akn
Musclechemistry Member
Adenosinetriphosphate (ATP) is more than the chemical our bodies utilizes to
fuel muscular contractions and nerve impulses. Obviously we would die without it.
However, our ATP level and function also dictates how muscular and fat we are to a
great extent.
As we know, the body needs a constant supply of ATP. When ATP is utilized as
energy, it loses a phosphate molecule which creates Adenosine Diphosphate (ADP).
ADP turns to creatine phosphate (CP) stores for the missing phosphate molecule and
ATP is again manufactured. This is of course why creatine products aid in strength
and lean tissue gains.
The body can produce ATP from proteins, glucose, or fats. This is possible due
to cellular mitochondria. When cellular ATP stores are low, such as after a heavy set of
squats, and cellular "ADP" levels rise, the cells must undergo oxidative
phosphorylation and electron transfer to restore ATP.
Oxidative phosphorylation is the process of adding a phosphate group to ADP
to make ATP. Electron transfer is the process or way in which this happens.
Mitochondria pump hydrogen ions from the interior to the exterior of our cells. This
creates an imbalance where there are a greater number of hydrogen ions on the
outside of the mitochondria which results in the pairing of ADP with an extra
phosphate group. Shazam!: We have ATP and cellular energy, which allows us to live
and train another day.
The electrons for electron transfer come from NADH, which is made from
macronutrients. As you know, macronutrients are protein, carbohydrates, and fats.
Which obviously become circulatory cell food: amino acids, glucose/glycogen, and
fatty acids. So the series goes like this:
1. NADH donates electrons to the mitochondria for transfer.
2. The electron transfer creates a hydrogen ion imbalance.
3. The imbalance powers the "coupling" of ADP and a phosphate group resulting in
ATP. (Again; Shazam!)
No doubt you remember the term "coupling" during the ADP/ATP process of
oxidative phosphorylation. Well, "uncoupling" is in simple terms a method of making
this whole process harder. In the case of oxidative phosphorylation, it is a matter of
making the mitochondria work very hard to create the hydrogen ion imbalance.
The little goodies responsible for this uncoupling are uncoupling proteins,
which are found in both muscle cells and brown fat cells. When these uncoupling
proteins make their way into the mitochondria, the resulting reaction is that the
mitochondria must work overtime trying to pump hydrogen ions from the inside to
the outside of the cell. This is due to the effect of uncoupling proteins allowing the
hydrogen ions to migrate back in. Since the process wasted the electrons from NADH
and no ATP was made, the process has to start all over again.
Uncoupling proteins in muscle cells act to regulate free fatty acids in the
myocytes. And uncoupling proteins in brown fat has a regulatory effect upon body
temperature/ thermalgenesis. The result of this uncoupling is that the mitochondria
uses up much more fatty acids, and to a lesser extent, more glucose to normalize and
regenerate ATP levels. When all this takes place, obviously an athlete burns more
calories (most of which come from fat stores) and becomes much leaner.
The chemically enhanced beasts had utilized many drugs that influence the
uncoupling process: DNP, Thyroid hormones T-4/T-3, amphetamines, ephedrine,
norephedrine (phenylpropanolamine) and caffeine to name a few. Before I go on, let
me say that amphetamines are a really bad idea under any circumstances. They are
very illegal, they sucked at burning fat, and they screwed up people's minds.
On top of this, they were dirty. Most black-market "meth" was and is
manufactured using red phosphorus as part of the process. This is not properly
removed or purified at any point in the process. Red phosphorous is cancer causing
and destroys immune function factors! Users commonly get weird sores and seem to
catch every cold and flu they come within 50 yards of. Picture that on contest day!
EPHEDRINE-NOREPHEDRINE-CLENBUTEROL
All three of these compounds are called beta -agonists, which means that they
stimulate beta receptor sub typesl,2, and 3. Clenbuterol is a beta-2 receptor specific
agonist. This means that its fat burning effect is due to specific stimulation of beta-2
receptors. Ephedrine is a non-specific beta-receptor agonist. Meaning its effects are
due to stimulation of beta 1,2,and 3 receptors. Norephedrine (phenylpropanolamine)
is a non-specific beta-receptor agonist as well, but seems to effect beta 2 receptors in
a slightly different way.
