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Bulletin #18 – Growth Hormone: The Ultimate Weapon

In this bulletin we’re pulling out theultimate weapon — growth hormone. Thisis the most important hormone for body-builders, acting as a powerful stimulus formuscle growth and fat loss. Many of theeffects of exercise in increasing musclemass and decreasing body fat are medi-ated by growth hormone. The most ef-fective training strategies are those whichmaximize growth hormone release. ParrilloPerformance knows exactly how to eatand how to train to maximize this mostimportant controller of nutrient partition-ing. And like always, we’re here to showyou how. If you’re willing to train hardenough, we’ll help you reach the stars.Every athlete who has struggled tobuild muscle is painfully aware of the factthat you have to lift weights to do it. Infact, you have to lift weights very in-tensely and consistently over a period ofsome time (months to years) to accumu-late significant increases in muscle mass.Since muscles are made from nutrients inthe food we eat, you may logically askwhy can’t we build muscle just by eatingthe right foods?

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The answer to this ques-tion takes us back to the theme of thisseries: hormones.Hormones are ultimately responsiblefor the process of tissue remodeling —that is, the process of laying down newmuscle tissue. Although you can exertgreat control over some hormones by dietalone (refer back to the previous bulletinsin this series), exercise is required to gen-erate the complete hormonal spectrumwhich will result in muscle gain and fatloss (1,2). Furthermore, the damage tomuscle tissue which results from exer-cise training (especially the eccentric, orlowering phase of muscle contraction)serves as a stimulus to the muscles moreresponsive to the growth-promoting ef-fects of anabolic hormones (1).Growth hormone (GH) is the mostanabolic substance in the human body(3,4). In a study of old men (whosegrowth hormone levels are diminished),it was found that GH administration pro-moted an increase in muscle mass and adecrease in body fat even in the absenceof exercise training (3,4). Growth hor-mone is anabolic, meaning that it acts topromote incorporation of nutrients intonew body tissues. This includes increas-ing protein synthesis in the muscle tissue(5,6). Part of this effect is believed to bedue to GH promoting transport of certainamino acids inside muscle cells (5). No-tably, insulin also acts to transport a dif-ferent set of essential amino acids, so youneed adequate amounts of GH an insulinpresent at the same time to stimulatemuscle growth (5). GH also has a lipoly-tic effect, which means it mobilizes bodyfat from adipose depots and increases theuse of fat for energy (5,6). This in turnspares carbohydrates so glycogen storesare preserved (5,6). GH is probably themost important hormone for bodybuild-ing since it has powerful actions in build-ing muscle and burning fat.The most important role of growthhormone is in promoting growth duringchildhood. Without GH, normal adult stat-ure will not be achieved (5,6). Growthhormone acts to promote growth of alltissues of the body except the nervoussystem. GH levels reach maximal levelsin the late teens and gradually decline withage.

The high levels of GH and testoster-one in young adult males explain why mostbodybuilders make their best gains dur-ing their late teens and twenties. This againunderscores the central role of hormonesin bodybuilding.Although I’ve discussed this before,it is so important as to bare repeating: thecentral reason behind all of your body-building activity, including both diet andtraining, is to manipulate your hormonelevels so as to promote muscle gain andfat loss. Your body’s level of muscle massand body fat are determined by hormonesand by the set point of your hypothala-mus. By following the guidelines in thisseries and in the Parrillo Nutrition andTraining Manuals you will adopt a lifestylewhich optimizes anabolic drive and setsup the proper hormonal environment forachieving a top physique.During the next couple of  bulletins Iwill explain in detail the physiology ofgrowth hormone, including its mecha-nisms of release, its actions and what youcan do to control your GH levels for maxi-mum results. As you know by now, hor-mones do not work alone in the body. Itis the combined interaction of all the hor-mones which generates the physiologicaladaptations to exercise. Therefore, I willdiscuss growth hormone in the contextof the other hormones with which itsynergizes to produce its effects. I havedecided to organize this discussion aroundsome of the most basic and importantquestions about growth hormone. If thediscussion sounds a little medical inplaces, bear with me. You will come awaywith a thorough understanding of growth hormone and how to control it. Get readyto annihilate the competition.1. Exactly what is growth, and whatis the difference between lineargrowth, mass increase and obesity?The common feature of growth is anincrease in mass (body weight). The com-mon definition of growth refers to theorganized addition of new tissue that oc-curs normally in development from infancyto adulthood (6). Bodybuilders are a bitunusual in that they continue to grow af-ter reaching adulthood. This is largely dueto the effects of intense exercise in in-creasing growth hormone. Normal growthinvolves both linear growth (increase inbody length or height) and mass increase(increase in body weight). Obesity spe-cifically refers to growth of fat stores outof proportion to the rest of the body. Quan-titatively, anything above 30% body fat iscommonly considered obese. Growth isnormal and healthy; obesity is not. Ab-normal growth can becaused by an excess ordeficiency in growth hor-mone.

