real life monsters by all accounts. It's been suggested that the reasoning behind this is the intense cold water. Note these organisms also have tiny metabolism's.

Apparently, water at freezing temperatures permits a far higher density of O2 within it, and its this extreme availability of oxygen that allows these organisms to grow so large.

Theres studies floating around on pubmed showing how Nitric Oxide ( from arginine ingestion or beet root juice ) enhances exercise, most likely through the vasodilation and therefore allowing a higher density of oxygen to come through.

It may therefore be beneficial to ingest beet root juice / arginine along with Niacin for the flush (which also causes vasodilation) post-workout to maximise the uptake of oxygen and post-workout feeding nutrients.

I'm not sure how long Nitric Oxide remains elevated after arginine / beet root juice, but the niacin flush lasts only 30mins-2 hours. This is when it could be best to consume those post-workout nutrients.

UPDATE :- upon further thinking, this could also be where the beneficial effects of stretching come into play, by increasing blood flow through the muscle. Stretching just before bed might be effective in promoting more nutrient influx to your exercised muscles.

UPDATE II :- I stumbled on some research suggesting stretching actually induces hypoxia in muscle. Therefore I dont recommend it before bed or after exercise, but it may help before exercise.

Wednesday, 8 September 2010

HIIT and resistence exercise may not work well together

It seems performing HIIT style exercise before resistence exercise may interfere with the anabolic response of the resistence exercise.

Muscle biopsy was only taken 3 hours after exercise. But this study could be a good indication that if your attempt to build muscle, then go to the gym just for that. Dont do anything else there. Including HIIT. Keep that for another session.

L-arginine and IGF-1

Interesting, IGF-1 is a powerful muscle anabolic, however systemic hormones are usually not anabolic towards muscle. More work is needed I guess.

Tuesday, 7 September 2010

Bicarbonate and Acidosis

Very interesting study, basically bicarbonate is a alkaline buffering agent, ingesting it prior to exercise apparantly delayed the onset of acidosis in muscle. The delay in acidosis would ofcourse mean the PCr is regenerated faster and therefore allow you to do more volume in the exercise.

I would like to see a resistence exercise study like this and measurements of mTOR and P70S6k taken!

This would move us one step closer to determining if it is volume or acidosis in the muscle that determines hypetrophy.

Saturday, 4 September 2010

Substrate turnover as the initiator of Hypertrophy

After a discussion over at, I was posed the question as to what I think actually causes muscular hypertrophy, and it suddenly occured to me that from a cellular and signalling perspective the initiator has to be substrate turnover. ( By substrate turnover I mean the total amount of molecules burned for energy, and in particular, the amount of anaerobic energy used. )

There is alot of evidence to support this. There are those studies showing much higher increases in mass and strength gains when rest between sets is extended, such as in this one.

There are also all those studies showing that a greater of sets are more anabolic compared to a smaller number. I.E. that volume matters hugely. Obviously, it takes more substrate turnover to do 4 sets than it does to do 2 sets.

Not to mention we have the famous 30FAIL > 90 FAIL study. The investigator's explained thier findings with the suggestions that the size principle was behind the greater muscle protein synthesis.

While I am a firm believer in the importance of the size principle, I think it doesnt tell the story of WHY the 30FAIL group got more muscle protein synthesis. The answer I'm almost certain was becuase of a higher substrate turnover allowed in the smaller motor unit muscle fibres.

Lastly, there is the evidence that mTOR is sensitive to the redox reaction.

UPDATE - having given more thought to it, theres a chance that the initiator could be also be the degree of PCr / glycogen exhaustion. In most situations the degree of substrate usage and PCr exhaustion will be closely related, except for sets of reps that are not taken sufficiently close to failure. In reality, it is probably a combination of the 2 effects as this explains the gains that happen when working with very high % or 1RM (90% and over )

Friday, 3 September 2010

Speed of movement in Resistence exercise again

I myself have found a good way to do reps is 3 seconds concentric and 1 second eccentric. (with a momentary pause at the top and bottom of the rep of about 0.5-1 seconds, just go with what feels natural and comfortable with you ) Focusing on eccentric motions really only increases strength in the eccentric motion but in addition is causes extreme pain, severe DOMS, and limits the total number of reps you perform.

