Animal study: vitamin C protects prostate of steroids users

A daily dose of 1 – 1.5 g Vitamin C may protect steroids users against prostate cancer. Lower doses may protect the prostate of non-users, conclude researchers at Seoul National University College of Medicine after doing tests on rats.

Vitamin C

The reason that the Koreans examined whether Vitamin C cancels out the undesirable effect of testosterone on the prostate is a theoretical one. According to recent research, the prostate grows because cells that are influenced by androgens produce more of the transcription factor HIF-1alpha. This leads to an increase in the production of VEGF, a hormone that stimulates the creation of new blood vessels. If the prostate grows and prostate cells start to divide, the risk of errors occurring in the genetic material of the cells increases. And if that happens, cancer cells may start to form.

HIF-1alpha is deactivated by HIF-1-prolylhydroxylases. And the more Vitamin C there is in the cells, the harder these enzymes work.

But the proof of the pudding is in the eating. So the researchers injected rats with testosterone. The dose was 10 mg/kg/day. Some of the rats were also given a dose of Vitamin C [T+VC]. A control group was given nothing at all [C]. The figure below shows that testosterone increases the production of the prostate cancer protein PSA, and that vitamin C reduces this. The more PSA men have in their blood, the greater the chance of them developing prostate cancer.After four weeks of supplementation, the researchers observed that the vitamin had reduced the growth of the prostate. The effect was noticeable but somewhat disappointing. The left-hand prostate in the photo below is from a C rat, the one in the centre is from a T rat, and the right-hand prostate comes from a Testosterone+Vitamin C rat. The researchers suspect that a longer course of vitamin C than the four weeks of the experiment would have had a greater inhibitory effect.

The rats in the Testosterone group, exactly as the theory predicted, started to produce more HIF-1alpha. The addition of Vitamin C reduced this effect.

Vitamin C works primarily through the enzyme PHD2, the Koreans discovered during the experiment.

They believe that their discovery explains why, in epidemiological studies, men who consume large quantities of fruit and vegetables in their diet develop prostate cancer less often. They also think that their study will be of interest to doctors who treat prostate cancer, as it shows that high doses of vitamin C administered through a drip can help fight prostate cancer. We at Ergo-log thought of those of our readers who, for whatever reason, have higher levels of androgens in their bodies.

Thyroid Hormone T2 T3 T4 for Losing Weight and Dieting

Before jumping right into a discussion of the use of thyroid hormone for fat loss, a little review of thyroid function and physiology might be in order. The thyroid gland secretes two hormones of interest to us, thyroxine (T4) and triiodothyronine (T3). T3 is considered the physiologically active hormone, and T4 is converted peripherally into T3 by the action of the enzyme deiodinase. The bulk of the body’s T3 (about 80%) comes from this conversion. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in the hypothalamus. This is analogous to testosterone production, where GnRH from the hypothalamus causes the pituitary to release LH, which in turn stimulates the testes to produce testosterone.

In addition to T3, it has recently been recognized that there exist two additional active metabolites of T3: 3,5 and 3,3’ diiodothyronines, which we will collectively call T2. Studies have shown that 3,3’-T2 may be more effective in raising resting metabolic rate when hypothyroid subjects are treated with T3, than when normal (euthyroid) subjects are given T3. Therefore in normal subjects 3,5-T2 may be the principal active metabolite of T3.

Like the hypothalamic-pituitary-gonadal axis, the thyroid gland is under negative feedback control. When T3 levels go up, TSH secretion is suppressed. This is the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. There is a difference though between the way anabolic steroids suppress natural testosterone production and the way T3 suppresses the thyroid. With steroids, the longer and heavier the cycle is, the longer your natural testosterone is suppressed. This is not the case with exogenous thyroid hormone.

An early study that looked at thyroid function and recovery under the influence of exogenous thyroid hormone was undertaken by Greer. He looked at patients who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids quickly returned to normal.

Increased Oxidative Energy Metabolism

Thyroid hormone has long been recognized as a major regulator of the oxidative metabolism of energy producing substrates (food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The mitochondria are often called the “cell’s powerhouses” because this is where foodstuffs are turned into useful energy in the form of ATP. T3 and T2 increase the flux of nutrients into the mitochondria as well as the rate at which they are oxidized, by increasing the activities of the enzymes involved in the oxidative metabolic pathway. The increased rate of oxidation is reflected by an increase in oxygen consumption by the body.

T3 and T2 appear to act by different mechanisms to produce different results. T2 is believed to act on the mitochondria directly, increasing the rate of mitochondrial respiration, with a consequent increase in ATP production. T3 on the other hand acts at the nuclear level, inducing the transcription of genes controlling energy metabolism, primarily the genes for so-called uncoupling proteins, or UCP (see below). The time course of these two actions is quite different. T2 begins to increase mitochondrial respiration and metabolic rate immediately. T3 on the other hand requires a day or longer to increase RMR since the synthesis of new proteins, the UCP, is required.

There are a number of putative mechanisms whereby T2 is believed to increase mitochondrial energy production rates, resulting in increased ATP levels. These include an increased influx of Ca++ into the mitochondria, with a resulting increase in mitochondrial dehydrogenases. This in turn would lead to an increase in reduced substrates available for oxidation. An increase in cytochrome oxidase activity has also been observed. This would hasten the reduction of O2, speeding up respiration. These and a number of other proposed mechanisms for the action of T2 are reviewed by Lannie et al.

What is the fate of the extra ATP produced during hyperthyroidism? There are a number of ways by which the increased ATP promotes an increase in metabolic activity, including the following:

Increased Na+/K+ATPase. This is the enzyme responsible for controlling the Na/K pump, which regulates the relative intracellular and extracellular concentrations of these ions, maintaining the normal transmembrane ion gradient. Sestoft has estimated this effect may account for up to to 10% of the increased ATP usage.

Increased Ca++-dependent ATPase. The intracellular concentration of calcium must be kept lower than the extracellular concentration to maintain normal cellular function. ATP is required to pump out excess calcium. It has been estimated that 10% of a cell’s energy expenditure is used just to maintain Ca++ homeostasis.

Substrate cycling. Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in fat cells. The stored triglycerides are broken down into free fatty acids and glycerol, then reformed back into triglycerides again. This is an energy dependent process that utilizes some of the excess ATP produced in the hyperthyroid state. Futile cycling has been estimated to use approximately 15% of the excess ATP created during hyperthyroidism.

Increased Heart Work. This puts perhaps the greatest single demand on ATP usage, with increased heart rate and force of contraction accounting for up to 30% to 40% of ATP usage in hyperthyroidism.

Mitochondrial Uncoupling

As mentioned, the mitochondria are often characterized as the cell’s powerhouse. They convert foodstuffs into ATP, which is used to fuel all the body’s metabolic processes. Much research suggests that T3, like another much more potent agent DNP, has the ability to uncouple oxidation of substrates from ATP production. T3 is believed to increase the production of so called uncoupling proteins. Uncoupling protein (UCP) is a transporter family that is present in the mitochondrial inner membrane, and as its name suggests, it uncouples respiration from ATP synthesis by dissipating the transmembrane proton gradient as heat. Instead of useful ATP being produced from energy substrates, heat is generated instead. There are conflicting studies about the importance of T3 induced uncoupling. Animal studies have demonstrated an actual increase in ATP production commensurate with increased oxygen consumption as we discussed above. Other studies in humans have shown that in fact uncoupling in skeletal muscle does occur. This would contribute to T3 induced thermogenesis, with a resulting increase in basal metabolic rate.

To make up for the deficit in ATP production (as well as provide fuel for the extra ATP production discussed above) more substrates must be burned for fuel, resulting in fat loss. Unfortunately, along with the fat that is burned, some protein from muscle is also catabolized for energy. This is the downside of T3 use, and the reason many people choose to use an anabolic steroid or prohormone during a T3 cycle to help preserve muscle mass. Studies have shown this to be an effective strategy. (Muscle glycogen is also more rapidly depleted, and less efficiently stored during hyperthyroidism. This may account for some of the muscle weakness generally associated with T3 use.)

Countering T3 induced muscle loss with anabolic steroids or prohormones makes sense from a physiological viewpoint as well. Thyroid hormone muscle protein breakdown is mainly mediated via the so-called ubiquitin-proteasome pathway. (There are several independent metabolic pathways of protein breakdown in the body. For instance, another pathway, the lysosomal pathway, is responsible for the accelerated rate of muscle protein breakdown during and after exercise.) Testosterone administration has been shown to decrease ubiquitin-proteasome activity. So anabolic steroids specifically target the muscle protein breakdown process stimulated by T3.

What may not be an effective strategy to maintain muscle mass during a T3 cycle is the use of exogenous growth hormone (GH). Studies have shown that when GH and T3 are administered concurrently, the increased nitrogen retention normally associated with GH use is abolished. This has been attributed to the observation that T3 increases levels of insulin like growth factor binding protein, reducing the bioavailability of IGF-1. Nevertheless, GH has fat burning properties independent of IGF-1, so using GH with T3 would act additively to speed fat burning, but with little if any preservation of lean body mass. So again, if GH is used in conjunction with T3, anabolic steroid/prohormone use would be indicated.

Andregenic Receptor Modulation

Administration of T3 has been shown to upregulate the so-called beta 2 adrenergic receptor in fat tissue. What is the significance of this effect for fat loss? Before fat can be used as fuel, it must be mobilized from the fat cells where it is stored. An enzyme called Hormone Sensitive Lipase (HSL) is the rate-controlling enzyme in lipolysis, or fat mobilization. The body produces two catecholamines, epinephrine and norepinephrine, which bind to the beta 2 receptor and activate HSL. The upregulation of the beta 2 receptor due to T3 results in an increased ability of catecholamines to activate HSL, leading to increased lipolysis.

Bodybuilders often use drugs like Clenbuterol, which bind to the beta 2 receptors and activate them in the same way as the body’s endogenous catecholamines. The use of Clenbuterol along with T3 can produce an additive lipolytic effect: T3 increases the number of receptors, while Clenbuterol binds to the receptors activating HSL and increasing lipolysis. Since clenbuterol itself downregulates the beta 2 receptor, most bodybuilders use Clenbuterol in a two week on/ two week off cycle, the rationale being that this minimizes downregulation and allows receptor recovery. Another option is to use the antihistamine ketotifen concurrently with the Clenbuterol. Studies have shown that ketotifen attenuates the beta 2 receptor downregulation caused by Clenbuterol. Moreover, research in AIDS patients has shown that ketotifen blocks the production of the proinflammatory and catabolic cytokine TNF-alpha. This may be of relevance to bodybuilders since there is evidence showing TNF lowers both testosterone and IGF-1 levels quite significantly, while strenuous exercise elevates TNF levels.

Besides increasing beta 2 receptor density in adipose tissue, T3 upregulates this receptor in human skeletal muscle. This has some very intriguing if somewhat speculative implications for the combined use of Clenbuterol and T3. Animal studies have shown that catecholamines, particularly Clenbuterol, inhibit Ca++ dependent skeletal muscle proteolysis. Like the lysosomal and ubiquitin-proteasome pathways discussed above, Ca++ regulated proteolysis is yet another way for the body to degrade muscle protein. Again the implications are enticing: Increased beta 2 receptor density from T3 use, coupled with the beta 2 agonist Clenbuterol, could slow this pathway of muscle catabolism.

