em certo ponto ele diz que tomar um suplemento de carboidratos durante o treino aeróbico faz parar a queima de gordura ... If you drink a carb drink during
aerobic exercise, for example, the slight increase in insulin will decrease fat mobilization despite
high levels of catecholamines.
não sei se fica bom jogando no google tradutor mas não custa tentar... to lendo o livro todo não tem como traduzir ee escrever em portugues, demora muito ... tem sempre tanta coisa a ser lida e estudada...
The Ultimate Diet 2.0 (acha fácil o livro pdf completo pra download pelo google)
by
Lyle McDonald
Chapter 6: Fat cell metabolism
The ultimate goal of a diet is to lose bodyfat of course so let's look at the processes
controlling that. That means examining the steps involved in mobilizing fat from fat cells and
burning them off.
First, let me elaborate on what it means to lose or "burn" bodyfat. What this means is
that the fat stored in your fat cells is removed from those cells and converted to energy elsewhere
in the body. Most tissues in the body (there are a few exceptions such as the brain) can use fatty
acids for fuel, but the main ones we are interested in are skeletal muscle and the liver. I want to
mention that even though the brain can't use fatty acids directly, it can use ketones which are
made from fatty acid metabolism in the liver.
Let's look at the mechanisms underlying the process of fat loss. Although the process can
be further subdivided, we are only interested in three major steps of fatty acid metabolism:
mobilization, transport, and oxidation (burning).
Step 1: Mobilization
The first step in burning off bodyfat is getting it out of your fat cells. You might even argue
that this is the most important step since, if you can't get it out of the fat cell, you can't burn it
off.
Recall from last chapter that bodyfat is primarily stored triglyceride, with a small amount
of water and some enzymatic and cellular machinery. Mobilizing bodyfat requires that we first
break down the stored triglyceride into three fatty acids and a molecule of glycerol. The rate
limiting step in this process is an enzyme called hormone sensitive lipase (HSL).
So what regulates HSL? Although a number of hormones such as testosterone, cortisol,
estrogen, and growth hormone have modulating effects on HSL activity (mainly increasing or
decreasing total levels of HSL in the fat cell), the only hormones that we need to be concerned
with in terms of HSL activity are insulin and the catecholamines.
The primary inactivator of HSL is the hormone insulin and it only takes very tiny
amounts (depending on insulin sensitivity) to have an effect. Even fasting insulin levels are
sufficient to inactivate HSL by nearly 50%. Small increases in insulin (from either protein or
carbohydrate intake) inactivate HSL further. Additionally, the mere presence of triglycerides in
the bloodstream (via infusion or by just eating dietary fat by itself) also inhibits HSL activity so
this isn't as simple as just blaming insulin. One way or another, any time you eat, HSL is going
to be inactivated, either by the increase in insulin from protein or carbs or the presence of fat in
the bloodstream from eating fat.
The primary hormones which activate HSL are the catecholamines: adrenaline and
noradrenaline. Adrenaline is released from the adrenal cortex, traveling through the bloodstream
to affect numerous tissues in the body. This means that blood flow to fat cells has an impact on
how much or how little adrenaline will reach fat cells. Noradrenaline is released from nerve
terminals which interact directly with the cells.
More technically, both insulin and the catecholamines affect levels of cyclical AMP (cAMP)
in the fat cell which is what really determines how active HSL is. When cAMP levels are low,
HSL activity is also low and fat breakdown is low. When cAMP levels are high, HSL activity is
high and fat breakdown increases.
Insulin lowers levels of cAMP and the catecholamines, in general, raise levels of cAMP (I'll
explain this statement in a second). The higher the level of cAMP, the more active HSL is and
the more bodyfat that gets broken down and released from the fat cell. It should be clear that,
from a fat loss standpoint, we want high levels of cAMP.
A tangent: all about adrenoreceptors
To understand some of the cryptic remarks above, I need to back up a bit and explain how
the catecholamines send their signals. All hormones work through specific receptors and the
catecholamines are no different, they have their own specific receptors called adrenoreceptors.
There are two major classes of adrenoreceptors: beta and alpha, which are found all over
the body. This includes the brain, liver, skeletal muscle, fat cells, heart, blood vessels, etc.; you
name it and there are probably adrenoreceptors there.
Now, there are at least 3 (and maybe 4) different beta receptors called, imaginatively:
beta-1, beta-2, beta-3, and beta-4 (or the atypical beta-3). Alpha-adrenoreceptors come in at
least two flavors, alpha-1 and alpha-2. There are additional subtypes of each adrenoreceptor but
this is more detail than we really need. Tangentially, beta-3 receptors (and drugs called beta-3
agonists) became a huge research project when it was found that beta-3 activation caused major
fat loss in animals; it was hoped that the drugs would work in humans as well. Unfortunately,
beta-3 receptors are found primarily on brown fat cells which, as I said, animals tend to have lots
of and humans don't.
The main receptors we need to worry about in human fat cells are alpha-2 receptors and
beta-1 and beta-2 receptors, both of which actively bind the catecholamine hormones. When
catecholamines bind to beta-1,2 receptors, they increase cAMP levels, which increases fat
breakdown. Great. However, when the catecholamines bind alpha-2 receptors, they decrease
cAMP levels which decreases fat breakdown. Not great. But it means that catecholamines,
which I told you were fat mobilizers, can actually send both fat mobilizing and anti-fat mobilizing
signals: by binding to either alpha- or beta-receptors.
So why does this matter? Different areas of bodyfat have different distributions of alpha-2
and beta-2 adrenoreceptors. For example, women's lower bodyfat (hips and thighs) have been
found to have 9 times as many alpha-2 receptors as beta-2 receptors. Some research indicates
that men's abdominal fat is similar, with more alpha-2 than beta-2 receptors. Now you know
part of why its so difficult to reduce these stubborn fat areas; with a greater number of alpha-2
receptors to bind catecholamines, it's that much more difficult to stimulate fat breakdown in
those fat cells.
Other factors affect adrenoreceptor function as well. Androgens and thyroid tend to
increase the sensitivity of beta-2 receptors to the catecholamines. This may be part of why men
(who have higher androgens and higher thyroid, on average) lose fat more easily. The factors
controlling alpha-2 adrenoreceptor function aren't as well elucidated.
Back to mobilization: summing up
I should note that insulin pretty much always wins the battle over fat cell metabolism.
That is, even in the face of high catecholamine levels, if insulin is elevated, fat mobilization will be
impaired. As it turns out, this generally doesn't happen under normal conditions. Typically when
insulin is high, the catecholamines are low and vice versa (e.g. during exercise, insulin levels drop
as catecholamine levels go up). There are exceptions of course. If you drink a carb drink during
aerobic exercise, for example, the slight increase in insulin will decrease fat mobilization despite
high levels of catecholamines.
Just remember the following: insulin inhibits fat mobilization and the catecholamines
(generally) increase it. Insulin always wins the battle. So when insulin is high and the
catecholamines are low, fat tends to be stored. When insulin is low and the catecholamines are
high, fat will be mobilized. A bit simplistic? Perhaps. But good enough for the time being. The
real take home message is that, from a fat mobilization standpoint, we want low insulin and high
catecholamine levels. Both can be readily accomplished by altering diet (lowering carbohydrates
and calories) and exercise (which increases catecholamines).
Step 2: