by Mike Arnold
In attempting to define the bodybuilding physique there are two physical characteristics that stand out above all the rest. One of these is extreme muscular development. As the calling card for bodybuilders worldwide, an exaggerated level of muscle mass is usually the first thing people notice when viewing a bodybuilder for the first time. But this isn’t the only feature vying for attention. Bodybuilders also display an almost alarmingly low level of bodyfat, particularly when in contest shape. This is crucial for allowing them to display the unique appearance they are known for and is the primary differentiating factor between those who train for looks and those who train for function (i.e. powerlifters, strongmen, etc). In fact, one could even argue that in the absence of this distinctive trait, the individual is no longer a bodybuilder at all.
While not everyone can walk around in the off-season at 6% bodyfat (at least not without great difficulty), the point here is that one must exhibit an sufficiently low level of bodyfat in order to be considered a bodybuilder. This prerequisite all but ensures rigorous attention to diet, cardio, and the occasional use of fat-loss drugs/supplements, but regardless of whether we are getting ready for a show or just trying to maintain a respectable off-season appearance, no one wants to sacrifice muscle mass in order to achieve this. Although there may be certain instances in which this scenario is unavoidable (starting contest prep with too much bodyfat, for example), for the most part it is an unnecessary evil.
There are numerous different factors which influence our ability to retain lean mass, but only a few of them are completely within our control. One of these is the use of fat loss drugs (from this point forward I will refer to all OTC, prescription, and blackmarket products as “drugs”). Unfortunately, not all fat loss drugs are created equal when it comes to their effects on lean mass retention. Some of them have a positive effect on tissue growth/maintenance, while others have a neutral effect, and some others have a negative effect. These differences do not necessarily make one better than the other, but it does require us to be aware of their effects and utilize only those products which are ideally suited to our own particular needs.
Oddly, some of the most frequently used fat loss drugs are those which have a potentially detrimental effect on muscle mass. This includes nearly all stimulants and T3. Stimulant-based drugs are probably the single most popular category of fat-burner on the market…and for good reason. Not only are they effective, but they are cheap, usually legal, and provide an energizing high that many find helpful when trying to overcome the energy deficit that accompanies low-calorie dieting. To top things off, they even help reduce food intake/cravings via appetite suppression.
On the surface they seem like an almost perfect complement to one’s fat loss program…and in many ways they are. But, as with most drugs, they also cause their fair share of problems. When used responsibly this is a non-issue, but chronic/long-term use can induce a plethora of unwanted effects which includes, but is not limited to: cortisol elevation, vasoconstriction, adrenal fatigue, dietary insufficiency via appetite suppression, and sleep cycle dysregulation. All of these have a negative effect on lean mass retention/accumulation, but it doesn’t stop there.
While stimulants have been shown to increase the rate of lipolysis (the release of fatty acids from fat cells into the bloodstream), much of their fat-burning potency is attributable to an overall increase in calorie burning; an effect which is largely indiscriminate in nature. In other words, they are not very selective when it comes to their preferred source of calorie burning, making them more likely to draw calories from muscle tissue than many other types of fat loss drugs. This makes them a comparatively poor choice for almost anyone trying to build muscle tissue, or for those who struggle to hold onto lean mass while dieting. Keep in mind that I am talking about chronic use here. In general I see no problem with intermittent use during growth phases, but if you are someone who needs to take stimulants before every workout just to train hard, get up in the morning, or just to function during the day, then you have much bigger problems than fat loss to worry about.
T3 is similar to stimulants in that it also burns fat primarily by increasing metabolic rate, while retaining the same indiscriminate, calorie burning nature of stimulants. The only time I feel off-season T3 use is justifiable is when the individual has a below average metabolism and is using the drug to normalize T3 levels, not to push them into the supraphysiological range. As effective as T3 is for fat loss, it is one of the most surefire ways to kill your gains, especially when employing moderate to high doses. A great example would be a client I worked with late last year. In this particular case his prior coach had him using an absolutely atrocious dose of T3 (150-200 mcg/day if I remember correctly) during the off-season so that he could “stay lean” as he built muscle mass. Unfortunately, this is not what happened. Rather than growing while he kept the fat off, he actually started to shrink without making any significant reductions to his bodyfat percentage. In his own words “I became a smaller version of myself”.
