ANABOLICS BY BODYGUARD


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Like it or not, anabolic steroids are here to stay in the dog game. Include track and field, professional football, weightlifting, and other sporting endeavors. It is a simple indisputable fact of life. The sports agent for the disgraced Canadian Olympic sprinter Ben Johnson was recently quoted as stating that 99% of elite track and field athletes use illegal substances. One of my closest friends is a former world class high jumper who would agree with that statement. Despite the great genetics enabling him to reach world class status, he could not scale the mountain to Olympic “elite” because of his choice not to use anabolic steroids. I can assure you his decision to not use anabolic steroids put him in the minority among world class track and field athletes. Unfortunately, unlike professional sports where testing for banned substances attempts to enforce the ban on anabolic steroid usage, there is no such testing in the dog game. Nor would such testing be practical. The best that drug testing in sports has accomplished thus far is controlling the abuse of steroids-not their illicit use. So, if you are currently using anabolic steroids on your dog or, if you intend to use them, the best advice I can give you is to read and learn as much as you can about the subject. Then read some more.

And keep reading. And experiment before an actual keep. Unfortunately for the dogman, although canines have been used in the laboratory to study the effects of various anabolic steroids, the studies are generally not helpful to the dogman whom desires to use anabolic steroids during the keep and needs to know the specific means (compound, duration, dose, etc.) to use them successfully. The existing studies generally examine the effects of a certain steroid on a specific canine bodily organ or function like the liver, reproductive organs, prostate, etc. Sadly, the canine is too often used as a laboratory tool to study what afflicts and ails we human Increasing your dog’s strength and its ability to recover faster during the keep is not a mainstream medical concern-veterinary or otherwise-and never will be. To further complicate matters, the mainstream veterinary community is not unlike the human medical community in its avoidance and condemnation of anabolic steroids for ergogenic (“Ergogenic” means “tending to increase work output”.) benefit. Consider the ongoing debate in the human medical community regarding the validity of any ergogenic benefit of anabolic steroids and you understand what is guiding the prejudice against anabolic steroids in the veterinary community. Further consider that within the last decade the human medical community is only now slowly acknowledging the potential ergogenic benefits of anabolic steroids, most notably while working with AIDS patients and the elderly. Now consider that anabolic steroids were developed in the 1930’s and you will begin to understand the long history of resistance in the medical and veterinary community to these compounds. Generically, the term “steroids” refers to a group of hormones including cortical hormones (gluco and mineralcorticoids, etc.), female sex hormones (estrogen, etc.) and male sex hormones (androgens). In this column we will discuss the use of anabolic/androgenic (androgens) steroids and other related ergogenic compounds.

Anabolic steroids are synthetically manufactured compounds similar to the male sex hormone testosterone. Anabolic or, “anabolism”, means “any constructive metabolic process by which organisms convert substances into other components of the organism’s chemical architecture”. Huh? Simply put, anabolism is generally considered the good guy of the anabolic/androgenic equation. Think growth and recovery. The anabolic characteristics of a steroid accelerates lean tissue buildup (skeletal muscle growth), increases formation of red blood cells, accelerates recovery (regeneration) from exercise, injuries or illness, slows down the breakdown of body tissues (catabolism), and stimulates the metabolism. Androgenic means “producing masculine characteristics”. Think of androgenic as the raging hormones of a male teenager; oily skin, pimples, aggression, frequent erections, etc. To further illustrate in human terms, the androgenic properties of a steroid hormone are responsible for the increased growth of body hair, beard growth, deepening of the voice, increased production of sebaceous glands, development of the male sex organ, aggressiveness, libido, etc. Generally, the androgenic effects of a steroid are considered to be negative and often manifest themselves as unwanted “side effects”. Considerable effort has been expended to manufacture a steroid without the corresponding androgenic effect. However, this has never been achieved. Thus we are left with various compounds with their own unique anabolic to androgenic balance. The balance between the anabolic and androgenic properties of a given steroid can be important in your choice of very compound. Read that last sentence again. It’s importance to you will become clear in the following months when I present and discuss different anabolic steroids. For example, testosterone scores very high in both androgenic and anabolic properties while the steroids of the nandrolone family (think Deca-Durabolin, etc.) score high in its anabolic properties but relatively low in androgens. At first glance, you would come to the conclusion that the nandrolone family of steroids are a better choice than testosterone.

They are highly anabolic (good) and only moderately androgenic (the “bad stuff’). So I should use Deca over testosterone right? I only wish it were that easy. Hopefully, I will be able to bring you enough information in the coming months to make those decisions on your own. As you will learn in the coming months, the androgenic properties of a steroid are not altogether bad. Whatever their benefit, anabolic steroids are not a magic bullet. They are an aid that can be used during the conditioning of your animal and, more importantly, to assist in the recovery from injuries sustained during a match, kennel accident or, as they are conventionally used in veterinary medicine-for specific illnesses. Anabolic steroids will not make your dog game if your dog is not game, nor will they increase any existing gameness. But, with proper selection and usage, they may just give you the edge you need before hitting the box. Hopefully, I can bring to you some of the information you will need to make intelligent choices. Good luck and keep scratchin.

