Tatyana

The combination of weight training, aerobic exercise and sound eating habits have shown to be the most effective for fat loss and toning. Toning is simply the simultaneous decrease of fat and restoration of muscle.





Every year after the age of 25, the average American gains one pound of body weight yet loses one third to one half pound of muscle. Consequently, our resting metabolism decreases approximately one half of a percent every year. Proper exercise and sound eating habits can reverse this process.


While aerobic exercise burns fat during exercise, anaerobic exercises, like weight training or sprints (see HIIT), utilize fat hours after exercise.


Weight training can also increase the metabolic rate a second way. It restores muscle tissue that had been lost over the years from a sedentary modern life-style, thus improving the aesthetics of the body by accentuating its curves and shape.



Furthermore, one pound of muscle burns approximately 30-50 Calories per day. In contrast, a pound of fat only burns about three Calories per day. This may not seem significant considering one pound of fat contains 3500 Calories. Although, over the course of years, it adds up.



Weight training exercises that use large muscle groups (e.g. Gluteus Maximus, Quadriceps, Hamstrings, Chest, and Back exercises) with a progressively greater resistance have the most potential for restoring lean body weight and raising the metabolism hours after exercise.

Most people do not have to be worried about getting too big when training with weights. Evidence suggests that less than 20 percent of men and very few women can develop large muscles even if they wanted to, regardless what program they follow.




Bodybuilders seen on TV typically, have trained for years, poses a certain degree of genetics, and most likely, have used anabolic steroids sometime in their careers.


When beginning an exercise program, muscle mass increases may initially out pace fat loss, resulting in a very small temporary weight gain. When exercise can be increased over time, more significant fat loss can occur. Unless an exerciser is highly motivated, actual weight loss is usually only seen with particular dietary improvements.


Most of you missed this as I titled the thread 'toning with weights'.

I think that this is important for people to see, learn to love the skin they are in.

I am not saying don't train or try to improve your physique, but this thing about getting big AT ANY COST is really not good.

Young kids taking steroids, we see the ignorance every day on this board.

I know some are responsible, however, I have been reminded at how irresponsible 18 year olds can be as I currently have an 18 year old flat mate.

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Tatyana

I have run into a few big brain biochemists etc and I have asked about this.

My thoughts were that it was true, and it set off some sort of memory pathway in my brain (I read New Scientist, Scientific American, British Medical Journal, New England Journal of Medicine like some women read HELLO) however, as I read so MUCH (+ uni) I don't always remember everything! Also, as I have no time to loads of extra medline searches.......................................... .....I took advantage of their knowledge base

Here are a few of their replies.

My own opinion is that it is more or less accurate in the absence of AAS. Most people can get fit and healthy with the correct diet and workout regimen but the vast majority do not have genetics that lend themselves to the bulky BB physique. In fact, most people are glad they can't get that look. The freakish BB look doesn't appeal to the majority of people.

Now, chemicals like AAS, growth hormone, insulin, and even creatine make that goal attainable by a larger percentage of the population but if they stop using those drugs, they will eventually lose much of the mass they attained while using them. It may take a long time for some if they continue to pay attention to their diet and workout correctly; years even. But eventually, they will lose it. The genetics to support that physique just aren't there. With proper diet and exercise, some of the added mass can be kept but that is highly variable between individuals. Some are able to keep more than others


And another

This is 100% true, and the reason is myostatin. Which basically the genetic regulator of how big you can be. it does this by basically regulating the myoD level in your stem cells. This directly effects their ability to reproduce and join existing muscle cells.

there are methods through training to reduce myostatin experssion though. The whole manipulation of the physiological pathways for hypertrophy is the whole basis of my new research based training method GTP for those who havent read about it yet.

So the answer is this is about 99% true. But there a few that can/will find a way to get beyond this factor by using GTP type training and supps/drugs

Tatyana

Too much testosterone kills brain cells

POSTED: 3:23 p.m. EDT, September 27, 2006

WASHINGTON (Reuters) -- Too much testosterone can kill brain cells, researchers say, in a finding that may help explain why steroid abuse can cause behavior changes such as aggressiveness and suicidal tendencies.

