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iSteroids Newsletter

Issue # 12

This month in steroids


If you’ve been keeping up with current events in the world of anabolic steroids, you’ve probably heard of three major events this month.

The first is that the largest underground lab in the world (International Pharmaceuticals) has been caught producing BD (British Dragon) counterfeits. Although I made this announcement on several major message forums at the request of British Dragon themselves, I didn’t actually discover it personally. They made the discovery themselves, and attempted to contact IP for an explanation, but didn’t receive one- prompting them to contact me to make the announcement on the major boards. At this point, IP copped to the allegations, offering an apology to everyone. Not surprisingly, on several boards where IP is popular, the moderators jumped to his defence, saying that it didn’t matter if the products weren’t the genuine article, as long as they contained what they were supposed to contain. Personally, if I bought a watch I thought to be a Rolex, I would be pretty pissed to find out that it wasn’t- even if the damn thing contained all of the gears and springs that it was supposed to contain.

The second major event in the world of steroids this month was the huge bust that recently happened in Germany and Poland. There was a steroid dealing cartel operating in the EU, with an estimated six-figure monthly sales figure. $90k dollars in cash was seized as well as carloads of steroids, and even some marijuana. I believe the initial report was that there were 52 separate buildings that were raided in a joint strike combining Polish as well as German law enforcement…and of course, there were no athletes involved, but rather sales were announced to be exclusively bodybuilding-related, and in part internet-related. If you happen to purchase your anabolics from a source in either Germany or Poland, I suspect you may have difficulty with that soon…

And finally, on a note that will his close to home for many, the owner of the anabolic steroid message board with the initials “WWBB” was busted for possession, importation, and distribution of anabolic steroids as well as recreational drugs. Predictably, he rolled, and gave the police at least one name in an effort to get himself out of trouble - perhaps several. Needless to say, I’m not surprised.

All of this makes me glad that I am not buying my anabolics from some online source, but rather, I get them legally from my doctor who has me on Hormone Replacement Therapy. Granted, the cost is a bit more than underground/black-market gear, and the selection is much more limited-but that’s fine with me. Anyone who has ever been to prison knows that a few cycles is not a good reason to go back, and anyone who has never been there certainly doesn’t want to pay a visit to one. With the recent busts, and controversy in the world of the underground/black-market, this is the perfect time to be on HRT for me…additionally, it’s nice to have my blood work and physicals monitored by a physician. It just makes much more sense to me to keep both your body safe as well as your freedom.

I can only hope that some people follow my example, and pursue legal alternatives to running around on the black market, buying gear that may not be the brand that it’s supposed to be, and facing possible health and legal consequences. If not, I suspect that more than one person who is reading this might be the topic of my next “This Month in Steroids” article…

Basic Pharmacological Concepts

AUTHOR: James Daemon, Phd

“Corpora non agunt nisi fixata”

“A drug will not work unless it is bound”

The background, and the central principles:

Synthetic chemicals introduced in the 1920’s.

Biotechnology has become a major source of new therapeutic agents, antibodies, enzymes and regulatory proteins, hormones and growth factors. These are produced in a different way to conventional drugs but the principles of pharmacology are largely unaltered.

Molecules must exert some chemical influence on one or more of the constituents of cells to produce a pharmacological response. These constituent cellular molecules in the organism vastly outnumber the drug molecules, and if the ligands were distributed at random the chance of interaction with any particular class of cellular molecule would be negligible. Osmotic diuretics, antacids, and chelating agents are the notable exceptions.

An understanding of binding sites and the mechanism by which the association of a drug molecule with these sites, constitutes the major thrust of pharmacological research.

Drugs mainly bind to protein molecules. Even anaesthetics. The only important exceptions to proteins as target sites is DNA, on which certain anti tumour and anti microbial drugs and certain mutagenic and carcinogenic agents act.

4 kinds of regulatory proteins are normally involved as primary drug targets:
  • -Enzymes
  • -Carrier molecules
  • -Ion channels
  • -Receptors
Also, plasma proteins which ensure distribution.
Receptor: Interactions of the regulatory type where the small molecule (ligand) may function either as an antagonist or agonist.

Drug specificity: For a drug to serve a useful purpose (like training) it must act selectively on particular cells and tissues. This is called binding site specificity. Conversely, proteins that function as the target for drugs generally show a high degree of ligand specificity.

A small chemical change such as the conversion of one of the amino acids from ‘L’ to ‘D’ form, or removal of one amino acid from a chain, or moving the functional group by one carbon atom, can completely inactivate the molecule since the receptor fails to recognise/ bind the altered form. The complementary specificity of ligands and binding sites gives rise to the very exact molecular recognition properties of proteins, and is central to explaining many of the phenomenon of pharmacology.

It is no exaggeration to say that the ability of proteins to interact in a highly selective way with other molecules-including other proteins- is the basis of living machines.

No drug acts however with complete specificity- this is why all drugs have side effects. In general the lower the potency of the drug and the higher the dose that is needed the more likely it is that sites of action other than the primary one will assume significance.

Receptor classification: Classified on the basis of the effects of particular drugs.
Several different criteria are used: The first of these was direct measurement of ligand binding to receptors, which allowed many subclasses to be defined. Molecular cloning has revealed the amino acid sequence of many receptors which provides a completely new basis for classification at a much finer level of detail than can be reached through standard pharmacological analysis.

Finally, analysis of the biochemical pathways that are activated in response to receptor activation shows patterns that provide yet another basis for classification. Receptor classification has become much more detailed with a proliferation of receptor subtypes for all the main types of ligand. Alternative molecular and biochemical classifications began to spring up which were incompatible with the accepted pharmacologically receptor classes. IUPHAR compendium of receptor characterization and classification.