GH causes parti-tioning of nutrients to thelean compartment andaway from fat stores. Ad-ministration of GH will in-crease muscle mass anddecrease body fat, and adeficiency of GH will re-sult in excess fat accumu-lation.2. What are the main stages ofnormal growth and the hormones thatstimulate growth in each?Prenatal: Hormonal control duringprenatal development is largely unknown,but insulin is believed to be important (6).Human placental lactogen, hPL, is prob-ably also involved.Infantile (0-1 years): Insulin is re-quired and possibly other unknown hor-mones as well (6). Interestingly, GH andT3 (thyroid hormone) are not requiredduring prenatal and infantile growth (6).Juvenile (1-12 years): GH is the mostimportant, but there is also a strict require-ment for T3 and insulin (5,6). Vitamin Dis also required.Adolescent (age 10-14 for females,12-16 for males): The sex steroids areresponsible for the adolescent growthspurt, closure of the epiphyseal plate (seebelow) and attainment of final adult height.GH, T3, vitamin D and insulin are still re-quired for normal growth during this time.Glucocorticoids are also required in nor-mal levels for normal growth but its ac-tion is mainly permissive (6). Permissiveactions of hormones describe effects ofhormones on enzyme systems so as toallow other hormones to exert their regu-latory effects. The permissive hormonesdo not stimulate growth directly, but ratherallow other growth-promoting hormonesto be active.3. What is the difference betweengrowth-regulating hormones and localgrowth factors?Hormones are released into the blood-stream to exert their effects on target tis-sues throughout the body, while growthfactors act mainly locally (as autocrinesor paracrines) to stimulate growth. Themost important growth-regulating hor-mones are GH, T3, insulin and the sexsteroids. Most growth factors act as regu-lators of local processes such as woundhealing, tissue repair, regeneration or or-dinary replacement of aged cells, but someare found in the circulation and may func-tion as true hormones. IGF1 (somatome-din C) is especially important in this re-gard in mediating many of the actions ofGH. See the below for more informationon IGF1.4. What are the other require-ments for normal growth in additionto hormones and growth factors? Proper nutrition (including energy,amino acids, vitamins, minerals and es-sential fatty acids) rest, and a good psy-chosocial environment are all requirementsfor growth (6). Mental state (emotionalstate) can directly influence normalgrowth in humans. No doubt this effectis mediated by the hypothalamus, since itconnects the endocrine system to themind. If you’re eating and training right,but are totally stressed out about work orsome personal problem, you’re probablynot going to make very good gains. Themind in very important to bodybuilding.You must maintain a positive and aggres-sive attitude and not be distracted by out-side stresses.5. What are catch-up growth andcompensatory growth?Catch-up growth is a period ofgrowth at greater than the normal rate torecover from a time when growth wasretarded, as during illness. Notably, in-creased levels of hormones (includingGH) are NOT required during catch-upgrowth. Compensatory growth is growthof an organ to compensate for damage tothat organ or its pair.