As a competitive powerlifter and aspiring dogman, I am exposed to many entertaining discussions on the subject of AAS. The lack of genuine information by athletes and dogmen alike is surprising. It is rare that a conversation about AAS does not contain some basic misunderstanding or outright fairy tale about what AAS really do-and can not do. So, let us start with the beginning. We will discuss how AAS work within the organism. What follows is a very difficult subject but I will try to present it as clearly and as simply as possible. You would require a Ph.D. to understand the complete technical explanation. Fortunately, for our needs, only a basic understanding of the process is necessary. Androgen sensitive tissue contains what is known as androgen receptors (AR). Basically, a receptor is a specific molecule on the surface or within the cytoplasm of a cell that recognizes and binds with other specific molecules. AR recognize and bind with AAS. The concentration of AR provides an indication of how sensitive the tissue is. AR are present in a number of organs and skeletal muscle. For example, the human prostrate may have up to 25 times more AR than skeletal muscle. This partially explains why the prostrate is susceptible to enlargement during AAS use. Now I want you to think of AR as either a young dog that isn’t started or a dog that is fully turned on. An AR either has an AAS bound to it and is thereby “turned on” or, it does not have an AAS bound to it, and is thereby “cold”. When AAS is transported to the muscle cell (a very complex process beyond the scope of this article), it binds to an AR and forms what is commonly referred to as a steroid-receptor complex. The steroid-receptor complex has a strong affinity for the nucleus of the cell. The complex is translocated into the nucleus and then binds to the cellular DNA. Once inside the nucleus, the steroid appears to enhance transcription of specific genes resulting in increased protein synthesis. It is also believed, though not fully understood by science, that catabolic (tissue breakdown) inhibition occurs. So, what did we just say there? Essentially, AAS bind with skeletal muscle cells and increase protein synthesis and quite possibly interferes with catabolism. By now, you should have a good understanding of why you should be thinking of AAS in terms of enhanced recovery and improved performance for your canine. The effect of this process is both anabolic and androgenic. Last month, we described in detail the meaning of anabolic and androgenic. Another interesting effect of AAS is the stimulation of the hormone erythropoietin (a glycoprotein hormone secreted chiefly by the kidney in the adult and by the liver in the fetus, which acts on stem cells of the bone marrow to stimulate red blood cell production). Red blood cells are responsible for transporting oxygen. Too good to be true right? Well, if it were such an easy deal, everyone would use AAS on their dogs and be successful. Unfortunately, with the positive effects of AAS there are corresponding negative “side effects”. This is why I preach that you research and learn as much as you can before using AAS on your dog. With proper knowledge, negative side effects can be minimized. The following is a list of commonly reported positive and negative effects of AAS use. The list is intended for human application but, as we pointed out last month, all too often the canine is used to study what afflicts and ails we humans so, many of the effects apply to both human and canine. But remember, as discussed last month, each AAS compound has its own distinct anabolic to androgenic properties. The following list encompasses all known effects of AAS in general. Not all of the following apply to any one particular AAS.

Commonly Reported Positive Effects

• Increased leanness / muscle definition

• Increased muscle mass / weight

• Increased strength

• Increased effectiveness of training

• Improved recovery rate

• Euphoria

• Increased aggressiveness

• Increased sex drive

Commonly Reported Negative Effects

Both Sexes

• Increased risk of mood disturbances including mania and depression

• Increased risk of psychosis

• Increased risk of aggressive acts which may injure self or others

• Increased risk of cardiovascular disease • Increased risk of liver disease and cancer

• Increased risk of kidney disease and cancer

• Acne

• Bad breath

• Decreased sex drive

• Baldness

• Water retention

• Muscle cramps

• Aching joints

• Increased risk of muscle tears

• Increased risk of tendon injuries

• Increased risk of nose bleeds

• Insomnia

• Decrease in immune system effectiveness

• Infertility

Men

• Increased risk of prostate enlargement and cancer

• Decreased testicular size

• Gynecomastia (growth of breasts)

Women

• Increased risk of cervical and endometrial cancer

• Increased risk of osteoporosis

• Irreversible enlargement of the clitoris

• Irreversible hoarsening and deepening of the voice

• Irreversible increase in facial and body hair

• Decreased breast size

• Amenorrhea

• Uterine atrophy

So where are we heading with all this? There will be many of you out there reading this saying to yourself that you don’t need AAS. You and your dogs did fine without them before, why do I need to mess around with them now? Why should I risk harming my dog? If asked, I would reply you have a valid point. Some of you may go even further and state AAS are for ex “muscleheads” and the pit is not a bodybuilding contest. Here, I would point out you have a fundamental misunderstanding of what AAS can do and that is the reason for this column. For those on the fence about this subject, let me leave you with some food for thought. In 1995, a study was conducted by the UCT Medical School in South Africa. Forty male rats were randomly divided into either a sedentary control group or an exercising group caged in specially designed running wheels in which the rats were able to run spontaneously. After 4 weeks, both groups were further divided into two groups receiving either nandrolone phenypropionate or saline. After 8 weeks, the rats receiving the AAS ran 41% longer. The study didn’t state the rats became 41% more muscular or, 41% heavier. The rats receiving the AAS ran 41% longer than those that did not receive AAS. Got your attention? Good. Because my opinion on AAS is irrelevant. Giving you the factual information needed to make your own informed decisions is.

