Announcement

Collapse
No announcement yet.

Thoughts on Thyroid Hormones & Function

Collapse
X
 
  • Filter
  • Time
  • Show
Clear All
new posts

  • SisterSteel
    replied
    Thyroid Hormone for Weight Loss: Physiologic and Metabolic Effects

    Introduction


    It has been over 100 years since the discovery by Magnus-Levy that thyroid hormones play a central role in energy homeostasis, and 75 years since the hormones were first used for weight loss. Despite this great length of time, the precise mechanisms by which thyroid hormones exert their calorigenic effect are not completely characterized, and still actively debated. Despite numerous clinical studies having shown that the administration of thyroid hormone induces weight loss, it is not currently indicated as a weight loss agent. This is probably due to the number of side effects observed during thyroid hormone use at the relatively high doses used in the majority of obesity treatment studies. These deleterious effects include cardiac problems such as tachycardia and atrial arrhythmias, loss of muscle mass as well as fat, increased bone resorption and muscle weakness. Nevertheless, thyroid hormones, particularly triiodothyronine (T3) are a mainstay in the arsenal of drugs used by bodybuilders for fat loss. The widespread underground use of T3 warrants an understanding of its mechanism of action, as well as a knowledge of how it is most effectively and safely used, with an eye to minimizing side effects.



    Thyroid Function and Physiology



    Before jumping right into a discussion of the use of thyroid hormone for fat loss, a little review of thyroid function and physiology might be in order. The thyroid gland secretes two hormones of interest to us, thyroxine (T4) and triiodothyronine (T3). T3 is considered the physiologically active hormone, and T4 is converted peripherally into T3 by the action of the enzyme deiodinase. The bulk of the body's T3 (about 80%) comes from this conversion. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in the hypothalamus. This is analogous to testosterone production, where GnRH from the hypothalamus causes the pituitary to release LH, which in turn stimulates the testes to produce testosterone.

    In addition to T3, it has recently been recognized that there exist two additional active metabolites of T3: 3,5 and 3,3' diiodothyronines, which we will collectiv

    ely call T2. Studies have shown that 3,3'-T2 may be more effective in raising resting metabolic rate when hypothyroid subjects are treated with T3, than when normal (euthyroid) subjects are given T3. Therefore in normal subjects 3,5-T2 may be the principal active metabolite of T3 (1)

    Like the hypothalamic-pituitary-gonadal axis, the thyroid gland is under negative feedback control. When T3 levels go up, TSH secretion is suppressed. This is the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. There is a difference though between the way anabolic steroids suppress natural testosterone production and the way T3 suppresses the thyroid. With steroids, the longer and heavier the cycle is, the longer your natural testosterone is suppressed. This is not the case with exogenous thyroid hormone.

    An early study that looked at thyroid function and recovery under the influence of exogenous thyroid hormone was undertaken by Greer (2). He looked at patients who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids quickly returned to normal.

    Here is a remark about Greer's classic paper from a later author:


    "In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days" (3)

    These results have been subsequently verified in several studies.(3)(4) So contrary to what has been stated in the bodybuilding literature, there is no evidence that long term thyroid supplementation will somehow damage your thyroid gland. Nevertheless, most bodybuilders will choose to cycle their T3 (or T4 which in most cases works just as well) as part of a cutting strategy, since T3 is catabolic with respect to muscle just as it is with fat. As previously mentioned, long term T3 induced hyperthyroidism is also catabolic to bone as well as muscle.

    The proviso about T4 vs T3 for weight loss alluded to above needs some elaboration. There have been a number of studies that have shown that during starvation, or when carbohydrate intake is reduced to approximately 25 to 50 grams per day, levels of deiodinase decline, hindering the conversion of T4 to the physiologically active T3.(5) From an evolutionary standpoint this makes sense: during periods of starvation the body, teleologically speaking, would like to reduce its basal metabolic rate to preserve fat and especially muscle stores. However, a recent study demonstrating the effectiveness and safety of the ketogenic diet for weight loss recorded no change in circulating T3 levels.(6) So this issue not completely settled. Nevertheless, persons contemplating thyroid supplementation during ketogenic dieting might prefer T3 over T4 since the bulk of the research does suggest a decline in the peripheral conversion of T4 to T3 during low carb dieting.

