akn
Musclechemistry Member
by Mike Arnold
Most bodybuilders tend to view estrogen as a fat storage hormone, but its actions on adipose tissue are not so simple. In excessive amounts it can indeed lead to body fat acquisition, but in quantities compatible with male physiology it has a positive effect on bodyfat, making it both more difficult to store fat and easier to lose fat. It does this by up-regulating the Ce3 gene, which is responsible for mediating lipase independent lipolysis (the release of fatty acids from fat cells). This is the same mechanism through which growth hormone stimulates fat loss and the first step in the fat loss process. Now that we are aware of estrogen’s effect on both glycogen synthesis and fat loss, are there any practical applications we can take away from this?
First and foremost, I want to discourage bodybuilders from going crazy with the A.I’s, although what is considered optimal (in terms of estrogen levels) will vary depending on the circumstances. I already touched on the issue of off-season estrogen levels earlier in this article (see Part #1), but I have not yet addressed estrogen levels in contest prep. Conventional wisdom dictates that we should attempt to lower estrogen levels as much as possible during the last few weeks of prep in order to become as dry as possible. Some have even gone so far as to over-suppress estrogen levels during the earlier stages of prep, as they believe this will eliminate estrogen’s pro-fat storage effects and allow them to get leaner easier.
While this all sounds plausible in theory it doesn’t work out that way in the real world. For one, as we have already seen, lowering estrogen levels too far will actually have a negative effect on fat loss by reducing lipase independent lipolysis via the down-regulation of Ce3. For this reason, regardless of whether it is off-season or pre-contest, I recommend keeping estrogen levels around 30 pg/ml. This doesn’t change until the bodybuilder enters the later stages of prep—the final 2-3 weeks. At that point it would be beneficial to lower estrogen to around 15 pg/ml. This will allow the individual to eliminate any estrogen-induced subcutaneous water retention, while still leaving enough estrogen floating around to facilitate adequate glycogen synthesis. At this point I have experimented with several different estrogen control strategies during prep and this approach seems to produce the best results.
When it comes to muscle growth, few endogenous molecules have as profound of an effect as IGF-1. Stimulating hypertrophy directly and indirectly through at least a half-dozen different mechanisms, IGF-1 is considered one of the big dogs of the PED world. In fact, the main reason most people use growth hormone is because of its ability to substantially increase IGF-1 levels. Anyway you look at it, IGF-1 is an important part of the muscle growth process…and one more reason not to over suppress estrogen production.
While most estrogen-mediated effects are pretty cut and dry in terms of what to expect, its impact on IGF-1 mediated muscle growth is less clear. Some studies show elevations in IGF-1 levels with estrogen supplementation, while others show no increase. Still, some others show a decrease in IGF-1 levels. This discrepancy is due to the route of administration, rather than some unknown variable causing test results to fluctuate. In reality, only oral administration has been shown to adversely affect IGF-1 production (and increase IGFBP-1 levels), while estrogen which is present as a result of aromatization has a positive effect on IGF-1 levels and no affect on binding proteins.
There is some bad news, though. Even when estrogen is produced via aromatization, estrogen tends to reduce local IGF-1 expression in muscle tissue. In other words, although IGF-1 levels may go up, the muscles’ ability to respond to IGF-1 is diminished. Think of it as a form of desensitization—same principle, but a different process. Although both of these effects (IGF-1 elevation and reduced gene expression) are relatively mild in terms of intensity, we can’t really weigh them in the balance simply because we have no way of obtaining an accurate measurement for either of them. Although this might sound like a big deal it’s real not. As mentioned earlier, not only is this effect very mild, but it will be counteracted through AAS use—a class of drugs that nearly every estrogen-concerned bodybuilder is using. I am sure you’re waiting for an explanation, so here goes. Many steroids, including DHT, decrease the expression of a gene referred to as Grb10. This gene is a negative regulator of IGF1, so by suppressing it, the body’s ability to respond to IGF-1 is enhanced. This directly counteracts estrogen’s mild negative effect on IGF-1 expression, making it null and void. So basically, anyone who uses steroids is unknowingly eliminating the issue.
Another cool effect associated with estrogen is the ability to enhance growth potential by increasing androgen receptor density. In laymen’s terms, this means that estrogen increases the number of androgen receptors in muscle tissue. Being that AR activation is the main pathway through which steroids initiate their beneficial effects on muscle growth, the more ARs we have, the more AAS one can effectively utilize before reaching receptor saturation. While most people aren’t going to use an amount of AAS capable of filling up all available receptors, there are plenty of bodybuilders out there who will and do. In these cases, an increase in AR density can pay dividends by allowing the individual to take advantage of larger doses of anabolics.
Out of all the positive effects estrogen has on our bodybuilding efforts, this next one is my favorite. I am talking about the ability to increase muscle strength. Recent studies reveal that this effect is not mediated by an increase in muscle size, but through a direct effect on muscle function, which researchers refer to as an improvement in muscle “quality”. More specifically, estrogen improves a muscle’s ability to generate force by causing myosin to bind to actin more strongly during the contraction process. Evidence reveals that this effect is almost certainly mediated through estrogen receptor binding, rather than some poorly understood or yet to be identified non-genomic effect. While an increase in muscle strength is not necessarily correlated with muscle growth, it can stimulate growth indirectly by allowing the individual to lifter heavier weights within the hypertrophy rep range. As we all know, heavier weights leads to increased muscular stress, muscular stress then leads to a greater growth stimulus, and a greater growth stimulus then leads to increased hypertrophy.
Despite possessing a much lower levels of testosterone in the bloodstream, research has repeatedly shown that women experience less muscle damage after weight training and tend to recover more quickly than their male counterparts. When attempting to determine the underlying cause for this gender specific anomaly, researchers traced the cause back to…you guessed it…estrogen. Acting as a muscle protectant, estrogen helps prevent exercise induced muscle damage through 3 different mechanisms: a reduction in muscle oxidative damage, reduced production of pro-inflammatory compounds, and the increased production of heat shock proteins.
When it comes to inhibiting oxidation, one of the ways in which estrogen benefits us is by increasing the expression of genes involved the glutathione metabolic pathway that protect cells from oxidative damage. Of these, the most influential of the bunch of is the Gpx3 gene. When estrogen up-regulates this particular gene, it not only prevents muscle cell oxidation, but also improves skeletal muscle insulin sensitivity by mediating the antioxidant effect of PPARg. To sidestep for a second, a recent report revealed that myosin (one of the two main contractile proteins in muscle fiber) is susceptible to oxidation and that this oxidation significantly impairs contractile function. Therefore, up-regulating Gpx3 also preserves muscle strength. As you can see, estrogen enhances strength through multiple mechanisms, making it an important hormone for strength athletes and all others attempting to maximize strength levels.
In addition to inhibiting oxidation, estrogen also blunts the production of interleukin-6 and interleukin-8; two inflammatory compounds produced in response to weight training and which are largely responsible for the development of delayed onset muscle soreness (D.O.M.S) the day after a hard workout. Heat shock proteins, which are activated by various forms of muscle stress (ex. heat, exercise, trauma, etc.), provide a further level of protection by facilitating muscle protein assembly and working to maintain protein structure. Through the manipulation of all these processes (oxidation, inflammation, and HSP activation), estrogen can protect muscles from damage, accelerate recovery rate, increase muscular strength, and improve growth rate.
While I have touched on several of estrogen’s most important bodybuilding related benefits, this article is by no means exhaustive. Rather, my purpose here was to provide the reader with a general idea of just how extensive this hormone’s role is in the overall bodybuilding process. Going forward, we should dispense with silly notions which peg estrogen as a decidedly “female” sex steroid and rather, view it as it really is—a unisex hormone with a wide variety of beneficial and even pro-male effects. So long as levels remain within a male appropriate range, feminization will remain a non-issue, just as much as testosterone does not promote masculinization in women when levels remain in a female appropriate range. Never the less, the over-suppression of estrogen should be strictly avoided, as it provides no benefits and a multitude of unwanted side effects.