Tests on brain cells in lab dishes showed that while a little of the male hormone is good, too much of it causes cells to self-destruct in a process similar to that seen in brain illnesses such as Alzheimer's.

"Too little testosterone is bad, too much is bad but the right amount is perfect," said Barbara Ehrlich of Yale University in Connecticut, who led the study.

Testosterone is key to the development, differentiation and growth of cells and is produced by both men and women, although men produce about 20 times more of the hormone.

It can also be abused, and recent scandals have involved athletes who use the hormone, or steroids that turn into testosterone in the body, for an unfair advantage.

"Other people have shown that high levels of steroid can cause behavioral changes," Ehrlich said in a telephone interview.

"We can show that when you have high levels of steroids, you have high testosterone and that can destroy the nerve cells. We know that when you lose brain cells you lose function."

Ehrlich's team tried the same thing with the "female" hormone estrogen, just to be fair.

"We were surprised, but it actually looks like estrogen is neuroprotective. If anything, there is less cell death in the presence of estrogen," she said.

Writing in the Journal of Biological Chemistry, Ehrlich and colleagues said their findings meant people should think twice about supplementing with testosterone, even if it does build muscle mass and aid recovery after exercise.

"These effects of testosterone on neurons will have long-term effects on brain function," they wrote.

"Next time a muscle-bound guy in a sports car cuts you off on the highway, don't get mad -- just take a deep breath and realize that it might not be his fault," Ehrlich said in a statement.

The cells die via a process called apoptosis, also known as cell suicide or programmed cell death.

"Apoptosis is an important thing for the brain -- the brain needs to weed out some of the cells. But when it happens too frequently, you lose too many cells and causes problems."

A similar process is seen in Alzheimer's disease, the most common cause of dementia in the United States, affecting an estimated 4.5 million Americans, and Huntington's disease, another fatal brain illness.

"Our results suggest that the responses to elevated testosterone can be compared with these pathophysiological conditions," the researchers wrote.

Copyright 2006 Reuters. All rights reserved.This material may not be published, broadcast, rewritten, or redistributed.
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Tatyana

The counter reply from my 'deep throat' big brain biochemist


Ok this is like the 5th board I have had to tend to thsi issue on

this is very important to consider for those of you that take your brain out at night and put it in a jar of testosterone. The rest of us however have a blood brain barrier as well as steroid hormone binding globulins that regulate the amount of free testosterone everywhere as well as what can cross over to the brain. Our cells are not sitting in a dish expose to serum steroids

For you non biology students, the blood in your body is not the same as that around the brain. it has a special "filter" if you will that prevents most things from the blood actually ever making it to the brain.

That being said this is not a full proof system. but its still much different than cells in a dish
http://www.pubmedcentral.nih.gov/art...i?artid=372100
Transport of Steroid Hormones through the Rat Blood-Brain Barrier
PRIMARY ROLE OF ALBUMIN-BOUND HORMONE

William M. Pardridge and Lawrence J. Mietus
Department of Medicine, University of California at Los Angeles School of Medicine, Los Angeles, California 90024
Division Endocrinology & Metabolism, University of California at Los Angeles School of Medicine, Los Angeles, California 90024

Small right arrow pointing to: This article has been cited by other articles in PMC.
Abstract

These studies were undertaken to investigate (a) the permeability properties of the blood-brain barrier (BBB) to the major gonadal and adrenal steroid hormones, and (b) the role of the binding proteins of plasma (albumin and specific globulins) in the regulation of BBB steroid hormone transport.