Meanwhile, focusing a bit more on the concentric is beneficial for overall strength, the slow movement means you maintain a higher degree of motor unit activation thoughout the range of motion and you get a deep feeling of contraction and which is satisfactory and lets you know that the targeted muscle group is really getting a good workout.

Working with a 3 second concentric phase will also probably mean that you are working with a lighter weight overall, which I dont think matters aslong as you go close to failure.

Wednesday, 1 September 2010

Drop-sets and the size principle

I came to the conclusion sometime ago that drop-set's are pretty much the most intense way to do resistence exercise. Done properly you can fatigue pretty much every type II fibre in the muscle. Recovery time after 1 drop-set is noticably longer than for example just working with a weight at your 10RM.

I began experimenting with drop-sets on my biceps to test thier effectiveness as predicted by the size principle and I have some observations to report.

I have only been resistence training seriously now for about 6 weeks, the first time I did a drop-set on my biceps (went close to failure at each weight), it took about 5 days to recover from 1 set! During the recovery period there was extreme pain and discomfort, I would have to keep the bicep muscle in a maximal extended position in order to relive some of the DOMS. I guess this was just becuase I was not used to working out.

Its now been about 2.5 weeks since then and now my recovery time for for 1 drop-set on biceps is about 36 hours. Muscle mass has gone up significantly, strength a bit.

More interesting though, I had assumed that drop-sets would be superior to just doing high reps with a low load to fatigue all fibres, mainly becuase overall it should of meant doing less reps in total.

However it seems that isnt true, instead I found myself doing the same total number of reps in a drop set compared to just doing straight reps to failure with the lowest weight I would use in the drop-set.

Recall to neurons are exactly like logic gates, either they are firing or they arent, there is no "half" firing. With the above anecdote in mind, this suggests that fibres have a fixed and finite "firing" time before they become totally fatigued. This is also independent of the weight you are lifting.

Still, I think there is a bone density advantage to using heavy weights atleast 50% of the time, as stress on bones is higher with higher weight. And we know from Wolff's law that bone stress determines bone density.

Tuesday, 31 August 2010

Hypertrophy and Obesity the same thing?

I have noticed some similarities in how muscle cells and fat cells behave. Perhaps they can both be viewed as adaptive responses whereby morphological changes take place in cumlative fashion with the goal of leading to an enchanced ability to maintain homeostasis when being exposed to a certain stimulus.

With muscles, the stimulus is exercise and muscle fibres increase in size and number in order to reduce the overall level of fatigue that that particular exercise induced.

With obesity, that stimulus is hyperglycemia, hyperinsulinemia. With fat cells, they multiply in number ( Hyperplasia ) in order to increase the total surface area of insulin receptors that are
exposed to the bloodstream.

Everyone knows that post obese people have an extreme tendency for weight re-gain. This is attributed to the increased number of fat cells that were produced during obesity. I have seen a study on PubMed that showed that a fat cell's insulin sensivity was inversely related to its size. I.E., large full fat cells have low insulin sensitivity. And empty small fat cells have high insulin sensitivity.

When you loose weight, you dont change the number of fat cells you have, you change thier size only.

Likewise, this could predict that in muscle, after loosing strength and mass during a period of inactivity, you retain the number of new muscle fibres you made during hypertrophy, but what happened is that the number of myofibrials in each muscle fibre decreased.

As with the post obese, there is alot of anecdotal evidence floating around that it is easier to re-gain muscle mass once youve 'been' there before. This also fits in with the threshold theory of cellular behaviour, in that hypertrophy comes before hyperplasia.

That is, muscle fibres increase in myofibrials ( cross-sectional area ) before increasing in number. Indeed this is what happens with fat cells, they increase in size and reach a critical mass before new ones are made.

In the opposite direction, how does one loose weight? Well the way one looses muscle mass is by inactivity. They stop exposing thier muscles to the stimulus that made them become the size they did. This can be done by either reducing intensity of the exercise, reducing the frequency, or both.

With regards to obesity, low-carb diets can be seen as reducing the intensity of the stimulus ( reducing insulin spikes ), while intermittant fasting can be seen as reducing the frequency.

We know that its very easy to gain body fat by eating very often and if each of those meals spikes insulin high with lots of carbs. This happens even in the face of potentially low calories, I.E. low-fat.