Most bodybuilders tend to view estrogen as a fat storage hormone, but its actions on adipose tissue are not so simple. In excessive amounts it can indeed lead to body fat acquisition, but in quantities compatible with male physiology it has a positive effect on bodyfat, making it both more difficult to store fat and easier to lose fat. It does this by up-regulating the Ce3 gene, which is responsible for mediating lipase independent lipolysis (the release of fatty acids from fat cells). This is the same mechanism through which growth hormone stimulates fat loss and the first step in the fat loss process. Now that we are aware of estrogen’s effect on both glycogen synthesis and fat loss, are there any practical applications we can take away from this?
First and foremost, I want to discourage bodybuilders from going crazy with the A.I’s, although what is considered optimal (in terms of estrogen levels) will vary depending on the circumstances. I already touched on the issue of off-season estrogen levels earlier in this article (see Part #1), but I have not yet addressed estrogen levels in contest prep. Conventional wisdom dictates that we should attempt to lower estrogen levels as much as possible during the last few weeks of prep in order to become as dry as possible. Some have even gone so far as to over-suppress estrogen levels during the earlier stages of prep, as they believe this will eliminate estrogen’s pro-fat storage effects and allow them to get leaner easier.
While this all sounds plausible in theory it doesn’t work out that way in the real world. For one, as we have already seen, lowering estrogen levels too far will actually have a negative effect on fat loss by reducing lipase independent lipolysis via the down-regulation of Ce3. For this reason, regardless of whether it is off-season or pre-contest, I recommend keeping estrogen levels around 30 pg/ml. This doesn’t change until the bodybuilder enters the later stages of prep—the final 2-3 weeks. At that point it would be beneficial to lower estrogen to around 15 pg/ml. This will allow the individual to eliminate any estrogen-induced subcutaneous water retention, while still leaving enough estrogen floating around to facilitate adequate glycogen synthesis. At this point I have experimented with several different estrogen control strategies during prep and this approach seems to produce the best results.
When it comes to muscle growth, few endogenous molecules have as profound of an effect as IGF-1. Stimulating hypertrophy directly and indirectly through at least a half-dozen different mechanisms, IGF-1 is considered one of the big dogs of the PED world. In fact, the main reason most people use growth hormone is because of its ability to substantially increase IGF-1 levels. Anyway you look at it, IGF-1 is an important part of the muscle growth process…and one more reason not to over suppress estrogen production.
While most estrogen-mediated effects are pretty cut and dry in terms of what to expect, its impact on IGF-1 mediated muscle growth is less clear. Some studies show elevations in IGF-1 levels with estrogen supplementation, while others show no increase. Still, some others show a decrease in IGF-1 levels. This discrepancy is due to the route of administration, rather than some unknown variable causing test results to fluctuate. In reality, only oral administration has been shown to adversely affect IGF-1 production (and increase IGFBP-1 levels), while estrogen which is present as a result of aromatization has a positive effect on IGF-1 levels and no affect on binding proteins.
There is some bad news, though. Even when estrogen is produced via aromatization, estrogen tends to reduce local IGF-1 expression in muscle tissue. In other words, although IGF-1 levels may go up, the muscles’ ability to respond to IGF-1 is diminished. Think of it as a form of desensitization—same principle, but a different process. Although both of these effects (IGF-1 elevation and reduced gene expression) are relatively mild in terms of intensity, we can’t really weigh them in the balance simply because we have no way of obtaining an accurate measurement for either of them. Although this might sound like a big deal it’s real not. As mentioned earlier, not only is this effect very mild, but it will be counteracted through AAS use—a class of drugs that nearly every estrogen-concerned bodybuilder is using. I am sure you’re waiting for an explanation, so here goes. Many steroids, including DHT, decrease the expression of a gene referred to as Grb10. This gene is a negative regulator of IGF1, so by suppressing it, the body’s ability to respond to IGF-1 is enhanced. This directly counteracts estrogen’s mild negative effect on IGF-1 expression, making it null and void. So basically, anyone who uses steroids is unknowingly eliminating the issue.