The permeability of the BBB to [3H]-labeled progesterone, testosterone, estradiol, corticosterone, aldosterone, and cortisol, was measured relative to [14C]butanol, a freely diffusable reference, in the barbiturate anesthetized rat using a tissue sampling-single injection technique. The isotopes were rapidly injected in a 200-μl bolus of Ringer's solution (0.1 g/dl albumin) via the common carotid artery and the percent extraction of unidirectional influx of hormone was determined after a single pass through brain: progesterone, 83±4%; testosterone, 85±1%; estradiol, 83±3%; corticosterone, 39±2%; aldosterone, 3.5±0.8%; and cortisol, 1.4±0.3%. The selective permeability of the BBB was inversely related to the number of hydrogen bonds each steroid formed in aqueous solution and directly related to the respective 1-octanol/Ringer's partition coefficient.

When the bolus injection was 67% human serum, >95% of the labeled steroid was bound as determined by equilibrium dialysis. However, the influx of the steroids through the BBB was inhibited by human serum to a much less extent than would be expected if only the free (dialyzable) hormone was transported; progesterone, estradiol, testosterone, and corticosterone transport was inhibited 18, 47, 70, and 85% respectively, or in proportion to the steroid binding to plasma globulins. Rat serum (67%) only inhibited the transport of these four hormones, 0, 13, 12, and 69%, respectively, reflecting the absence of a sex hormone-binding globulin in rat plasma. However, neonatal rat serum (67%) inhibited progesterone, testosterone, and estradiol transport 0, 0, and 91%, respectively, consistent with the presence of an estradiol-binding protein in neonatal rat serum.

The binding of steroid hormone to bovine albumin in vitro (as determined by equilibrium dialysis) was compared to albumin binding in vivo (as determined by the single injection technique). The ratio of apparent dissociation constant in vivo, KD(app), to the in vitro KD was: ≫200 for progesterone, >200 for testosterone, 120 for estradiol, and 7.7 for corticosterone. Assuming the steady-state condition, the KD(app)/KD was found to be proportional to the BBB permeability for each steroid.

These data demonstrate (a) the selective permeability properties of the BBB to the major steroid hormones is proportional to the tendency of the steroid to partition in a polar lipid phase and is inversely related to the number of hydrogen bond-forming functional groups on the steroid nucleus; (b) the presence of albumin in serum may bind considerable quantities of steroid hormone, but exerts little inhibitory effects on the transport of steroids into brain, whereas globulin-bound hormone does not appear to be transported into brain to a significant extent. Therefore, the hormone fraction in plasma that is available for transport into brain is not restricted to the free (dialyzable) fraction, but includes the larger albumin-bound moiety.
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Robsta

Seem to be seeing a lot of anti-steroid info from you lately T....not having a go or owt x

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Robsta

Tatyana

Just latest research stuff. I have more bad news.

Hell, I sort of have to. The other natties were getting annoyed with me cause I play more with all you gear heads.

You know it is cause I love you guys and I want to make sure you have all the info so you can make educated choices.

Just want to take care of the lads

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How T3 works and its negative effects on Muscle
<HR style="COLOR: #8080a6" SIZE=1><!-- / icon and title --><!-- message -->The Problem with T3

For a long time we have known that thyroid hormones played a role in gene transcription during myoblast proliferation and differentiation. The regulation of gene expression by thyroid hormone (T3) involves binding of the hormone to nuclear receptors [thyroid hormone receptor (TR)] acting as T3-dependent transcription factors encoded by TRalpha (NR1A1) and TRbeta (NR1A2) genes. This in turn leads to the desired increase in the SERCA1 and SERCA2a mRNA proteins we all want because these cod for the Ca++ pumps on the muscle cell that cause use to burn extra calories through increased active Ca++ transport. However new research in spring 2006 revealed an regulatory mechanism that might not make you so happy. In this study, they identified another transcript, TRalpha-DeltaE6, produced by alternative splicing with microexon 6b instead of exon 6. This splicing leads to the synthesis of a protein devoid of a hinge domain. And what this new factor was found to be responsible for was that although TRalpha-DeltaE6 did not bind DNA, its expression induced a TRalpha1 sequestration in the cytoplasm. Functional studies demonstrated that TRalpha-DeltaE6 inhibits the transcriptional activity of TRalpha1 and retinoic X receptor-alpha, but not of retinoic acid receptor-alpha. We also found that TRalpha-DeltaE6 efficiently decreased the ability of TRalpha to inhibit MyoD transcriptional activity during myoblast proliferation. Consequently, when overexpressed (like when people take synthetic T3) in myoblasts, it stimulated terminal differentiation. This suggest that TRalpha-DeltaE6 may act as down regulator of overall T3 receptor activity, including its ability to repress MyoD transcriptional activity during myoblast proliferation.