    Now that we have reviewed a little about thyroid function, let's consider just how it is that thyroid hormone exerts its fat burning effects.



    Increased Oxidative Energy Metabolism


    Thyroid hormone has long been recognized as a major regulator of the oxidative metabolism of energy producing substrates (food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The mitochondria are often called the "cell's powerhouses" because this is where foodstuffs are turned into useful energy in the form of ATP. T3 and T2 increase the flux of nutrients into the mitochondria as well as the rate at which they are oxidized, by increasing the activities of the enzymes involved in the oxidative metabolic pathway. The increased rate of oxidation is reflected by an increase in oxygen consumption by the body.

    T3 and T2 appear to act by different mechanisms to produce different results. T2 is believed to act on the mitochondria directly, increasing the rate of mitochondrial respiration, with a consequent increase in ATP production. T3 on the other hand acts at the nuclear level, inducing the transcription of genes controlling energy metabolism, primarily the genes for so-called uncoupling proteins, or UCP (see below). The time course of these two actions is quite different. T2 begins to increase mitochondrial respiration and metabolic rate immediately. T3 on the other hand requires a day or longer to increase RMR since the synthesis of new proteins, the UCP, is required (1).

    There are a number of putative mechanisms whereby T2 is believed to increase mitochondrial energy production rates, resulting in increased ATP levels. These include an increased influx of Ca++ into the mitochondria, with a resulting increase in mitochondrial dehydrogenases. This in turn would lead to an increase in reduced substrates available for oxidation. An increase in cytochrome oxidase activity has also been observed. This would hasten the reduction of O2, speeding up respiration. These and a number of other proposed mechanisms for the action of T2 are reviewed by Lannie et al.(7)

    What is the fate of the extra ATP produced during hyperthyroidism? There are a number of ways by which the increased ATP promotes an increase in metabolic activity, including the following:

    Increased Na+/K+ATPase. This is the enzyme responsible for controlling the Na/K pump, which regulates the relative intracellular and extracellular concentrations of these ions, maintaining the normal transmembrane ion gradient. Sestoft(7) has estimated this effect may account for up to to 10% of the increased ATP usage.


    Increased Ca++-dependent ATPase. The intracellular concentration of calcium must be kept lower than the extracellular concentration to maintain normal cellular function. ATP is required to pump out excess calcium. It has been estimated that 10% of a cell's energy expenditure is used just to maintain Ca++ homeostasis. (1)


    Substrate cycling. Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in fat cells. The stored triglycerides are broken down into free fatty acids and glycerol, then reformed back into triglycerides again. This is an energy dependent process that utilizes some of the excess ATP produced in the hyperthyroid state (8). Futile cycling has been estimated to use approximately 15% of the excess ATP created during hyperthyroidism (8)


    Increased Heart Work. This puts perhaps the greatest single demand on ATP usage, with increased heart rate and force of contraction accounting for up to 30% to 40% of ATP usage in hyperthyroidism (9)



    Mitochondrial Uncoupling


    As mentioned, the mitochondria are often characterized as the cell's powerhouse. They convert foodstuffs into ATP, which is used to fuel all the body's metabolic processes. Much research suggests that T3, like another much more potent agent DNP, has the ability to uncouple oxidation of substrates from ATP production. T3 is believed to increase the production of so called uncoupling proteins. Uncoupling protein (UCP) is a transporter family that is present in the mitochondrial inner membrane, and as its name suggests, it uncouples respiration from ATP synthesis by dissipating the transmembrane proton gradient as heat. Instead of useful ATP being produced from energy substrates, heat is generated instead. There are conflicting studies about the importance of T3 induced uncoupling. Animal studies have demonstrated an actual increase in ATP production commensurate with increased oxygen consumption as we discussed above. Other studies in humans have shown that in fact uncoupling in skeletal muscle does occur. This would contribute to T3 induced thermogenesis, with a resulting increase in basal metabolic rate.(10)