Quantitive aspects of drug receptor interactions: The first step in drug action on a specific receptor is the formation of a reversible drug receptor complex- being governed by the law of mass action. (The rate of a chemical reaction is proportional to the product of the concentrations of reactants.)

Agonist concentration effect curves.
The binding of drugs in tissues can be measured directly, and has been shown to obey equations, based on the law of mass action. Usually however, it is a biological response, such as a rise in blood pressure, contraction or relaxation of a strip of smooth muscle in an organ bath, or the activation of an enzyme that is actually measured and plotted as a concentration effect or dose response curve. Though they appear similar to the theoretical concentration-occupancy curves, they cannot be used to measure the affinity of agonist drugs to their receptors, since the physiological response produced is not, as a rule, directly proportional to occupancy.

Another rather blindingly obvious issue, is that whilst the concentration of drug molecules in the organ bath is easy to calculate, the concentration of drugs molecules at the receptor is more often than not, not known.

The agonist is subjected to many factors before it reaches the receptor such as enzymatic degradation or uptake by non target cells, so at best you can account for these as percentage wastage and ..guess! Governs therapeutic window.

Competitive antagonism: Only one drug molecule can bind to the receptor at one time, after a while, the molecule may in the main leave the receptor and leave it free, but whilst its there, that’s it. The higher the affinity of a drug for the receptor, the lower the concentration at which it will produce a given level of occupancy

Partial agonists and the concept of efficacy: The ability of a drug to activate a receptor is a graded, rather than an all or none property. If a series of chemically related agonist drugs (i.e. AAS) acting on the same (AR) receptor is tested on a given biological system, it is often found that the maximal response differs from one drug to another, some compounds (full agonist) can produce a maximal response, whereas others (partial agonists)can only produce a sub maximal response. When we recall that only one drug molecule can bind to any given receptor at one time- you have the basis for QID dosing. A partial agonist will not produce a maximal response even at 100% occupancy…

Direct measurement of drug binding to receptors.
Not really honed down to a replicable and classified science yet. It is one of the most talked about concepts in AAS- but the pharmacological basis for it is scant. Usually performed with radioactive molecules, and time is taken to see when equilibrium is reached. However, non specific binding takes place, and all the algebra in the world to date hasn't’produced 100% reliable figures.

Antagonism: Frequently the effect of one drug is diminished or completely abolished by the presence of another (see QID) Competitive antagonism we have touched upon.
Chemical antagonism is uncommon where two substances combine in solution so that the effect of the active drug is lost. e.g.: Chelating agents

Pharmacokinetic antagonism: Where the presence of the ‘antagonist, or partial agonist’ reduces concentration of the intended agonist at the site of action. This will increase the rate of metabolic degradation of the agonist.

Antagonism by receptor block: Reversible or irreversible antagonism, think anti aromatase and HPTA.

Non competitive antagonism: Antagonist blocks at some point the chain of events that leads to production of response by the agonist.

Physiological antagonism: Loose term describing the interaction of two drugs in the body whose opposing effects tend to cancel each other out. Occurs naturally, central concept to homeostasis and things like nitrogen balance. Without either hormone, production or reduction will continue exponentially.

Desensitisation and tachyphalaxis: In the human body, the effect of a drug gradually diminishes when the subject is exposed to it continuously or repeatedly. This is an effect that applies loosely to psychology, pain, and adaptation response to training.

These two terms are synonymous used to describe this phenomenon which can happen in a few minutes. The term tolerance is conventionally used to describe a more gradual decrease in responsiveness to a drug, taking days or weeks to develop, but the distinction is not a sharp one.
The term 'refractoriness' is also sometimes used mainly to a relation to a loss of therapeutic efficacy. Drug resistance is a term used to describe the loss of effectiveness of anti microbial or anti tumour drugs. Many different mechanism can give rise to this type of phenomenon:

Change in receptors Loss of receptors

Exhaustion of mediators

Increased metabolic degradation.

Physiological adaptation.

Active extrusion of drug from cells.

In receptors coupled to ion channels desensitisation is rapid and pronounced. At the neuromuscular junction there is evidence that the desensitised state is caused by a slow conformational change in the receptor resulting in tight binding of the agonist molecule without the opening of the ion channel.

A similar change is thought to occur in B adrenoreceptors which become unable to activate adenylate cyclase though they can still bind the agonist. It is also believed that phosphorylation of specific residues in the receptor protein is responsible for many types of desensitisation.

Prolonged exposure to agonist often results in a gradual decrease in the number of receptors as measured by binding studies.

This occurs with Beta adrenoreceptor and appears to be a slower process than the uncoupling from adenylate cyclase mentioned above in studies on cell cultures the number of b2 adrenoreceptors can fall to about 10% of normal in 8 hours in the presence of low concentrations of isoprenaline recovery to normal takes several days similar. This is the reason that Clenbuterol doses spiral upwards, and gives rise to notion of 2 days on, 2 off. Having reviewed the literature which points to Clenbuterol’s main effect on fat (and calcium channel mediated protein) catabolism being greater over extended periods, it would be useful if there was an adjunctive treatment that could be administered to prevent such huge down regulation of the receptor, and allow the dose to remain fairly consistent.. There is.

Unsurprisingly, it is an adjunctive treatment for asthma, given (much to the mystery of English physicians and even the authors Ritter Dale Rang) called Ketotifen. It is medically used to allow doses of salbutamol (a molecule known to act in a weaker, but virtually identical way to Clenbuterol- theoretically similar to the relationship between T3 & T4) It posses a much shorter half life than Clenbuterol, but this seems to be a positive effect, coupled with its delivery method in inhaler format) to remain effective without large scale increases. Medicine has not linked the reason for spiraling doses and this medication yet.

