1MoreRep
MuscleChemistry Registered Member
Learn everything you will ever need to know about testosterone and how it works. Find out the basics, how it reacts in the body, the difference between steroids and testosterone and much more...
<!-- Social Header Widget --><!-- The goal in this article is to prime the body for an intensive two week program of twice-a-day training and hardcore eating that could result in a shocking amount of new muscle. But don't jump into this program...
-->By: Virtual Muscle Sep 10, 2003
From Rogue To Vogue
If you had asked a doctor 10 years ago about bumping testosterone into the high-normal range to enhance one's physique, chances are slim you would have gotten a positive response. "Testosterone is bad for you," he would probably say. "It will shrink your grapes to raisins, give you liver disease and make you backhand your Grandma!"
Enter 1996 and the legal availability of androstenedione (a-dione) and other prohormones. For the first time, "steroids" were legally available over the counter and testosterone became user-friendly. It could not only enhance strength and muscle size, but also improve body composition, bone density, libido, and immunocompetence. Some research even suggested T could make you smarter! Unfortunately, as supplement sales skyrocketed, so did marketing hyperbole. And so, too, did the bull about which company had the most potent prohormone concoction and how effective these "legal steroids" were.
If you are tired of being confused by "diones", "diols" and "19-nor" something-or-others - and want to know the real benefits and risks associated with testosterone boosting - read on. The information presented may just clear some of that fog in your noggin'.
The Basics
Testosterone is a 19-carbon steroid hormone produced primarily by the Leydig cells of the testes (in men) and the ovaries (in women). Smaller amounts are produced in the adrenal glands of both sexes. As a "steroid", testosterone belongs to the androgen class of hormones that also includes dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA), androstenedione, and androstenediol. Six other classes of steroid hormones exist, including estrogens (the bane of male bodybuilders), progestins (some female contraceptives are made of these), mineralocorticoids (which help control water balance), glucocorticoids (mainly anti-inflammatory compounds), vitamin D, and bile acids.
In men, approximately seven mg of testosterone is produced each day, and blood levels range between 300 and 1000 ng/dL (10-28 nmol/L). Females, on the other hand, produce about 1/15th of this amount, leading to average blood levels of only 25 to 90 ng/dL (1-2.5 nmol/L). All steroid hormones are derived from the sterane ring structure, composed of three hexane (6 carbon) rings and one pentane (5 carbon) ring.
A-diol has the same ring structure as testosteron.
In healthy humans, the "rate-limiting" step in testosterone biosynthesis is the conversion of cholesterol into a hormone called pregnenolone. This hormone is then first converted to either DHEA or progesterone before being further degraded in a stepwise fashion to testosterone. Schematically, the two possible pathways look like this: (Enzymes have been omitted for clarity.)
After testosterone is secreted into the bloodstream, 96-98 percent is bound to proteins called albumin and globulin. This binding is thought to serve three purposes: 1) it makes testosterone soluble for transport within the blood, 2) it protects testosterone from degradation by the liver and kidneys, and 3) it serves as a reservoir or storage depot that can be used to dampen fluctuations in plasma testosterone.
The two to four percent not bound to plasma proteins is known as "free testosterone" and is thought to represent the biologically active fraction of the hormone; in other words, the amount that is capable of interacting with cells to cause physiological changes. And although recent data suggest this is most likely an oversimplification, we'll leave that discussion for another time.
Regulation of testosterone levels is governed by two factors: the total amount of testosterone in the blood, and the binding capacity of the plasma proteins. Obviously, as binding capacity goes up blood levels of free testosterone go down. Not surprisingly, certain drugs (anabolic-androgenic steroids, insulin, etc.) and perhaps nutritional supplements (like avena sativa, urtica dioica, etc.) can reduce the binding capacity of the blood and result in higher free-testosterone levels. [Editors' Note: Nutrition is also a factor in testosterone regulation; see our March discussion on this topic in Experiments vs. Experience.]
There is also mounting evidence that some types of pollution and pesticides can do the opposite. So much for running sprints in downtown Detroit! Also, testosterone production from the testes occurs the entire period of fetal development until about 10 weeks after birth. Then the gears screech to a stop until puberty - a time when men know all-too well their T levels are screaming.