    To make up for the deficit in ATP production (as well as provide fuel for the extra ATP production discussed above) more substrates must be burned for fuel, resulting in fat loss. Unfortunately, along with the fat that is burned, some protein from muscle is also catabolized for energy. This is the downside of T3 use, and the reason many people choose to use an anabolic steroid or prohormone during a T3 cycle to help preserve muscle mass. Studies have shown this to be an effective strategy (11). (Muscle glycogen is also more rapidly depleted, and less efficiently stored during hyperthyroidism. This may account for some of the muscle weakness generally associated with T3 use.)

    Countering T3 induced muscle loss with AAS or prohormones makes sense from a physiological viewpoint as well. Thyroid hormone muscle protein breakdown is mainly mediated via the so-called ubiquitin-proteasome pathway. (12). (There are several independent metabolic pathways of protein breakdown in the body. For instance, another pathway, the lysosomal pathway, is responsible for the accelerated rate of muscle protein breakdown during and after exercise.) Testosterone administration has been shown to decrease ubiquitin-proteasome activity. (13) So AAS specifically target the muscle protein breakdown process stimulated by T3.

    What may not be an effective strategy to maintain muscle mass during a T3 cycle is the use of exogenous growth hormone (GH). Studies have shown that when GH and T3 are administered concurrently, the increased nitrogen retention normally associated with GH use is abolished. This has been attributed to the observation that T3 increases levels of insulin like growth factor binding protein, reducing the bioavailability of igf-1 (14). Nevertheless, GH has fat burning properties independent of igf-1, so using GH with T3 would act additively to speed fat burning, but with little if any preservation of lean body mass. So again, if GH is used in conjunction with T3, anabolic steroid/prohormone use would be indicated.



    Andregenic Receptor Modulation


    Administration of T3 has been shown to upregulate the so-called beta 2 adrenergic receptor in fat tissue. What is the significance of this effect for fat loss? Before fat can be used as fuel, it must be mobilized from the fat cells where it is stored. An enzyme called Hormone Sensitive Lipase (HSL) is the rate-controlling enzyme in lipolysis, or fat mobilization. The body produces two catecholamines, epinephrine and norepinephrine, which bind to the beta 2 receptor and activate HSL. The upregulation of the beta 2 receptor due to T3 results in an increased ability of catecholamines to activate HSL, leading to increased lipolysis.

    Bodybuilders often use drugs like clenbuterol, which bind to the beta 2 receptors and activate them in the same way as the body's endogenous catecholamines. The use of clenbuterol along with T3 can produce an additive lipolytic effect: T3 increases the number of receptors, while clenbuterol binds to the receptors activating HSL and increasing lipolysis. Since clenbuterol itself downregulates the beta 2 receptor, most bodybuilders use clenbuterol in a two week on/ two week off cycle, the rationale being that this minimizes downregulation and allows receptor recovery. Another option is to use the antihistamine ketotifen concurrently with the clenbuterol. Studies have shown that ketotifen attenuates the beta 2 receptor downregulation caused by clenbuterol (15). Moreover, research in AIDS patients has shown that ketotifen blocks the production of the proinflammatory and catabolic cytokine TNF-alpha (16). This may be of relevance to bodybuilders since there is evidence showing TNF lowers both testosterone and IGF-1 levels quite significantly (17) (18), while strenuous exercise elevates TNF levels. (19)

    Besides increasing beta 2 receptor density in adipose tissue, T3 upregulates this receptor in human skeletal muscle (12). This has some very intriguing if somewhat speculative implications for the combined use of clenbuterol and T3. Animal studies have shown that catecholamines, particularly clenbuterol, inhibit Ca++ dependent skeletal muscle proteolysis (20). Like the lysosomal and ubiquitin-proteasome pathways discussed above, Ca++ regulated proteolysis is yet another way for the body to degrade muscle protein. Again the implications are enticing: Increased beta 2 receptor density from T3 use, coupled with the beta 2 agonist clenbuterol, could slow this pathway of muscle catabolism.