All beta agonist affect the fat burning process through mild thermalgenesis,
which of course involves the process of uncoupling.
Clenbuterol administration tended to cause down-regulation of beta-2 receptor
activity. Since beta 2 receptors are a major regulator of the fat break down (lipolysis)
process, this sucked.
Continuous administration of Clenbuterol allowed the drug to lose its CNS
effectiveness after only a few weeks. Regardless of dosage. For this reason, a 2 day
on-2 day off protocol was necessary during Clenbuterol use. This approach slowed
the adaptive down-regulating response by beta-2 receptors.
Please be patient. I will explain all the "receptor" stuff in a few minutes.
Unlike Clenbuterol, Ephedrine and Norephedrine did not cause an excessive
adaptive response and therefore continued to effect thermalgenic activity for months.
Both induce the release of "Noradrenaline", which in turn stimulates all three
beta receptor sub types, and both can stimulate the same receptor-sites directly to
some degree. Ephedrine products induce the thermalgenic effect by stimulation of all
3 receptor sub types, but 35-40 % of their stimulatory effects are upon type 3 beta
receptors.
This is significant because the response governing activity down-regulation of
beta 2 receptors is not possible with beta 3 receptors. So ephedrine products have
potential long term effectiveness. Simple? Beta-3 receptor stimulation increases the
break down of fats. This also results in an increase in uncoupling protein levels. It
should be noted that Ephedrine products increase the conversion of T-4 to T-3 by the
liver. (Yup!!)
CAFFEINE
When beta agonist compounds are utilized, the body releases adrenaline and
nor-adrenaline, which is secreted due to stimulation of the sympathetic nerves.
Ultimately, the body has an adaptive response which regulates the long term activity
of beta agonist and therefore their thermalgenic value (fat burning effect).
Methylxanthines such as caffeine, enprofylline, forskolin, and theophylline,
block or inhibit the body's adaptive response to a respectable degree. Coadministration
of methylxanthines with Clenbuterol, ephedrine or norephedrine
resulted in a longer and more potent effect/result period. Normally the most effective
ratio of ephedrine or norephedrine to caffeine was about 1 to 1 0. (20 mg of Ephedrine
to 200 mg of caffeine.) The chemistry behind this is quite complex, but the basic
action is this:
More Science Geek Stuff
Beta agonists modulate their fat break-down signal through an energy
precursor within the cell called cyclic adenosine monophosphate (cAMP).
Compounds called phosphodiesterases counter-act this by breaking down cAMP
and the fat loss signal decreases or stops. Methylxanthines either inhibit or block
phophodiesterase which is the enzyme that degrades the phosphate in cAMP.
Therefore the fat burning effect/thermalgenic value of the chosen beta-agonist signal
continues.... (Sorry, but you made me do the science geek thing.)
RECEPTORS
Most cells and organs in the body possess a distribution of andrenergic
receptors. These receptors have sub types: ALFA sub-land 2, and beta sub-1,2,3 and
4. The receptors we are interested in initially for fat loss/thermalgenesis are alfa-sub-
2, and beta-sub-2 and 3. These are the andrenergic receptors having the greatest
initial effect upon fat loss.
Stimulation of beta-sub-2 receptors creates an anti-catabolic response meaning
protein sparing. Unfortunately beta-sub-2 receptors down-regulate after 2-3 weeks of
continuous stimulation. Action/Reaction, remember?
Stimulation of Alfa-sub-2 receptors blocks the mobilization of fat stores.
Blocking these receptors with Yohimbine increases fat expenditure.
Interesting fact: Women have greater numbers of Alfa-sub-2 receptor (and
estrogen receptors) in their lower bodies when compared to males. Hey, they bit the
apple, and I didn't design the receptor distribution ratio. This is why women have so
much trouble losing fat in these areas. (Which really sucks)
If I had designed the receptor ratio and distribution, the women of this world
would have significantly higher ratios of Alfa-sub-2 andrenergic and estrogen
receptors in the breast with few anywhere else. I would also greatly reduce 16-ahydroxyestrone
production so women could have great racks, lower incidence of
breast cancer, and remain lean while eating cookies and ice cream. But that is another
story...and lots of hate mail, no doubt.