This may suggest that in order to rapidly gain muscle mass we must apply the stimulus frequently with a certain minimum intensity, and that the calories of the exercise ( I.E. the number of sets we perform ) can thus be a secondary consideration. I intend to experiment with exercising once every 48 hours with 1 drop-set. As opposed to performing 4 sets of reps every 72-96 hours.

With fat mass, like muscle mass, if we want to loose it, we need to stop sending it the stimulus that made it that way. Ketogenic diet combined with intermittant fasting. However I think that carb re-feeds will still be helpful because they help boost leptin and change the critera for homeostasis adapation on a ketogenic diet will incude, I.E. the famous weight loss plateau.

Monday, 30 August 2010

Carb Re-feeds - What to Re-feed on?

Well this study would suggest that refeed's should be done with carbs but still keeping fat low. Fat over-feeding only caused a 18% rise in fat oxidation, meanwhile Carb over-feeding caused a 74% rise in carb oxidation.

Over-feeding with things like Icecream and chocolate may then be quite counter-productive.

Friday, 27 August 2010

Postwork out Feeding again, Myostatin look

This study shows how mTOR and P70s6K are highly elevated post workout with a protein drink. We know that the effects of BCAA and resistence exercise are additive, however if you note the 48hour mark, there is virtually no difference for P70s6K, although mTOR is still up a bit.

What these results dont show that I think is important is area under curve. Although the cross-sectional area of the protein group was higher when measured.

Interesting to see how protein stopped the myostatin decrease, but it also totally blunted the testosterone response. And we have seen how Testoserone can negatively regulate Myostatin, perhaps this is where the connection is.

Thursday, 26 August 2010

Post Workout Feeding - Overhyped?

Another workout today, although I didnt do it fasted (had a protein shake earlier in morning because I had already fasted 16 hours ), I did not consume any BCAA or any type of food/calories until 2 hours after.

This just works so much better for me, I dont feel hungry upon just finishing exercising, and consuming post workout nutrition just made me stiff, bloated, and clunky.

Waiting 2-3 hours makes all the difference, I feel more supple then, and notice I get full faster from the food. Like I said before, all the research "suggests" that immediate post workout is most optimal, but there is something that just feels so wrong and unnatural about it.

I will continue delaying my post workout nutrition for 2-3 hours for a few weeks and see how it goes.

Exercising Fasted - Leangains site

I spotted a somewhat old post over at and it was very refreshing to see a post ( and link to a clinical study ) showing not only that exercising fasted didnt result in lower anabolic responses, but actually increased anabolic signalling post workout, our old friend P70s6K!

There is a current stigma in thinking that one should not exercise fasted, especially if its high intensity, because your body will catabolise muscle for energy. It was interesting to see Martin at Leangains speculate on the theory of anabolic rebound and this is something I truely believe is real.

Basically, if your body needs to break down extra muscle protein during working out for energy, this breakdown actually creates a cellular "debt". And, that debt is repaid later with interest. Not only does the study that links to suggest this, but this actually happens in other circumstances that were already aware of.

What happens in extreme short term fasting? You loose weight, but as soon as you go back to eating, you gain the fat back and more! Your adipocytes saw that weight loss as a short term loan, and they forced you to repay the debt with interest by manipulating the hormones that make you feel hungry and full.

Again, the same cellular behaviour is seen with regards to sleep. If you get little sleep one night, you tend to oversleep the next night.

This is why I firmly believe that muscle cells are also "educated" on the behaviour of cellular debt.

Wednesday, 25 August 2010

L-arginine gene expression

These 2 studies suggest benefits of L-Arginine dietary supplementation, with increased HSL expression.

Fed to pigs at 1%

Testosterone and Heart Attacks

This study suggests that Testosterone activates HSL in the heart, since fatty acids are a major energy source for the heart, letting your Testosterone levels drop can help lead to heart problems.

Post workout feeding - I'm not convinced

Countless studies have shown not only the benefit but perhaps the requirment to feeding immediately or atleast very shortly after working out for increased muscle protein synthesis.

From a Hunter-Gatherer perspective, it does not make sense because the kill would need to be dragged back to camp and cooked before we can ingest protein, and I expect this would take up to 3 hours.

While in the wild, animals eat almost immediately upon making a kill. Anyway, this study suggests that hormone sensitive lipase remains acutely elevated after exercise for up to 3 hours.

Remember that as soon as you eat, insulin is going to shut off HSL. There goes your fat burning. Meanwhile, there have been some studies suggesting that anabolic signalling in muscle remains elevated for 36hours, and that the eating anabolic window can remain open for 24 hours.

Therefore if ones goal is fatloss, I expect it to be beneficial to wait 3 hours after working out before eating. If you want to loose weight you need to stop sending your adipocytes the signal to get bigger, and that is insulin.

Saturday, 21 August 2010

Stuart Philips - Pubmed RE study points

This guys name brought up a selection of interesting studies from pubmed, summary points are...

Phillips Stuart[au] - The now famous low load high volume recruits more muscle motor units study - 3 Sets of an exercise stimulates more muscle protein synthesis than 1 set, but we already knew that from the earlier study done on 1,3,5 sets and P70s6K. - Exercising in a glycogen depleted state can increase the oxidation and turnover of protein during pro-longed high intensity exercise. - 20g of protein was enough to maximally stimulate post work-out MPS. However only 1 muscle group was exercised, this number will obviously go up as multiple muscle groups are usually exercised during a workout.

Friday, 20 August 2010

Whole Milk and Whey as Workout supplements

15g why pre and post workout gave higher anabolic signalling. But worse myostatin decrease

Whole milk gave higher anabolic signialling.

P70S6k occurs mostly in Type II fibres.

This suggests that type II fibres hypertrophy to a greater extent than type I.

P70S6k may also remain elevated for up to 36 hours after resistence exercise.

P70S6k is maximally stimulated some 3-6 hours after exercise. From an evolutionary sense this is suspected, as after a hunt, they probably would not have eaten until 3-6 hours later.

Testosterone and Exercise induced muscle increases are independent?

Well that is what this study seems to suggest,

Androgen Anabolic Muscle Growth

These results suggest that androgen responsiveness of skeletal muscles is determined by the level of androgen receptor protein in a particular muscle and that androgen receptor protein content is regulated by translational or post-translational mechanisms

Altogether, androgens seem to have strong negative impact on myostatin expression, which might be a key factor in the weight regulation of LA muscle

Muscle growth and Testes

Points of note from this study are...

- Testosterone is known to act differentially on skeletal muscle from different regions, Sexual dimorphism in muscle growth relates to the protein anabolic effect of testicular hormones.

- Testosterone through the androgen receptor can stimulate local IGF-1 which increases muscle mass independent of myostatin.

Wednesday, 18 August 2010

The number of reptitions perfomed at a given % of 1RM is a constant

It made sense to me intuitively, but here is a study that even shows it!

Myostatin and muscle force

Perhaps messing with myostatin may not be such a good idea afterall. Decreased muscle force and less muscle oxidative capacity.

Androgens, Testosterone, and Receptors

Every man wants high Testosterone. The problem is serum levels are usually tightly regulated to stay in a certain range by the body.

Increasing your serum levels via drugs/injections/supplements is doomed to fail in the long run becuase your body will down regulate its own production of T.

The key is actually to increase the androgen receptor's on your cells. They will suck Androgens out of the serum and by the bodies self regulatory system, it will sense low T and therefore increase its own production.

Afterall, theres no point having the T levels of a horny bull if your cells aint expressing any androgen receptors.

Anyway, it was interesting to see this study suggests a link between androgen receptor expression and P70S6k.

More investigation to follow.

P70S6k and exercising Fasted

Im a big fan of exercising fasted, it feels more natural, I feel I have more energy and can my mind is more clear.

However this study seems to suggest that P70S6k is even more elevated after exercise with a pre-workout feeding. Sigh.

Carb feeding after exercise may alter muscle metabolic adaption

This study seems to suggest that carb feeding after exercise may influence the oxidative capacity of skeletal muscle.

When attempting to loose fat, it may therefore be beneficial to not consume carbs post work out, as free fatty acids can only undergo oxidative respiration

The other question is, does carb feeding after a work out therefore effect gains in Type I vs Type II fibre? Since Type I fibre is highly oxidative.

Friday, 13 August 2010

Stretch induced Hypertrophy and Muscle Contraction Speed

Birds with Chronic Stretch induced muscle hypertrophy exhibited greater force and strength but perhaps alarmingly had slower maximal velocity muscle contractions.