Changes have been described for other types of receptors including those for various peptides such a HGH and insulin. It is believed that the vanishing receptors are taken into cells by endocytosis. This type of adaptation is common of hormone receptors and has obvious relevance to the effects produced when drugs are administered for extended periods-like a cycle. Receptor desensitisation is generally and unwanted complication, but it can be exploited clinically. For example GRH is used to treat endometriosis or prostatic cancer. Given continuously this hormone paradoxically inhibits gonadotrophin release in contrast the normal stimulatory effect of the physiological secretion, which is pulsatile.

Exhaustion of mediators: Desensitisation of is associated with depletion of an essential intermediate substance. Drugs such as amphetamine and ephedrine, act by releasing tissue stores of adrenaline and nor adrenaline and other amines from the nerve terminal-tachyphalaxis occurs because the releasable stores of nor adrenaline become depleted.

Increased metabolic degradation: Tolerance to some drugs e.g.: barbiturates and Ethanol occurs partly because the repeated administration of the same drug produces a progressively lower plasma concentration. The degree of tolerance that results is generally slight, and in the case of the above other mechanisms contribute to the substantial tolerance that occurs.

Physiological adaptation:
A drugs decreasing effects may occur because it is nullified by a homeostatic response. This homeostatic measurement is very common and if they occur slowly the result will be a very gradually developing tolerance. It is a common experience that many side effects of drugs such as nausea and sleepiness tend to subside even though administration is continued. We may assume that kind of physiological adaptation is occurring though little is known at this time about the mechanism involved.

P450 cyctochrome-responsible for 70% of drug elimination inhibited by unknown factor in grapefruit juice. CYP2A1 is responsible for metabolising testosterone into a useless conjugate by the addition of a 7 alpha OH group. The CYP2A2 is responsible for metabolising testosterone by the addition of an OH group on carbon 15 in the alpha position. Activity of these two enzymes is responsible for metabolism of around 75% of steroid hormones and subsequent excretion. They are inactivated by an unknown factor in grapefruit juice. This means the active steroids will be passed back into serum via enterohepatic circulation.

This should not be attempted with certain blood pressure raising medications such as Prozac, ephedrine, amphetamine etc. Also, Prozac and ephedrine in conjunction are quite a lethal combination. And quite an unpleasant one to sit out the increased half life.

Only drugs can stop the sports cheats" Reprinted From August's New Scientist

AUTHOR: Michael Le Page

Only drugs can stop the sports cheats" Reprinted From August's New Scientist- By Michael Le Page.

THE Finnish cross-country skier Eero Mantyranta won two gold medals in the 1964 Olympics and accumulated an impressive tally of medals during his career. Later it turned out that he has a mutation in a gene called EPOR that means he produces up to 50 per cent more red blood cells than normal.

The east African runners who dominate distance events have also been shown to have at least one genetic advantage: their lower legs are thinner and weigh on average 400 grams less than those of Danish athletes, which translates into a massive 8 per cent energy saving. Other people have distinct genetic disadvantages. For instance, 1 in 5 Europeans cannot produce the alpha-actinin-3 protein found in fast-twitch muscle fibres. Very few people with this genotype excel at power sports such as sprinting.

So much for fairness in sport. The World Anti-Doping Agency says its aim is "to protect the athletes' fundamental right to participate in doping-free sport and thus promote health, fairness, and equality for athletes worldwide". Such notions are a quaint hangover from the amateur age. Sports are inherently unfair. Genes alone do not make you a winner, of course, but some people's genes give them a massive advantage with which others struggle to compete no matter how young they start or how hard they train.

There is a way to level the playing field: allow athletes to make up for their natural disadvantages by taking performance-enhancing drugs. There is not yet a "foot growth potion" for the rivals of Australian swimmer lan Thorpe, who has size-17 feet, but an estimated i million Americans have already taken human growth hormone, which in the US can now be prescribed for children with "idiopathic short stature" - effectively anyone who is very short. No one knows how many average-sized people have used growth hormone to help them make the national basketball team, but would it really be fair to exclude such people as cheats when, for example, players such as Pavel Podkolzin or Sun Ming Ming owe their great height to pituitary tumours that resulted in an excess of growth hormone?

Or take the mutation that boosted Mantyranta's red blood cell count. All athletes know that there are ways of equalling or surpassing his natural advantage: take the hormone EPO, indulge in blood doping (injecting extra red blood cells), train at high altitude or sleep in a low-oxygen tent. Only the last two are allowed, of course, but the effect is the same. So the consequence of the ban on EPO and blood doping is to give an unfair advantage to athletes who can afford to train at altitude or invest in an altitude chamber - or on cunning doctors who can help them beat drug tests.

If we were really serious about making sport fair, we would try to ensure some sort of equality in the resources athletes have access to. And when genetics becomes advanced enough, we would introduce different divisions or some kind of handicapping system based on people's inherited advantages or disadvantages. After all, people who lack a Y chromosome already compete separately from those who have one. Will it happen? Unlikely.

There is one decent argument against performance-enhancing drugs: safety. Many drugs taken by cheating athletes are dangerous, and allowing their use would force all athletes to take them to have any chance of winning. But the rules as they stand are clearly not designed with the safety of athletes in mind. A good example of this is the lack of any safety limit on the concentration of red blood cells, which beyond a certain level considerably increases the risk of heart attacks and strokes. Dehydration resulting from exercise makes matters even worse. Yet doping authorities allow athletes to compete no matter how high their blood cell concentration, as long as it is not due to doping. So it is fine for athletes to risk death, just as long as it is a natural death.