There are a few compounds that block Alfa-sub-2 receptors (antagonists) and
therefore prevent the fat loss inhibiting effect. Pure Yohimbine is a good example. It
actually inhibits the negative feed-back loop that inhibits continued fat loss.
Unfortunately, the effects of Yohimbine are mitigated by insulin release (or
administration). This means that yohimbine is only effective as an Alfa-sub-2 receptor
antagonist if the athlete utilizes it in a fasted state (like before breakfast).
Chiseled SGR (Site Reducing Gel)
As stated earlier in this book, AGR Nutrition (www.agrnutrition.com) has a very
effective fat-burning topical product called "Chiseled SGR (Site Reducing Gel)", which
contains pure Yohimbine and other goodies that prevent insulin from getting in the
way of Yohimbine doing its job.
It is in a gel form intended for topical site-specific application with an amazing
absorption rate. Most note benefits in the first few days to a week of application. It is
actually so effective that users are suggested to apply the product to only one site at
a time (abs, lower back etc) to prevent an over accumulation of newly freed fatty acids
from entering the circulatory system too quickly. (I truly enjoyed working on this one)
As stated prior, ephedrine products modulate 35-40% of their fat
burning/thermalgenic effect through activation of beta-sub-3 receptors. However, to a
lesser degree, they do stimulate thermalgenesis through activation of the beta-sub-1
receptors. Since beta-sub-2 receptor activity significantly down-regulates after only a
few weeks of continuous stimulation, the question of "how long before beta-sub-land
3 receptors down-regulate activity" should come to mind.
After about four weeks of ephedrine/caffeine use, thyroid hormone levels
increase. At about 12 weeks of use thyroid hormone levels decrease below normal
levels. As stated prior, Ephedrine products increase T-4 conversion to the more potent
T-3 thyroid hormone. Unfortunately, this too has a negative feed-back loop that kicks
in at about 12 weeks of continuous ephedrine use.
Guess what? We have beta-sub-4 Andrenergic receptors which over-ride the
rest and continue the fat burning process even with lower circulatory thyroid hormone
levels. In fact, the thermalgenic effects of an ephedrine /caffeine stack is better at 12
weeks of use and remains significantly effective for up to 50 weeks.
This is due to the body's ability to increase the number of beta-sub-3 and 4
receptors in response to down regulation of beta -sub-1 and 2 receptors. Cool! By the
way, the enzyme that converts T-4 to T-3 thyroid hormone is 5-deiodinase. Low
selenium intake greatly reduces this enzyme's effects.
Note: most athletes experienced a 3-10% gain in strength and anaerobic capacity when using beta
agonist. This resulted in more lean mass gains due to greater muscle fiber recruitment... potentially.
There are two readily recognized thyroid hormones. T-4 (thyroxine) and T-3
(triiodothyronine). In response to TSH, (Thyroid Stimulating Hormone) the thyroid
gland releases T-4 hormone, and to a lesser degree T-3 hormone.
Daily T-4 production is normally about 76 mcg, and T-3 production is about 26
mcg daily. The majority of T-3 hormone production is due to the conversion of T-4 to
T-3 by the enzyme 5-deiodinase primarily in the liver and kidneys. T-3 is about 5-10
times more active or potent (depending upon which research paper the statistic
originated from) than T-4.
Remember that only unbound or free testosterone can initiate a reaction? Well
about 0.02 % of circulatory T-4 is unbound and about 0.30% of T-3 is unbound or free.
Only free or unbound thyroid hormones can merge with and activate thyroid hormone
receptor sites.
Thyroid hormones increase the levels of uncoupling proteins. They also
increase ATP turn over by stimulating enzymes that effect nerve impulse conduction.
A great deal of research supports the idea that thyroid hormone receptor-sites are
directly linked to the genes that regulate the amount of uncoupling proteins
produced. It should seem evident that thyroid hormones played a significant role in a
chemically enhanced beast's contest prep in most cases.
My opinion was that a few weeks of exogenous thyroid hormone use was far
healthier than long periods of calorie restriction. But that was only my opinion and
not a recommendation. As stated prior, beta agonist aid in the conversion of T-4 to T-
3 so there was an existing synergy when referring to fat loss or lean mass gains.
author L Rea
fuel muscular contractions and nerve impulses. Obviously we would die without it.