When discussing AAS esters, we are broadly addressing the subject of “drug delivery” into an organism. Generally, there are three conventional forms of drug delivery; oral (tablets, capsules), topical/dermal (creams, ointments, patches) and injections. Specifically, we are addressing a component in the drug delivery of injectable AAS. Understanding esterification and the actions of specific esters will affect three critical decisions when administering AAS: “selection”, “dose” and “duration”. When you understand the actions of various AAS esters, your drug “selections” (choice of compound) will be more intelligent. Your understanding of esters will impact your strategy regarding “dose” (the amount of the drug administered) and “duration” (the length of time or “cycle” in which you administer the drug). Manipulating both “dose” and “duration” will be discussed at length in future columns. All AAS are chemical derivatives or “analogues” (a chemical compound with a structure similar to that of another but differing from it in respect to a certain component) of the male sex hormone, testosterone. Without esterification, testosterone has a very short biological half-life (the time required for a living tissue, organ or organism to eliminate one-half of a radioactive substance which has been introduced into it or simply, the time in which it takes the body to eliminate half of the AAS introduced into it). Testosterone’s short half-life poses two problems; (1) frequent administration of the drug would be required to have the desired effect and (2) it would be extremely difficult to maintain desired concentrations of the drug in the organism. These problems and others have been addressed by modifying oral steroids by alkylation and injectable steroids by esterification. Essentially, esterification of AAS slows its release from the injection site or depot (a body area in which a substance, e.g., a drug, can be accumulated, deposited, or stored and from which it can be distributed). AAS are injected intra-muscularly where a deposit forms and is released into the general circulation. Esterification makes an AAS less water soluble and increases its lipid (fat) solubility. This causes a deposit of the drug to form within the muscle. The release of the drug into the general circulation allows the drug to reach the desired androgen receptors (AR). Esterification of an AAS modifies its chemical structure to make it last longer in the body. See the illustration below for an example of esterification, or the modification, of the testosterone molecule. The example above illustrates the esterification of a testosterone molucule by adding a propionate ester chain. If you examine the two, you will see they are identical with the exception of the propionate ester chain. Esterification temporarily renders the AAS inactive. The esterification chain makes it impossible for the AAS to bind to an androgen receptor (AR). When not bound to an AR, the AAS cannot exert any activity in the body. As the body metabolizes the AAS, it removes the ester chain, allowing the AAS to bind with an AR. There are numerous esters in use today with more on the horizon as science makes drug delivery advances. Inasmuch as the type of ester determines its duration in the organism, you must have a passing familiarity with the various esters in order to make decisions regarding “selection”, “dose” and “duration”. The following are brief profiles of the common AAS esters in use today.

Acetate

Also referred to as Acetic Acid; Ethylic acid; Vinegar acid; vinegar; Methanecarboxylic acid. Acetate esters delay the release of a steroid for only a couple of days.

Propionate

Also referred to as Carboxyethane; hydroacrylic acid; Methylacetic acid; Ethylformic acid; Ethanecarboxylic acid; metacetonic acid; pseudoacetic acid; Propionic Acid. Propionate esters will slow the release of a steroid for several days.

Phenylpropionate

Also referred to as Propionic Acid Phenyl Ester. Phenylpropionate extends the release of active AAS a few days longer than propionate.

Isocarpoate

Also referred to as Isocaproic Acid; isohexanoate; 4-methylvaleric acid. Isocaproate is similar to enanthate in terms of release. The duration is shorter, with sustained AAS concentration levels of approximately one week.

Caproate

Also referred to as Hexanoic acid; hexanoate; n-Caproic Acid; n-Hexoic acid; butylacetic acid; pentiformic acid; pentylformic acid; n-hexylic acid; 1-pentanecarboxylic acid; hexoic acid; 1-hexanoic acid; Hexylic acid; Release duration is similar to isocaproate and enanthate.

Enanthate

Also referred to as heptanoic acid; enanthic acid; enanthylic acid; heptylic acid; heptoic acid; Oenanthylic acid; Oenanthic acid. Enanthate is one of the most popular testosterone esters. Enanthate will release AAS for approximately 10-14 days.

Cypionate

Also referred to as Cyclopentylpropionic acid, cyclopentylpropionate. Its release duration is almost identical to enanthate (10-14 days).

Decanoate

Also referred to as decanoic acid; capric acid; caprinic acid; decylic acid, Nonanecarboxylic acid. Release time up to one month.

Undecylenate

Also referred to as Undecylenic acid; Hendecenoic acid; Undecenoic acid. This ester is very similar to decanoate. Release duration is very similar (approximately 2-3 weeks).

Undecanoate

Also referred to as Undecanoic Acid; 1-Decanecarboxylic acid; Hendecanoic acid; Undecylic acid. Not a common ester. Only known use is the nandrolone preparation Oynabolan, and oral testosterone undecanoate (Andriol). Release duration is approximately 2-3 weeks.

