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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
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
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
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
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
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
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
Change in receptors Loss of receptors
Exhaustion of mediators
Increased metabolic degradation.
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
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
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
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
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
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
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
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
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
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
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
The human body as an organism is not a perfectly sequential or
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
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
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
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
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
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
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
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
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
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
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
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..?
Wastage is a key concept and is pertinent to every attempt at improving
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
And the first trade off to happen to reach an elite, but un-rounded
development, is health. “Health ends where high performance
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
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
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 …?”
“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
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
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
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
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