Another adrenergic receptor important to lipolysis is the alpha 2 receptor, which impedes fat mobilization by counteracting the effects of the beta 2 receptor. There are some conflicting studies about the effects of T3 on the alpha 2 receptor, with studies showing either a downregulation or no effect. If T3 does in fact downregulate alpha 2 receptors, this would further aid lipolysis.

Decreased Phosphodiesterase Expression

In hyperthyroid patients as well as in normal subjects given T3, levels of the enzyme phosphodiesterase are lowered in fat cells. When lipolytic hormones like epinephrine (adrenaline) bind to the beta 2 receptor described above, they initiate a signaling cascade mediated by the so called “second messenger” cyclic AMP (cAMP). cAMP in turn acts on other cellular enzymes to initiate and maintain lipolysis. The original signal is terminated when cAMP is degraded by the enzyme phosphodiesterase. Clearly, maintaining elevated cAMP levels, by lowering phosphodiesterase concentrations with T3, will prolong lipolysis. As an aside, caffeine is thought to exert at least a portion of its lipolytic action by lowering phosphodiesterase in fat cells. Interestingly, Viagra and Cialis are also phosphodiesterase inhibitors but their action seems to be limited to relaxing vascular smooth muscles.

Increased Growth Hormone Secretion

In vitro, animal, and human studies have all demonstrated that T3 administration increases growth hormone production. Since GH is calorigenic aside from any increase in IGF-1, elevated GH may contribute to some of the fat burning associated with T3 administration. This effect may obviate the need for the use of expensive recombinant HGH, as mentioned above.

Decreased Insulin Secretion

Insulin is well known as a lipogenic hormone. It promotes fat storage by facilitating the uptake of fatty acids by adipocytes, and reducing lipid oxidation in muscle tissue. Several studies have shown that thyroid hormone is associated with glucose intolerance resulting from decreased glucose stimulated insulin secretion.

This defect in insulin secretion is believed to result from an increase in the rate of apoptosis (programmed cell death) of pancreatic beta cells as a direct effect of thyroid hormone excess. This process is reversible, since when thyroid hormone is withdrawn the rate of beta cell replication increases until homeostasis returns. However, there are conflicting studies regarding the effects of T3 on insulin. For example, Dimitriadis et al showed a decrease in glucose stimulated insulin secretion, consistent with, but an increase in basal insulin. They also observed increased insulin clearance, with a compensatory increase in basal insulin secretion.

So if in fact the hyperthyroid state is associated with lower insulin levels, this could explain a portion of hyperthyroid stimulated lipolysis. The obvious downside here is that insulin is also an anabolic hormone. Basal insulin concentration is thought to limit the action of the ubiquitin-proteasome degradative pathway of muscle protein breakdown. Of course supplementing with insulin during T3 use would be counterproductive. However, as mentioned above, anabolic steroids inhibit ubiquitin-proteasome activity, so their use could counter any loss in muscle anabolism resulting from a drop insulin levels.

Insulin Levels and Fat Loss

Insulin is responsible for pushing nutrients to their respective targets and if necessary creating fat. It also inhibits fat loss. So given a negative caloric balance while trying to achieve fat loss with adequate protein fish oils and say 100 grams of carbs, how does the body bypass insulin’s effect on fat loss inhibition?

Does the insulin just deplete itself and fat oxidation resumes?
What about differences in GI and its effect on insulin.

Does equal carb intake of say white rice vs .brown rice elicit the same insulin response but at different portions varying over time?

If both white rice and brown rice are equal in calories and nutrients and let’s say right before bed I consume it, but still consuming at negative caloric balance. Would I still burn the fat equally to brown rice?

Possibly a bit lengthy but I would appreciate a response if you could. An insulin column would be fantastic on your new site and would eliminate a lot of repetitive questions! nice job on the site and thanks for all you do.

Lyle McD: This is going to be a long answer because, frankly, there is a lot of misinformation and misunderstanding about insulin and, as usual, I got a lot to say.

This is because, in a lot of ways, insulin is a schizophrenic hormone. Depending on what folks read (e.g. bodybuilding literature), they will be told that insulin is great, it’s the most anabolic hormone in the body, it’s key to getting big. And if you read other stuff (a lot of mainstream dieting literature), you’ll hear that insulin is the devil, it makes you fat and ruins your health. Who’s right? Well, everybody…sort of.

As the question above states, it’s best to think of insulin as a generalized storage hormone rather than being good or bad; and what it does, as always, depends on the context. I should mention that insulin not only affects peripheral tissues such as the liver, muscle and fat cell; it also has central effects in the brain.

When elevated insulin pushes nutrients into cells. So insulin stimulates glycogen storage in the liver, it also enhances glycogen storage in skeletal muscle. And while insulin isn’t that critically involved in protein synthesis per se, it does decrease protein breakdown, this is important for maximal increases in muscle mass. So far so good.

But insulin also is involved in fat storage which is where it gets its ‘bad’ characterization. Insulin activates an enzyme called lipoprotein lipase which is involved in breaking fatty acids off of chylomicrons for storage. However, this isn’t the only important step in fat storage.

Contrary to popular belief (espoused by people still reading literature from the 1970’s), insulin is neither the only nor single most important hormone involved in fat storage. Rather, a little compound called acylation stimulation protein (ASP) has been described as “the most potent stimulator of fat storage in the fat cell”. And ASP levels can go up without an increase in insulin (although insulin plays a role).

As another effect of insulin on body-fat levels, and this is discussed in some detail in The Stubborn Fat Solution, insulin drastically inhibits lipolysis (fat mobilization) from fat cells. Even fasting insulin levels inhibit lipolysis by up to 50%, even small increases essentially turn off lipolysis completely. Some could easily interpret this as meaning that ‘eating carbs stops fat loss’. Or it might lead them to conclude that a carbohydrate based diet would make fat loss impossible.

Tangentially I’d note, and one weird little study supports this, that spiking insulin (and letting it crash back down) might be superior for fat loss than the standard strategy of trying to keep insulin low but stable all day long. The reason is that even tiny amounts of insulin block lipolysis, if you keep insulin low but stable all day, you are effectively impairing lipolysis. But the study in question showed that blood fatty acid levels came back up much faster when insulin was spiked (which crashed blood glucose back down, lowering insulin). The drawback, mind you, is that rapidly falling blood glucose tends to make people hungry and calorie control would be nearly impossible with this strategy. And, as you’ll see below, in a hypocaloric situation, it probably doesn’t matter a bit.

Anyhow, despite the sometimes seen mentality that you must ‘cut carbs to get lean’, four decades of practical experience (and endless clinical research) show that that is simply not the case: bodybuilders (well, some bodybuilders) have gotten plenty lean on carb-based diets (of course, others have failed miserably) so it’s obviously not as simple as many would make it. That’s because whether a high-carb, moderate-carb, or low-carb diet is most appropriate for someone depends on the circumstances.

Which brings me the long way around to the first question above. What is happening in terms of fat loss on a diet that is hypocaloric (below maintenance levels, that is the person is burning more calories than they are consuming) but contains sufficient protein and essential fatty acids but with say 100 grams of carbohydrate? Don’t the carbs prevent fat loss by raising insulin? What’s going on?

To understand what’s going on, I need to explain two terms which are the post-prandial and post-absorptive phases.

Post-prandial phase: this is just a technical term for ‘after you’ve eaten a meal’. In this situation, nutrients are being absorbed and digested from the gut and released into the bloodstream, a whole host of hormones are being released (depending on the macronutrient content of the meal) and the body will generally be in an anabolic state (meaning that more nutrients are being stored than are being released from storage).

Post-absorptive stage: This is what happens between post-prandial phases. Eventually what you’ve eaten has all been digested, absorbed and either burned for energy or stored in various tissues. When this happens, hormone levels change an the body starts shifting to an overall catabolic state.

So throughout the day, the body is shifting between the post-prandial phase and the post-absorptive phase as you eat, that food gets digested and absorbed, and the body starts to draw on stored nutrients (hopefully stored fat in fat cells).

And when you lower caloric intake, over a 24 hour period, the body will end up spending relatively more time in the post-absorptive (remember: body burning stored nutrients) than post-prandial (remember: body storing ingested nutrients) phase. This is simply a consequence of having less nutrients coming in relative to what’s being burned.

On a diet, meals are smaller (or activity is higher, or both) so any given meal will only maintain an anabolic state for so long (and that time period will be shorter than if the person were eating more) before the body shifts back to burning stored nutrients. So even in the face of dietary carbohydrate intake, the body still will tap into stored fat; hence fat loss.

I’d note that theoretically this might mean that eating less frequently would improve fat loss, since the body would spend more time between meals in the post-absorptive stage. Of course, this is probably offset by each meal being larger and therefore taking longer to digest and I tend to doubt it matters in the long-run. Some interesting research into intermittent fasting suggests that there is more to it than that but that’s another topic for another day.

And this brings me to the second part of the above question, the glycemic index (GI) and insulin. Which requires another long explanation. The GI was developed back in the 80’s to help with diabetic meal planning. Basically it involves feeding folks a fixed amount of a reference carbohydrate (studies have typically used either 50 grams or 100 grams of digestible carbs and while glucose was the original test food, they now use white bread) with blood glucose being measured over a several hour period. The glucose response to the reference food is defined as having a GI of 100.

Then, whatever food was being tested (again either 50 or 100 grams of digestible carbs were given) and blood glucose was measured, researchers compared the blood glucose response of the test food to the reference food. If the blood glucose response was say, 80% of the reference food, the test food was given a GI of 80. If the blood glucose response was 120% of the test food, that’s a GI of 120. You get the idea. And lower GI values basically meant that the test food was generating a smaller blood glucose response than the reference food.

GI is far from perfect, there is massive individual variability, many foods will show a different GI depending how you cook them and, as soon as you start mixing foods or adding things like protein, fiber and fat, GI changes (almost always going down). So GI in and of itself ends up not saying very much in the big scheme of things. An additional confound is training. 

Now, it was always pretty much assumed that the GI was indicative of the insulin response and that lower GI foods caused a lower insulin response than higher GI foods; this is part of where dieters originally got fixated on the issue. However, it looks like it’s not quite that simple. While there was some brief interest in an Insulin Index (II) which measured the insulin response to foods in the same way GI does, research seems to have stopped as soon as it started.

That is, it’s important to realize that the blood glucose response of a food is determined by both its rate of digestion and entry into the bloodstream as well as the rate of glucose storage in tissues such as muscle. And it looks like low GI foods are not necessarily digesting more slowly but that a fast initial insulin response is clearing more blood glucose. To quote from the summary of that research article:

Question: “Bran cereal has a low GI because a more rapid insulin-mediated increase in tissue glucose uptake attenuates the increase in blood glucose concentration, despite a similar rate of glucose entry into the blood.”

Lyle McD: In this regards, I’d note that adding protein to carbs has been known to lower the GI for a couple of decades. However, it’s also been established that adding protein to carbs increases the insulin response. Which is consistent with the conclusions of the paper above, by increasing insulin, protein lowers blood glucose levels giving a lower effective GI. Just not for the reason that most people think. And I daresay that most of the ‘insulin is evil’ people are going to argue that eating more protein hurts fat loss, yes protein increases the insulin response to carbs. While increasing the insulin response. Go figure.