Laurate

Also referred to as Dodecanoic acid, laurostearic acid, duodecyclic acid, 1-undecanecarboxylic acid, and dodecoic acid. Longest releasing ester used in commercial steroid manufacture. However, longer acting esters do exist. Release duration of Laurate is close to one month.

Finally, even though esterification of an AAS increases its duration in the organism, fluctuations in drug hormone levels are still an issue. This is where the fine art of manipulating dose and duration are crucial. In the coming months, we will provide you with more pieces to the puzzle. As I stated in Introduction to Anabolic Steroids Part I. we do not intend to promote the use of AAS, illegal or otherwise. However, acknowledging that AAS are a part of the dog game and that knowledge is power, we will provide you with as much information as possible. Starting last issue, I shared with you a scientific abstract that studied the effects of AAS administration to a control group of rats and its positive effect on endurance. Each issue, I will attempt to provide you with at least one relevant study for your review. This issue, I present to you a study demonstrating the potential application of AAS in treating muscle trauma. This would seem to be of particular interest to those of us “active” in the square. As I have stated before, the potential benefits of AAS are not limited to the “keep”.

The effect of an anabolic steroid (nandrolone decanoate, 20 mg/kg) and a corticosteroid (methylprednisolone acetate, 25 mg/kg) on healing muscle injured with a drop-mass technique in a reproducible muscle contusion injury model in the rat was studied. Healing was determined by measuring active contractile tension in each muscle and histologic analysis. At day 2, the corticosteroid group showed significant improvement in both twitch and tetanic strength relative to the controls. At day 7, this effect was reversed and the corticosteroid muscles were significantly weaker than the control muscles, but there was still no significant effect seen in the anabolic steroid group. At day 14, the corticosteroid muscles were totally degenerated, with disorganized muscle fiber architecture. The anabolic steroid muscles were significantly stronger in twitch, and a similar trend was seen in tetanus relative to control muscles. The results indicate that in an animal model corticosteroids may be beneficial in the short term, but they cause irreversible damage to healing muscle in the long term, including disordered fiber structure and a marked diminution in forcegenerating capacity. Anabolic steroids may aid in the healing of muscle contusion injury to speed the recovery of force-generating capacity. Although anabolic steroids are considered renegade drugs, they may have an ethical clinical application to aid healing in severe muscle contusion injury, and their use in the treatment of muscle injuries warrants further research.

First, a brief review of esterifî- cation in general (For a more detailed review, see Volume 13, Issue 6). Esterifîcation of an injectable AAS slows its release from the injection site by decreasing its water solubility and increasing its lipid (fat) solubility. Remember, testosterone, without an ester chain, has a very short biological half-life. With esterifîcation, a deposit of the compound forms intramuscularly at the injection site and is released into the bloodstream and metabolized by the organism. The speed at which the AAS is released into the bloodstream and metabolized is largely dependent on the type of ester. The rate at which a drug metabolizes is often referring to as its half-life or simply, the time in which it takes the organism to metabolize half the compound. In Volume 13, Issue 6, we profiled numerous esters for your reference. Notwithstanding pharmacology’s estimations of half-life and drug clearance times, the clock or calendar does not govern metabolism. In other words, it is, by its very nature, an inexact science. The published half-life estimates of various compounds are just that-estimates. However, these estimates are sound enough to guide your dosage strategy and provide you with the means for estimating and managing blood concentrations of a given compound. To illustrate the importance of proper dosage management, I have constructed two imaginary AAS cycles (FIG 1 and FIG 2). FIG 1 represents a 10-week cycle. The imaginary AAS administered has an estimated halflife of 7 days (Remember, half of our AAS is metabolized every seven days; therefore we lose available AAS at an approximate rate of 50% every seven days). Because the potency of most veterinary AAS compounds are 50 milligrams per milliliter (1cc), we will assume a dosage of 50 milligrams, or one cc, every 7 days. FIG 1 clearly illustrates that blood concentrations of the compound did not peak and are not constant until week number five. Applying our theoretical AAS cycle to a keep, the dog in question does not receive the complete ergogenic benefit of the compound until week number five when blood concentrations are predicted to be highest. This would not appear to be problematic until you consider that exogenous (meaning, developing or originating outside the organism) administration of AAS suppresses endogenous (meaning, growing from within) production of testosterone.