    Another adrenergic receptor important to lipolysis is the alpha 2 receptor, which impedes fat mobilization by counteracting the effects of the beta 2 receptor. There are some conflicting studies about the effects of T3 on the alpha 2 receptor, with studies showing either a downregulation (21) or no effect (22). If T3 does in fact downregulate alpha 2 receptors, this would further aid lipolysis.

    Studies in rats have shown that inducing hyperthyroidism increases the lipolytic beta 3 receptor density in white adipose tissue by 70% (23). Beta 3 receptors are abundant in human white adipose tissue as well, and if T3 administration has the same effect in humans, this could could contribute significantly to T3 induced fat loss. This might also argue for taking a currently available beta 3 agonist such as octopamine along with T3 and perhaps clenbuterol.



    Decreased Phosphodiesterase Expression


    In hyperthyroid patients as well as in normal subjects given T3, levels of the enzyme phosphodiesterase are lowered in fat cells (20). When lipolytic hormones like epinephrine (adrenaline) bind to the beta 2 receptor described above, they initiate a signaling cascade mediated by the so called “second messenger” cyclic AMP (cAMP). cAMP in turn acts on other cellular enzymes to initiate and maintain lipolysis. The original signal is terminated when cAMP is degraded by the enzyme phosphodiesterase. Clearly, maintaining elevated cAMP levels, by lowering phosphodiesterase concentrations with T3, will prolong lipolysis.

    As an aside, caffeine is thought to exert at least a portion of its lipolytic action by lowering phosphodiesterase in fat cells. Interestingly, Viagra and Cialis are also phosphodiesterase inhibitors but their action seems to be limited to relaxing vascular smooth muscles.



    Increased Growth Hormone Secretion



    In vitro, animal, and human studies have all demonstrated that T3 administration increases growth hormone production. (24)(25) Since GH is calorigenic aside from any increase in igf-1, elevated GH may contribute to some of the fat burning associated with T3 administration. This effect may obviate the need for the use of expensive recombinant HGH, as mentioned above.



    Decreased Insulin Secretion


    Insulin is well known as a lipogenic hormone. It promotes fat storage by facilitating the uptake of fatty acids by adipocytes, and reducing lipid oxidation in muscle tissue. Several studies have shown that thyroid hormone is associated with glucose intolerance resulting from decreased glucose stimulated insulin secretion (26).

    This defect in insulin secretion is believed to result from an increase in the rate of apoptosis (programmed cell death) of pancreatic beta cells as a direct effect of thyroid hormone excess.(27) This process is reversible, since when thyroid hormone is withdrawn the rate of beta cell replication increases until homeostasis returns. However, there are conflicting studies regarding the effects of T3 on insulin. For example, Dimitriadis et al (28) showed a decrease in glucose stimulated insulin secretion, consistent with (25), but an increase in basal insulin. They also observed increased insulin clearance, with a compensatory increase in basal insulin secretion.

    So if in fact the hyperthyroid state is associated with lower insulin levels, this could explain a portion of hyperthyroid stimulated lipolysis. The obvious downside here is that insulin is also an anabolic hormone. Basal insulin concentration is thought to limit the action of the ubiquitin-proteasome degradative pathway of muscle protein breakdown (29). Of course supplementing with insulin during T3 use would be counterproductive. However, as mentioned above, anabolic steroids inhibit ubiquitin-proteasome activity, so their use could counter any loss in muscle anabolism resulting from a drop insulin levels.



    The Future



    As mentioned at the beginning of this article, a major roadblock in the adoption of T3 by the medical community as an antiobesity agent is its deleterious effect on the heart. Recent research has identified two isoforms of the thyroid hormone receptor, TRalpha and TRbeta. The TRalpha-form may preferentially regulate the heart rate, and an experimental agent, GC-1, has been developed that selectively binds the TRbeta receptor, with minimal effects on the heart (30). The distribution and actions of TRalpha and TRbeta throughout the body are not yet well characterized. However should it turn out that TRalpha is specific to the heart, then drugs like GC-1 may turn out to be effective fat burning agents with a much safer profile that T3 or T4.