If these arguments do not convince you that we need to rethink the ban on drugs in sport, there is a more pragmatic one: the existing regime is not working. Clearly, many top athletes still resort to drugs. And the situation is only going to get worse. In the not too distant future, gene therapy could be used to boost the strength of muscles. The only way to detect such modifications may be to remove and test a piece of muscle. Are we really going to inflict that on athletes?

There is another way: allow the use of drugs, and have sports authorities focus on testing the health of athletes rather than their use of drugs. This is the suggestion of ethicists Julian Savulescu at the University of Oxford and Bennett Foddy at the University of Melbourne, Australia. They argue that any drugs that are safe should be permitted, whatever their effect on performance. Authorities would set a safe level for, say, red blood cell concentration, and anyone exceeding it would not be allowed to compete, whether their result was due to doping, altitude training or genetics.

Savulescu says he would prefer it if there were no drugs in sport. But the drugs are out there and they are not going to go away. So let's adopt the policy that is best for athletes and best for sport. We cannot live in fantasy land. Savulescu thinks doping authorities will have to adopt his idea sooner or later. Sooner would be better.*

"According to the existing sporting rules, it is fine for athletes to risk death.justas long as it is a natural death"

Michael Le Page.


The Synergistic approach to individually optimal exercise prescription:

AUTHOR: James Daemon, PhD

By James Daemon, PhD


(From the Editor: This month we have the benefit of including 2 articles from James Daemon, PhD. This particular one concerns training paradigms and preiodization. It’s a rather long and in-depth look at the proper way to incorporate training, rest, and other variables into a proper and synergistic routine. I highly recommend reading it from start to finish and actively working to incorporate the ideas presented into your current training- many of the ideas are drawn from pillars of the field, and you’ll find them in many successful powerlifting and bodybuilding routines. If you don’t own all of the major texts on training, this is a great introduction to many of the concepts presented in them. Enjoy.)

Part 1: The Problem….

Periodization, the schematic organization of training utilized by the athlete, sports person, and fitness enthusiast, is based on the manipulation of training variables to achieve a specified goal as part of a long term plan. Over the past twenty years the applied concept of periodization has revolutionized the training of athletes, and the prescription of exercise.

Traditionally, volume and intensity are varied throughout the long term training period based on an inverse relationship, if volume levels are high intensity is low and vice versa.

Initially developed for swimming, weight lifting and athletics in Eastern Europe, it was observed that the successful athlete ’s long term training followed a distinctive pattern. Early in the training year, training was of low intensity but was high in volume, and as the year progressed volume would decrease linearly as intensity would increase. At the point of competition, intensity would be at its highest and volume, it’s lowest. From this observation, the periodized model was developed.

Seyle’s General Adaptation Syndrome provides the framework on which periodization was conceptualized.

G.A.S stipulates that adaptations follow 3 phases, initially the shock phase wherein the body encounters a new stimulus that it is not accustomed to, progressing from this is the adaptation phase occurs as a response to the shock or stimulus of the initial phase and finally staleness occurs as the shock/stimulus has been adapted to and no longer provides any stimulus to adapt to. This may lead to a plateau or overtraining.

Periodization aims to provide a linear step like progression, as once the stimulus has been adapted to, and the stimulus no longer provides the shock element- the stimulus becomes altered so that the shock will occur and adaptation will take place once more.

The traditional periodized model conceptualized by Matveyev, separated the training program into specific periods of time with differing goals and purposes.

These cycles consist of the long-term macro cycle (e.g., the training year), which is broken into separate meso-cycles (a period of several months) which are further subdivided into micro cycles which may represent a period of 1-4 weeks. The meso and micro cycle components implemented into the macro-cycle provide the time scale for variance, the mode of variance depends on the training focus, and is determined by what phase of training the cycle is part of.

The traditional European model consists of the general preparatory phase to provide underlying physical conditioning for the competition phase wherein training intensifies and skills become perfected: Finally there is the transition phase(s) which serve to provide the necessary recuperation necessary for both the physical and psychological stresses of training and competition, whilst simultaneously providing the necessary stimulus to prevent de-training.

There have been many adaptations and additions to this model.The Western adaptation version, hypothesized by Stone, O’ Bryan and Garhammer, for strength/power sports in 1981 furthered Matveyevs model and is typified by significantly smaller fluctuations of the volume and intensity variables due to the smaller adaptation window of advanced athletes, and necessity to maintain higher intensity of training during the high volume periods, to ensure no detriment to performance occurs: thus the 3 phases of training become subdivided further.

The high volume/ low intensity preparation phase is delineated into 3 further sub phases of differing emphasis. The initial sub phase called the hypertrophy phase provides the initial muscular and metabolic conditioning for the further phases. It is typically of 1-6 week’s in duration. From this there is the strength phase, typically training becomes focused around the strengthening of sports specific muscle groups which leads to the transition into the strength/power phase.

Here the focus of training narrows further towards sports specific condition as training intensifies. The competition phase displays the maximal development of physical ability culminating in the “peaking” of performance.

The transition phases provide the active recovery, ordinarily these are positioned pre and post competition phase.

The periodization model purported by Bompa again is developed from the initial European model. Bompas model depicts the delineation of the preparatory period ,into general physical preparation, and specific preparation and further sub phases to develop physical conditioning and increase the physical abilities- and muscular attributes specific to the sport. The period before the competition phase, serves to peak performance for specified competition(s). The traditional European model resulted in peaking for a single key competition in the calendar, displaying stark contrasts in volume and intensity.