Which is a long way of saying that I don’t think the GI and insulin response matter much (although see my final comments below). If there is much effect of GI on fat loss, it’s more likely to be mediated through food intake and fullness as lower GI foods generally make people feel fuller and often cause decreased food intake. This is the typical confound in these types of studies: certain food types often make people spontaneously eat less, causing fat and weight loss and people confuse the food itself with the reduction in food intake that it causes.

Question: “Apparently, the glycaemic index-induced serum insulin differences are not sufficient in magnitude and/or duration to modify fuel oxidation.”

Lyle McD: Basically, at least outside of the absolute extremes (where it’s possible that some of this stuff might matter), it just doesn’t really seem to matter much outside of any influence on food intake (e.g. if a certain food keeps you fuller and you eat less, it’s good for fat loss; if it doesn’t, it’s not). Basically:

The GI doesn’t truly indicate the insulin response in the first place, if it does it appears that low-GI foods may be generating a faster initial insulin response in the first place, and none of this seems to meaningfully impact on fuel utilization anyhow. Certainly any tiny differences in GI between brown and white rice are going to be utterly irrelevant for 99% of cases.

Now, to wrap this up, I’d note that most studies done on this topic are drawing conclusions from average responses and emerging evidence suggests that it’s a bit more complicated than this. In the article Insulin Sensitivity and fat loss, I detail some recent work suggesting that the insulin sensitivity of a given individual interacts with diet; the punchline of that article is that individuals who are insulin resistant (and/or show a pronounced early insulin response to food intake) seem to get superior results from a lower GI/lower-carbohydrate diet. In contrast, individuals with high insulin sensitivity show superior results on a carb-based diet. 

Ok, I know that was long but, as noted initially, there’s a lot of confusion over insulin and I have a lot to say on the topic. Hopefully I answered your question.

Do You Want to Have Great Glutes?

Whether you are a guy or a girl, it is always an asset to have some nice glutes. The main exercise that will help you develop your glutes the most is obviously the squat. Look at those who have the highest squat numbers. ‘Nuff said.

There are some other exercises that will help a good bit, but the squat will always be the king glute exercise. Before going on to mention the top exercises, we will inform you on some information about the glutes.

Like mentioned above, squats are the king of glute exercises. They are without a doubt the single best exercise you can use to develop your glutes. I would even go as far as saying that you would not even need to do another single exercise for them; squats are really that good! However, there are always some other exercises that would be good to experiment with.

The Gluteus Medius and Minimus lies directly beneath the Gluteus Maximus. The Gluteus Maximus starts along the pelvic bone crests and attaches to the rear of the femur. The Gluteus Medius and Minimus start in about the same spot as the Maximus, but they attach to the side of the femur. The Iliotibial Band is made of connective tissue. It serves to transfer the force of abduction to the leg. The main function of the Gluteus Maximus is hip extension, which means moving the thigh to the rear. The Gluteus Medius and Minimus serve to abduct the leg.


The lift: Start by putting a 45 lb barbell on your shoulders. You will then step back until you have enough room. You will want to get a wider stance than you shoulders with your feet pointed outward. When you begin squatting down, you will want your knees to track out toward your toes. While doing this, you will want to look straight forward. Once you hit parallel, you will want to drive your butt off while pushing through the floor.

This is mainly a leg exercise, but it is so good that it will hit your lower back really well.

For a change of pace, try one legged squats or pistol squats. When you start these you will probably need to hold onto something so you don’t fall over, unless you have exquisite balance.

Walking Barbell Lunges

The lift:You will start this exercise out by putting a standard 45 lb barbell on your back, much like the squats starting position. After stepping back to give yourself room, you will need to start the exercise out by stepping one foot forward while bending the back leg to the point where the thigh of the back leg is perpendicular to the floor, and the shin is parallel. The thigh of the front leg should also be parallel to the floor, while the shin should be perpendicular.

Walking Lunge – Immediately use your front leg to pull your body and back leg forward. Contract the front leg glute hard when stepping forward to really target that muscle. Bring your back leg up, even with the front leg. Now repeat the same movement with the other side. That’s one rep. By continuing this movement for the prescribed number of reps, you will appear to be “walking”.

Standard Lunge – Once in the lunge position, you will use the front leg to step back into your starting position. For the next repetition, you will step forward with your other foot. Here is a good video demonstration to help you better understand this exercise.

A good alternative to the barbell lunge, is the dumbbell lunge. This is often a better option for women who have more difficulty getting a barbell on their shoulders if they don’t have access to a squat rack or power rack.

Step-back lunge. Rather than stepping forward with one leg, you start the exercise by stepping backwards. Then use the front leg to pull yourself forward, back to the start position.


This is why they call deadlifts and squats a compound exercise. They are just so effective; you must have them in your workout!

The lift:You will start by placing a standard 45 lb barbell on the floor. You will then position your feet at about shoulder’s width apart and placing your hands on the bar outside of your feet. From there, you will need to put your back in a good position to pull the bar up without rounding your back.

To pull correctly, drop your butt and pull the bar up while it “scrapes” your shins. You don’t have to literally scrape your shins, but the bar should be mere millimeters away from your body. Once you pull the bar to the top, drop it back down at a reasonable speed to the floor all while keeping the bar close to your body.

Also, you may want to try the single leg dumbbell deadlift to really isolate each side of the buttocks. Squeeze on the way up.

You might also consider the sumo deadlift, which is performed with the feet spaced a foot wider than shoulder width on each side. Grab the bar with both hands at shoulder width and deadlift like you normally would, keeping your upper body as straight as possible.

Step Ups

The lift: This is a fairly simply exercise. First, you will need a pair of dumbbells to choose for. After that, you will need to find a platform in order to do this exercise on. The platform should be a little bit lower than knee height or so. You are now prepared to start the lift.

Begin by stepping your right foot up onto the platform and follow your left foot with that one. After you successfully step up onto the platform, you will step off. For the next repetition, you will use the other foot to lead the movement. Do this for 8-12 reps on each leg.

Stiff Leg Deadlifts or Romanian Deadlifts

Stiff leg deads are a compound exercise and one of the best mass building exercises for the hamstrings. Form is especially important to avoid becoming the next victim of lower back injury. Make sure to practice stiff leg deads with lighter weight until you master the form.

Setup similar to a conventional deadlift except that your feet should be set in a narrower stance and your knees should just barely be bent. Use a pronated grip until you get strong enough that an alternating grip is warranted.

The lift: do not use your back! This should be another exercise where you drive with your hips and glutes using a straight back. The hips should move out and back to allow you to descend. Do NOT round your back or ‘bend over’ so to speak. Lower the weight down as far as you can without straining your hamstrings or compromising your spine.

Romanian Deadlifts

The lift: the Romanian deadlift is another good compound ham exercise. Again, form is of essence. While similar to the stiff leg deads in the sense that you have to move your hips back during the descent, but the difference is that you can bend the knees a little more through the movement. This often allows one to go lower and lift heavier weight but takes some of the focus directly off the hamstrings. Romanian deads are a bit safer for the lower back.

Honorable mentions: good mornings, reverse hyper-extensions, “butt blaster” movements (don’t ask), weighted hip bridges.

Reverse Hyper-extensions

I feel I’m reaching with this exercise, but it was suggested to me by several people, so I’ll recommend it and explain it. However I feel the above 5 exercises and their variations are a thousand time better if you want to build great glutes.

If you have bad knees, this may be a good exercise for you to try out. Squats will blow these out of the water and the comparison isn’t even close, but they can still be a fairly good exercise if used effectively.

The lift: Start by lying down on the platform with the bottom part of your torso off the platform. You should attach your feet into the lock where you will lift the weight up. Once you do this, you will raise your legs up focusing on using your glutes in doing so, and come back down you’re your legs hit a straight line with the rest of your body. Here is a video demonstration to help you better understand this exercise; excuse the weird music.

To work these exercises into your routine, simply use a good workout routine that already includes standard squats, and standard or sumo deadlifts. Then select either step ups, lunges, stiff leg deadlifts, or one of the single-leg variations of squats, deads, and stiff legs. Every once in a while, use good mornings in place of stiff leg deads or Romanian deadlifts.

Flat Bench Press vs. Incline: Which Is A Better Chest Builder?

The granddaddy of all exercises, let alone the chest builder that displays upper body strength and swells ego-laden heads all around the world is the unparalleled barbell bench press. Of course if done properly and said ego was left home to wither away in self-pity, the uncrowned king of the weightlifting world is a very effective tool for adding upper body strength and muscle.

Little compares to the ability to properly lift an impressive amount of weight off your chest with a loaded barbell. Others can sub in for this beast of a movement using such exercises as dumbbell press and machine press, but they don’t measure up to the sheer brutality of the barbell variation.

But what about the close relative of the flat bench, the incline bench barbell press? Sure, we all know the obvious difference of placing more stress to the upper pec region, but how does it compare as an overall chest builder? What are the real differences when taking mechanics, angle of stress and efficiency into consideration?

Flat bench barbell press

As mentioned earlier, the flat bench version of the barbell press doesn’t need a formal introduction due to its popularity. We all know it’s the very first exercise performed on Mondays around the world. Despite its fame, few actually execute this exercise properly.

Lie down on the bench with an arch in your lower back, with your glutes and upper back in contact with the bench. Keeping your entire body tight, lower the bar with your elbows at roughly a 45 degree angle from your torso. When the bar touches (not bounces) your lower chest area drive the bar back up to the start position with a slight bend in your elbows.

Be sure to drive through your feet but not so much that your butt comes off the bench. Also, during the lift, shift your shoulders down to the floor and toward your waist to place the focus on your pecs and to protect your shoulders.

Pros: Because it is one of the elite upper body multi-joint movements, the flat bench press can pack on mass and strength. Utilizing the majority of muscle tissue from the pecs, shoulders and triceps, this exercise is not only effective but efficient as well. Few upper body moves exist where so much weight can be used for so many muscle groups. The flat bench press develops muscle, strength and power.

Cons: Of course, when done improperly and letting the ego sneak into your program, the flat bench press can be a devil in disguise. Too much weight, loose form and a contortionist back can spell certain injury. The key is to not treat the bench press like some sort of max day every day. Look at the flat bench press like any other exercise to help build muscle safely and effectively. Performing the exercise properly is paramount when considering your longevity with resistance training.

Incline bench barbell press

Always reserved for upper pec work, the incline bench barbell press is a far more difficult and challenging move for most. Despite the difference in angle the incline version still has its need for proper form and technique. Often relegated as a secondary exercise, the incline press can do the job of packing on upper chest mass quickly.

Lie on an incline bench similarly to the flat bench version with your upper back and glutes contacting the bench and a slight arch in your lower back. Squeeze your shoulders back toward the floor and your rib cage expanded up toward the ceiling.

Lower the bar down to your upper pec area just below your neck and your elbows at a slight angle to your torso. Touch (not bounce) the bar to your upper chest and press the bar back up to the starting position without locking your elbows.

Pros: As I mentioned, the incline bench barbell press can pack on some serious mass to the upper pecs. When performed properly the incline press places a tremendous stretch on the upper pec region requiring a bit less weight lifted than the flat bench version. Although this exercise falls into the upper chest builder category, it will still stress the entire pec region to some extent. And since the upper chest area is often neglected on many physiques, a comprehensive chest program that includes the incline press will effectively shore-up any weaknesses.

Cons: As with every exercise (especially ones for the chest) ego must be something left at the gym door. Too much weight used can not only be detrimental to your gains but also sets you up for potential injury and subsequently burnout.