    One alleged “futuristic” agent that is here now is T2, or 3,5-Di-iodo-L-thyronine, the T3 metabolite discussed above. Unfortunately, this product does not live up to its hype. It has been claimed to be as or more effective that T3 for fat burning with minimal suppression of endogenous thyroid production. Regarding the relative effectiveness of T2 as a lipolytic agent, and its effect on TSH, this topic was thoroughly covered in a recent article by Bryan Hay**** in Muscle Monthly:




    All of my research into this subject has led me to the same conclusion reached by Mr. Hay****. That is, T2 is only slightly less suppressive of TSH than is T3, and only packs a portion of the lipolytic punch of T3, with no ability to increase the expression of the UCPs, which is a major determinant of the action of thyroid hormone.



    Summary



    We have discussed a number of ways by which T3, and its active metabolite T2 act to increase resting energy expenditure. Also discussed were some drawbacks of T3 use, such as cardiac stress, as well as the potential loss of muscle mass. It is ironic that the latter may be of more concern to many bodybuilders that the other more serious potential impacts on health. Nevertheless, used moderately and for short periods (a couple of months or less) in people with no preexisting cardiovascular disease T3 has a relatively safe medical profile, compared to other lipolytic agents like DNP. Perhaps most importantly we have presented substantial evidence that even the long-term use of supraphysiological levels of T3 does not damage the thyroid gland.

    Leave a comment:


  • SisterSteel
    started a topic Thoughts on Thyroid Hormones & Function

    Thoughts on Thyroid Hormones & Function

    Maybe it's a well-kept secret that nobody wants to share, or perhaps it's a rare jewel that lies hidden and awaits discovery. Regardless of the reason, if you're a bodybuilder who is interested in hormones that affect growth and metabolism, this baby could be the Holy Grail. The nectar that awaits in this cup is called the thyroid hormones, and they can unleash the power of metabolism in muscles. But why is it that nobody has yet to realize its importance to the sport of bodybuilding?

    The most likely explanation for people not talking much about the thyroid and its hormones is that it has just been taken for granted. The close association between the thyroid hormones and metabolism has long been recognized in the field of medicine. If a person is hypothyroid-a condition where one produces too lithe thyroid hormone-there is a loss of appetite, they become easily fatigued, have weak muscles, suffer from weight gain and have a low body temperature due to their reduced metabolism. On the other hand, if one is hyperthyroid and produces too much thyroid hormone, they tend to lose weight despite a good appetite due to their increased metabolism. They are also restless, unable to sleep and have higher body temperatures.

    These two extremes show just how powerful the thyroid hormones are. In fact, it should make one stop and consider whether this awesome power should be tampered with at all. But these two conditions represent disease states where the thyroid gland has gone out of control. What we are interested in is optimizing the body's daily output of thyroid hormone to our advantage. Like all glands that produce hormones, the thyroid produces its hormones within a normal range that varies from high to low. Our goal is to increase this gland's normal production of thyroid hormones and keep them in the high end and working to maintain our anabolic edge.

    THE THYROID HORMONES

    The thyroid is a gland that wraps itself around the larynx just behind the trachea. It produces two active hormones known as triiodothyronine and thyroxine. Triiodothyronine and thyroxine are each composed of two amino acids of tyrosine and only differ by the amount of bound iodine. Triiodothyronine has three iodides bound to it while thyroxine has four. This is why they are called T3 and T4.

    T3 and T4 are released by the thyroid into the blood where they bind to specialized proteins that carry them to other parts of the body. for the most part, both hormones have identical functions but must be released from their binding proteins to be active. T3 is the more powerful of these twins; although it is present in amounts that are 30-60 times lower than T4. However, many cells are capable of removing one of the iodides from T4 and converting it to the more active T3.

