converting stored fat to energy. vets and experts needed.

[leancuisine]

with scientific evidence, can anybody explain how the body converts stored fat for energy?

i'm a little confused about muscle clycogen and liver glycogen.

thanks.

 

[Burning_Inside]

do a search on google

 

[Lee]

its called ketosis, put that in yer google and smoke it.

 

[leancuisine]

do a search on google

it didnt even once occur to me that there's such a beautiful thing called google.

no shit about google and ketosis..

more interested in liver glycogen and the process that takes place converting that glucose into energy and ultimately depleting liver glycogen without sacrificing muscle tissue in the process.

search THAT in google!

 

[Ron Ritzman]

with scientific evidence, can anybody explain how the body converts stored fat for energy?

i'm a little confused about muscle clycogen and liver glycogen.

thanks.

Actually, the fat cells are always futile cycling (both storing and releasing fat) to some degree. In the fed state, insulin inhibits lipolysis (fat release) so the body is burning mostly dietary carbohydrates, storing dietary fat in fat cells and excess glucose as glycogen in liver and muscles (and in fat cells if glycogen stores are full)

In the fasting state, insulin levels drop and glucagon levels rise. This causes the liver to break down it's glycogen stores and release glucose into the bloodstream. At the same time the fat cells release more fat into the bloodstream saving the limited supply of glucose for the brain which can't burn fat. When the liver runs out of glucose, it starts making glucose out of non carbohydrate sources such as protein and turning some of the fat it's burning into ketone bodies which the brain can use as fuel further conserving glucose and reducing the need to break down protein.

Muscle glycogen is different. It can only be used by the muscles storing it when they are exercised. However, if the exercise is anaerobic then the liver can convert the lactic acid it generates into glucose for use by any tissue.

The ECA stack changes this a bit. The higher catecholamine levels promote increased fat utilization and antagonize the insulin receptors on fat cells. In this situation the body is burning the fat and storing the carbs. In most people this results in a higher metabolic rate, more stable blood sugar levels, and a reduced appetite making diet and weight loss easier.

--
Ron Ritzman
http://www.panix.com/~ritzlart

 

[MS]

Fat burning in adipose tissue is controlled by an enzyme (called hormone-sensitive lipase) which is dependent on the intracellular cAMP level (in other words useable energy in the cell).
In human adipose tissue, cAMP level is increased by catecholamines such as ephedrine (through beta-adrenoceptor stimulation) or decreased by insulin, catecholamine (through alpha 2-adrenoceptor stimulation), neuropeptide Y, prostaglandins and adenosine. The mobilization of lipids from adipose tissue is an adaptative mechanism in response to starvation or hypocaloric diet, which involves REDUCTION of the anti fat-burning effect of insulin and the increase of catecholamine sensitivity. So as long as you are eating less than you burn, your fat loss efforts will be less affected by other hormones such as insulin, and increased by drugs such as ephedrine. If you are eating more than you burn, then drugs such as ephedrine may paradoxically make you MORE resistant to the effects of carbohydrates on your insulin sensitivity. Note: ephedrine also increases thermogenesis more in 'dieting' folks than in folks who eat higher calorie meals. Increased thermogenesis also=more fat-burning. All of the above is true whether or not you are in ketosis if you average out lipolysis over a 24 hour period based on energy intake versus energy expenditure. In other words, you may burn more fat while your liver glycogen is low compared to after a high carb meal, but over an entire day (unless you are already severly insulin resistant) it all balances out to the same fat lost for the same calorie intake. And as Ron Ritzman pointed out, muscle glycogen has no effect on your ability to burn fat, so anything that can preferentially fill muscle glycogen (such as muscle glycogen depletion with weight training followed by timed carbohydrate consumption) is a great thing for bodybuilders. Carbs stored in muscles cannot inhibit fat-burning in the classical sense.

 

[leancuisine]

RON RITZMAN.....

exellent stuff. that's exactly the kind of material i need.
do you have any more similiar references?

thanks again.

MS...

good stuff. appreicate that.

now, it occurs to me that perhaps the quickest and most efficient method of fat loss while, at the least, sparing muscle in through TKD - targeted ketonic diet.

correct me if i'm wrong but on such diet, your liver glycogen levels will remain low except pre and post workout.

so, you'll have plenty of energy for an efficient workout and the rest of the day (due to low liver glucose levels) the main source of energy will inevitably come from stored fat????????????????

allright experts

 

[Ron Ritzman]

In human adipose tissue, cAMP level is increased by catecholamines such as ephedrine (through beta-adrenoceptor stimulation) or decreased by insulin, catecholamine (through alpha 2-adrenoceptor stimulation)

Something I have been wondering about. It has been argued that ECA used continuously (without cycling) enhances fat burning even more because the constantly stimulated alpha-2s downregulate but the beta-3s don't.

If this is true then would stopping ECA after being on it for a very long time possibly cause a "yohimbe like" rebound fat burning effect? (if this makes any sense)

 

[MS]

TKD or TNKD (Targetted NON-ketogenic diet) may be the ideal diet for bodybuilders IMHO. Ketosis is not necessary to reap the benefits of targeted carb intake, but either way (ketogenic or not) this ensures that muscle glycogen is optimized and insulin inhibition of fat-burning is minimized.

There is no doubt in my mind that the fat lost with long term EC use will be quickly regained (and then some) when it's discontinued. I think this is both due to downregulation of A2 ARs, as well as the loss of appetite suppression. This downregualtion of the A2s is one of the reasons they say you shouldn't mix EC plus yohimbine. However, as a female I know for sure that my thighs will never get lean from EC alone, and I'm sure there are a lot of guys out there who know the same when it comes to getting that 6-pack to show. So I don't think the downregulation is absolute-just relative. There may be other, more subtle changes in noradreneric signalling as well, and there is some evidence that EC supps merely return an obese or dieting person's impaired sympathetic output to 'normal'. There may also be changes in fluid balance associated with long term EC use that disappear leading to a return to more fluid weight. No one is 100% certain what the long term fat loss effects are from taking EC, but in general diets don't work long term anyway, so you might as well throw some EC at the problem. The best bet though is to wait until you're well into your diet (far enough that metabolism has slowed and cAMP levels have dropped) before you start your EC stack.

Maybe even a better bet is to never get to a state where you need to diet ??????

 

[MS]

Oops, I should add that there is some evidence (not yet conclusive though) that chronic EC treatment actually increases Beta-3 ARs in obese people, while reducing leptin levels (and prolly reducing leptin resistance). Again, I'm not sure what this means after discontinuation of the drugs, but it is clear that obese folks (compared to lean, non-dieting folks) have lower levels of Beta-3 ARs and, again, EC use may just 'normalize' their metabolism. I suspect this would also be true for lean dieters with a diet induced metabolic slow down.