So, when he first approached me complaining of a lackluster rate of progress, diagnosing the problem was easy. To make a long story short, this individual put on about 40 pounds of lean tissue within just 2 months of working together, while maintaining the same low bodyfat percentage he had started with (probably around 8%). While he was overly impressed with his progress and extremely grateful for the guidance he received, the truth is that I did very little to earn such praise. The dramatic growth he experienced was attributable almost entirely to a single change—the removal of T3 from his program, rather than any profound advice provided on my part. For the first time in over a year his body was actually able to use the calories he was eating to synthesize new muscle tissue, rather than cannibalizing his muscle in order to support his self-induced, hyper-metabolic state.
Now, I don’t want to come across as sounding like I am anti-stimulant/T3 because I am not. I think both drugs have several effective applications and I often recommend them as part of a more comprehensive fat loss program. However, I just don’t think they are a wise choice (in most cases) for the off-season bodybuilder trying to maximize muscle growth. So, rather than discuss the potential applications that these drugs have to offer, I want to focus on an area of research that has garnered a lot of attention in recent years. More specifically, I want to talk about the appropriate use of fat loss drugs during growth phases. As most of you know, maintaining a ripped appearance while adding muscle new muscle tissue is an exceedingly difficult task; one usually only possible for those with the most gifted genetics. Fortunately, there are many things we can do in order to make this whole process significantly easier, but if you are expecting some type of new or revolutionary insight into the realm of fat loss, you are going to be sorely disappointed. The truth is that most of what I will cover here today has been known for decades, yet the majority tends to dismiss this information in favor of a more radical approach—often to their own detriment. For those of you who want to improve your ability to stay lean while building muscle mass, you may want to consider adopting the recommendations provided below.
In short, there are a number of products available today that provide both body fat reducing and growth promoting effects without any acute or long-term toxicity. Some of them even impart notable health benefits. Perhaps the most well known of these drugs is growth hormone. Although extremely complex in its actions, GH’s fat loss effect is mediated mainly through its ability to increase lipolysis, while its IGF-1 elevating effect is responsible for the bulk of its growth promoting effects. Regardless, GH has proven to be a valuable addition to just about any bodybuilding program…and it doesn’t take much to begin noticing its benefits. As little as 3 iu daily has been shown to be effective for eliciting noticeable improvements in body composition, while higher doses will provide the same benefits in a more rapid, exaggerated fashion.
Although exogenous growth hormone has long been considered the Gold Standard for elevating growth hormone/IGF-1 levels, it is not the only option available. GH peptides/secretagogues are also a viable alternative. In fact, a secretagogue like MK-677 (which stays active for 24 hours and is equivalent to roughly 3-4 iu of GH per day in terms of production) can provide effects on par with exogenous growth hormone. It is also significantly less costly than growth hormone, which will help reduce the blow to your bank account. For many individuals it will end up being the most sensible choice. Regardless of the source, growth hormone is one of the best possible options for minimizing fat gain as you add lean mass.
Traditionally, bodybuilders have focused on diet, training, cardio, and also the manipulation of hormones when attempting to get /stay lean. As mentioned above, growth hormone has long been part of the bodybuilder’s fat loss arsenal, but when it comes to the manipulation of other endocrine hormones, most of them, outside of T3/T4, have received comparatively little attention. This is a mistake, as our body composition isn’t determined by a single molecule, but by a panoply of tightly regulated, inter-related hormones. The more of these hormones we can manipulate in our favor, the less likely we are to store calories as bodyfat, thereby bringing us one step closer to becoming the muscle building, fat destroying machine we all want to be. To this end both insulin and cortisol management is critical.
When insulin first hit the scene bodybuilders viewed it mostly as a muscle building agent, while relatively little emphasis was placed on its negative effect on fat cells. Things remained this way for a little while…until people started to realize they were getting fat. You see, insulin is a double-edged sword in that it not only promotes recovery and growth, but it also stimulates fat storage. The more of this hormone we are exposed to, the fatter we will get (assuming all other variables are equal). This is because insulin has a direct, negative effect on fat cell function by inhibiting lipolysis. In laymen’s terms, this means that it orders fat cells to stop releasing stored fat. However, insulin’s effect on fat cells is not unique. As the body’s primary storage hormone, insulin signals multiple cell types (fat, muscle, brain, etc) to not only accept incoming glucose, but to stop currently stored fatty acids from being released into the bloodstream. Needless to say, this makes fat loss much more difficult.