The first four weeks of our imaginary cycle could amount to a mere replacement dose of normally occurring endogenous testosterone production. A replacement dose would not yield any ergogenic benefit. Alternately, the suppression of endogenous production could be such that the resulting concentrations of testosterone are less than previous endogenous output. This would obviously yield an undesirable effect. The latter scenario is clearly an example of where the potential to harm your animal is possible when working with AAS-particularly when the goal of AAS administration is increasing recovery and performance. At the very best, the initial four weeks of this example show the dog working for four weeks under less than desirable conditions. To achieve an ergogenic benefit one must administer a dosage high enough and frequent enough to replace and exceed endogenous testosterone production. We will address the subject of endogenous testosterone suppression secondary to exogenous administration of AAS in the next future issue. should now be clear that dosage management can profoundly affect blood concentrations of a compound over the course of a cycle-to the benefit or detriment of the animal. FIG 2 represents an alternative to the model illustrated in FIG 1, This cycle assumes a blood concentration of approximately 100 milligrams of active AAS is the amount necessary to replace and exceed endogenous testosterone production, thereby producing an ergogenic result. Frequency of administration is the same as FIG 1-every seven days. Significantly, although our maintenance dose remained at 50 milligrams per week, we immediately achieved the desired blood concentration of the compound by administering 100 milligrams in week number one followed by a maintenance dose of 50 milligrams per week. Further, the desired blood concentration is constant for the full ten weeks. The first four weeks of our theoretical keep is no longer potentially compromised as illustrated in FIG 1. The potential improvement over the cycle illustrated in FIG 1 is significant when considered in the context of working a dog during a keep. Using the cycle in FIG 1, your dog potentially loses the first four weeks of conditioning. Depending on whether your dosage management amounted to a replacement dose or unwanted suppression together with the stress of the keep, your dog may never recover sufficiently to make a good showing come match time. Think for a moment; how many dogmen and women have unknowingly made such a mistake and for reasons unknown, their dog just was not right come ShowTime. Well, I stated in the beginning that if you use AAS incorrectly, you would cause harm to your dog. I have just provided you with one example of the potential harm you can cause your dog by mismanaging dosage strategy. I hope the two examples of dosage management provide you with some useful strategies in the future. Dozens of dosage strategies exist and, as the saying goes, “performance and mileage may vary”. The dosage strategy that is right for your dog depends on the particulars of your keep and the needs of your dog.

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Our example illustrated that the animal was not receiving the desired peak concentrations of AAS until week 5 of the keep or cycle. I hope the illustration and example got your attention. I doubt anyone would want to work his or her dog under anything but optimal conditions. The entire purpose of our keep is to optimize all conditions in favor of our animal. This is why we use supplements and superior feed during this time. It is also why some of us use AAS during this time. However, merely missing the maximum benefits of AAS administration is the least of our challenges. I have heard many a fairy tale about AAS causing a dog to “run hot” or not perform well. I can almost guarantee you the problem do not lie with AAS alone, but rather with incorrect AAS selection, improper dosage management and failure to monitor and manage important blood and liver profile markers in the animal! Unfortunately for the novice, successful use of AAS is a bit more complicated than loading the syringe and shooting your dog once a week. Yet, that is the very approach that is most common-even among experienced dogmen and conditioners. Even with this uninformed approach, many will still succeed with AAS. This just illustrates how powerful these compounds can be.

Successful administration and management of AAS encompasses multiple considerations; dosage management, blood profiles (red cell count in particular), liver enzymes, etc. Although these issues will be addressed in the future, I want to impress upon you that until you have a fundamental understanding of how to manage all the basic issues successfully, you are playing Russian Roulette with your keep. The failure to manage the important variables is the number one reason for failure with AAS. One of the most common questions I receive regarding AAS usage in dogs is:

How much? Specifically, how much AAS per day, per week, per keep, is the right amount? I am going to give you my opinion based on all of my knowledge; everything I have read on the subject, my consultations with experts in the field and, personal experience and observation. As the saying goes, “opinions are like rectums, everyone has one.” However, at least I will give you an informed opinion and not a guess.

Many erroneously believe the question of dosage or “how much” would have a relatively simple an – swer. Simply put it does not and I will explain some of the reasons why. First, although many AAS com – pounds are available for human and/ or veterinary consumption, drug companies and licensed profession – als do not specifically manufacture or routinely prescribe their use to achieve a performance enhancing benefit. In other words, the manu – facturers of AAS, and in all likelihood your veterinarian, are not manufac – turing or prescribing AAS with your dog’s performance in mind. They are manufactured, both for human and veterinary use, to treat specific medical conditions. Thus, the dos – age instructions accompanying the package insert (assuming you have a package insert and have not ob – tained the AAS from a black market source) are not entirely suitable for the purposes of eliciting a perfor – mance advantage. I say “not entirely” suitable because some benefit can be received. However, an optimal benefit equal to a substantial perfor – mance improvement will not occur.A reasonable dosage for purposes of improving your dog’s performance is 1 milligram of AAS per kilo of lean bodyweight per day for male dogs, half that amount, or, .5 milligrams per kilo of lean body – weight for female dogs. Very impor – tant: When I state “per day”, I mean, “amount of AAS released per day”. This is where knowledge of drug halflives are important (see our last issue for an in depth discussion of drug half lives). Drug half-life estimations are required to make reasonable dosage predictions on a per day, per week basis. This information is crucial.