However, our ATP level and function also dictates how muscular and fat we are to a
great extent.
As we know, the body needs a constant supply of ATP. When ATP is utilized as
energy, it loses a phosphate molecule which creates Adenosine Diphosphate (ADP).
ADP turns to creatine phosphate (CP) stores for the missing phosphate molecule and
ATP is again manufactured. This is of course why creatine products aid in strength
and lean tissue gains.
The body can produce ATP from proteins, glucose, or fats. This is possible due
to cellular mitochondria. When cellular ATP stores are low, such as after a heavy set of
squats, and cellular "ADP" levels rise, the cells must undergo oxidative
phosphorylation and electron transfer to restore ATP.
Oxidative phosphorylation is the process of adding a phosphate group to ADP
to make ATP. Electron transfer is the process or way in which this happens.
Mitochondria pump hydrogen ions from the interior to the exterior of our cells. This
creates an imbalance where there are a greater number of hydrogen ions on the
outside of the mitochondria which results in the pairing of ADP with an extra
phosphate group. Shazam!: We have ATP and cellular energy, which allows us to live
and train another day.
The electrons for electron transfer come from NADH, which is made from
macronutrients. As you know, macronutrients are protein, carbohydrates, and fats.
Which obviously become circulatory cell food: amino acids, glucose/glycogen, and
fatty acids. So the series goes like this:
1. NADH donates electrons to the mitochondria for transfer.
2. The electron transfer creates a hydrogen ion imbalance.
3. The imbalance powers the "coupling" of ADP and a phosphate group resulting in
ATP. (Again; Shazam!)
No doubt you remember the term "coupling" during the ADP/ATP process of
oxidative phosphorylation. Well, "uncoupling" is in simple terms a method of making
this whole process harder. In the case of oxidative phosphorylation, it is a matter of
making the mitochondria work very hard to create the hydrogen ion imbalance.
The little goodies responsible for this uncoupling are uncoupling proteins,
which are found in both muscle cells and brown fat cells. When these uncoupling
proteins make their way into the mitochondria, the resulting reaction is that the
mitochondria must work overtime trying to pump hydrogen ions from the inside to
the outside of the cell. This is due to the effect of uncoupling proteins allowing the
hydrogen ions to migrate back in. Since the process wasted the electrons from NADH
and no ATP was made, the process has to start all over again.
Uncoupling proteins in muscle cells act to regulate free fatty acids in the
myocytes. And uncoupling proteins in brown fat has a regulatory effect upon body
temperature/ thermalgenesis. The result of this uncoupling is that the mitochondria
uses up much more fatty acids, and to a lesser extent, more glucose to normalize and
regenerate ATP levels. When all this takes place, obviously an athlete burns more
calories (most of which come from fat stores) and becomes much leaner.
The chemically enhanced beasts had utilized many drugs that influence the
uncoupling process: DNP, Thyroid hormones T-4/T-3, amphetamines, ephedrine,
norephedrine (phenylpropanolamine) and caffeine to name a few. Before I go on, let
me say that amphetamines are a really bad idea under any circumstances. They are
very illegal, they sucked at burning fat, and they screwed up people's minds.
On top of this, they were dirty. Most black-market "meth" was and is
manufactured using red phosphorus as part of the process. This is not properly
removed or purified at any point in the process. Red phosphorous is cancer causing
and destroys immune function factors! Users commonly get weird sores and seem to
catch every cold and flu they come within 50 yards of. Picture that on contest day!
EPHEDRINE-NOREPHEDRINE-CLENBUTEROL
All three of these compounds are called beta -agonists, which means that they
stimulate beta receptor sub typesl,2, and 3. Clenbuterol is a beta-2 receptor specific
agonist. This means that its fat burning effect is due to specific stimulation of beta-2
receptors. Ephedrine is a non-specific beta-receptor agonist. Meaning its effects are
due to stimulation of beta 1,2,and 3 receptors. Norephedrine (phenylpropanolamine)
is a non-specific beta-receptor agonist as well, but seems to effect beta 2 receptors in
a slightly different way.