As previously mentioned the small adaptation potential of higher caliber athletes, coupled with the necessity to maintain performance capabilities (as ability increases the maintenance of performance becomes more important) stipulates the application of such a model be suitable for beginners or novices only.

This model too would be unsuitable for sport requiring frequent competition. Bompa advocates the use polycyclic patterns for more advanced athletes and team sports, wherein performance is peaked and maintained for a period of time.

Periodized models display a linear transition from high volume, to high intensity sessions. The non-linear approach utilizes the integration of high volume and high intensity training within each micro-cycle to maintain a higher level of performance for a sustained period opposed to the systematic peaking for a specified event. The non-linear ‘undulating’ model (it is postulated), avoids the accumulation of fatigue caused by the linear increases in magnitude of training intensity.

The principal of specificity provides the fundamental training focus of both the individual sessions, and the programming or arrangement of the training cycle. Each sport has specific characteristics and seasons from which all training protocol is specified to.

The preparatory phase usually corresponds to the off season and pre-season, the competition phase applies to the in-season phase- the transitional phase represents a portion of the off season.

It becomes apparent that training provides the stimulus for sports improvement, and once an individual has advanced beyond the beginner/novice status, then the capacity to improve becomes diminished and necessitates the systematic variation of the adaptational stimuli.

The smaller the window for adaptation (the more advanced the athlete, or how close to their genetic ceiling) the more sophisticated the training program necessary to keep delivering adaptations.

The modern western adaptations and of Matveyevs periodized model solidified the commonly held perception of periodization’ superiority. Periodization advocates purport this superiority based on the apparent calculated application of training principles (specificity, overload, progression etc) formulated by the precise quantification of intensity and volume for each individual cycle, phase, sub phase and session.

However, the analytical and calculated precision of the construct becomes flawed. Human beings are not mathematically programmed, and all behavior is subject to many, many variables-not accounted for in anything but an ancillary fashion in this model Typically these calculated/computed-training programs (in a bid to provide application of specificity) are prescribed based on analysis of the athlete and the specific protocol of the sport and its sporting calendar.

It is here that we first encounter one of the fundamental flaws of periodization.

The human body as an organism is not a perfectly sequential or pre-determined system.

Individual responses cannot be pre-established; the application of the fundamental concept “homeostasis” elucidates that the human body will adapt to a stimulus.

We can see how periodization applies to this, it appears that periodization manipulates this ability to achieve positive adaptation, and indeed it does, however, its ultimate downfall is the lack of consideration for any other possible stimuli external to the volume and intensity variables. Variables such as age, training status, genetic predisposition, nutritional and psychological status, plus a multitude of environmental, societal and cultural factors amongst many others may influence the training effect. Therefore the organization of training to manipulate the body to produce a peak in performance may ultimately be flawed due to its lack of consideration of individual responses and how external factors can influence the productivity of training and the athlete.

It has been pointed out by many authors that it would be more logical to organize the training scheme to match the ongoing demands of the sporting season and that the use of expressions such as non-linear etc serves only to provide a smokescreen for periodization concepts.

It has become apparent within modern society that the magnitude of achievement and level of competition has increased. Sports are evolving, higher demands are placed on the athletes, more competitions are organized to increase revenue and increasingly higher purses / salaries are awarded reflective of the capitalistic nature of western society.

Periodization has proven itself to be an important development in the sphere of sports performance. It’s success is mirrored in the achievements of the old Eastern European athletes and most modern-day records.

However we must remember that periodization was from inception to its development, created in an era where the sporting arena was entirely different in terms of standard, status, magnitude and professionalism.

Periodization as a concept was established for weight-lifting, swimming and track and field events in the 1950s. If we consider the previous point, and note that as an athlete develops in ability, the window of adaptation or development potential decreases.

Also, that the athletes who periodization was initially conceptualized for, existed in an era where sports standards where significantly lower. In unit-dimensional predictable sports, its limitation as a template is evidenced. Much of the success of the eastern European athletes was displayed during a time where sports performers were less advanced and pre-dated the onset of the professional era.

It has been speculated that since the introduction of periodized training into the British sports training agenda, there has been a noticeable decline in achievement internationally.

The original periodized model was formulated under the influence of communism and its ideology. The cycles of training are reflective of the productivity cycles of the communist regime, and do not consider the effect of weather, seasons and biological rhythms. The quantification of the volume and intensity variables served to facilitate logic and science whilst eliminating what was perceived to be weaknesses- such as emotion and apperception.

In Eastern European society, the periodized model has proven to be successful.

Conversely however, the success of many African nations in sports may be attributed to environmental conditions, genetics, society and culture- the dominance of Kenyan athletes in endurance events highlights this.

Kenyan athletes habitually train at altitude, which serves to increase the haemoglobin content in the blood facilitating O2 transport and waste product removal; they do not follow a periodized scheme.

Periodization has proven itself; its limitation lies in the lack of qualitative considerations.

The specific delegation of a regime based singularly on the sports specifics fails to account for individual responses and nuances of the athletes- the effect of culture, society, and training environment amongst many, many others.

As a result of its quantitative nature, periodization does not holistically utilize the concept of specificity. Periodization highlighted the necessity to manipulate training protocols such as loading to elicit adaptations.

Much like the modern athlete, the periodization concept must now evolve to the modern arena, with the application of scientific advances and with the integration of a more definitive variable pool inclusive of quantitative and qualitative considerations: If it can adapt- periodization may provide a more comprehensive framework for athletic training.