Another all too often mistake during the incline press is the use of a short range of motion. When the bar is stopped several inches or even half way down you neglect the all too important stretch of the muscle tissue. More stretch equals more contraction and in the end that spells more mass and strength. Use less weight, a full range of motion and see better gains.

The verdict

As these are two exercise are very similar in execution they have a few significant differences in effect. Common sense would tell you that the flat version stresses the middle and lower portions of the pecs and the incline would stress the upper area. Well, the truth is that they do stress their respective areas of the chest; however, they still both stress the entire area to some degree. When done properly and the shoulders are set as described both will do their jobs in packing on the mass to the entire chest.

The incline bench barbell press does seem to stretch the chest more requiring a longer range of motion. This is usually why less weight is needed and bad form is sometimes used when ego creeps in. In many cases the incline barbell press is rarely used with any regularity by most gym-goers with the flat bench version always included in most programs. Weak upper pecs and a larger, stronger middle and lower chest seem to be the norm in most gyms.

Be sure to use both versions in your program even starting with the incline press first in your routine. Starting your next chest program with a focus on upper pec work will slowly but surely shore-up your weakness and balance out your chest for a fully proportioned upper body.

How To Build Monster Arms

Guys want big arms. That’s never more apparent than when you see lines forming at the preacher bench and press-down stations. Most lifters don’t come prepared with a plan of attack other than doing as many sets as possible and repeating it again a few days later.

These four common mistakes create a mile-wide gap between people wanting big biceps and triceps and people actually stretching out shirtsleeves. Let’s fix them and put together a routine that’ll deliver monster results and an even more ferocious pump!

Mistake №1 - Thinking just about any exercise works well as the first movement in your workout. Not sure where to start your arm-day workout? Anyone leading off with concentration curls or triceps press-downs as their preferred mass-building move makes a big mistake.

The fix:
Choose mass-building exercises early in your workout when your energy levels are highest. What are the best mass-building moves? Good question. They’re typically the ones in which you can push the most weight. Multi-joint exercises which recruit secondary muscle groups fall into this category (one reason you start your chest workouts with presses and thigh workouts with squats). For triceps, there are a number of multi-joint moves to choose from, but not so for biceps. Basic standing curls allow the biceps to move the most weight.

"Basic standing curls allow the biceps to move the most weight".
Mistake №2 not working the target muscle from various angles
When training arms, “angles” refers to your arm position relative to your torso as well as your grip. If you always do your curls or triceps extensions with your arms locked by your sides, you limit your gains.

The fix
For biceps, with your arms in front of your torso (think preacher curls), you target more on the biceps’ short head; when your arms are behind your torso (think incline bench dumbbell curls), you better focus on the long head. Likewise, using a neutral grip (hammer curls) and taking a closer or wider grip on the barbell during standing curls each recruits the arm flexors in slightly different ways.

For triceps, when your arms are overhead you better target the long head, while going from an overhand to an underhand grip (as when doing press-downs) shifts the emphasis from the lateral to medial head.

In sum, using a variety of grips and arm positions better emphasizes the various heads of your bis and tris for more complete development

Mistake № 3 following the same rep sequence
Many trainees choose a weight, usually one in which they can do for a set of 10, rest and repeat. That’s another mistake.

The fix
"Pick challenge weights to reach muscle failure at the lower end".
Recall that heavier weights for low reps (fewer than 6) promote optimal increases in strength, and moderate weights for moderate reps (8-12)—as long as they’re done to failure—are best for muscle growth.

The target musculature quickly becomes accustomed to doing the same rep sequence, such as when you do all your sets to 10 reps. Since you’re stronger earlier in your workout, that’s the time to challenge your muscles with heavier weights on the best mass-building moves you already selected.

Pick challenging weights to reach muscle failure at the lower end (as few as 6 reps). Over the course of your workout, select slightly lighter weights so you fail at 8, 10 or even 12 reps; this allows you to work the muscle with different relative intensities. Hence, you progress from very heavy weights on the mass-building moves to lighter weights to pump the muscle on the isolation exercises.

Mistake №4 failing to push past failure
Do you do the same workout over and over again and expect different results? That’s a common mistake some would call insane.

The fix
Your body eventually adapts to a particular routine—even if it worked great in the beginning. Most people need to make changes in their workouts at least every 6-8 weeks to help progress through a training plateau.

One way to push past a plateau is to include advanced training techniques that require you to work past muscle failure on 1-2 sets per exercise. Among the techniques you can try are forced reps, dropsets, rest-pause, and negatives.

Supersets—the technique presented below—require that you do two exercises back-to-back with no rest in between; you rest only after you finish both exercises. While you might not consider supersets a mass-building technique, in this workout you do them joining antagonist muscle groups—while one is flexed, the other is stretched—which forces even more blood into the target region.

Close - grip bench press

And research even backs up that when you precede a move by one for its antagonist, the second one is actually stronger! So doing a set of press-downs before a set of curls actually makes you stronger on the curls. Just make sure you reverse the pattern of which exercise comes first in your next workout.

Another advantage of supersets is that they’re a great time saver, substantially reducing rest times. Rather than having you run all over the gym, the superset combinations in this arm routine utilize the same pieces of equipment for each of the two exercises.

The Monster Arm Workout fixes the four most common mistakes on arm day, combining the best mass-building moves with a progressive rep sequence while combining the mass-building benefits of supersets. Faster workout, best mass moves, intensity-boosting techniques … this could be the one workout that finally splits those shirtsleeves!

Monster Arm Workout
Close-Grip Bench Press
3 sets of 6-8 reps
Standing Barbell Curl
3 sets of 6-8 reps
Seated Overhead Dumbbell Extension
3 sets of 8 reps
EZ-Bar Preacher Curl
3 sets of 8 reps
Cable Kickback
3 sets of 8-10 reps
Standing One-Arm Cable Curl
3 sets of 8-10 reps
Rope Press-Down
3 sets of 10-12 reps
Rope Hammer Curl
3 sets of 10-12 reps


  • The next time you do this workout, do the biceps moves first in the superset sequence.
  • Warm-up sets are not listed; do as many as you need but never take warm-up sets to muscle failure.
  • Choose a weight so you reach muscle failure by the target rep.

Superset 1
Equipment: Flat bench-press station, barbe
Superset 2
Equipment: Preacher bench with seat, EZ-curl bar, dumbbell
Superset 3
Equipment: Lower cable with D handle
Superset 4
Equipment: Rope with adjustable cable

Deca Durabolin Tips To Avoid Side Effects

Deca Durabolin, which is also known as Deca and Nandrolone decanoate, is one of the best performance enhancing drugs and anabolic steroids when it comes to stimulating endurance and muscle function gains.

The steroid is popular among both amateur and professional sportsmen when it comes to improving the levels of recuperation time between workouts, protein synthesis, and nitrogen retention. The fact that the use of Nandrolone decanoate is not related to side effects like oily skin, male pattern baldness, and prostate complications means that it can even be used by those who are prone to these side effects.

Since this steroid has a very low rate of aromatization that is approximately 20 percent the rate of testosterone, it does not result in estrogenic or androgenic side effects and gives ample opportunities for sportsmen and others to stay high on the sense of well being, lean muscle mass, and unmatched body strength and muscle mass.

Deca Durabolin is best used in doses of 600 mg per week for 12-16 weeks by men for bulking cycles and 400 mg per week for 12-16 weeks by men in cutting cycles or in doses of 300-800 mg per week for men (or 2 mg per lb of body weight) and 50-100 mg per week for women.

This anabolic steroid is commonly stacked by sportsmen with steroids and performance enhancing drugs such as testosterone cypionate, testosterone suspension, testosterone enanthate, testosterone propionate, Anadrol, Dianabol, and Sustanon 250 and should always be used under medical supervision and for legal purposes as Deca Durabolin abuse can lead to side effects atrophy of the breasts, early epiphyseal closure, hypercalcaemia, hypercalciuria, withdrawal of ovarian action, decreased ejaculatory volume, and more-than-average increase in bone development, suppression of ovarian activity, oedema, and depression.

Use of this steroid is not recommended to those suffering prostate cancer, breast cancer, testicular cancer, high blood pressure, stroke, liver damage, kidney damage, jaundice, hepatic carcinoma, or renal failure.

Women and Nolvadex use

This remedy is somewhat different from others since it is not an anabolic/androgenic steroid. For male and female bodybuilders, however, it is a very useful and recommended compound which is confirmed by its widespread use and mostly positive results.

Nolvadex belongs to the group of sex hormones and is a so-called antiestrogen. The normal application of Nolvadex is in the treatment of certain forms of breast cancer in female patients. With Nolvadex it is possible to reverse an existing growth process of deceased tissue and prevent further growth. The growth of certain tissues is stimulated by the body’s own estrogen hormone. This is especially true for the breast glands in men and women since the body has a large number of estrogen receptors at these glands which can bond with the estrogens present in the blood. If the body’s own estrogen level is unusu-ally high an undesired growth of breast glands occurs. However, in healthy women and particularly in men this is not the case. Despite this, it is mostly male bodybuilders who use Nolvadex, and fewer women. At first sight this seems somewhat inconceivable but when taking a closer look, the reasons are clear. Bodybuilders who take Nolvadex also use anabolic steroids at the same time. Since most steroids aromatize more or less strongly, i.e. part of the substance is converted into estrogens, male bodybuilders can experience a significant elevation in the normally very low estrogen level. This can lead to feminization symptoms such as gynecomastia (growth of breast glands), increased fat deposits and higher water retention.

The antiestrogen Nolvadex works against this by blocking the estrogen receptors of the effected body tissue, thereby inhibiting a bonding of estrogens and receptor. It is, however, important to understand that Nolvadex does not prevent the aromatization but only acts as an estrogen antagonist. This means that it does not prevent testosterone and its synthetic derivatives (steroids) from converting into estrogens but only fights with them in a sort of “competition” for the estrogen receptors. This characteristic has the disadvantage that after the discontinuance of Nolvadex a “rebound effect” can occur which means that the suddenly freed estrogen receptors are now able to absorb the estrogen present in the blood. For this reason the combined intake of Proviron is suggested. Nolvadex is also useful during a diet since it helps in the burning of fat. Although Nolvadex has no direct fat burning effect its antiestrogenic effect contributes to keeping the estrogen level as low as possible. Nolvadex should especially be taken together with the strong an-drogenic steroids Dianabol and Anadrol 50, and the various testosterone compounds. Athletes who have a tendency to retain water and who have a mammary dysfunction should take Nolvadex as a prevention during every steroid intake. Since Nolvadex is very affective in most cases it is no wonder that several athletes can take Anadrol 50 and Dianabol until the day of a competition, and in combination with a diuretic still appear totally ripped in the limelight. Those who already have a low body fat content will achieve a visibly improved muscle hardness with Nolvadex.

Several bodybuilders like to use Nolvadex at the end of a steroid cycle since it increases the body’s own testosterone production. These can occur after the discontinuance of steroids when the androgen level in relationship to the estrogen concentration is too low and estrogen becomes the dominant hormone. A very rare but all the more serious problem of Nolvadex is that in some cases it does not lower the estrogen level but can increase it. Another disadvantage is that it can weaken the anabolic effect of some steroids. The reason is that Nolvadex, as we know, reduces the estrogen level. The fact is, however, that certain steroids especially the various testosterone compounds can only achieve their full effect if the estrogen level is sufficiently high. Those who are used to the intake of larger amounts of various steroids do not have to worry about this. Athletes however, who predominantly use mild steroids such as Primobolan, Winstrol, Oxandrolone, and Deca-Durabolin should carefully consider whether or not they should take Nolvadex since, due to the compound’s already moderate anabolic effect, an additional loss of effect could take place, leading to unsatisfying results.

A rarely observed but welcome characteristic of Nolvadex is that it has a direct influence on the hypothalamus and thus, by an in-creased release of gonadotropine, it stimulates the testosterone production in the testes. This does not result in a tremendous but still a measurable increase of the body’s own testosterone. This effect, however, is not sufficient to significantly increase the testosterone production reduced by anabolic/androgenic steroids.


The side effects of Nolvadex are usually low in dosages of up to 30 mg/day In rare cases nausea, vomiting, hot flashes, numbness, and blurred vision can occur. In women irregular menstrual cycles can occur which manifest themselves in weaker menstrual bleeding or even complete missing of a period. Women should also be careful not to get pregnant while taking Nolvadex. It is important for fe-male athletes that Nolvadex and the “pill” not be taken together since the antiestrogen Nolvadex and the estrogen-containing pill negatively counterfeit each other.


The normal daily dosage taken by athletes corresponds more or less to the dosage indications of the manufacturer and is 10-30 mg/day To prevent estrogenic side ef-fects normally 10 mg/day are sufficient, a dosage which also keeps low the risk of reducing the effect of simultaneously taken steroids. Often it is sufficient if the athlete begins this preventive intake of Nolvadex only three to four weeks after the intake of anabolics. Athletes who have tendencies toward gynecomastia, strong water retention, and increased fat deposits with steroids such as Dianabol, Testosterone, Anadrol 50, and Deca-Durabolin usually take 20-30 mg/day The combined application of Nolvadex 20-30 mg/day and Proviron 25-50 mg/day in these cases leads to excellent results. The same is true for athletes who are in competition, and for women. Women, however, should do without the intake of Proviron or at least reduce the dose to one 25 mg tablet per day. Unfortunately, in most cases, a very pronounced gynecomastia (“bitch tits”) cannot be reduced by taking Nolvadex so that often surgery is required, surgery which is not paid for by health insurance. First signs of a possible gynecomastia are light pain when touching the nipples. The tablets are usually taken 1-2 x daily, swallowed whole without chewing, with some liquid during meals.

Deca Profile. Deca-Durabolin helps joints.

Deca Durabolin is actually the brand name for Organons version of the compound Nandrolone Decanoate. Deca-Durabolin is a 19-Nor compound (some would say that it is the 19-nor compound), and as such, it shares basically the same characteristics with all of them. One thing unique to Deca Durabolin, above nearly all steroids, is the mystique it has had for the last quarter of a century. On a personal level, Ive included Deca Durabolin in cycles at doses ranging from 100mgs/week to 2,000mgs per week.

First of all, Deca Durabolin (and Nandrolone in general) doesnt produce many estrogenic or androgenic side effects. This is because Deca Durabolin has a very low rate of aromatization (conversion to estrogen via the aromatase enzyme), roughly equal to 20% the rate of testosterone.

Deca Durabolin stores water in connective tissue, thus alleviating joint pain. I have no idea what “storing water in the joints” means. I have no idea how to really quantify that statement, or where it started. However, in one study of postmenapusal women, Deca Durabolin impoved collagen synthesis, and in another study Deca Durabolin increased bone mineral content.

Both of these studies used VERY low doses, which were far too low to promote muscle growth. In my estimation, based on these 2 studies, an athlete attempting to use Deca Durabolin only for these two effects (increasing bone mineral content and collagen synthesis) should be using 100mgs of Deca Durabolin every week. Thats actually a higher dose than those two studies used successfully. Even at of this dose, in HIV+ patients who have experienced significant wasting, a 100mg/E2W (every 2 weeks) injection of Deca Durabolin resulted in a “significant increase in weight”. Id never recommend that low of a dose for an athlete, but its evidence of Deca Durabolin strong anabolic properties. Deca Durabolin is a very nice anabolic, causing nice (albeit slow) gains in quality muscle. This could be due to its moderately strong binding to the Androgen Receptor, or its many positive non-Androgen-Receptor mediated effects. One such effect is nitrogen retention, which is a major factor in muscle growth and lean mass gains; in one study, with low-doses (65 mg/week) and high-doses of Deca Durabolin (200 mg/week), both low-doses and high-doses resulted in significant nitrogen retention (33-52 g nitrogen/14 days, representing gains of 0.5 to 0.9 kg lean tissue/week), and body weight increased by 4.9 +/- 1.2 kg, including 3.1 +/- 0.5 kg lean body mass, and treadmill exercise performance (cardiovascular fitness) also improved. Need I say that the higher doses in this study produced more gains?

Deca Durabolin also has a very long active life. We can see from the chart below that a 100mg shot Deca Durabolin produced relatively active and stable plasma nandrolone levels until day almost 10, hence once a week shots are all thats necessary for stable levels of nandrolond Deca-Durabolinnoate (as a side note, the nandrolone phenylpropionate used in this study was active, and only experienced a severe drop off around day 5, shooting NPP every 4th day is the way to go). Youll also note that higher blood plasma levels of Nandrolone are found with Gluteal injections as opposed to Deltoid injections.

In another study of HIV+ men we can see that Deca Durabolin ( 200mgs on week 1, 400 on week 2 and 600mgs for weeks 3-12) caused NO negative side effects in total or LDL cholesterol, triglycerides, or insulin sensitivity and there was a reduction of HDL cholesterol (8-10 points) in both groups. Also, in most studies with HIV+ subjects, Deca Durabolin also improved immune function.

So what do we know so far about this compound? So far, we know that Deca-Durabolin is a very safe drug for long term use, will help with joint problems, could improve immune function, and is highly (!) anabolic, and not very androgenic.

Deca Durabolin Side Effects

Many members of also complain of water-retention with this drug, and again, Im inclined to agree. Letrozole seems to be a preferred choice to combat this, and its my favorite for this use. This water retention would seem to make Deca Durabolin more suitable for bulking rather than cutting, although it can be successfully used for either.

Now for the worst news: Deca Durabolin is a progestin (as are all nandrolones), unfortunately; it happens to stimulate the progesterone receptor 20% as well as progesterone itself, and this opens the door for many possible unwanted side effects (water retention, acne, etc…). It must be noted that most of those are rare, though. This also may be the major reason that Deca Durabolin is such a suppressive drug when it comes to your natural testosterone levels. We can see from the chart below that a simgle measly 100mg injection of Deca Durabolin caused a total (100%) reduction of natural testosterone levels, and it took roughly a month to return those testosterone levels to baseline! All from 100mgs of Deca Durabolin!

The moral of this story? Always use Testosterone with your Deca Durabolin! I suggest 200mgs, minimum, to avoid impotence and sexual dysfunction. For an anabolic effect from that Testosterone, I recommend at least double that, with an equal amount of Deca Durabolin (minimum). Id also recommend taking an anti-progesteronic drug with Deca Durabolin.

Deca Durabolin Cycle

So where are we? Well, Id be comfortable recommending Deca Durabolinfor use in a bulking cycle at up to 600mgs/week for an extended duration (12-16 weeks), or up to 400mgs/week in a cutting cycle (again, for 12-16 weeks), as long as something to combat water retention is present. Whichever purpose you decide to use Deca Durabolin for, you still need to include Testosterone in your cycle and have some anti-progesteronic drugs on hand just in case.

Post Cycle Therapy (PCT), though beyond the scope of this profile, needs to be commented on. Due to the highly suppressive nature of Deca Durabolin, I will speculate that testosterone in a Deca Durabolin-inclusive cycle needs to be run for at least 2 additional weeks upon cessation of Deca Durabolin. We remember from the chart above that baseline testosterone levels took roughly a month to return. Hence, a nice long estered testosterone should be run about 2 weeks longer than Deca Durabolin, to prevent having a lag in time when the Deca Durabolin is not producing an anabolic effect, yet is still suppressing your natural testosterone levels. Id also suggest that a particularly aggressive PCT be run after your cycle; Nolvadex, HCG, and perhaps Clomid should all be utilized in an effort to restore your natural hormone levels as quickly and efficiently as possible.

Turn Up The Heat For Muscle Mass!

According to a new study that shows that heating muscle may increase muscle mass through the expression of heat shock proteins. The following research may persuade bodybuilders to use the sauna and hot tubs more often for muscle recuperation and muscle growth. Researchers reported that the muscles of animals exposed to heat stress stimulated increases in heat shock proteins, which not only caused the activation of satellite cells (skeletal muscle stem cells are responsible for the repair and hypertrophy of skeletal muscle), but also increased protein synthesis during the regeneration of injured skeletal muscle. It was strongly suggested by the researchers that the application of heat to injured or damaged muscle may facilitate recovery and enhanced satellite cell activation leading to enhanced muscle mass.

Want more? Also researchers reported that intermittent heat application (30 minutes on alternating days) to the muscles of rats enhanced muscle hypertrophy. You might want to go steal grandma’s heating pad after reading these research papers! Heat shock proteins have previously been shown to increase muscle protein synthesis and increase muscle mass. In fact, a single bout of heat stress has been demonstrated to increase muscle mass and protein synthesis. Heat shock proteins are stimulated by many factors, but originally were discovered to be increased by the application of heat, hence “heat shock proteins.”

Heat shock proteins (HSPs) are a group of proteins whose expression is increased when the cells are exposed to elevated temperatures or other stress. The exercise-related stressors that have been shown to induce HSPs are: elevated temperature, decreased glucose availability, increased intracellular calcium levels, increased catecholamines and reduced blood flow to muscle. Consequently, HSPs are also referred to as “stress proteins” and their upregulation is sometimes described more generally as part of the stress response because they are increased in response to numerous stressors. HSPs provide cellular protection and work together with the antioxidant system to prevent further damage to cells. Thompson28 observed a large HSP response to high-force eccentric exercise, but a reduced HSP response following a repeated bout of high-force eccentric exercise. Thus, the increases in HSPs after high-force eccentric exercise may have reduced further damage to muscle.

HSPs have recently been shown to be important for increasing muscle protein synthesis and muscle hypertrophy. Scientists believe that heat stress-associated muscle hypertrophy may be induced by calcium-related intracellular signals. It is speculated that the application of heat stress to muscles may activate the intracellular signals, which stimulates the protein synthesis and/or modifies the protein breakdown. Therefore, heat stress may modify the intracellular Ca2+ level in skeletal muscles. Others have reported that Ca+ signaling is important for mediating muscle hypertrophy. For example, Oishi et al. recently reported that muscle hypertrophy induced by muscle overload was associated with an increased intracellular calcium level and that treatment with a drug that blocks calcium signaling reduced muscle hypertrophy during muscle overload. Activation of calcium may be one of the intracellular signals for skeletal muscle hypertrophy in response to IGF and increased loading. Preheating of skeletal muscles is being experimented on as a means of preventing muscular atrophy during bed rest inactivity and also the possibility of exposing astronauts to heat stress to reduce anti-gravity-related muscle atrophy.