All beta agonist affect the fat burning process through mild thermalgenesis,
which of course involves the process of uncoupling.
Clenbuterol administration tended to cause down-regulation of beta-2 receptor
activity. Since beta 2 receptors are a major regulator of the fat break down (lipolysis)
process, this sucked.
Continuous administration of Clenbuterol allowed the drug to lose its CNS
effectiveness after only a few weeks. Regardless of dosage. For this reason, a 2 day
on-2 day off protocol was necessary during Clenbuterol use. This approach slowed
the adaptive down-regulating response by beta-2 receptors.
Please be patient. I will explain all the "receptor" stuff in a few minutes.
Unlike Clenbuterol, Ephedrine and Norephedrine did not cause an excessive
adaptive response and therefore continued to effect thermalgenic activity for months.
Both induce the release of "Noradrenaline", which in turn stimulates all three
beta receptor sub types, and both can stimulate the same receptor-sites directly to
some degree. Ephedrine products induce the thermalgenic effect by stimulation of all
3 receptor sub types, but 35-40 % of their stimulatory effects are upon type 3 beta
receptors.
This is significant because the response governing activity down-regulation of
beta 2 receptors is not possible with beta 3 receptors. So ephedrine products have
potential long term effectiveness. Simple? Beta-3 receptor stimulation increases the
break down of fats. This also results in an increase in uncoupling protein levels. It
should be noted that Ephedrine products increase the conversion of T-4 to T-3 by the
liver. (Yup!!)
CAFFEINE
When beta agonist compounds are utilized, the body releases adrenaline and
nor-adrenaline, which is secreted due to stimulation of the sympathetic nerves.
Ultimately, the body has an adaptive response which regulates the long term activity
of beta agonist and therefore their thermalgenic value (fat burning effect).
Methylxanthines such as caffeine, enprofylline, forskolin, and theophylline,
block or inhibit the body's adaptive response to a respectable degree. Coadministration
of methylxanthines with Clenbuterol, ephedrine or norephedrine
resulted in a longer and more potent effect/result period. Normally the most effective
ratio of ephedrine or norephedrine to caffeine was about 1 to 1 0. (20 mg of Ephedrine
to 200 mg of caffeine.) The chemistry behind this is quite complex, but the basic
action is this:
More Science Geek Stuff
Beta agonists modulate their fat break-down signal through an energy
precursor within the cell called cyclic adenosine monophosphate (cAMP).
Compounds called phosphodiesterases counter-act this by breaking down cAMP
and the fat loss signal decreases or stops. Methylxanthines either inhibit or block
phophodiesterase which is the enzyme that degrades the phosphate in cAMP.
Therefore the fat burning effect/thermalgenic value of the chosen beta-agonist signal
continues.... (Sorry, but you made me do the science geek thing.)
RECEPTORS
Most cells and organs in the body possess a distribution of andrenergic
receptors. These receptors have sub types: ALFA sub-land 2, and beta sub-1,2,3 and
4. The receptors we are interested in initially for fat loss/thermalgenesis are alfa-sub-
2, and beta-sub-2 and 3. These are the andrenergic receptors having the greatest
initial effect upon fat loss.
Stimulation of beta-sub-2 receptors creates an anti-catabolic response meaning
protein sparing. Unfortunately beta-sub-2 receptors down-regulate after 2-3 weeks of
continuous stimulation. Action/Reaction, remember?
Stimulation of Alfa-sub-2 receptors blocks the mobilization of fat stores.
Blocking these receptors with Yohimbine increases fat expenditure.
Interesting fact: Women have greater numbers of Alfa-sub-2 receptor (and
estrogen receptors) in their lower bodies when compared to males. Hey, they bit the
apple, and I didn't design the receptor distribution ratio. This is why women have so
much trouble losing fat in these areas. (Which really sucks)
If I had designed the receptor ratio and distribution, the women of this world
would have significantly higher ratios of Alfa-sub-2 andrenergic and estrogen
receptors in the breast with few anywhere else. I would also greatly reduce 16-ahydroxyestrone
production so women could have great racks, lower incidence of
breast cancer, and remain lean while eating cookies and ice cream. But that is another
story...and lots of hate mail, no doubt.