This is also the reason why low-carb diets tend to burn bodyfat more quickly than those which contain larger amounts of carbs—because carbohydrates are insulinogenic by nature. They increase blood glucose levels, which in turn stimulates the pancreas to secrete insulin as a means of blood sugar regulation. When muscle and fat cells come in contact with this newly secreted insulin, a transporter protein known as Glut-4 (which is located inside muscle and fat cells) rises to the cell surface and immediately shuttles any available glucose inside the cell. When this glucose is absorbed by muscle cells it promotes glycogen replenishment, accelerates recovery rate, increases performance, and leads to bigger, fuller muscles. But when it is absorbed by fat cells it is converted to fatty acids for future use (i.e. stored as bodyfat).
Furthermore, the more insulin that insulin receptors come in contact with (which are located in muscle, fat, etc), the less sensitive they become to its actions. This is called insulin resistance. As a result, the pancreas must produce more insulin in order to transport an equal amount of glucose inside the cells. Why is this bad for fat loss? It’s really simple and can be summed up in the following sentence. Muscle cells become resistant to insulin’s signal (i.e. they lose sensitivity) more quickly than fat cells! This means that long after our muscle cells have stopped efficiently absorbing glucose, our fat cells are still doing a wonderful job, which is the exact opposite of what we want. In the end, a larger percentage of glucose ends up getting absorbed by our fat cells and converted to fat. So, if we want to make it as easy as possible for our body to lose fat, we have to keep our overall insulin sensitivity as high as possible, so that our muscles’ capacity to absorb glucose is never diminished. This is the only way to minimize the amount of glucose that gets absorbed by our fat cells.
When first learning that we must minimize overall insulin levels in order to improve our ability to stay lean, some bodybuilders express concern that this will have potential negative ramifications on muscle growth. They figure that by reducing levels of such a powerful anabolic and anti-catabolic hormone, that their body’s muscle building machinery will be weakened, resulting in impaired growth. On the surface this logic seems to make sense…until one realizes this is not necessarily true. In fact, chronically elevated insulin levels, whether it takes place through excessive pancreatic production or irresponsible exogenous administration, can have the exact opposite effect. This is because insulin resistance makes it more difficult for our muscles to absorb glucose, it reduces the rate of protein synthesis via the decreased phosphorylation of insulin-dependent enzymes, and increases proteasomal protein degradation. When it comes to reaping maximum benefits from insulin (either exogenous or endogenous), it all comes down to how well our bodies respond to the hormone, rather than how much we are able to pump into our system. Not only can we grow more quickly and stay leaner by doing things this way, but it is a much healthier-safer approach and also less likely to result in aesthetic imbalances (Note: visceral fat storage, which results in stomach distension, is caused by insulin resistance).
Earlier I addressed a particular conundrum that most of us face at one point or another during our bodybuilding journey—attempting to stay lean while maximizing muscle growth. Inevitably, many have found that trying to accomplish both at once results in one or the other (and sometimes both) being compromised. But rather than accept this plight as an unalterable, in-born physiological limitation, I wanted to explore some of the measures that could be taken in order to help make this whole process a little bit easier.
Eventually, I ended up on the topic of insulin sensitivity and its role in bodyfat management. I concluded by asking the reader how ewe could manipulate this hormone to our advantage. But before answering this question, I encourage anyone who hasn’t yet read Part #1 to go back and do so, as we are picking up right where we left off without re-laying any of the groundwork. With that said, what can we do to help improve this vital component of metabolic health? The most obvious course of action is decrease our carb intake, but for those who require a lot of carbs in order to maximize muscle growth, this approach will only hinder muscle gains. This is not something most bodybuilders are interested in.
Fortunately, there are a number of things we can do in order to accomplish this goal, but when it comes to employing drugs/supplements there are literally 100’s of compounds which have been clinically proven to provide insulin sensitizing effects. Not all of these are readily available to the general public, but this is of no concern, as there are plenty of effective options at our disposal. Of these, metformin and berberine may be the most potent. Although metformin is available by prescription only, both drugs are pretty much equal when compared on a mg to mg basis. They are also inexpensive, especially metformin, which costs less than $10 per month even without insurance. Although I prefer berberine (mostly because I believe it provides greater number of health benefits), I think both drugs are great options for anyone looking to improve their insulin sensitivity via OTC/pharmaceutical means. In my opinion, nearly everyone should be using some type of insulin sensitizer, especially during the off-season when consuming large quantities of carbohydrates. With all the benefits that increased insulin sensitivity has to offer (we didn’t even scratch the surface), it would be foolish to bypass this category of supplementation simply because you don’t want to invest a few extra dollars into your supplement regimen.
