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:

A insulina inibe a lipólise, ou seja, a quebra dos triglicerídeos nas células de gordura. Por isso ingerir carboidrato faz você parar de utilizar gordura. Mas é um processo temporário (o simples fato de fazer exercício já induz uma redução nos níveis de insulina, que foram elevados pela ingestão de carboidrato).

eu tava tentando explicar isso mas nao sabia como, o martin explicou praticamente o que eu ia falar

eu ainda iria dizer que eu acho besteira suplementar carbos principalmente pelo fato de voce estar consumindo calorias ao meu ver desnecessarias.

edit :

ta ae um texto do Rodolfo Peres sobre carbos pra quem quer perder gordura

01 - Uso de repositores energéticos durante atividade aeróbica, quando o objetivo é a redução da gordura corporal.

É muito comum encontrarmos alguém fazendo esteira e/ou bicicleta ergométrica, com o objetivo de perder gordura corporal, ingerindo repositores energéticos como se fosse água. O conteúdo do rótulo, afirmando que é uma bebida repositora para praticantes de atividade física, associado a um sabor agradável, tende a estimular o consumo. Mas vale lembrar que essas bebidas só devem ser ingeridas, durante a atividade aeróbica em duas situações específicas: quando o objetivo for um aumento na performance - devido ao efeito poupador de glicogênio -ou para repor eletrólitos em exercícios com duração superior a uma hora. Ou seja, os vinte ou trinta minutos de esteira que você faz buscando otimizar a queima de gordura não terão o efeito esperado se você consumir repositores energéticos durante a atividade.

Editado 29/06/2013 às 00:20 06/29, 2013 por falange- (veja o histórico de edições)

sim, isso mesmo

então tem que proibir dextrose ou malto durante os treinos, princpalmente aeróbico, pra galera que ta em cutting...

se gastar energia de gordura nesse momento, as calorias depois serão melhores aproveitadas reconstruindo parte dos musculos e diminuindo o catabolismo...

agora acredito ainda mais na possiblidade que defendi no tópico sobre crescer seco de acordo com uma melhor divisão dos macronutrientes durante o dia...

mesmo que o balanço energética defina o ganho ou perda de peso, os horários dos macros podem sim mudar o quanto se perde e ganha de gorduras e músculos.

copnsiderando que o Lyle McDonald esteja certo

repito: me parece mais certo ainda a possibilidade de manipular via nutrição a relação entre o que o corpo gasta de gordura e perde de musculos contra o que ele estoca em musculos e estoca em gordura...

O Lyle diz que apenas uns 20% disso poderá ser feito e que 80% é genética, mas pode fazer diferença em quanto se perde de massa magra em cutting e quanto se ganha de gordura em bulk

Editado 29/06/2013 às 00:27 06/29, 2013 por planeta (veja o histórico de edições)

cara, eu acredito que da pra ganhar massa muscular enquanto perde gordura tendo um conhecimento mais aprofundado (coisa que eu nao tenho) pelo menos se o cara estiver longe do 'limite genetico' dele.

Eu acredito que pra quem conhece bem o timing dos nutrientes vai alguma coisa sim no resultado final, mas a diferenca nao vai ser absurda.

concordo

passei da metade do livro

1- o cara manja demais, se ele não tá inventando ueahuehae

2- ele tb fala legal sobre treinos, vale muuito a pena ler isso