Im optimistic that big muscles doesnt give slow reflexes however since this hypertrophy was purely stretch induced. And we have the anecdote that sprinters are extremely muscular.

Thursday, 12 August 2010

HIIT increases fat oxidation

Note there was also a decrease in glycogenolysis, probably becuase fat oxidation increased.

Training to Failure not Good

This study suggests how training to failure results in less serum resting Testosterone and less IGF-1.

Wednesday, 11 August 2010

Speed of movement in RE

performing eccentric movement at 180deg per second gave the most hypertrophy.

This study also shows that once again, muscle gets stronger for how you train it.

P70s6 is associated with hypertrophy

This study shows show muscle hypertrophy is strongly associated with an the expression of an enzyme called P70s6.

This study shows how P70s6 varies strongly with training volume.

5 sets of 6 reps was 100% more effective than 3 sets of 6 reps, even though the volume increased by 66%.

Tuesday, 10 August 2010

BCAA enchances muscle building

Saturday, 7 August 2010

A new design for Maximal Strength Gains

This study suggests that lifting 85% of 1RM and doing 8 sets per week was most optimal.

Together with the moderate volume data, I will experiment with 7 reptitions per set.

Moderate volume better than high or low for gains

Again, muscle adapts to however you train it

A strength increase for the CON group but not the ECC group.

Eccentric training overrated?

Given it was performed in women, but the Eccentric group got last fast twitch fibre.

Muscle gets better at whatever you train it to do

Just like fat loss, perhaps there is no magic bullet for building muscle. ( aside from myostatin manipulation )

Low-rep high weight produced the best strength gains.

Upper Body Strength is harder to build

Not surprising given how big your legs are compared to other muscles on your body.

Stretching helps build muscle

30 mins stretching 2 times per week can significantly help muscle hypertrophy from lifting.

Friday, 23 July 2010

Myostatin goes up during fasting

It took 2 days of fasting to increase myostatin levels significantly, 1 day of fasting did not affect myostatin.

Glutamine prevents Myostatin hyperexpression

More support for glutamine supplementation.

Friday, 16 July 2010

Eating Animal Adipose Tissue

Bacteria ferment plant material into short chain fatty acids.

Barry mentions how prized fatty meat was in our past. So lets all eat more animal adipose tissue, something that so rarely happens these times.

Adaption : Reminder to myself

Your bodies metabolism will ultimately adjust to whatever diet your consuming. Regardless of macronutrient content.

To break a weight loss plateau, change from high protein to high fat or vice versa if you was doing the other. Always try to keep it ketogenic however!

Body Fat Set Point

Muscle is controlled by the protein myostatin. Your expression of myostatin is genetic. Therefore your set point of musculature is also primarily genetic.

You can change how much muscle you have by doing exercise, your body compensates by building more muscle. Or you can lower muscle mass by being extremely sedentary. This change in activity must be maintained, for once it is abandoned, you slowly but surely go back to your muscle "setpoint".

Bone density is essentially the same. Bone will change its mass and density dynamically, depending on what happens to it.

So is adipose tissue size the same as the analogy above? Is there really a fundamental genetically determined setpoint controlled by some mysterious gene or protein.

Thursday, 15 July 2010

Going to bed in a insulin sensitive state

Im still intrigued by the study posted recently were lean subjects got a spike in ghrelin during sleeping hours and obese subjects didnt.

In the study, the subjects were eating high carb meals all day, in the last 2 meals they had a blunted response to ghrelin, suggesting that they may be insulin resistent at this point. Going to bed in an insulin resistent state is perhaps not sufficient to make a ghrelin response becuase ghrelin itself will cause a kind of physiological insulin resistence so that we can switch to FFA for fuel.

This is just trial and error and speculation at the moment, tomorrow I will look for more studies to piece together the puzzle of ghrelin.

High Intensity Exercise boosts Adiponectin

Their definition of high intensity exercise is 80-85% of 1RM. 3 Sets of each exercise were performed with 6 mins rest between!

Thats alot of rest, but then again the subjects were elderly.

Adiponectin was raised for 24hrs following this.

My Dandruff has vanished

Its been a problem for most of my life.