Along with insulin, cortisol is another hormone that we need to keep tabs on (this is especially true if we are dealing with heightened levels of stress at work, home, etc). For most of us, stress is a daily reality that we just can’t get away from…and you don’t have to be dealing with a divorce, job loss, or the death of a loved one in order to be afflicted with elevated cortisol levels. Even moderate stress can result in a significant boost in cortisol production, leading to impaired fat loss and crippling your ability to respond to growth stimuli. But what exactly does cortisol do that is so bad? A lot! While this hormone is absolutely essential to the maintenance of human life, excess production results in a barrage of negative physiological effects in a multitude of areas relevant to bodybuilders.
First off, cortisol promotes fat gain by interfering with thyroid function. It does this by both lowering overall thyroid output and hindering the conversion of T4 to T3 (the more active form of the hormone). It also decreases insulin sensitivity via an increase in blood glucose concentrations and by inhibiting the translocation of Glut-4. What about muscle growth? Well, it messes with amino acid metabolism in just about the worst possible way—by promoting protein breakdown (the destruction of muscle tissue) and also by stopping essential amino acids from entering the muscle cell (if aminos can’t get into the muscle, they can’t recover and grow). It would be bad enough if cortisol caused just one of these side effects, but causing both at once is nothing short of an all-out assault on muscle growth. Making matters worse is that cortisol acts as an indirect vasoconstrictor by increasing sensitivity to the adrenal hormones epinephrine and norepinephrine, which are themselves potent vasoconstrictors. This reduces blood flow to muscles, resulting in diminished muscle pumps and a potential decrease in nutrient delivery. Any way you look at it, cortisol is an anti-bodybuilding hormone, promoting both muscle loss and fat gain.
When it comes to cortisol, eliminating the hormone is not wise—unless you want to die, but for all others the proper management of this hormone involves a delicate balancing act that brings levels down into the low-normal range without over-suppression. While cortisol levels are affected by virtually any type of stress (physical, mental or emotional), as well as diet, drugs, various hormones, and many other things, there are a few OTC products that have been proven effective for reducing cortisol levels without overdoing it. This is critical. Some old-school bodybuilding drugs, such as Cytadren, developed a reputation for causing severe cortisol suppression and have since fallen out of favor, but this hasn’t stopped some bodybuilders from continuing to experiment with the drug—oftentimes with disastrous results. In addition to its potent cortisol lowering properties, it is also known for causing dramatic cortisol rebound upon discontinuation, which can stimulate significant muscle loss while the body fights to restore homeostasis. These days few bodybuilders use the drug not only because of its poor availability, but because we have learned that taking such extreme measures are unnecessary. Of all the OTC products available today, 7-Keto DHEA and phosphatidylserine are two of the most noteworthy.
Both have been clinically shown to provide significant benefits in terms of cortisol management without causing any of the negative side effects associated with stronger pharmaceutical preparations. Typical doses involve 200 mg of 7-ketho DHEA (split into two evenly divided doses), and phosphatidylserine at 600 mg/day (split into 2-3 equally divided doses).
Estrogen management is another area of supplementation that most bodybuilders are pretty well educated in, but the drug is usually employed as a means of avoiding certain cosmetic side effects (i.e. gyno and water retention) rather than avoiding estrogen’s negative effect on bodyfat levels. In many instances, as long as the individual isn’t experiencing an unacceptable amount of sub-q water retention or starting to develop gynecomastia, they don’t really care what their estrogen level is. However, estrogen tolerance can vary tremendously from one individual to the next, with some people avoiding gyno even when their estrogen levels have climbed into the supraphysiological range. But just because you may be avoiding certain side effects, it does not necessarily mean your fat cells aren’t being negatively affected. Elevated estrogen levels, even when in the lower-end of the supraphysiological range, still tend to stimulate lipogenesis (the formation of bodyfat) and increase estrogen receptor density. This is one of the main reasons why women tend to carry more fat than men, particularly in areas like the hips glutes, thighs, and breasts. Don’t be fooled into thinking that just because you don’t resemble a water-balloon or have gyno that estrogen is not negatively affecting your ability to stay lean.