Back in 1995, researchers were examining how reduced blood flow or so-called tourniquets could increase muscle hypertrophy. They performed surgical procedures on rats to reduce blood flow to their legs; surprisingly, the rats’ legs grew in size due to reduced blood flow. Muscle fibers were 34 % larger from the reduced blood flow in the experimental group. The content of HSPs also increased in muscle, which the researchers speculated may be important for muscle hypertrophy. Additionally showed that overload of muscle caused muscle hypertrophy in rats and increased both myosin heavy-chain protein (a consequence of muscle cell remodeling) and HSP expression in the hypertrophied leg muscle compared to the control leg. Taken together, these data demonstrate a relationship between protein synthesis, muscle cell remodeling and HSP expression. HSPs are not only increased by heat and exercise, but also can be increased pharmacologically. Clenebuterol has previously been shown to cause an increase in HSPs in muscle, which may be a molecular pathway in which clenebuterol increases protein synthesis and increases muscle mass.

In a recent study, researchers were looking specifically at how the expression of HSPs affect muscle protein content and muscle differentiation (process in which precursor muscle cells become mature muscle fibers. It’s a necessary process for muscle growth). Both processes are important for increasing muscle mass. The researchers examined heat stress, GGA or heat stress plus GGA. The researchers found that the administration of the anti-ulcer drug, GGA, as well as the heat stress, increased the expression of HSPs and protein content in muscle cells. It was suggested that GGA may activate intracellular growth signals, which stimulates muscle growth and protein synthesis. The researchers concluded that the administration of GGA could be one of the useful tools to gain muscular mass not only in athletes, but also in patients during rehabilitation. Why, all of a sudden, do all bodybuilders feel a burning sensation in their chest?

If you are in the gym busting your ass, and your legs are on fire from the high intensity, then that burning sensation is more than determination— but rather HSPs being expressed! The degree of HSPs expressed in muscle seems to be influenced by the total amount of work performed in the gym. Researchers investigated the HSP response in trained humans exposed to four weeks of rowing exercise by taking serial muscle biopsies after each week of training. The expression of HSPs increased in relation with increasing amounts of exercise, and they suggested that the HSP response was related to the total amount of exercise. The same research group then revised this statement and found that more importantly than just total work volume, HSPs are also stimulated to a greater extent during high-intensity exercise. For example, elite male rowers had muscle biopsies performed during two parts of their training season and post-season. During the training season, the sessions were divided so that the volume was the same, but one group performed at a low intensity and the other group performed at a high intensity. At the end of the study, there were the largest increases in HSPs being expressed during the high-intensity training season while HSP levels declined during the post-season when training volume and intensity were reduced. A recent study also found that HSP was correlated with the concentration of blood lactate levels during exercise, which may be the reason for higher HSP expression during high-intensity exercise.

HSPs seem to be increased with exercise sessions that cause muscle damage. Protocols that are higher in intensity and performed eccentrically elicit significant increases in HSPs. A recent study showed that a single bout of maximal eccentric exercise increased HSPs by 203 % within 23 hours of exercise. Interestingly, heating muscle and intense exercise causes a greater rise in HSPs than either one alone. One study looked at two forms of eccentric training and HSP expression. Researchers compared high-force eccentric barbell curls and moderate aerobic-intensity downhill running for 30 minutes. HSPs increased during high-force barbell curls but not during aerobic downhill running. The study demonstrates that a high-force eccentric stimulus promotes HSP responses that are not seen following a moderate, mixed-contraction exercise modality such as downhill running. The researchers concluded that the lower training intensity used in downhill running failed to increase HSP levels because of insufficient training intensity. Additionally, it has been suggested that the eccentric overload causes an increase in HSPs, which play an important role in the regulation of muscle mass. Performing eccentric contractions seems to be a better stimulus of HSPs than concentric contractions. Eccentric contractions are known to promote more hypertrophy than concentric contractions. Although the mechanisms of why eccentric contractions increase muscle hypertrophy is not clear, it is known that the process of hypertrophy involves long-term changes in protein synthesis, and several suggests that increases of HSPs are involved in these processes. Thus, HSPs are stimulated by high-intensity training. High-intensity exercise can increase testosterone levels as well; it should be of no surprise that when testosterone is administered, there is an increase in HSP expression in fast-twitch muscle fibers.Remember that fast-twitch muscle fibers have the most potential for muscle growth! Testosterone increases muscle mass, so could testosterone be increasing protein synthesis by activation of HSPs?

For many years, heat treatment has been used as a therapy for muscle injuries. There are several different heat modalities, such as heat packs, whirlpools, ultrasound and recently, microwave hyperemia. Molecular mechanism responsible for muscle hypertrophy in response to various stimuli, such as strength training and bodybuilding, is still unclear. Recently, the application of heat stress has been found to induce hypertrophy in muscle cells and facilitate the recovery of muscle atrophied following muscle unloading. Although we generally don’t think of a sauna as anabolic, it could possibly be for bodybuilders. Heat stress has been shown to reduce muscle atrophy and increase muscle protein synthesis. For example, Naito et al. reported that heat stress before an eight-day period of hindlimb unloading (unloading causes rapid muscle atrophy) in rats reduced muscle atrophy. Compared with sedentary cage control rats, hindlimb unloading resulted in a 25 % atrophy and a 40 % decrease in the level of HSPs. When muscle unloading was pretreated with heat stress, muscle atrophy was only 17 % and had >20 % higher HSP levels than control after eight days of unloading. It was postulated that the elevated levels of HSPs could have retarded muscle atrophy by both maintaining protein synthesis and decreasing the rate of protein breakdown. Other researchers have reported similar findings; it was reported that if animals underwent hindlimb unloading and then were immediately exposed to heat stress, thereafter the muscle exposed to heat stress had accelerated protein synthesis and muscle mass as compared to animals that had nothing.

A direct role of HSPs in protection of skeletal muscle has been demonstrated in both animals and humans. An increase in HSPs may also be able to increase strength the day after a heavy workout. For example, animals that overexpress HSPs by 20 times greater than normal had a 63 % lower rate of strength decline as compared to normal animals three days after a session of lengthening contractions. High-intensity resistance training increases HSP in muscles of both older and younger individuals— although the average relative increase of HSP expression appears to be larger in the young. The HSP response to exercise is lower in older rats with more hypertrophy-prone fast-twitch muscle fibers, which may play a part in why older people don’t have the same increase in muscle mass as younger people. Others have demonstrated the failure of successful recovery of skeletal muscles of older animals is due to a blunted activation of HSPs following muscle damage and suggests that abnormal activation of HSPs may play a major role in the defective regeneration seen in muscles of old mice. The defect in HSPs may provide strong evidence for the protective role of HSPs in preventing damage and strength loss in skeletal muscle during the aging process.

It is known that exercise and heat stress induce muscle fiber injury or protein breakdown. Because HSPs function to maintain cellular function under stressful conditions, it is speculated that HSPs are involved with the repair of injured skeletal muscles exposed to stress. The exposure to heat, muscle damage by eccentric exercise and high-exercise intensity are potent stimulators of HSPs. HSPs are currently being examined as a possible anabolic treatment to athletes, as the British Journal of Sports Medicine researchers found that microwave hyperthermia to muscle increased HSPs in the legs of subjects. Who knows? Maybe you can get big by lying out in the sun and getting a tan! As far as supplements, glutamine may also enhance HSP expression. Researchers examined the role of glutamine in muscle under two environments: heat stress and resting. Glutamine has a stimulatory effect on the rate of protein synthesis in skeletal muscles subjected to heat stress, while it has no effect on the rate of protein synthesis in normal muscle fibers. Glutamine increases HSP expression only in heat-stressed muscle fibers. Therefore, HSPs may play a role in the mechanism by which glutamine enhances the rate of protein synthesis in heat-stressed muscle fibers. One final bit of wisdom— stay away from alcohol if you want to increase HSPs, as alcohol consumption blunts HSP expression in muscle.

Key Points:

  • Heat stress activates satellite cell activity, increases muscle mass and enhances muscle rejuvenation.
  • HSPs provide cellular protection and protects against further damage.
  • HSPs are increased in response to training intensity.
  • Eccentric exercise is a potent stimulator of HSPs.

Injectables Guide For Ladies

Ladies that have tried at least one mild oral steroid and now wish to add more mass to their bodies.

The chances of contracting side effect, and potential virilization, are higher with injectables than with anavar. Anavar is the mildest steroid for ladies without a doubt…too bad it is not in an injectable form.

Most common sides seen with the ladies are as follows and in no particular order. Some negatives can also be positives as you will note below

NEGATIVE SIDES - Ance, oily skin, clitoral enlargement beyond minimal, aggression, hair loss..male style, hair growth especially on upper lip and chin, hair loss, darkened hair growth, quickened hair growth on legs and arms, lowering of voice tone, distruption of normal menstral cycle, aggression.

MOST COMMON NEGATIVE SIDES - Oily skin, some hair growth, a little acne, some alteration in normal menstral cycle, minimal voice tone lowering, darkening body hair

PRECURSER TO VOICE LOWERING - If you get a squeaky voice, hoarse throat or voice, scratchy thoat, raspy throat or voice, a cough, or any ache in the throat then stop the steroid immediately as these are common warning signs of voice alterations

PERMANENT NEGATIVE SIDES - Voice lowering may improve immediately after a cycle A LITTLE but will NEVER return to normal. Some girls are affected minimally and still sound like a women and others end up sounding like a man if they continue with the steroid. Clit growth remains…androgenic swelling goes away but the GROWTH remains. Some long time and heavy users have grown a little penis(TRUE!)

POSITIVE SIDES - Feelings of well being, increased energy, decreased recovery time, aggression, heightened sex drive with small amount of clit enlargement, Muscle gain, strength gain, some reports of decreases in estrogenic fat ie”upper legs, butt, upper arms, abdomen.

PERMANENT POSITIVE SIDES - Mass and strength will largely remain IF you train and eat properly post cycle. Better sex, due to clit growth, but sex DRIVE returns to normal except for the possible increase in sex drive as a result of heightened enjoyment.

Pure anabolics vs androgenic anabolics.

There are only two injectables that are nearly pure anabolics and they are Nandrolone and primobolan. They are somewhat androgenic but one could classify them as anabolics. The more androgenic the hormone the greater are your chances for sides including virilization, but the greater your chances are for great muscle growth. The most androgenic hormones are Test and Tren and then perhaps winny, although some would disagree with me on the winny.

PRIMOBOLAN - Used by many ladies as it, along with nandrolone, is probably the least androgenic roid. CAREFUL….Primobolan is in the long acting ester enenthate and it clears slowly. Many ladies have experienced very bad sides from this roid due to the fact that they take too much per week (above 50-75mg). Injectable Primobolan is not our drug of choice because it is long acting and if sides come on that you don’t like then you have to ride them out until the roid clears your system and by the time it does permamnent sides may have set in. Daeo’s wife had a bad experience with Primobolan. If you start low you shouldn’t have too much trouble, if any, IMO as it is quite mild androgenically. Just remember though that it will not give quick muscle gains at all. The gains seen are usually quality muscle built at a slow steady rate. If more and quicker gains are needed then I would recommend Nandrolone.