Simply, if you have a male dog with a lean bodyweight of 47 lbs., then its weight in kilos is approximately 21 kilos. If you cannot determine the dog’s lean body mass, its true pit weight should suffice as a reasonable estimate. The target dosage for this dog would be 21 milligrams of released AAS per day or, 147 milligrams per week. For example, let us assume our AAS has a half-life of ten days and we administer an injection of 100 milligrams. Approximately 50 milligrams of AAS metabolizes in the first ten days based on its halflife. Thii equals approximately 5 milligrams of AAS released per day. Thus, over the first seven days, the initial 100-milligram injection will release approximately 35 milligrams of AAS. Notice my continuous use of the word “approximate”. Those of you whom read our last installment know I use the word “approximate” because AAS half-lives are estimations and not absolute. The halflives of many drugs are the subject of disagreement among scientists. However, the existing estimates are more than accurate enough for our purposes. Now we have tackled the “how much” or dosage question. However, other challenges remain; our first challenge is to achieve peak AAS levels quickly so as not to compromise any portion of our keep. This can be accomplished one of two ways; First solution, by initially administering any one of various short acting AAS compounds that deliver very quickly into the organism or, by beginning your AAS cycle before your actual keep work. The second solution is feasible and simple but one I do not recommend. Starting your AAS cycle before your keep, or even during pre-keep, means administering AAS to your dog for a longer period. This is not necessarily in the best interest of your animal. It unnecessarily increases the length of the AAS cycle and the corresponding period during which you may have to manage potential problems associated with AAS administration. The shorter the duration of the cycle, the less side effects, if any, you are likely to encounter. A close correlation between length of cycle and unwanted side effects exists. As the cycle grows longer, unwanted side effects are more likely to manifest. Furthermore, organisms like humans and animals have a tendency to be adaptive to many drugs. After a certain period, the organism’s adaptive responses begin to treat certain drugs in a fashion similar to a foreign entity; the enzymatic processes of the organism become more efficient in an effort to degrade the drugs more effectively. In essence, prolonged AAS administration is vulnerable to the law of diminishing returns. Greater quantities and longer cycles are not a good solutionespecially with AAS. In my opinion, the first solution is the way to go and we will discuss this in detail in the near future. Our second challenge, and one of the more technically complex issues, is managing the androgenic to anabolic ratio of the AAS we select. This relates to another “most frequently asked” question : Which specific AAS to use? I know this is confusing to many of you. You are saying to yourself, “why can’t I just shoot this damn dog up with some deca every week?” Well, the answer is you can. Moreover, if done correctly, your dog will probably respond favorably to a degree. That does not mean that this approach is best nor is it without disadvantages. There is a better approach. As we discussed in previous issues, each AAS compound has its own distinct androgenic to anabolic ratio and its corresponding advantages and disadvantages. Czech scientists have determined that if anabolism (growth, repair, etc.) is the goal of AAS administration, then the ideal ratio of anabolic to androgenic compounds is 70% anabolic to 30% androgenic. Although this target ratio can be flexible, based on the science currently available it is a credible and meaningful target. It is, without question, a better approach than haphazardly administering any AAS and hoping for the best. In our next installment, we will continue to explore the complexities of dosage management and discuss anabolic to androgenic ratios and selection of AAS further. I sincerely hope that those of you whom follow this column closely are beginning to appreciate the complexities of the subject matter and the depth of knowledge required for administering AAS successfully. I will continue to do my very best to provide you with the information necessary for you to make the best possible decisions for your dog.