    Once these hormones reach the muscles, they are released from their binding proteins and are carried inside the cells by receptors on the cell membrane. Inside the cell, there are two targets where T3 can exert its effect. One is the nucleus where it can bind to the genes and increase protein synthesis. The other is the mitochondria, which are the power factories that burn calories in the presence of oxygen to produce adenosine triphosphate (ATh). It is believed that T3 can increase the mitochondria's ability to burn calories and thus raise the basal metabolic rate (BMR). In addition, T3 will also cause an increase in the number and size of the mitochondria, which will further serve to increase BMR.

    THYROID HORMONE ACTION

    The effects of the thyroid hormones are many and can be most advantageous to the bodybuilder. Every bodybuilder knows that muscles look their best when you're ripped and there's no excess bodyfat to obscure the striations. This is where T3 really excels by helping a person burn away those puffy little fat cells. T3 increases the BMR in nearly every cell of the body, especially the muscles, It does so by causing the fat cells to release free fatty acids into the bloodstream where they are taken up by the tissues. Here they are burned by the hyperactive mitochondria to make the ATP that drives muscle contractions. This energy can then be used to support muscle contractions for exercise and protein synthesis for growth. Another benefit is that although T3 increases the level of free fatty acids in the blood, it lowers cholesterol and triglyceride levels.

    T3 is so effective at cranking up the metabolic fires and using fat to feed these fires that it can actually increase the BMR by 60- 100%. So if one can increase their T3 levels just a little it can have a profound effect on metabolism. Since one of the bodybuilder's prime concerns is keeping off bodyfat, T3 easily earns its title of master of metabolism for bumping up the BMR. even if it did nothing else at all.

    But T3 does more than function as a terminator for fat cells. Another site of action for T3 is the muscles, where slight increases in this hormone causes the muscles to react to increased resistance with greater vigor. It accomplishes this by increasing the number of sarcoplasmic reticulum, which control contractions, and the energy- producing mitochondria that provide the muscle with the energy to do work. T3 has also been shown to cause an increase in the muscle's production of myosin, which is one of the major contractile proteins in muscle. Much of this accomplished by T3's ability to activate genes and cause an increase in protein synthesis in the muscles.

    Nothing escapes the influence of T3, since it can also stimulate almost all aspects of carbohydrate metabolism. It can increase the absorption of glucose by the intestinal tract, increase the uptake of glucose by the cells, and increase glucolysis. In glycolysis, the excess glucose that is not needed for glycogen production is broken down and burned by the mitochondria to produce even more ATP.

    T3 also has the ability to influence other hormones. Because it can cause blood sugar levels to rise, this causes a release of insulin from the pancreas to deal with the flood of glucose. As we have seen in the previous parts of this series, rapid rises in insulin can lead to hypoglycemia, which induces the production and release of growth hormone. T3 also causes a greater release of lactate and a lowering of blood pH. Acidic blood conditions are another mechanism by which growth hormone is induced. The induced growth hormone in turn causes the synthesis of insulin-like growth factor several hours later. All these hormones working in concert can produce an anabolic environment that will give maximum support to muscle growth and repair after an intense workout.

    In addition to providing a rich anabolic setting for muscle growth, T3 has no tolerance for catabolic conditions. It acts directly on the liver to increase the rate of destruction of the adrenal glucocorticoids, such as cortisol, which are responsible for protein breakdown. This decrease in cortisol will allow for greater recovery and uninterrupted muscle growth.

    There are other effects of T3 that are worth mentioning in brief. The increased BMR causes the muscles to demand increased oxygen to keep up with the greater burning of fats and energy production. To do this, T3 increases the respiratory capacity by increasing the depth of respiration and allows better oxygen utilization by the lungs. It also increases the strength of the heartbeat, increases blood volume and elevates blood pressure in the arteries. It also causes the vessels to expand and lower blood pressure. This decrease of blood pressure in the vessels offsets the rise in the arteries, so overall blood pressure remains unchanged. The result is greater amounts of oxygen-rich blood available to bathe the muscles with oxygen and nutrients and carry away waste metabolic by products.