ESTERS AND DOSE SCHEDULES. - An ester is a compound made up of hydrogen and carbon atoms. They are added to pure steroids or testosterone in order to slow the release of the active agent. Some esters have a short chain of hydrogen and carbon and others have longer chains. The longer the chain the longer the time release of the steroid. Propionate is a short ester and Decanoate is a long chain ester. 50mg of Nandrolne in a Phenylprop ester has more actual steroid than 50mg of Nandrolone in the Decanoate ester as some of the 50mg weight is taken up by the longer ester. THE DIFFERENCE IS MINIMAL! Never let anyone tell you that one type of steroid is more powerful than another type of the same steroid. These are myths . There is a myth that Testosterone Cypionate is more powerful than Testosterone Enanthate and this is a myth. In actuality the enanthate ester has one less carbon atom and 50 mg of the test will have a tiny amount more test than 50mg of cyp.


Most conservative…..Inject 50 mg of steroid or testosterone once and then let it completely clear the system. ie: Testosterone Propionate 50mg then wait a week before doing another injection. OR…Testosterone Cypionate 50mg and then wait for two weeks before injecting again. This system will give you some results and is very safe in regard to sides.

The next method is recommended by Bill Llewellyn and others. In this system one injects a dose and then lets it partially clear the system. It is thought that this clearance will not allow androgens to build up over time which of course can cause sides and virilization. This sytem will give better results and liitle sides. Examples are 25- 50mg Testosterone Propionate every 5-7 days or 50mg of Testosterone Cypionate every 10 days.

The last system will give best results. This system is favored by many and requires injecting AT LEAST as frequently as a male.
In this system you try to inject at least twice per half life. This keeps hormone spikes to a minimum. These more even blood levels result in better gains. There is also some evidence to suggest that spiking hormone levels cause more sides. Here is an example of this system…Testosterone Propionate 15mg every second day or 20 mg every third day. Also Testosterone Cypionate 20-25 mg twice per week or every forth day at most. Simply put the longer you are “on” the greater are your chances for virilization. An 8 week cycle is a good start. latter cycles can be longer once you get a feel for the hormone. A long low dose cycle of 12 weeks or more can be great.


Testosterone 25-50mg
Primobolan 50-75mg
Winistrol 50-70 mg 7-10mg per day INJECT DAILY for best results
Nandrolone 25-60mg
EQ 25-60mg

These doses will give you great gains with little chance of serious sides. If you are top level competitor then obviously these doses are quite moderate. I would not recommend any women go much above these doses unless they are darn serious about being competitive!


We do not recommend that you use more than one hormone at a time unless your are a top competitor. If you do stack your voice will almost certainly lower and other sides will be worse. If you MUST stack than we would recommend using a small dose of anavar with the injectable at perhaps 10mg per day, 5mg in the am and 5 mg in the pm.

While trying to increase mass while on injectables you must increase your protein intake to about 2 grams per pound of body weight. If you do not do this then your gains will be likely be less . I recommend a good low fat whey protein shake betwee three regular meals. Some people seem to get great gains with less but it is safer to go higher. Caloric intake also needs to go and the increased protein intake will help.
You can get good strength gains ,and some muscle gain, while on anavar, and not eat that much in the way of protein or calories, but this is not the case when trying to build some serious muscle.

The anabolic/catabolic diet

First, lets look at the ABCDE diet. Originally ABCDE Diet (Anabolic Burst Cycling of Diet and Exercise) was proposed by Torbjorn Akerfeldt in an old issue of Muscle Media 2000. Basically, you ate your heart out for two weeks, which would elicit all sorts of different anabolic responses and cause you to add muscle. Then for the next two weeks, you would turn things around by going on a strict Low-Caloric diet. Done correctly, you’d lose the fat you gained during your hog fest and keep most of the muscle. That’s of course in “theory” meaning it works like crap with the average bodybuilder. ABCDE diet is great for people who do not easily gain fat or who easily lose fat. But what if you rapidly gain fat and cannot seem to be able to get rid of it? What will happen is that by feasting for 2 weeks you will accumulate a tremendous amount of fat.

This accumulation occurs in two forms:

Each fat cell will hypertrophy. Once fat cells reach critical size they release certain growth factors which, in turn, build up new fat cells. This hyperplasia will occur in a matter of days if your adipocytes are already big enough, i.e; as you are fat in the first place. Of course, as the diet state, you can diet down the hypertrophy, but you cannot get rid of newly formed fat cells. As you repeat the ABCDE cycles you will add new fat cells. Intense training (because of cortisol) plus a high carb and high fat diet is a great way to induce adipose tissue hyperplasia in people who are prone to gain fat.

Your body fat percentage is the reflection of the size of the fat cells multiplied by their number. You can shrink fact cell size but only up to a certain point. You’re not able to lose fat cells. In other words, as you start a low calorie diet, you will only have a single variable to play with (reducing fat cell size). But once you have reduced fat cell size up to a point (which is quickly reached) they won’t shrink anymore. So you will not have any variables left.

The diet stops working and you are stuck at a high bodyfat percentage. The only way to lose fat cells is to use weird drugs, or to undergo liposuction. I think the concept of the ABCDE diet is valid but not appropriate for fat people or drug users. For those people I propose a variation of this diet that I have been using for some time. I call it the anabolic/catbolic diet (let’s call it ACD diet).

It is based on the fact that there is a constant turnover of protein in our muscles. We are constantly adding protein (anabolism) but also losing protein (catabolism). It is the balance between the two which determines the size of our muscles.

So whenever someone complains of only gaining 5 pounds a year, this is not strictly true. He gained maybe 200 pounds of muscle but he also lost 195 pounds. This (contrived) example points out that we are able to gain a tremendous amount of muscle every year. As we cannot hold on to those 100 pounds, it means we are doing something really wrong. As its name implies, the ACD diet is composed of two distinct phases.

An anabolic phase lasting 10 to 20 days and a catabolic phase lasting 5 to 10 days. When I say a catabolic phase, I really mean it; we do whatever it takes in order to lose muscle. Our body will detect something is very wrong and will attempt to stop this rapid muscle loss. It will deactivate the ATP-dependent proteolytic pathways. So far, almost no drug that I know of can do this. The more catabolism you seek, the more your body will fight it. After the catabolic phase, we will be in a position where both anabolism and catabolism are very low. But anabolism is ready to be accelerated to catch up growth while catabolism is reduced to a minimum for a while no matter what. During the anabolic phase, we will try to boost anabolism as much as possible.

During the first week, catabolism will stay very low. So, there will not be an anabolic catch up, there will be an overshoot. How do we do that? During the catabolic phase, the goal is to lose as much fat as possible no matter what the cost is for the muscle mass. I mean a low carbohydrate, low fat and low protein diet. If you are using creatine stop it. Oral anabolics will be stopped 48 hours before the beginning of this phase while 5 days before the injectables are stopped. Thyroid medication (T3) will be started at day one. Clenbuterol will be used at day one and maybe on day four or fine at massive doses (15 to 20 tabs). Of course, if you are new to Clenbuterol do not use that much. At that dose, used acutely you should feel sore all over which will only enhance catabolism.

Overtraining is a must and don’t forget about the daily (at least) one hour of aerobics. During your first few catabolic cycles, please do not play with so many variables. Avoid too much aerobics and don’t be too hard on the diet. Make it last only 5 days. As you get used to it, add days and variables. The following anabolic phase will start with either a carb load or a fat load lasting only on and a half days. But be careful about not eating too much. Many people get sick whenever they try to load on food after starving themselves. On the other hand, one or two days sick in bed is a good way to end up the catabolic phase but only if you are very advanced. The fat load consists of the following: on the last day of the catabolic phase do 2 hours of low intensity cardio. I like the rowing machine since it involves both lower and upper body. Repeat this cardio workout again on an empty stomach before the fat load.

As its name implies the fat load consists of eating fat with some proteins but no carbs at all. This will direct the fat inside the aerobically trained muscles not in the subcutaneous adipocytes. Whenever you are eating carbs along with fat, this fat will tend to be esterified in the subcutaneous adipose tissue not inside the muscles. I know the ABCDE diet tells otherwise, but oh well¦. Even though you are not eating carbs, don’t forget the creatine. It will find its way in the muscles without insulin. The oral anabolics will be started ruing the first day while the injectables will be used as late as possible the day before. Along with the carb up, use creatine and ALA. In the first few days, eat a high carb, low fat and moderate protein diet. The protein should be of the highest quality possible to make up for the moderate amount. The more protein eaten the sooner the ATP-dependent proteolytic pathway will recover.

Of course the thyroid medication, the Clenbuterol, the aerobics and the overtraining are stopped. In fact, it is better to reduce training to a bare minimum in the first few days. During the remainder of this phase, do not eat too much. Unless you want to gain fat cells, you should just eat over maintenance and no more. I do not think overfeeding builds up muscle. My belief is that the measuring techniques are biased.

Whenever you eat too much and gain weight, they are going to tell you have gained muscle mass along with the fat. But whenever you diet it down, the bias will take place the other way around. The apparatus will tell you that you have lost muscle along with the fat. Your overfeeding gains just evaporated.

The length of the anabolic phase is determined by the length and the severity of the catabolic phase. The shorter the latter is, the shorter the former should last. Of course, this kind of radical cycling is much more appropriate for steroid users than for drug free bodybuilders. It allows anabolics to keep working for a long time as it is frequently stopped during a short catabolic phase. This will fully restore their potency. In case you are a drug free bodybuilder, it is better not to go to the extreme. Shoot for a moderate catabolism not an extreme one.

Nandrolone PhenylPropionate by Accordo RX - Explained

Nandrolone Phenylpropionate was never really all that popular simply because of availability issues. Many of the pharmacy grade Nandrolone Phenylpropionate products range between 25mg-50mg/ml and are extremely expensive.

Nandrolone Phenylpropionate vs Decanoate.

Let’s calculate the amount accumulated in the body after 6 weeks of 500mg/deca. Let’s say you inject it once a week and we’ll give it a 1.5-week half-life. Note that injection frequency makes a huge difference in blood concentration stability but no difference in amount of esterified in the system

E (greek letter “sigma”) 500*e^(ln(1/2)n/1.5) from n=0 to n=6. So after 6 weeks, about 1300mg of esterified nandrolone remain in the body.

Now lets see how long, after the initial injection, it takes to reduce to a small enough amount that permits recovery.

1300*e^(ln(1/2)n/1.5) After 3 weeks, 325 mg of esterified remaiт after 6 weeks, 81 mg of esterified remain After 8 weeks, 32mg of esterified remain.

Nandrolone Decanoate is a long acting depot; it takes quite a while for it to “kick in” and clear out of the system. Depending on how much is used; it will take at least 4-6 weeks after the last shot for Deca to clear out. It also takes about 4 weeks for active blood levels to stabilize. This can easily add up to 8-10 weeks of “dead time” i.e. periods of time when blood levels are not consistent. These numbers apply to reasonable use of Nandrolone Decanoate; between 200-400mg a week. The more you use, the worst it gets. So a 10-week cycle of Deca can easily end up been a 16-week cycle when you account for clearance time (active blood levels). The first 4 weeks are also somewhat of a waste of time.

So that 10-week cycle ends up been 16 weeks; 6 weeks of optimal blood levels and 10 weeks of dead time. Not a very effective way to cycle.

With Nandrolone Phenylpropionate, you can bypass all that dead time. 19-Nortestosterone based drugs are known to shutdown HPTA very easily - think Trenbolone. Most bodybuilders will use Tren for around 6 weeks at the beginning of a cycle. Nandrolone Phenylpropionate should be used in a similar manner.