I t just seems some of us can not rid our minds of the bulging over-inflated muscles of the bodybuilding world when the subject of AAS arises. Instead of Ben Johnson and his world record performance in the 100 meters, we think Arnold Schwarzenegger. Instead of the Olympic Cyclist or Marathon runner, we think of Lee Haney (seven times Mr. Olympia-not quite as famous as Arnold). Too many of us mistakenly limit our perception of AAS to “muscle hypertrophy” (hypertrophy means, “the enlargement or overgrowth of an organ or part due to an increase in size of its constituent cells) without including “performance” enhancement. Of course, AAS successfully induces muscle hypertrophy-if that is the goal of administration. However, athletes in track and field, cycling, running, swimming, etc., have a long history of successfully using AAS to enhance “performance”. Before we get to this issue’s topic matter, allow me to debunk the misunderstandings expressed by my friend-whom I happen to hold in the highest regard for his knowledge of canine nutrition and conditioning. First, there is no published material contraindicating AAS for endurance type training. There is not even any anecdotal real-world evidence. In past issues, we have discussed in detail how AAS improves recovery and raises work capacity. Manipulated properly, these two factors can greatly influence endurance training. The error in my friend’s thinking was not putting more strength into a hard biting, barnstorming type dog but rather his thinking that AAS would hinder performance for the “marathon” or extended match. His second mistake was that AAS would cause the dog to become heavier due to muscle gain. This is simply misleading and I will briefly explain why. For an organism to gain weight, caloric consumption must be greater than caloric depletion. In other words, the body needs to “save” more than it “spends”. It is a rather simple equation no matter how much mumbo jumbo you read about carbohydrates, protein, fat and the various fad diets that abound today. Caloric surplus equals weight gain. Caloric deficit equals weight loss. If you properly manage workload, hydration (water intake) and feed rations, AAS will not affect this equation. AAS will certainly enhance the metabolism of certain nutrients like protein (enhanced protein synthesis and positive nitrogen balance). AAS may even affect the basic metabolic rate of the organism. Although AAS certainly increases extra-cellular fluid volume resulting in an average weight gain in human subjects of about 3%, this is not especially problematic and its successful management is not too difficult. However, AAS does not change the basic caloric rule as stated earlier. Bodybuilders are able to gain incredible amounts of muscle mass because they ingest an equally incredible amount of calories along with AAS. Simply put, you cannot gain weight or muscle without an excess of calories-with or without AAS. Notwithstanding, if you fail to manage feed, work load and hydration (water), you may have a weight problem. However, the challenge of successful weight management while using AAS is not much more difficult than without AAS. As we all know, weight management and bringing a dog to the box on the agreed weight is one of the most difficult tasks to meet. With AAS, weight management merely requires some extra attention on your part. However, to believe that administering AAS to your dog will cause your dog to become muscle bound and heavy is just plain wrong. Furthermore, numerous studies have demonstrated that endurance type training has a negative impact on lean body mass (muscle). Simply put, you cannot run ten miles per day and build bigger muscles. It just does not happen. Given the amount of treadmill work, roadwork, etc., in a typical keep, your chances of significantly increasing muscle mass are zero. Enough said! Let us move on to the main topic. If you are serious about properly using AAS in your keep, something we reported last issue should have stuck in your mind; “Czech scientists have determined that if anabolism (growth, repair, etc.) is the goal of AAS administration, then the ideal ratio of anabolic to androgenic compounds is 70% anabolic to 30% androgenic.” To reach this “Holy Grail”, it often becomes necessary to stack or combine two or more AAS. Most AAS compounds available are either too androgenic or too anabolic to give optimum results. However, not only do we desire to reach the ideal androgenic/anabolic ratio, we want to combine the correct AAS, in precise amounts, to induce “synergy”. The technical definition of Synergism is ” the joint action of agents so that their combined effect is greater than the algebraic sum of their individual effects”. Simply put, synergism is the successful combination of two different substances that when combined, work better than either substance alone. For instance, by combining 100 milligrams of Drug A with 100 milligrams of Drug B, the combined effect of the two together is greater than 200 milligrams of Drug A or Drug B alone. Unfortunately, it is not as simple as combining equal amounts of two are more drugs. One must understand each compound’s unique properties, strength and half-life to combine the compounds correctly. A more accurate example might be combining 60 milligrams of Drug A with 80 milligrams of Drug B. Then we would need to determine the frequency of administration for each drug. I never said this stuff was going to be simple! As you now know, each parent AAS compound has its own distinct anabolic to androgenic ratio, esters, potency, half-life, etc. In addition to these variables, AAS act on the organism at the cellular level other than just via the Androgen Receptors (AR). Science is only beginning to understand the multiple cellular actions and influences of AAS. Without getting into a detailed scientific explanation, it is important to understand that certain AAS compete against each other at the cellular level and certain AAS compliment each other. In the former, we have what amounts to a waste of your hard-earned cash and good drugs and, in the latter, we have “synergyw-a big difference! The challenge to achieving synergy between two or more AAS is selecting complimentary AAS and then properly managing the dose and of each drug. Why is this important you ask? Because every AAS has both positive and negative characteristics and no single AAS alone is better than the correct two combined. For example, a common drug like nandrolone (Deca), widely regarded as one of the safest and most effective AAS, is lacking alone but combined with a complimentary AAS and voila! You have magic. Since the inception of this column, we have covered a lot of ground. I understand AAS is a complex and confusing subject matter. Let us review what we have given you so far:

01 in our first installment, we provided you with a basic introduction to AAS and important terminology like anabolic and androgenic. We emphasized the anabolic actions of AAS like recovery and tissue regeneration and its potential usefulness during the keep;

02 Part 2 covered the role of the Androgen Receptors (AR) and both the positive and negative effects of AAS. We shared a study demonstrating that AAS increased running duration by 41% for a group of tested rats;

03 Part 3 discussed AAS esterification and its impact to “selection”, “dose” and “duration”. The concept of half-life is explained and various esters are profiled;

04 In part 4 and 5 we illustrated two sample dosing strategies illustrating the potential pitfalls of under-dosing;

05 Finally, last issue we provided a basic dosage strategy for male and female dogs-essentially “how much” AAS to administer.