OK what did I just say????
By taking T3 you basically up regulate a regulatory mechanism that regulates the effect of T3 not by effecting the adult muscle cells, but it actually kills off you muscle stem cells before they have a chance to join with the adult muscle cell. These are the same cells that MGF and IGF and AAS increase, and are the same cells that your body recruits for growth and repair.

In addition say you take MGF, and IGF, and AAS with your T3 to try and combat this effect. (btw I have no research to suggest these would significantly help the situation and people that say they lose less by using them may be an alternative mechanism etc. so you still might be losing the effect of recruitment of muscle stem cells)
T3 up regulates these SERCA1 proteins right. Here is a question that always bothered me, because these proteins have a long half life and t3 itself isn’t increasing your metabolism like a stimulant… you shouldn’t need to slowly come off it. It should be that the slow loss of the CA++ pumps would serve as a slow decline on its own. Here in lies the other problem. Your body responds to up regulated SERCA1 proteins with another group of hormones to catabolize them. Corticosteroids!!! Like the all famous cortisol.
This is done in part by the corticosteroids causing an increase in sarcolipin mRNA which decrease the activity of the SERCA1 pumps. So not only are you losing the energy burning pumps after you come off t3, you are decreasing the effectiveness and levels of the ones you naturally would have and your increasing corticosteroid levels. That makes for a hell of a rebound effects….

So how do I cut then???
Here is an idea.
If you use T4 you are going to have a small conversion to T3, and reduce the negative effects. If you use HGH in with your T4 they will synergistically benefit you and HGH will help reduce the increase in cortisol through negative feedback. Then after you or towards the end of you T4 cycle you should add IGF. This increases the half-life of the SERCA1 proteins making them last longer so there is no fall off effect. If you are going to use T3 I recommend all the above and staying at a low dose as well as adding a cortisol blocker at the end. T3 with a cortisol blocker should have a synergistic effect due to increased SERCA1 activity which means more energy burning.

To be safe you are best not using T3 if you are competitive athlete who depends on performance and can not afford loss of strength or increased risk of injury.

But I will add some more information for those still considering the compound.

How does T3 actually work, here is the non science definition

T3 increases you metabolism by causing your muscle to use more atp to maintain proper calcium levels. It does this by increasing the number of calcium pumps on the surface of your muscle cells. Because of the change in Calcium levels in the muscle it actually puts your muscles in a more relaxed state. This may atribute to the sudden loss of strength some users see while taking T3.
There are no current studies that indicate long term use of T3 results in the permant shut down of the thyroid. However long term use is deterimental for the muscle tissue. T3 can cause protein loss and decreases myotuble formation. Long term use can also result in a rebound effect where a user gains more fat afterwards because it take the body longer to return to its normal basal metabolic rate.

T3 with IGF-I not only increases these effects but prolongs the effect.