Here’s an example of a balanced cycle consisting of Nandrolone Phenylpropionate

Week 1-6: Dianabolbol
Week 1-6: Nandrolone Phenylpropionate
Week 1-8: Test Prop

It is a good idea to run Test 2 weeks past the Nandrolone Phenylpropionate, however; Nandrolone Phenylpropionate can be used as a stand-alone. Earlier, I compared Nandrolone Phenylpropionate to Tren. They are similar in some ways but Tren is much more androgenic and stronger in general.

Nandrolone Phenylpropionate shares some of the same sides associated with Deca (they are after all the same base compound). It should be noted that most of the sides that come with Deca are a result of its long ester. Decanoate ester is very hard to control and Nandrolone side effects are not easily countered like Testosterone related sides (Tamoxifen, anastrozole, finasteride…) Overall, Nandrolone is a milder compound than Testosterone and is better mg for mg (but that’s a matter of opinion)

Nandrolone Phenylpropionate should be injected at least every 3 days. A typical dose is 350mg-700mg a week for 5-8 weeks. It stacks very well with Winstrol, Dbol, Test, EQ, Anavar It does not stack well with Tren and especially Anadrol

Here are some good cycle suggestions:

Fast Acting Classic Test/Deca/Dbol cycle:

Week 1-6: Dianabol 30mg ED
Week 1-6: Nandrolone Phenylpropionate150mg EOD
Week 1-8: Test Prop 150mg EOD

Highly Anabolic cycles

Week 1-6: Nandrolone Phenylpropionate: 200mg E3D
Week 1-8: Anavar: 30mg ED

Week 1-6: Nandrolone Phenylpropionate: 200mg E3D
Week 1-8: Winny: 50mg ED

A good First cycle:

Week 1-6: Nandrolone Phenylpropionate: 150mg E3D
Week 1-4: Dbol: 25mg ED
(Week5-8: Anavar: 30mg ED - optional)

Nandrolone Phenylpropionate in a typical cycle

Week 1-10: EQ 400mg a week
Week 1-9: Test Cyp 600mg a week
Week 1-8: Nandrolone Phenylpropionate 200mg E3D
Week 10-13: Test Prop 150mg EOD

Nandrolone got a very bad rap with many bodybuilders; there is no reason to use Nandrolone Decanoate if Nandrolone Phenylpropionate available aside from year-round juicer using it for joint pain. Nandrolone is a tremendous bodybuilding drug that can take your physique to a whole different level but many people shy away from it because of what they have heard or experienced with Deca.

When Can I Start Taking Steroids

The problem with this is that most young bodybuilders can’t grasp the concept of the future and how long the road ahead really is even with the use of steroids. How do you convince a 14 year old that it will take years before he can look like the Pro bodybuilders in the magazines, and that he may never look like that even with all the drugs available in the world.

At what age should you be, before you consider using anabolic steroids? This question is not as easily answered as you may think it is. You cannot randomly just pick an age and say that this is the point at which you can now start to consider using anabolic steroids.

Between the ages of 12 and 26 a male’s hormone levels are on a steady rise until the age of 26. This is when these levels slowly start to decline until they are almost nonexistent by the ripe old age of 40.

When puberty starts in males at the age of 12 there is a huge flux in hormonal patterns in the body, which cause the growth of male characteristics, (deepening of the voice, growth of body hair, growth in height, etc.). These hormone levels increase by themselves so much that they can be compared to that of a mild anabolic steroid cycle. Therefore trying to add to what the body is doing on its own by adding in exogenous (outside) anabolic steroids is very counter productive.

Whenever any extra amount of anabolic steroids is added to the body, the body recognizes this extra level through a feedback loop in the human body known as the hypothalamus. Once the hypothalamus recognizes the increase in hormones which happens usually between 14 and 21 days, the body will shut off its own production of hormones until these levels decrease, along with increasing hormones to decrease these extra levels in the body (cortisone, estrogen). Cortisone and estrogen are 2 hormones in the body that bodybuilders do not need any extra. The easiest way to try to explain this without getting to complicated, is that the more anabolic steroids you put in your body, the more your body will try to lower those levels. When this happens bodybuilders get all the side effects that are normally associated with anabolic steroids use, gynecomastia (growth of fatty tissue underneath the breasts in males), hair loss, kidney damage, liver damage, and high blood pressure, just to name a few).

Before you consider the use of anabolic steroids you should have already reached your genetic potential. What is your genetic potential? To figure this out you should first look at the weight, height and build of other members in your family. Is this exact, no, but it is somewhere to start. If every male on both sides of your family is approximately 5’7” and weighs between 150lbs and 170lbs and they are all bald by the age of 25, then it would be a good guess that you will also fall somewhere in those ranges by the time you stop growing. Now with working out and eating correctly for 4 years lets say, you would be able to put on 15 or more pounds of muscle tissue (that would mean you now weigh 165-185 lbs.). This is what your genetic potential would be. Now if you started to use steroids at that point, 165-185 lbs you may be able to put on another 15-20 lbs (180-200lbs). If you had started using when you were 125 lbs., and gained 25lbs through the use of anabolic steroids, you would still be well short of what you could have gotten naturally (150lbs as compared to 180-200lbs), and now it will be much harder to try to gain another 30-40lbs.

So for a starting point lets say that you need to be at least 18 years of age before you consider using anabolic steroids. Now that we have a starting point, lets look at a few other factors that should be considered. Steroids DO NOT IN ANY WAY, SHAPE, OR FORM makes up for a good diet and workout program. Most people who use anabolic steroids feel that this is the time where they can be a little more relaxed in their workouts and diet. Actually this is when they should be even more strict. So before you can think of using at the age of 18, you will need 3 more solid years of good training and eating habits. Minor changes in diet and workouts can result in great gains in mass and muscle as well as strength.

No matter how much assistance you get from anabolic steroids, without proper nutrition and workouts you will be lucky to have any gains at all, let alone keep them after the cycle is over. The goal of using any substance, legal or not should be that after you stop using it you don’t loose all of that which you have fought to get. What would be the point of spending all that money (steroids are not free) to gain that 30lbs when you will loose it after the cycle is over anyway?

So the better question to ask instead of when can I take anabolic steroids, should be, what can I do to get all that I can out of my body without needing anabolic steroids?. In order to calculate my progress, I need to talk with my family and doctors, before I try to make a choice like that.

We will start with the age range of 14-16; this is when your hormones are raging. Your body is in full swing of making the best steroids that you can ever get, and it does all this without you even needing to do a single thing. At this point you should start with a solid exercise plan and a basic supplement plan in addition to the regular food that you need to be eating on a regular basis.

For workouts focus on the basic compound movements (Bench Press, Squats, Deadlifts, Barbell Curls, etc.) Working out 4 days a week with at least 8 hours of sleep a night is a great start. Add to that the extra protein that you should be taking and you will definitely start seeing a difference in your body.

By the age of 16-18 you will have had most of your growth spurts and you will be ready to change a few more things in your overall plan. You workouts can become a little more specialized as you start using different exercises. 

Somewhere between 18 and 21 you should be just about done growing, so what should you do differently now? Add more protein! You should be getting at the very least, your body weight in grams of protein per day! And that?s at the very least! By now you will have been working out consistently for quite a while and should know your body very well. What will work and what won?t work should be old news. There isn’t really anything new to add to what is already a great program, other than Tribulus and maybe a pre-workout supplement such as Ultimate Orange. After this point, you can start to consider the use of steroids. What about them? Are they as terrible as everyone seems to think they are? As long as they are used correctly, I don?t think so. When considering their use, I feel that orals should be used as late as possible. These are most harmful on the body and therefore should not be used for a very long time.

Another thing to consider, other than the side effects I have already spoken of, is your sex drive. Some anabolic steroids will make your sex drive almost nonexistent and will have a big effect on your sperm count. These drugs in particular should try to be avoided. That leaves mild anabolics. Although they are the safest to use, they are expensive, illegal, and require the use of a needle. Which most first time users do not want to use.

I told you that this is not something that should be passed off very easily; you shouldn?t have to make the mistakes that most of us make by using steroids to early in your life. If used correctly, I think they are fine, but look at what it takes in order to use them correctly. Have you been working out for 5 years straight without more the 2 weeks off every 6 weeks? Do you eat every 2-3 hours, 6 times a day without missing a meal? Do you get 8 hours of sleep every night? This is something that can have a huge effect on your body for the rest of your life, so don?t make that choice in 10 minutes. Good luck and keep growing.

Deca Durabolin vs Equipoise

Deca Durabolin, also known as Deca and Nandrolone Decanoate, is an anabolic androgenic steroid that is used by bodybuilders to bulk up. While this steroid is second to none for stimulating dramatic improvements in terms of recuperation time between workouts, it also has the ability to promote nitrogen retention and protein synthesis. Not only this, Deca Durabolin is easy on the liver and unarguably one of the best performance enhancing drugs for promoting strength, muscle size, and wet gains.

Deca Durabolin is characterized by a very low rate of aromatization that makes it ideal even for athletes who are prone to estrogenic side effects, though progesterone sides (some prolactin) are usual. Moreover, they can expect slow but steady gains in terms of muscle mass, strength, and muscle tissue. Deca Durabolin is more suited to longer steroid cycles and is generally stacked with Testosterone Suspension, Testosterone Enanthate , Testosterone Propionate, Testosterone Cypionate, Anadrol, Dianabol, and Sustanon 250. Most athletes prefer stacking Deca Durabolin and Dianabol as they share a synergistic effect with each other.

Equipoise has come a long way from just being a veterinary drug to transform itself into one of the most popular and recommended bodybuilding drugs. This extremely anabolic and moderately androgenic steroid stimulates appetite and has the unmatched ability of increasing endurance. A perfect pre-contest drug, Equipoise can dramatically increase Hemoglobin and Hematocrit (the number of red blood cells and the percentage of red blood cells) that in turn promote greater “pumps” during intense workouts. One of the biggest advantages associated with Equipoise is that this anabolic androgenic steroid can stimulates the release of erythropoietin in the kidneys. A big majority of athletes prefer stacking Equipoise with Testosterone Enanthate, Testosterone Cypionate, Winstrol, Anadrol, Sustanon 250, and Testosterone Propionate.

Considered by a big majority of bodybuilders as a dream steroid, Deca Durabolin is superior to Equipoise. This is primarily because Deca Durabolin is better than Equipoise in terms of retention of muscle mass and body strength gains. However, Deca Durabolin users should always follow a very strict post cycle therapy with drugs such as Arimidex, Clomid , or Nolvadex to protect against excess estrogen. There is one issue with Deca Durabolin that’s a big downside, Deca Durabolin stays in the body for a long duration (approximately 2 years) and is therefore not the ideal drug for athletes who are tested regularly.

Equipoise, on the other hand, is preferred by experienced athletes and bodybuilders who can be satisfied with moderate gains that are sustaining in nature. While Equipoise is associated with androgenic side effects like hair loss, growth of body and facial hair, and acne, Deca Durabolin is often associated with gynecomastia and fluid retention. It is widely believed that Deca Durabolin is more suited for bulking cycles while Equipoise is more suitable for cutting cycles. The use of Equipoise is associated with slow but steady gains in terms of muscle mass and strength with very few estrogenic side effects. Equipoise can be a part of longer cycles. The fact that Equipoise promotes red blood cell production and stimulates appetite slightly puts it ahead of Deca Durabolin.