Currently the supplements im taking are...

l-glutamine + fizzy vit c in morning
Vitamin D 7500iu in morning
Butter Oil
Cod Liver Oil
Krill Oil 2g per day
ZMA at night before bed 4-5 times per week.
Niacin 500mg , few times a week, randomly

I started taking Inositol today aswell, will see how it goes.

I suspect it is the Vitamin D, since I only started taking large doses of it again recently and spending more time in the summer sun. Theres also a small chance it could be the krill oil, as I added it back to my supplement list at the same time as the D3.

Tuesday, 13 July 2010

Ghrelin and Adiponectin

First, in this study we see from the graphs that ghrelin increases dramatically in response to sleep for lean people, however it remains unchanged for obese people.

We also see a marked drop in adiponectin during sleeping for lean people, while for obese people, nothing happens to thier adiponectin levels.

For breakfast and lunch, the pattern of ghrelin remained the same for obese and lean people, then we get to dinner, ghrelin goes down markedly for lean people, but stays the same for obese people, then the evening snack comes, ghrelin goes up for obese people, while for lean people it stays low, right up until sleepy time.

Then we have the leptin graph, notice it stays the same for lean people constantly, while for obese people its shooting all over the place.

There is clearly something wrong with an obese persons adipocyte functions.

Unfortauntely the study doesnt say what the dinner consisted of, as this is when the trouble starts for the obese people with ghrelin.

This study offers a discussion on ghrelin and adiponectin,

Circulating ghrelin concentrations are also regulated by longer term changes in energy homeostasis. Ghrelin levels are lower in humans with higher body weight and rise after diet-induced weight loss (31). The usual postprandial fall in plasma ghrelin is absent or attenuated in the obese, suggesting that ghrelin may be involved in the pathophysiology of obesity (32, 33). We have shown that iv ghrelin administration stimulates appetite in obese humans, suggesting that they are not ghrelin resistant

2002 Food fails to suppress ghrelin levels in obese humans. J Clin Endocrinol Metab
2005 Postprandial plasma ghrelin is suppressed proportional to meal calorie content in normal-weight but not obese subjects

The above study showed that meals high in carbs didnt really do alot for ghrelin levels in the obese, but in lean people ghrelin was surpressed more as calories went up.

Now, we have already seen that fat digestion is needed for ghrelin supression after a meal, and we have also seen that carb rich meals make ghrelin bounce back, while protein rich meals supressed ghrelin for along time.

Today we also saw that obese people secret markedly lower bile acids after food.

Could it be that obese people are not properly digesting thier food?

Obese slower digestion of fat?

A while ago I posted how fat digestion was needed for ghrelin supression post meal.

This study shows how obese people secret markedly less bile salts for fat digestion.

Also note that lean people typically have higher levels of ghrelin in a fasted state.

Monday, 12 July 2010

The coming together of Leptin

This interesting thread links Leptin with Glutamate, its quite common for people to stall weight loss on ketogenic diets. And those very obese who loose weight tend to have very very low leptin levels after the weight loss.

On a ketogenic diet, gluconeogenesis is most likely massively increased. The liver, at all costs, needs to maintain normoglycemia as hypoglycemia is death very quickly. This would suggest that following a ketogenic diet, the pathway of gluconeogenesis is massively upregulated becuase the liver cannot afford to ever let the 5g of glucose in the blood drop too low.

Obviously, ketones reduce the need for glucose in the brain, but whatever way we swing it, that 5g of blood glucose rules the day. That must be maintained.

Anyway, there is lots of anecdotal evidence that one of the ways to break a fat loss stall on a ketogenic diet is to kind of carb binge for sometime. Such a carb binge will completely refuel liver glycogen and thus down regulate the pathway of gluconeogenesis, perhaps finally allowing glutamate to cause intense leptin secretion from white adipocytes.

With gluconeogenesis so high during a ketogenic diet, my theory is that glutamine is massively and preferentially turned into liver glycogen, instead of being turned into glutamate or reaching white adipocytes where we can crank up leptin.

I intend to experiment with honey and l-glutamine powder mega-dosing over the coming week.

Thursday, 8 July 2010

The body works on a system of thresholds

some may well be as good as none. and more may not be any better than some.

One thing that is prevalent in biology is that cell surface receptors for the most part determine what a cell will do.

There is no point in having high serum growth hormone for example if all your cells dont have the receptor for it to bind. Same for Testosterone. Same for ANY hormone.

With Testosterone there is a strong negative feedback loop, such that high serum T will cause your balls to churn out less. This has implications as increasing serum T through whatever means is largely a mission in futility, your testis will adjust accordingly.

Meanwhile, having the T cell surface receptor is upregulated does not have a negative feedback loop, infact, having your cells sucking in more T will ofcourse make your testis produce more as serum levels drop.

Sunday, 4 July 2010

Ghrelin Antagonism = Hypertension

Given that protein supresses ghrelin for the longest period of time, again intermittent fasting looks to be a magic bullet for reducing metabolic syndrome.

I have high blood pressure but I dont worry about it too much becuase its I tend to get dizzy quickly with even slight drops in blood pressure.

l-glutamine stimulates Growth Hormone

Basically it looks like glutamine taken in isolation supresses FFA in the blood, which once again stimulates a nice GH response.

They used 2g but I suspect its dose dependent, I would imagine 5-10g would be optimal depending on body weight.

The study author speculates that the the smaller GH spikes are more beneficial becuase of the negative feedback loops associated with the large spikes.

Area under curve is likely important, but his theory does need testing.

Friday, 2 July 2010

L-Glutamine induces insulin resistence in adipocytes

I remember when I first started my ketogenic diet again, the weight loss at the beginning was very dramatic and at the time I was still finishing off my bottle of l-glutamine. taking about 5g per day.

Its unclear how much glutamine the rodents in this study were getting per kg of body weight since I don't have access to the full article. But I think that in general obesity is characterised by an upregulation of fat storage compared to fat oxidation gene's.

Taubes comment on obesity being a disorder of excess fat accumulation rather than a result of over-eating mirror's this theory.

Thursday, 1 July 2010

Current Hormone Understanding

Leptin - So far this looks to be more of an anti-starvation hormone. The fact that it is highly elevated in obese people is irrelevant, probably due to the fact that receptor levels are saturated.

However, problems occur when Leptin is low, although it does not seem to affect percieved hunger it does have an effect of sex hormones and depression.

Ghrelin - It seems to this hormone is also not completely involved in hunger and apetite. - The satiating effect of dietary protein is unrelated to postprandial ghrelin secretion.

Leptin production is mainly regulated by insulin-induced changes of adipocyte metabolism -

I also found another eye opening study here -

Despite cutting out 95% of bypass patients stomach's, levels of circulating ghrelin remained in measurable quantities.

Wednesday, 30 June 2010

Fat digestion supresses ghrelin

Digestion of fat is needed to surpress ghrelin.

Ghrelin helps promote sleep

This could be why carb foods are notorious for inducing sleep, carb foods produce a temporary decline in ghrelin followed by a strong rebound 60 mins after meal

Meanwhile, protein supresses ghrelin slowly and for along time. Dont eat protein before going to bed!

Monday, 28 June 2010

Exercising while fasted or not?

According to this study, exercising while fasted upregulates fat burning genes, while exercising after a meal instead inhibits fat storing genes.

Basically, when trying to lose body fat, it should be more beneficial to exercise while fasted.

Sunday, 27 June 2010

DHA upregulates lipolysis

Note most fish oil supplments are considerably higher in EPA than DHA.

Friday, 25 June 2010

Insulin stays elevated after protein meal

The high protein meal kept ghrelin surpressed for the longest but it also kept insulin elevated for the longest.

There is a potential take home message here for fat loss in that consuming a 90% fat diet will keep insulin down.

Carbs suppress ghrelin the most, but it is temporary

Carbs supressed the hunger hormone ghrelin the most, but the investigators report that it was followed by a quick rebound.

Protein supressed ghrelin the least, and fat somewhere in between protein and carbs.

Interesting that the obese group reported more hunger following the carb meal.

Monday, 21 June 2010

Testosterone or Grwoth Hormone, I can't have both?

Confusing take home message from this study, they report that GH was significantly higher 1 min after resistence exercise for the 60sec rest groups COMPARED to the 120sec rest groups. No mention of the 90sec rest groups though. I guess 60sec and 90sec were NOT significantly different for GH.

Further down, we see that testosterone was 76% higher in 90sec groups compared to 60sec groups.

Overall 90sec rest intervals looks like a good average for both GH and Testosterone.