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.

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

http://www.ncbi.nlm.nih.gov/pubmed/10919929

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.

Postwork out Feeding again, Myostatin look

http://jap.physiology.org/cgi/content/full/106/5/1720

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.

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 Leangains.com 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 leangains.com 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.

http://www.leangains.com/2009/12/fasted-training-boosts-muscle-growth.html
http://www.springerlink.com/content/w8712615714k8150/

L-arginine gene expression

http://www.ncbi.nlm.nih.gov/pubmed/20619625

http://www.ncbi.nlm.nih.gov/pubmed/18683021

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

Fed to pigs at 1%

Testosterone and Heart Attacks

http://www.ncbi.nlm.nih.gov/pubmed/20691154

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.