This is a time when young men really blow past their female counterparts in body weight and muscularity - and get drawn toward sports like high school football, along with other aggressive pastimes. Sadly in many ways, testosterone levels begin to decline between the third and fourth decade of life. And by 80 (if we make it that long) we are only one-third the man we used to be, testosterone-wise.
The physiological actions of testosterone in males are far reaching. For example:
Of the "free" testosterone that interacts at the tissue level, much of it is converted within the cells to DHT - a more potent androgen - by the enzyme 5-alpha reductase. In the prostate, for example, this conversion is thought to be necessary for physiologic effects. Other tissues (like the epididymis, vas deferens, seminal vesicles, skeletal muscle, and bone) lack the 5-alpha reductase enzyme and therefore are thought to respond to testosterone directly.
The conversion of testosterone into estrogens (estriol, estrone and estradiol) is governed by the aromatase enzyme complex and occurs mainly in the liver, brain and fat tissue. Some bodybuilders attempt to avoid / reduce the conversion of testosterone to DHT or estrogens by maintaining low bodyfat and using drugs or nutritional supplements that block 5-alpha reductase and aromatase. Chrysin, saw palmetto and indole-3-carbinol are three examples of legal plant-derived supplements that may maximize testosterone levels by minimizing its conversion to DHT and estrogens. Unfortunately, the bio-availability of many "bioflavanoid" compounds when ingested is poor. Some cutting-edge supplement companies have trick "delivery systems" that attempt to address this problem.
It is important to recognize that blood levels of testosterone - all hormones for that matter - represent a dynamic balance between biosynthesis (which occurs in a pulsatile fashion) and biodegradation. As mentioned, the testes, adrenals and ovaries are responsible for testosterone biosynthesis, while the liver and kidneys are responsible for its biological degradation and excretion. So, for instance, increases in plasma testosterone commonly observed following a hard weight-training session are not just the result of increased production of testosterone from the testes, but also from a reduction in its clearance (blood flow to the liver and kidneys is reduced during exercise). Make sense?
This balance between synthesis and breakdown also make a single blood testosterone value extremely difficult to interpret. As noted decades ago, testosterone levels rise and fall throughout the day; therefore a single testosterone value could represent a peak or valley on the daily testosterone roller coaster.
Anabolic-Androgenic Steroids
So what is the difference between testosterone and anabolic-androgenic steroids (AAS)? Well, while testosterone is produced naturally in the body, AAS are synthetic analogs of testosterone that were first used medically in the US around the time My Three Sons and The Honeymooners were beaming with popularity.
<!-- <img src=catdeca.jpg align=right> -->By synthetic, I mean AAS are synthesized by guys in lab coats who, for most of their lives, have been taking science and chemistry courses. Several "relatively safe" AAS are used clinically to treat osteoporosis and muscle-wasting disorders. These are nandrolone decanoate (Deca Durabolin) and oxandrolone (Anavar), respectively. Examples of more potent, but potentially dangerous, AAS are fluoxymesterone (Halotestin), trenbolone acetate (Parabolan), methandrostenolone (Dianabol), and oxymetholone (Anadrol). In general, injectable steroids are more potent, safer and remain in the system longer than oral steroids. There are, however, a few exceptions.
Potential Side Effects From AAS Abuse
Though you may already be aware of potential side effects from testosterone abuse (note I said abuse and not use), here they are again: lowered HDL-cholesterol levels (good cholesterol), testicular atrophy, reductions in sperm count, prostate enlargement, liver damage (primarily with oral steroids that have been modified with a 17-alkyl substitution), menstrual irregularities, suppression of endogenous hormone levels (like LH and T), development of palpable breast tissue in men (also known as gynecomastia), clitoral enlargement, and acne. Whether an individual using AAS will develop any of these side effects is difficult to predict because of the complex interaction between factors like drug type, dosage, duration of use, and individual (genetic) differences. Suffice to say there are safer ways to boost testosterone levels and gain an edge in the gym. More importantly, there are legal ways - at least for now.
<!-- Social Header Widget --><!-- The goal in this article is to prime the body for an intensive two week program of twice-a-day training and hardcore eating that could result in a shocking amount of new muscle. But don't jump into this program...