There are a few compounds that block Alfa-sub-2 receptors (antagonists) and
therefore prevent the fat loss inhibiting effect. Pure Yohimbine is a good example. It
actually inhibits the negative feed-back loop that inhibits continued fat loss.
Unfortunately, the effects of Yohimbine are mitigated by insulin release (or
administration). This means that yohimbine is only effective as an Alfa-sub-2 receptor
antagonist if the athlete utilizes it in a fasted state (like before breakfast).
Chiseled SGR (Site Reducing Gel)
As stated earlier in this book, AGR Nutrition (www.agrnutrition.com) has a very
effective fat-burning topical product called "Chiseled SGR (Site Reducing Gel)", which
contains pure Yohimbine and other goodies that prevent insulin from getting in the
way of Yohimbine doing its job.
It is in a gel form intended for topical site-specific application with an amazing
absorption rate. Most note benefits in the first few days to a week of application. It is
actually so effective that users are suggested to apply the product to only one site at
a time (abs, lower back etc) to prevent an over accumulation of newly freed fatty acids
from entering the circulatory system too quickly. (I truly enjoyed working on this one)
As stated prior, ephedrine products modulate 35-40% of their fat
burning/thermalgenic effect through activation of beta-sub-3 receptors. However, to a
lesser degree, they do stimulate thermalgenesis through activation of the beta-sub-1
receptors. Since beta-sub-2 receptor activity significantly down-regulates after only a
few weeks of continuous stimulation, the question of "how long before beta-sub-land
3 receptors down-regulate activity" should come to mind.
After about four weeks of ephedrine/caffeine use, thyroid hormone levels
increase. At about 12 weeks of use thyroid hormone levels decrease below normal
levels. As stated prior, Ephedrine products increase T-4 conversion to the more potent
T-3 thyroid hormone. Unfortunately, this too has a negative feed-back loop that kicks
in at about 12 weeks of continuous ephedrine use.
Guess what? We have beta-sub-4 Andrenergic receptors which over-ride the
rest and continue the fat burning process even with lower circulatory thyroid hormone
levels. In fact, the thermalgenic effects of an ephedrine /caffeine stack is better at 12
weeks of use and remains significantly effective for up to 50 weeks.
This is due to the body's ability to increase the number of beta-sub-3 and 4
receptors in response to down regulation of beta -sub-1 and 2 receptors. Cool! By the
way, the enzyme that converts T-4 to T-3 thyroid hormone is 5-deiodinase. Low
selenium intake greatly reduces this enzyme's effects.
Note: most athletes experienced a 3-10% gain in strength and anaerobic capacity when using beta
agonist. This resulted in more lean mass gains due to greater muscle fiber recruitment... potentially.
There are two readily recognized thyroid hormones. T-4 (thyroxine) and T-3
(triiodothyronine). In response to TSH, (Thyroid Stimulating Hormone) the thyroid
gland releases T-4 hormone, and to a lesser degree T-3 hormone.
Daily T-4 production is normally about 76 mcg, and T-3 production is about 26
mcg daily. The majority of T-3 hormone production is due to the conversion of T-4 to
T-3 by the enzyme 5-deiodinase primarily in the liver and kidneys. T-3 is about 5-10
times more active or potent (depending upon which research paper the statistic
originated from) than T-4.
Remember that only unbound or free testosterone can initiate a reaction? Well
about 0.02 % of circulatory T-4 is unbound and about 0.30% of T-3 is unbound or free.
Only free or unbound thyroid hormones can merge with and activate thyroid hormone
receptor sites.
Thyroid hormones increase the levels of uncoupling proteins. They also
increase ATP turn over by stimulating enzymes that effect nerve impulse conduction.
A great deal of research supports the idea that thyroid hormone receptor-sites are
directly linked to the genes that regulate the amount of uncoupling proteins
produced. It should seem evident that thyroid hormones played a significant role in a
chemically enhanced beast's contest prep in most cases.
My opinion was that a few weeks of exogenous thyroid hormone use was far
healthier than long periods of calorie restriction. But that was only my opinion and
not a recommendation. As stated prior, beta agonist aid in the conversion of T-4 to T-
3 so there was an existing synergy when referring to fat loss or lean mass gains.
author L Rea