The in dept process
Thyroid hormone (L-tri-iodothyronine; T3) has major effects
on Ca2l homeostasis in heart and skeletal muscle [1,2]. One of the
most striking effects is the increased speed of muscle relaxation
in hyperthyroidism and the decreased relaxation rate in
hypothyroidism [3-6]. In the last decade it has become clear
through work by ourselves and others that T3-dependent changes
in the sarcoplasmic reticulum (SR) underlie these phenomena. T3
administration in vivo causes an increase of the amounts of Ca21
pumps (Ca2+-ATPase) and SR, thereby increasing the rate of
Ca2+ removal from the sarcoplasma as well as the capacity for
Ca2+ storage [7-11]. As a consequence of the increased Ca2+
release and re-uptake (Ca2+ cycling) the metabolic rate is
stimulated in skeletal muscle by consuming more ATP, which
contributes to the well known thermogenic effect of thyroid
hormone
This process works continuously because the cell has Ca++ channels that operate solely on the concetratoin gradient. There fore the result is a faster cycleing of Ca++ in and out of the cell.
Thyroid hormone (T3) is a major determinant of the fast-type
sarcoplasmic-reticulum Ca2+-ATPase (SERCAl) level in skeletal
muscle [1-4]. This Ca2+-transporting protein is responsible for
the removal of Ca2+ from the cytosol during a contractionrelaxation
cycle. The T3-induced increase in SERCAl expression
is mainly responsible for the enhanced muscle relaxation rate
which is characteristic of the hyperthyroid status [5-7]. Evidence
that T3 regulates SERCAI expression in vivo at least partly at a
pre-translational level was provided in one of our previous
studies, in which it was shown that T3increases SERCAI mRNA
levels in rat soleus and extensor digitorum longus muscle


More in depth on the IGF synergy
T3 administration in vivo causes an increase of the amounts of Ca21
pumps (Ca2+-ATPase) and SR (sarcoplasimic reticulum), thereby increasing the rate of Ca2+ removal from the sarcoplasma as well as the capacity for Ca2+ storage. The muscle cell has natural calcium channels that Ca2+ can flow through according to the gradient requiring no energy expenditure. As a consequence of the increased Ca2+ release and re-uptake (Ca2+ cycling) the metabolic rate is stimulated in skeletal muscle by consuming more ATP to run the pumps, which contributes to the well known thermogenic effect of thyroid hormone. T3’s mechanism of action occurs at the nuclear level upregulating the transcription of the mRNA’s for these Ca@= ATPase’s. IGF-I assist in the maturation of the SR where these pumps are located on the cell. It has alsop been reported that through an insulin like mechanism the IGF actually increases the stability of the mRNA. A quote from research:
“The SERCAI mRNA (the discussed above) half-life was twice as long in IGF-I + T3-treated cultures
compared with T3-treated cultures, which is in reasonable agreement
with the 1.6-fold greater increase in the SERCAI mRNA
levels by IGF-I + T3 compared with T3. T3 or IGF-I alone did not
affect the SERCAI mRNA half-life, which indicates that both T3
and IGF-I are involved in the process leading to the T3 + IGF-I
induced increase in SERCA1 mRNA stability.”
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Tatyana

I posted this on the natty board and so many were so offended, one even said he thought I was lost, and should go and talk to Ronnie, WTF?

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Toregar

You often time see this sort of behavior in people ... When their ideals are encroached upon by one of their own, and in their minds, defending the very ones they've come to look down upon. So, nattys vs juicers ... In the end, EVERYONE needs to keep an open mind. Read the studies out there, like you're doing, and you'll become a much more educated person. If they want to call you lost or whatever, F that. You're educated, which is a lot more than we can say for some of those other guys you tried to enlighten.

I myself am natural. I plan on starting a cycle in the not too distant future, and I SOAK UP this stuff. I'm like a human sponge I thank you very much for providing all of this information !

hackskii

Bumping this for later.

But when I take testosterone I feel my mind is clearer.
Lets not forget even if it was true, which I find a little hard to believe only 1%-3% of test is actually free test.

Deficiencies in Omega 3 fatty acids and specifically DHA probably play a more significant role in alzheimers.
Oh, they say smoking week actually lowers your risk of alzheimers (just heard that on a doc's show this weekend).

Lets not forget we use very little of our brains anyway.

Most guys that are savy will cycle their cycles and not just bang steroids all their lives.

I agree that guys that stay on for prolonged period of time can have some behavioral issues, I would be the first to say that but common sense will prevail here.