-->By: Virtual Muscle Sep 10, 2003
From Rogue To Vogue
If you had asked a doctor 10 years ago about bumping testosterone into the high-normal range to enhance one's physique, chances are slim you would have gotten a positive response. "Testosterone is bad for you," he would probably say. "It will shrink your grapes to raisins, give you liver disease and make you backhand your Grandma!"
Enter 1996 and the legal availability of androstenedione (a-dione) and other prohormones. For the first time, "steroids" were legally available over the counter and testosterone became user-friendly. It could not only enhance strength and muscle size, but also improve body composition, bone density, libido, and immunocompetence. Some research even suggested T could make you smarter! Unfortunately, as supplement sales skyrocketed, so did marketing hyperbole. And so, too, did the bull about which company had the most potent prohormone concoction and how effective these "legal steroids" were.
If you are tired of being confused by "diones", "diols" and "19-nor" something-or-others - and want to know the real benefits and risks associated with testosterone boosting - read on. The information presented may just clear some of that fog in your noggin'.
The Basics
Testosterone is a 19-carbon steroid hormone produced primarily by the Leydig cells of the testes (in men) and the ovaries (in women). Smaller amounts are produced in the adrenal glands of both sexes. As a "steroid", testosterone belongs to the androgen class of hormones that also includes dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA), androstenedione, and androstenediol. Six other classes of steroid hormones exist, including estrogens (the bane of male bodybuilders), progestins (some female contraceptives are made of these), mineralocorticoids (which help control water balance), glucocorticoids (mainly anti-inflammatory compounds), vitamin D, and bile acids.
In men, approximately seven mg of testosterone is produced each day, and blood levels range between 300 and 1000 ng/dL (10-28 nmol/L). Females, on the other hand, produce about 1/15th of this amount, leading to average blood levels of only 25 to 90 ng/dL (1-2.5 nmol/L). All steroid hormones are derived from the sterane ring structure, composed of three hexane (6 carbon) rings and one pentane (5 carbon) ring.
A-diol has the same ring structure as testosteron.
In healthy humans, the "rate-limiting" step in testosterone biosynthesis is the conversion of cholesterol into a hormone called pregnenolone. This hormone is then first converted to either DHEA or progesterone before being further degraded in a stepwise fashion to testosterone. Schematically, the two possible pathways look like this: (Enzymes have been omitted for clarity.)
- Cholesterol » pregnenolone » progesterone » androstenedione» T
Cholesterol » pregnenolone » DHEA » androstenediol » T
After testosterone is secreted into the bloodstream, 96-98 percent is bound to proteins called albumin and globulin. This binding is thought to serve three purposes: 1) it makes testosterone soluble for transport within the blood, 2) it protects testosterone from degradation by the liver and kidneys, and 3) it serves as a reservoir or storage depot that can be used to dampen fluctuations in plasma testosterone.
The two to four percent not bound to plasma proteins is known as "free testosterone" and is thought to represent the biologically active fraction of the hormone; in other words, the amount that is capable of interacting with cells to cause physiological changes. And although recent data suggest this is most likely an oversimplification, we'll leave that discussion for another time.
Regulation of testosterone levels is governed by two factors: the total amount of testosterone in the blood, and the binding capacity of the plasma proteins. Obviously, as binding capacity goes up blood levels of free testosterone go down. Not surprisingly, certain drugs (anabolic-androgenic steroids, insulin, etc.) and perhaps nutritional supplements (like avena sativa, urtica dioica, etc.) can reduce the binding capacity of the blood and result in higher free-testosterone levels. [Editors' Note: Nutrition is also a factor in testosterone regulation; see our March discussion on this topic in Experiments vs. Experience.]
There is also mounting evidence that some types of pollution and pesticides can do the opposite. So much for running sprints in downtown Detroit! Also, testosterone production from the testes occurs the entire period of fetal development until about 10 weeks after birth. Then the gears screech to a stop until puberty - a time when men know all-too well their T levels are screaming.