Human beings are subject to many factors which dictate their response to training programs. Some are internal (hormones), and some are external (sociological/perceived outcome status). However, before the external factors can impinge upon response and performance, they must first be recognised, and then the effects of the emotion mediated by chemical signals. For instance- an athlete may be under intense pressure from his parents to succeed in competition.

This can lead to anxiety on his part, and anxiety can raise arousal to the wrong side of the curve and thus, impair performance.

Anxiety, and indeed, all thoughts both conscious and unconscious are electrochemical signals, and if we leave out the manner in which we represent these to ourselves-we can certainly see that an ‘emotional’ impetus triggers a cycle of events that ultimately leads to relative changes in chemical levels. With the above example, it could be the child is unaware of the pressure, even though someone else may perceive it. To be more urbane, it is only when we are bothered about something, either for good or bad, that it causes a notable chemical response within us. Without the underpinning process of chemicals, there is no feeling, only the awareness of an emotional possibility.

A cycle is defined as a series of related events that are repeated. Biologically, it refers to genetically programmed hormone levels i.e.: menstrual cycle, gonadotrophin release cycle. There is also the sleep/wake cycle. These are referred to as circadian rhythms.

This is the body’s evolutionary mirror of the light/dark cycle that occurs in nature. In itself, it is a complete cycle for both sexes, unlike the sexual cycle, which occurs monthly for women-Not to be confused with “seasonal behaviour” which is a cosmological effect(!)

The body as an organism, we loosely assume to have evolved in vivo so to speak, even if we did start as interrelated microprobes delivered on rock. Nature, through the course of Aeons, has devised a system in response to its environment that has slight differences in people living in different degrees in relation to the poles.

Winter feels odd for many as the ratio of light and dark confuses and often depresses them. There is even a disorder named after this. It is aptly named Seasonally Affected Disorder.

The next item to consider is a training cycle. A conventional periodized training cycle is a collection of sessions forming six week blocks called mesocycles. Groups of mesocycles are arranged into yearly or quadrennial plans. This, as you may have guessed is just theatrical semantics. Yes, you need to train an ability for so long to see a notable adaptation.

But the body doesn’t recover from every training stress, it recovers from those it is subjected to in a day. Unelss you plan to spend years in KGB custody; you will not change your circadian rhythm.

The link between a biological circadian rhythm and a training cycle is that bio rhythms use hormone concentrations as markers. Hormone concentrations are what will ultimately dictate how well you will adapt to training.

Intensity is a concept that should be adjusted in response to the athlete both up and down, and not as a mathematical given. The body responds to different training doses, in different ratio’s, and long term attempts at singular bio motor abilities in isolation, does not take into account that the body has no singular stand alone system.

There are cardiovascular benefits to weight training for instance- it is possible to develop seemingly diametric abilities.The original studies that shocked bodybuilders out of running have not been replicated since, which throws a dubious light at the original.

Mitochondrial volume and capillary density are two separate effects, and one style of training will not develop the other directly-but equally, unless you are not doing the hours on your main skill-it will not hinder it.

Capillary density decreases as a result of the increase in muscular size and volume.

The increase in sarcoplasmic hypertrophy witnessed in bodybuilders results in a decrease in capillary density (due to there being more muscle not because capillaries disappear), in fact bodybuilding increases capillarization - bodybuilding is in essence high intensity endurance training. It’s only due to the massively high amounts of hypertrophy and hyperplasia in bodybuilders using AAS and HGH/IGF-1 -that decreased capillary density is observed.

Far from it- If you’re mitochondrial density improves, just because the effects are specifically produced in response to a singular cathexis of training stimuli, it doesn’t mean that one ability would be greater than if the other was not developed at all, and it would be lunacy to suggest that concurrent development won’t allow you to reach higher goals in your chosen sport.

The cellular apparatus is geared toward the stress it is adapted to, but having a strong ability to deliver blood, or produce ATP is obviously going to be a boost in any sport.

The difference between a runner and a bodybuilder are form following function, they are all the same muscular movements a human body performs, requiring the same energy source of ATP, and the only thing that changes is the amount of times a movement is repeated, and the force- but, both of these are limited if blood flow is reduced and if the mitochondria are short of ATP.

This archaic practice that gained credibility in the 70-s was interpreted as if you were to compete on competition day or week, in two different disciplines.

This isn’t the complete or holistic picture- it does not take into account that having strong cellular apparatus will gear you toward success in any discipline. Ok, a pro bodybuilder is never going to run a marathon, but if he avoids catabolism, whose to say that the oxygenation wont improve nutrient delivery and protein synthesis…? It is only of relevance to people over their genetic potential, who exist solely in the world of body building.

Obviously, specialised training will produce specialised improvements in performance, but as is becoming increasingly fashionable to note, is that physical preparedness forms the basis of technique and so the organism with the stronger cellular apparatus will have a greater chance of enduring higher stress, and thus improving by adapting.

Lets look at it from another angle- If you had abnormally large mitochondrial volumes, but had only done weight training, would that reduce your force output..?

The answer is so blatant it seems quite pathetic to type it out. There are non beneficial effects to doing endurance running if you are looking for pure mass- all exercise is proteolytic - and that protein loss can oppose the effect of looking for mass.

Capillary density is shown to decrease with hypertrophy training, but that doesn’t signal that the body is sacrificing one system at the expense of the other..?

These fallacies are the ‘logic’ that lead to the rationale behind the singular development of a bio motor ability.

When viewed holistically, this highlights a weak link in the chain to be addressed and strengthened-just like women need to train the upper body. An untrained women’s’ upper body is chronically weak and people shy away from hard resistance work saying

“We weren’t meant to be strong”- it is just like the older generation need RFD training.