Our more attentive readers may have noticed that not once have I addressed the application of oral AAS. This is not by mistake. Oral AAS are generally referred to as being “alkylated”. The only exception that comes to mind is Testosterone Undecanoate (an oral preparation of testosterone absorbed via the lymphatic system into the systemic circulation) and methenolone acetate. Common examples of alkylated oral AAS include Dianabol (D-bol), Anadrol-50, Oxandrolone (Oxandrin), etc. All oral AAS are alkylated with the exception of the two referenced above. There are three general types of modification of testosterone: esterification of the 17 beta-hydroxyl group (type A), alkylation at the 17 alpha-position (type B), and modification of the A, B, or C ring structures (chemistry mumbo jumbo). Most compounds actually contain combinations of ring structure alterations and either 17 alpha-alkylation or esterification of the 17 beta-hydroxyl. Generically, alkalization of an oral AAS protects the active ingrediente from the digestive system until it can reach the blood stream. However, the metabolic pathway of oral alkylated AAS is through the liver. Although sometimes exaggerated and certainly dose sensitive, the liver toxicity of oral AAS is well documented. Your liver is like a garbage disposal system for your blood. It acts as a filter. During times of stress and increased workload-like during a keep, your dog’s liver is working overtime processing metabolic waste, tissue breakdown, etc. The increased physical activity, feed, supplementation, etc., of a keep places increased demands on your dog’s liver. The additional burden of oral AAS is the last thing your dog’s liver needs during a keep. Remember a certain 4x winner that lost while “acting funny” and running hot? Supposedly was “rubbed” but was not. Well it turned out that dog had liver damage. Poor liver function will certainly compromise performance. This is why I do not recommend oral AAS to your dog. Administration of oral AAS to your dog is simply foolish inasmuch as suitable alternatives like injectables exist and are readily available. This is why we do not address the subject of oral AAS. I am not representing that oral AAS cannot be used safely and effectively in the absence of underlying liver disease or stress. However, administering oral AAS adds more variables that require management and monitoring. Liver values require monitoring (additional blood work and costs) and additional supplementation to protect the liver are needed. Simply, the risks and burdens outweigh the benefits in my mind. Like all AAS, oral AAS are especially unsuitably for novice experimentation.

I see dogs lose, in my opinion, because they did not have the enough strength and cardiovascular conditioning to win over a lesser dog. I have seen too many dogs blow hot ten minutes into a match to count. Hell, these dogs could not be much worse coming in off the chain. It is difficult to believe a conditioned dog, otherwise healthy and parasite free, can run hot in a mere ten minutes. I do not mean a bit “winded”. I am talking flat-out huffing and puffing from which they do not recover. A number of things could be the culAs I write this, I am reflecting on some matches I saw at a southern convention last month. I saw four matcheseight dogs. I saw a remarkable kill in one. However, I am not reflecting on the wins, the losses or the particular dogs and dogmen. I am reflecting on conditioning. The more matches I see, the more I see the better dog lose. By now, I guess I should not be surprised but I am. prit; not enough work (doubtful given the manner in which some dogmen work their dogs), not enough of the right type of work or, too much work. I know there are many other reasons why a dog may run hot but I am referring strictly to conditioning. My opinions regarding “not enough work” and the “wrong kind of work” are irrelevant to this column.

This column is not “The BodyGuard’s Keep”. However, I do want to discuss the negative effects of “too much work” and how to avoid it. When I say “too much work” I am referring to a condition commonly referred to as “over-trained”. What does this have to do with using AAS during the keep? Proper AAS administration can be like buying an insurance policy against over-training your dog. Believe me, once you understand how detrimental an over-trained state is to your dog, you will quickly realize that, within the confines of a six week keep, your dog is in serious trouble if it ever reaches this state. First, let us examine what is occurring to a mammal when it reaches a state of overtraining. The term “overtraining” is almost laughably simplistic when you consider that it is medically classified a neuro-endocrine disorder. Sound a bit more serious? Well, it is. In human athletes, science has studied this syndrome with exercise physiologic, psychological, and biochemical laboratory testing. These studies have shown decreased performance in exercise testing, decreased mood-state, and, in some, increased Cortisol. In previous columns, we have discussed that Cortisol is a catabolic hormone-not good. In addition, various studies have shown a decrease in testosterone, altered immune status, and an increase in the markers that measure muscle tissue destruction. In general, the over-trained body has a decreased ability to repair itself even during rest. Scientist generally believe that there are two forms of the overtraining syndrome. The sympathetic form is common to sprint and power sports and the parasympathetic form is common to endurance sports. In the parasympathetic form, there may be a lower heart rate during a given workload. Athletes training with a heart rate monitor may notice that they cannot sustain the workout at their usual “set point”.

Another difference between the two forms lies in resting heart rate. In the sympathetic form, the resting heart rate is elevated. However, in the parasympathetic form the resting heart rate is decreased. I want youto read that last sentence again. To the uninitiated, a decreasing resting heart rate is a sign of good conditioning and it is-except when the body is over-trained. There is one cure for over-training syndrome-rest. Rest is easy for the human athlete. However, sufficiently resting a canine in the middle of a sixweek keep is a challenge with little room for error. Simply, you may not have sufficient time for the dog to recover and be in a position to resume its work schedule to make progress or peak leading up to match time. Unfortunately, in the limited time of six weeks, over-training is more likely to occur closer to match time. Obviously, the best solution is never to reach this state but the line separating overtraining from progress is a thin one and easily crossed. I have heard the arguments from dogmen that the canine athlete can take much more stress and workload than a human can. Generally, I believe this to be true. However, the canine, being a mammal, is most certainly susceptible to this syndrome. Our endocrine systems are almost identical. With proper administration of AAS, you can buy insurance against over-training. At the very least, AAS will increase your margin for error. As we have discussed in the past, AAS raises work capacity and decreases the time needed to recover from work. The key to making progress in any type of program is sufficient recovery. I hope each of you is beginning to understand that AAS is not merely a “muscle drug”.

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