Another cool effect associated with estrogen is the ability to enhance growth potential by increasing androgen receptor density. In laymen’s terms, this means that estrogen increases the number of androgen receptors in muscle tissue. Being that AR activation is the main pathway through which steroids initiate their beneficial effects on muscle growth, the more ARs we have, the more AAS one can effectively utilize before reaching receptor saturation. While most people aren’t going to use an amount of AAS capable of filling up all available receptors, there are plenty of bodybuilders out there who will and do. In these cases, an increase in AR density can pay dividends by allowing the individual to take advantage of larger doses of anabolics.
Out of all the positive effects estrogen has on our bodybuilding efforts, this next one is my favorite. I am talking about the ability to increase muscle strength. Recent studies reveal that this effect is not mediated by an increase in muscle size, but through a direct effect on muscle function, which researchers refer to as an improvement in muscle “quality”. More specifically, estrogen improves a muscle’s ability to generate force by causing myosin to bind to actin more strongly during the contraction process. Evidence reveals that this effect is almost certainly mediated through estrogen receptor binding, rather than some poorly understood or yet to be identified non-genomic effect. While an increase in muscle strength is not necessarily correlated with muscle growth, it can stimulate growth indirectly by allowing the individual to lifter heavier weights within the hypertrophy rep range. As we all know, heavier weights leads to increased muscular stress, muscular stress then leads to a greater growth stimulus, and a greater growth stimulus then leads to increased hypertrophy.
Despite possessing a much lower levels of testosterone in the bloodstream, research has repeatedly shown that women experience less muscle damage after weight training and tend to recover more quickly than their male counterparts. When attempting to determine the underlying cause for this gender specific anomaly, researchers traced the cause back to…you guessed it…estrogen. Acting as a muscle protectant, estrogen helps prevent exercise induced muscle damage through 3 different mechanisms: a reduction in muscle oxidative damage, reduced production of pro-inflammatory compounds, and the increased production of heat shock proteins.
When it comes to inhibiting oxidation, one of the ways in which estrogen benefits us is by increasing the expression of genes involved the glutathione metabolic pathway that protect cells from oxidative damage. Of these, the most influential of the bunch of is the Gpx3 gene. When estrogen up-regulates this particular gene, it not only prevents muscle cell oxidation, but also improves skeletal muscle insulin sensitivity by mediating the antioxidant effect of PPARg. To sidestep for a second, a recent report revealed that myosin (one of the two main contractile proteins in muscle fiber) is susceptible to oxidation and that this oxidation significantly impairs contractile function. Therefore, up-regulating Gpx3 also preserves muscle strength. As you can see, estrogen enhances strength through multiple mechanisms, making it an important hormone for strength athletes and all others attempting to maximize strength levels.
In addition to inhibiting oxidation, estrogen also blunts the production of interleukin-6 and interleukin-8; two inflammatory compounds produced in response to weight training and which are largely responsible for the development of delayed onset muscle soreness (D.O.M.S) the day after a hard workout. Heat shock proteins, which are activated by various forms of muscle stress (ex. heat, exercise, trauma, etc.), provide a further level of protection by facilitating muscle protein assembly and working to maintain protein structure. Through the manipulation of all these processes (oxidation, inflammation, and HSP activation), estrogen can protect muscles from damage, accelerate recovery rate, increase muscular strength, and improve growth rate.
While I have touched on several of estrogen’s most important bodybuilding related benefits, this article is by no means exhaustive. Rather, my purpose here was to provide the reader with a general idea of just how extensive this hormone’s role is in the overall bodybuilding process. Going forward, we should dispense with silly notions which peg estrogen as a decidedly “female” sex steroid and rather, view it as it really is—a unisex hormone with a wide variety of beneficial and even pro-male effects. So long as levels remain within a male appropriate range, feminization will remain a non-issue, just as much as testosterone does not promote masculinization in women when levels remain in a female appropriate range. Never the less, the over-suppression of estrogen should be strictly avoided, as it provides no benefits and a multitude of unwanted side effects.