The next point in devaluing conventional training cycles is the singular development of bio motor abilities.

Power delivery is key to many sports. Power is composed of two components- speed and maximal strength. If one is sacrificed at the expense of the other, a less powerful athlete will be produced. Power is developed with light weights and RFD training, but if maximal strength doesn’t increase, the bar will only move in a very limited range of motion on the force curve.

This seems obvious, but what about endurance running…? Obviously cardiovascular training needs to occur- what if a cardio development program was figured into a strength training routine- as the ability to run is just a demonstration of ability of certain muscle groups to continuously produce force. No one aspect of human performance can be addressed by one variable.

Training in the conjugated method enables the athlete to continuously feel the benefits in term of increased skill and Proprioception, rather than the concept that after developing that you will do a six week cycle that will tie it all in and let you perform better- sounds like magic doesn’t it..?

Some simple facts about biological cycles; Abilities decline if not used. Strength declines in 3 days, reaching a substantial percentage after a week. So why spend half a year developing strength to let it decline to a maintenance level..? Why not continue to improve it..? Time…? Recovery..?

Wastage is a key concept and is pertinent to every attempt at improving muscular qualities.

Only elite level athletes can claim that they have no time for anything other than maintenance, as they have to devote all training to time to developing their critical and defining ability. This can be a little short-sighted as many muscular qualities go into producing just one sporting movement.

And the first trade off to happen to reach an elite, but un-rounded development, is health. “Health ends where high performance begins”

It is important when separating strength training from all sports, as has been prevalent, is to realise that a person who can move 100kg once, can move 50kg at least twice with no extra training. Obvious. But not obvious is the fact that the person who can move 50kg 20 times can move 100kg even once, without a large period to train this seemingly separate attribute. The muscular qualities are the same, but the nervous component is key here.

Does the ability to produce force repeatedly mean that a different process will occur than in a maximal lift..? No. It just repeats itself with less force. As maximal strength tiers into cyclic endurance sports, this should all seem relatively obvious.

The first concept, which isn’t new, is that of Conjugated training cycles.

The basis of the system is exercise selection, rotation, variable resistance. It basically integrates all training variables into one training regimen. There is no off period, as encountered in periodized macro or mesocycles.

Rather, training is continuous and progression constant. It completely de-values traditional progressive overload methods, most of which were developed in the wake of one factor theory.

For power lifting it works like this:

4 training days per week-

2 maximal effort (working up to 1RM and P.R if possible)

2 dynamic/ speed days (using sub maximal weights with maximal speed to increase rate of force development and explosive strength).

With power lifting you have essentially 3 lifts: Squat, dead lift and bench press. Squat and Dead lifting exercises are performed on the same day and bench exercises on a separate day.

Here's the unique part: Once an exercise is learned you cannot improve it by simply performing it over and over again. You have to select specific exercises to train your specific weaknesses and perform movements to address them. You never actually perform the 3 lifts.

Exercises are changed either each week or every 2 weeks at most, by rotating exercises constantly you help delay fatigue, however, all exercises are performed in the same reps/set pattern.

Max effort day: Main specific exercise(s) up to 1RM, then perform assistance exercises (submax 3-5% of 1RM, 4-6 sets).The same pattern is followed for both max effort days.

Dynamic: Bench day: 8 sets x 3 reps performed explosively

Squat / dead: 12 sets x 2 reps, after assistance exercises are performed

Rest periods on these days are kept to 45 -60 seconds between sets.

Training (on the dynamic days) is performed in 3 week waves:

Week 1: loads are 50% of 1RM

Week 2: 55% of 1RM

Week 3: 60% then back to 50%.

As progression is constant every time you go back to 50%, the load becomes slightly higher.

After 3 weeks of training a de-loading week is necessary, which means no maximal effort training for the week. Its not a week off as you can perform 4 sessions, but just don’t max out.

All training in this phase is sub maximal.

Many will dismiss these ideas as being unconventional.

Panic strategy takes over in these people thinking that every hour spent doing the same thing will produce the same increase- it won’t. And the time spent is not as great because people are driven to exhaustion in conventional periodization. If you follow a conjugated program, the benefit is that you can work strength out all year, but the body will respond continually rather than in peaks. Peaks can still be engineered pre contests, but this just super compensation of resources due to increased rest and shock loading.

Next concept is steroid cycles. Even when people use creatine they say “How long should I use it for?”

“What is it being used for …?”

"Erm…increased strength...”

“Ok, what training are you doing…?”

“Err... high reps…”

As indicated by our triangle, goals dictate training which is supported by diet and impinged upon by lifestyle. Creatine falls into the diet category. You are using it to assist improve a specific attribute, and as we know the ability to respond to a specific training stimulus optimally will decline at 8-12 weeks the program will have to be changed, and the dietary supplements should too.

Creatine specifically- it is not toxic, taking it increases the ability of the body to excrete it. If your training is all geared toward the same goal, there is no point coming off. It will not repress anything than the overall levels of cellular phosphate which you are replacing anyway, and the declining strength period that supplement manufacturers interpret as meaning its time to come off, is in fact just the body attenuating to a training stimulus.

Steroid cycles developed rather coincidentally at the same time periodization gained ground, mainly in Eastern bloc athletes. In Germany, there was actually a state sponsored initiative to systematically dope athletes- 4chlorodehydromethyltestosterone was given to athletes, the athletes were told they were vitamins. When an East German swimmer was asked why all the women looked so masculine and had eerily deep voices, she replied “We didn’t come here to sing”.