I bet there are far more brain cells in people that take drugs and alcohol and perscription medications that testosterone.

Now a bit for the ladies.
Estrogen and protesterone does not reverse osteoporosis, not calcium or even exercise. Testosterone actually reverses osteoporosis in aging women.
Now go put that in your pipe and smoke it

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Scott


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mrmasive

Bump for when i have a spare day to read it lol

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B:120 S:200 DL:230 @ 85kg

Toregar

I've read more than a fair share of information on this subject. I first heard about this back when I was 19 ish, 4 years ago. I had just got back into lifting after a 2 year layoff (military) ... I then found an article in a bodybuilding magazine ( Flex september 2006 ) that got me thinking about it again.

There is SO MUCH information out there about Myostatin. Even today, everything is not clear, due to the need of more testing to be done.

I'm not going to go into too much detail, but Myostatin definitely plays a role in the amount of skeletal muscle muscle one can attain (There's uncertainty as to whether or not the gene exists in internal organs).

Back in the 1800s, European farmers noticed some of their cattle were more heavily muscled than others. Naturally, they decided to breed these "super" cattle ... Today, we have the Belgain Blue and Piedmontese cattle. Turns out, these cattle have a defective myostatin gene. This translates into them being 30 % bigger than their cousins who don't possess the mutated gene.

Here's a picture of a Belgain Blue



Here's a picture of Piedmontese



Here's a picture of your normal, everyday cow.



Now, scientists have already expiremented with mice. In mice, they completely "knock-out" the gene. Mice end up being 200-300 % larger than normal mice.

Here is a diagram showcasing the differences between the two. If you couldn't guess ... the normal mouse is up top, the myostatin-less mouse, is on bottom.



Another Diagram



I apologize for those of you a little squemish :P

Here is a Wikki that gives a decent breakdown of myostatin.

http://en.wikipedia.org/wiki/Myostatin

Here is a much more in depth article on it.

http://images.google.com/imgres?imgu...lr%3D%26sa%3DG

Now, what does all of this mean ? Well, only time will tell really :P There's a ton of speculation out there, obviously. One medical doctor and author of several weight training articles asserts that over-expression of myostatin is to blame for weight lifters that have trouble gaining muscle mass. Another says that the rarest of defects, are what you see in the top bodybuilders of today. Hardgainers vs Mesomorphs (or ecto-mesomorphs and endo-mesomorphs) The important aspect being that all top bodybuilders are some form of mesomorph. The lack of myostatin expression, does make sense to me. Would explain why the top bodbuilders have a MUCH easier time gaining muscle than your average joe. It also falls in line with the whole "Genetics are god" thing in bodybuilding.

If myostatin does indeed live up to all of what is being said today ... We're going to see some really &*#ing huge BBers out there.

hackskii

Very nice post.

The rats are even more pronounced than the cows.
Those rats look way more muscular.


I am a firm believer in genetics, I see it every day in fact.

Couple of black guys at my work started training and week to week I see results in them. They have natural muscular bodies and man they got strong very fast.
Some of these dudes are benching just under 400 pounds and they are smaller than me.

One guy that just started 4 months ago did 11 reps with 225 lbs on bench and he is probably maybe 160 pounds. He is a natural.

But he does seem a little short in the brain department
He is a nice guy though and was benching every day till I gave him some direction.

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Scott


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Toregar

Yep, when mice eventually take over the world ... Atleast we'll know where it all started :P

I've never come across a TRUE mesomorph, in my time going to the gym. Mesomorphs typically don't need any guidance in building muscle. Their bodies are quite simply MADE for building muscle. Bastards ... :P

It's kind of sad when you think about it ... I know some athletes who have everything nailed down. Training/Nutrition/Supplemenation/Rest ... Everything. Yet, they don't look very impressive, in the least. I mean, in street clothes you wouldn't be like "Wow, he must lift weights". Shirtless, you can def tell, it just seems as if they're not genetically pre-disposed to carrying much muscle on their frames :(