In order to avoid estrogen-induced fat gain, some have gone so far as to reduce their estrogen levels as far as possible. This is another example of something that might seem like it makes sense on the surface, but which is actually counterproductive. Estrogen is an odd hormone in that both too much or too little will have a negative effect on body fat levels. Therefore, the goal should be to maintain estrogen levels within a normal range. Most of you will be familiar with the more commonly used A.I’s (aromatase inhibitors), such as letrozole, exemestane, and anastrozole. According to the research I have done, it appears there is no single best A.I., as each one has its own unique set of characteristics that makes it more or less suited to each individual. In steroid users and those at an increased risk for cardiovascular disease, I tend to recommend exemestane, as it typically has a milder effect on the lipid profile. But for those who respond negatively to exemestane, anastrozole is usually my next choice. Letrozole is normally only employed during the later stages of contest prep or to treat gyno, as it tends to provide a drier appearance than other A.I’s (as well as more side effects) and is more effective at eliminating gyno. On another note, bloodwork is essential for being able to determine when your estrogen levels are in the ideal range.
Another useful, although somewhat controversial drug is GW-501516. As a PPARδ agonist, GW-501516 is one of the few non-stimulant drugs capable of inducing fat loss via an increased rate of oxidation. There are two main steps involved in the fat loss process: oxidation and lipolysis. As stated previously, lipolysis is a term used to describe the release of fatty acids from fat cells into the bloodstream (where they are more likely to be used by the body for energy), while oxidation describes the burning of fat for energy. Both of these steps must occur in order for fat loss to take place. If fat is not first released from the fat cell, it cannot be used for energy. On the other hand, if newly released fat is not used for energy due to insufficient oxidation, it will simply be re-deposited into fat cells, leaving us back at square one.
If one of these processes (lipolysis and oxidation) begins to exceed the other, the slower process is said to be the rate-limiting factor. In other words, the rate of fat loss is “limited” by the weakest link. When it comes to fat loss, oxidation is usually the rate-limiting factor. Ideally, we want both lipolysis and oxidation to balance each other out perfectly, but rarely does that happen, nor is it even something we can accurately measure. However, what we can do is try to make sure that any potential imbalance is minimized. This make GW-501516 an excellent stacker with growth hormone, as its ability to increase oxidation pairs well with GH’s lipolytic effect. This accelerates the rate of fat loss beyond what can be achieved with growth hormone alone by strengthening the weakest link in the fat loss process.
But this is not the only reason GW-501516 makes a good match with growth hormone. As awesome as growth hormone is, most of you know that it can have some pretty significant downsides too, especially in terms of metabolic health. When used at replacement doses this is not something we need to worry about, but when used at normal bodybuilding doses its injurious effects on metabolic health (via insulin resistance) are undeniable. Growth hormone has been clinically demonstrated to cause insulin resistance even when used at doses as low as 5 iu/day. As mentioned above, insulin resistance has a barrage of negative effects on the body, including diminished fat loss.
At this point you may be wondering how growth hormone is able to cause such a significant reduction in bodyfat considering its potent, negative effect on insulin sensitivity. The explanation is simple. Growth hormone’s lipolytic effect is so powerful that it basically overpowers insulin resistance’s negative effect on fat loss. So, when using growth hormone to drop bodyfat it is like taking 2 steps forward and 1 step back. You will still end up in the green after all is said and done, but maximum results are not obtained. By stacking GW-501516 with growth hormone you are promoting fat loss through two primary mechanisms; by reversing GH’s negative effect on insulin sensitivity and by accelerating the body’s rate of oxidation.
There are a number of other fat loss agents on the market that have proven themselves effective both in the lab and in the gym (injectable L-carnitine is a good example). All of these can help you keep the fat off as you go about achieving your muscle building goals, but what makes the previously mentioned products special is the manner in which they promote fat loss. Not only do they lack any negative effects on lean mass accumulation/retention, but the majority actually have a positive effect on lean mass levels. This makes them completely suitable for anyone prioritizing muscle growth, as well as for those engaged in contest prep. Even better is that they don’t appear to cause any significant side effects (GW-501516 may be an exception, although the jury is still out), when used responsibly over the long-term. This is in significant contrast to other fat burners, most of which have an undesirable side effect profile and can only be administered for a relatively brief period of time.
You may notice that I left certain drugs out of the discussion, such as clenbuterol and ephedrine. I did this intentionally, as these drugs, despite the claim that they may help maintain or even build lean mass (I have not noticed this to be true in my experience), are not suitable for extended use. They simply have too many side effects on organ systems I would rather avoid, such as the cardiovascular system, adrenal system, etc. In my opinion, when trying to determine which drugs are ideal for long-term use they must meet the following criteria. One, they must support lean mass gains (or at worst have a neural effect). Two, they must promote improvements in overall health (or at worst, have a neutral effect). Everything mentioned here, including low-dose growth hormone, insulin management, cortisol management, estrogen management, GW-501516 (a PPARδ agonist), and injectable L-carnitine all meet this criteria.