When can safely assume that as PED’s have been used since the original Olympic games, that in the interests of competition, the practice established over thousands of years has not disappeared in the last few decades.

The concept of a steroid cycle is drawn from the standard periodization model. You do a six week mesocycle, you use X drugs for that period. The two go hand in hand, but the usage by recreational athletes doing the same style of training constantly falls short of science for a number of reasons. Periodization does not take into account all human variances, and neither do the drug programs used by professional athletes to support it.

As we will cover in depth later, natural hormone release is pulsatile in nature, and with ebbing concentrations of one hormone, comes the increased potential for adaptation with another. The body’s levels rise and fall in a concert lasting in men for a day, in women for a month. Different hormones the body releases are beneficial to it at different times of the day, and at different phases of recovery.

There are few related “ancillary” issues that we should explore as a grounding for the rest of this opus.

HCG is a lutenizing hormone analogue. Its use is central to the “homeostatic” steroid cycles plan that most follow.

Its action is to stimulate Leydigs cells to produce testosterone, and sperm to be produced in the seminifourous tubules.

It is prescribed to medically compensate for the lack of LH caused bylack of GnRH.

Its use in athletes is usually to restore endogenous testosterone production. It can also be used to mask certain doses of androgens, as it promotes epi-testosterone production.

During a certain level of drug administration, different for everyone, the bodies sensors on the HPTA detect that there is a relatively high concentration of steroid hormones (estrogen and progesterone included) in the blood, and that internal production is not needed.

After the drugs are withdrawn and the necessary half life calculations are performed, the dose and duration (up to saturation) dictates how long the body takes to restart hormone production.

In fact, hormone production can start in a few hours and be notable in a few days, but as there is a certain amount of atrophy to the testicles  when AAS have been administered at supraphysiological doses over long periods-they will not be producing at capacity.

This principle applies to an atrophied muscle. Normal size and function can be restored as long as negative feedback inhibition is effected.

This used to be with Clomiphene, but since Tamoxifen has been proven a fiercer agonist at the HPTA, and in the breast- it stands to reason that this molecules affinity for the “homeostatic” chemo-receptors is stronger.

In males, Interstitial cell stimulating hormone takes over from FSH- which stimulates follicular cells in women.

Anecdotally, this has proven to be true. Tamoxifen is supplied in a lower dosage than Clomiphene, 10mg and 50mg respectively, and the (subjectively) same, or greater effects have resulted from Tamoxifen administration at a substantially lower dose.

There are many theories about ancillary medication, but these do not seem to tally up with basic biochemistry.

The problem people face when coming off AAS is that as cortisone has been blocked from the receptor for so long, and as a certain degree of androgen attenuation has built up- that when the AAS are withdrawn the dominant hormone is cortisol, the body is hypersensitive to it, and thus catabolism can become pronounced.

As we will see later, cortisol could well be the cellular trigger that renews genetically mediated growth, but in the short term, catabolism is undesirable.

The user will obviously want to get natural testosterone levels back into the normal range as fast as possible, to retain as much lean mass as possible.

It is important to consider the whole hormonal package here. Estrogen and progesterone are especially notorious for initiating negative feedback, indeed, progesterone is the hormone that is used to initiate negative feedback in a women’s menstrual cycle, and the doses are monstrous- that much in a male will cause serious emotional disturbances in the limbic cortex.

So when increasing testicular output we must considered that overall estrogen levels will rise. If not catered for, it will counteract your best efforts to restore natural function.

People use Mesterolone as it is not believed to repress spermatogenesis-likewise Fluoxymesterone, but the nervous activity with Fluoxymesterone will most likely negatively affect size.

As do all stimulants.

The first thing that people overlook, is that in the absence of supraphysiological doses of AAS, endogenous testosterone production will start again, even with no ancillary medication-it will just take longer. A high dose of Tamoxifen has proven to be a very advantageous

synergist whilst using HCG in the normal way- endogenous testosterone recurs very fast with this combination of drugs. As mentioned, with dose and duration being important- the rebound (as less receptor disassociation must occur to return to homeostasis) of someone using 50mg of an oral a day will be much faster than someone who has had round the clock increases.

This delay in return to homeostasis leads to panic about speed of recovery, and masculinity because of diminished testicle size. The body providers a blueprint for everything, and even to further confuse the issue, the chemical properties of LH are well documented. Size will impinge on production, as an atrophied cell, or cell number isn’t going to be at peak performance-The goal is to return the body back to its natural method of functioning… This seems to provide a sound basis for using physiological doses that will subside quickly enough to prevent round the clock elevation, and thus suppression.

The standard dosing protocol insists that the testicles need to be shocked out their inactivity with a supraphysiological dose (i.e.: one never encountered naturally). Supraphysiological doses of anything you hope to encourage back into a natural pattern of secreting something that is tied to a negative feedback cycle, is utterly futile.

In the chemical world, absence really does make the heart grow fonder. Low concentrations of a drug make the bodies homeostatic mechanism operate to make the receptors more sensitive to the lower amount. This means that when relative concentration returns they will be hypersensitive, which will in turn activate negative feedback. HPTA suppression by AAS cuts of the natural output of LH. If a blanket cycle is adopted (steady blood levels round the clock) the endogenous production will dry up totally-atrophy takes time, but without endogenous testosterone production it will happen.

This means that after having none of this chemical for 12 weeks, that the body at this point is HYPER sensitive. A dosage higher than usual will not encourage the most efficient output. It will be patchy and sporadic as the half life of HCG, you will be a supraphysiological levels for too many hours in the day. The leydigs cells only become desensitized to LH and ICSH when they have been exposed to it constantly. As they are hypersensitive

 
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