The physiological actions of testosterone in males are far reaching. For example:
- Growth of the penis, scrotum and testes during puberty
- Enlargement of the larynx (voice box) that results in a deepening of the voice
- Formation of functional sperm
- Stimulation of hair growth - especially in the pubic area, chest, face, and, sometimes, the back
- Increases in skin thickness and darkness
- Increases in libido (sex drive)
- Increases in basal (resting) metabolic rate
- Increases in red blood cell number and total blood volume
- Promotion of sodium and water retention in the kidneys
- Increases in muscle protein synthesis resulting in increased muscle mass
- Reductions in muscle glycogen breakdown during exercise
- Increased calcium retention in bone
- Decreased growth of hair on top of the head
- Increased activity of the sebaceous (sweat) glands, sometimes resulting in acne
- Promote a narrowing and strengthening of the pelvis
Of the "free" testosterone that interacts at the tissue level, much of it is converted within the cells to DHT - a more potent androgen - by the enzyme 5-alpha reductase. In the prostate, for example, this conversion is thought to be necessary for physiologic effects. Other tissues (like the epididymis, vas deferens, seminal vesicles, skeletal muscle, and bone) lack the 5-alpha reductase enzyme and therefore are thought to respond to testosterone directly.
The conversion of testosterone into estrogens (estriol, estrone and estradiol) is governed by the aromatase enzyme complex and occurs mainly in the liver, brain and fat tissue. Some bodybuilders attempt to avoid / reduce the conversion of testosterone to DHT or estrogens by maintaining low bodyfat and using drugs or nutritional supplements that block 5-alpha reductase and aromatase. Chrysin, saw palmetto and indole-3-carbinol are three examples of legal plant-derived supplements that may maximize testosterone levels by minimizing its conversion to DHT and estrogens. Unfortunately, the bio-availability of many "bioflavanoid" compounds when ingested is poor. Some cutting-edge supplement companies have trick "delivery systems" that attempt to address this problem.
It is important to recognize that blood levels of testosterone - all hormones for that matter - represent a dynamic balance between biosynthesis (which occurs in a pulsatile fashion) and biodegradation. As mentioned, the testes, adrenals and ovaries are responsible for testosterone biosynthesis, while the liver and kidneys are responsible for its biological degradation and excretion. So, for instance, increases in plasma testosterone commonly observed following a hard weight-training session are not just the result of increased production of testosterone from the testes, but also from a reduction in its clearance (blood flow to the liver and kidneys is reduced during exercise). Make sense?
This balance between synthesis and breakdown also make a single blood testosterone value extremely difficult to interpret. As noted decades ago, testosterone levels rise and fall throughout the day; therefore a single testosterone value could represent a peak or valley on the daily testosterone roller coaster.
Anabolic-Androgenic Steroids
So what is the difference between testosterone and anabolic-androgenic steroids (AAS)? Well, while testosterone is produced naturally in the body, AAS are synthetic analogs of testosterone that were first used medically in the US around the time My Three Sons and The Honeymooners were beaming with popularity.
<!-- <img src=catdeca.jpg align=right> -->By synthetic, I mean AAS are synthesized by guys in lab coats who, for most of their lives, have been taking science and chemistry courses. Several "relatively safe" AAS are used clinically to treat osteoporosis and muscle-wasting disorders. These are nandrolone decanoate (Deca Durabolin) and oxandrolone (Anavar), respectively. Examples of more potent, but potentially dangerous, AAS are fluoxymesterone (Halotestin), trenbolone acetate (Parabolan), methandrostenolone (Dianabol), and oxymetholone (Anadrol). In general, injectable steroids are more potent, safer and remain in the system longer than oral steroids. There are, however, a few exceptions.
Potential Side Effects From AAS Abuse
Though you may already be aware of potential side effects from testosterone abuse (note I said abuse and not use), here they are again: lowered HDL-cholesterol levels (good cholesterol), testicular atrophy, reductions in sperm count, prostate enlargement, liver damage (primarily with oral steroids that have been modified with a 17-alkyl substitution), menstrual irregularities, suppression of endogenous hormone levels (like LH and T), development of palpable breast tissue in men (also known as gynecomastia), clitoral enlargement, and acne. Whether an individual using AAS will develop any of these side effects is difficult to predict because of the complex interaction between factors like drug type, dosage, duration of use, and individual (genetic) differences. Suffice to say there are safer ways to boost testosterone levels and gain an edge in the gym. More importantly, there are legal ways - at least for now.