    SERVANTS TO THE MASTER

    As mentioned earlier, thyroid hormones have a normal range that varies from high to low. So to get the full benefits of T3, we must provide the body with conditions that will keep this hormone in the high range of production. One way to do this is through exercise. Most studies agree that intense exercise causes a rise in serum T3 and T4 levels. Repeated bouts of exercise cause an increased turnover of thyroid hormones. This means that the destructive process for thyroid hormones increases and signals the pituitary gland to release more thyroid stimulating hormone (TSR). The TSH causes the thyroid to produce more thyroid hormones.

    This is somewhat of a slingshot effect, where the initial exercise pulls the thyroid hormones to the low end of the normal range. The body responds by cranking up the production of T3 and T4 to get levels back up to the normal range. This panic response by the body to the fall in thyroid hormones will result in their overproduction. and as the levels rise, they shoot past the midpoint and rise to the upper normal range. The result is that a person rcmains slightly hyperthyroid for a while until the turnover slows and thyroid levels fall back to the normal midrange.

    As mentioned, intensity is necessary to get this process rolling. Studies of people who switched from a sedimentary lifestyle to one of moderate exercise showed no increase in their thyroid hormone levels. However, when the amount of exercise was doubled, there was a significant increase in thyroid hormone secretion. As we know there are two ways to increase the amount of exercise we perform-work longer or work harder. For bodybuilders the greatest advantage comes from working harder. or increasing the intensity of the workout.

    Another factor that affects thyroid function is nutrition. People who go on a calorie-restricted diet cause the body to lower its BMR to conserve energy, and this causes a decrease in thyroid hormone production. If a person increases their food intake, thy- old hormone production increases to turn up the BMR and burn the extra calories. When a person exercises intensely, two independent changes occur. They burn calories during exercise and they increase their production of thyroid hormone, which raises their BMR and burns still more calories. However, if this energy burned during exercise isn't replaced, the production of thyroid hormones will decrease.

    Also see that you get plenty of zinc in your diet. Zinc is thought to possibly play role in thyroid hormone metabolism and aid in the conversion of T4 to T3.

    That's why it's important for bodybuilders to supplement their diets to replace expended energy. Two of the best nutrients for increasing the production of T3 and T4 are protein and complex carbohydrates. When people were led a protein/carbohydrate diet that was either low or high in fat. only the low-fat diet elevated thyroid hormone levels. It seems that carbohydrates and protein can stimulate T3 and T4, but fat inhibits their release. That's why sports supplements are an important tool in bodybuilding. They are designed to be high in protein and carbs, while extremely low in fat. This makes them obvious choices for replacing energy used during exercise and inducing T3 and T4.

    GET RIPPED WHILE YOU GROW

    Thyroid hormone loves muscle and hates fat. That's why it's a bodybuilder's best friend. Because muscles are the primary site of our body's BMR. T3 works to increase this lean mass so there will be increased BMR available to burn fat. To accomplish this, T3 virtually increases all aspects of protein synthesis in the muscles to allow growth to occur. It also increases the efficiency in which fat is burned. It can actually double the calories burned for each unit of work performed. That means twice the fat get burned while you train and grow. So as you can see, the thyroid hormones may well be one of bodybuilding's best kept secrets. And the good news is you don't have to travel to the distant ends of the earth like Indiana Jones to drink from this grail. Its benefits can always be summoned forth if one stimulates the muscles by using the principles and techniques of bodybuilding. while maintaining a proper diet that includes supplements. Do so. and the power of T3 will always be there for you.

    EPILOGUE

    As you conclude this write up on the hormones that affect your metabolism and anabolic state, it should be clear that htulding a world-class physique doesn't depend on a single hormone. Many hormones work together as a team to influence muscular development and fitness. These hormones depend on each other to get the job done by providing a stimulus that aids in growth and recovery, while influencing each other's production. But most important, these honnones depend on you. Remember, they can't do their job unless you do yours. So plan your workouts and timing of supplementation to take full advantage of your anabolic hormones and there will be no limits to what your body can accomplish.
Working...
X