For example, if onekidney is removed, the remaining kidneywill grow larger. Increased hormone lev-els are probably not needed for compen-sation by the liver and kidney, althoughIGF1 may be increased. Compensatorygrowth of the adrenal gland is accompa-nied by increased levels of ACTH (6).Many athletes who are over-trained orunder-nourished experience a growthspurt when they correct the problem. Inthe case of over-training, the problem islikely due to elevated cortisol levels, whichare catabolic.6. What are the roles of insulin,glucocorticoids, sex steroids and thy-roid hormone in normal growth? Howdo these relate to growth hormone?Insulin: Optimal concentrations ofinsulin are required for normal growthduring postnatal life. Insulin stimulatesprotein synthesis and inhibits proteinbreakdown. Without insulin, normal re-sponses to GH are not seen and protein breakdown is severe. Insulin promotesgrowth primarily by shuttling nutrients(glucose and some amino acids) insidecells, providing energy and the buildingblocks for protein synthesis. Note thatinsulin and GH must both be present atthe same time for normal growth to oc-cur. Guyton (5) suggests that this is be-cause insulin and GH each shuttle a DIF-FERENT compliment of essential aminoacids inside cells, and of course all of theessential amino acids must be present atthe same time for protein synthesis (andthus growth) to occur. Neither insulin norGH alone is sufficient to supportnormal growth — it takes optimallevels of all the body’s hormonesto produce optimal health and opti-mal gains. As noted in a previousbulletin, excess insulin cannot cre-ate muscle mass, but it will pro-mote fat storage. It’s not the calo-ries in sugar that make you fat —it’s the insulin response (7,8).Glucocorticoids: Glucocorti-coids (primarily cortisol) promoteoptimal function of a wide varietyof organ systems, but do not havedirect growth promoting actions.Excess GC’s inhibit growth by thecatabolic effects of cortisol (in-creased protein breakdown). Nor-mal levels of GC’s seem to be needed topermit optimal function of the other hor-mones. The concept here is that gluco-corticoids act to stimulate (or maintain)optimal levels (amounts) of metabolic en-zymes, whose activities in turn are regu-lated by the other hormones. GC’s sortof set the stage and make sure all of themachinery is in place. Cortisol functionsto make sure the key regulatory enzymesare present in sufficient amounts to allowallosteric regulation (enzyme regulation viasmall effector molecules such as meta-bolic intermediates) and enzyme regula-tion by other hormones.

Also, cortisol isimportant in maintenance of glucose lev-els and resistance to stress, which intu-itively would seem important for normalgrowth.Sex Steroids:Androgens: Androgens (such as tes-tosterone) are potent stimulators of lineargrowth in children whose epiphyses (thegrowing ends of bones) have not yetclosed. Androgens can promote somegrowth in the absence of GH, but com-bined treatment with androgens and GHtogether promote more rapid growth thanthe sum of the two hormones alone. Thisis an example of the synergistic action ofcertain hormones. Much of the growth-promoting action of androgen appears tobe mediated by increased GH secretion(6). Androgens increase the frequencyand amplitude of GH secretory pulses (6).In addition to promoting linear growth,androgens also stimulate growth ofmuscle, and this can occur in the absenceof GH or T3. Androgens bind to nuclearreceptors and the hormone-receptor com-plex in turn binds to chromosomes andactivates transcription of specific genes.Estrogens: In normal girls, theadolesent growth spurt usually occurs be-fore estrogen secretion is sufficient to ini-tiate breast development and is probablyattributable to very low concentrations ofestrogens (6). Paradoxically, concentra-tions of estrogen sufficient to promotebreast development actually inhibit growth(6). Stranger still is the fact the concen-trations of estrogens which inhibit growthincrease GH secretion. What is the basisfor the complex interaction between es-trogen and GH? High concentrations es-trogens appear to inhibit growth by inter-fering with the actions of GH (6). Estro-gens also antagonize the effects of GH onnitrogen retention. Of course, estrogen isalso responsible for the characteristic fe-male fat distribution. The differential ef-fects of estrogen and testosterone, as wellas their different interactions with GH, ex-plain why males on average contain 50%more muscle mass than females and whyfemales have a higher body fat percent-age.At the same time thatgonadal steroids stimulatelinear growth, they also ac-celerate closure of the epi-physes (the sites at the endsof the bones where boneelongation occurs) andtherefore limit the finalheight that can be attained.This is why linear growthstops a few years after pu-berty. GH and the sex ste-roids are still present andactive, but the ends of bonesare permanently sealed andcannot grow anymore. Flatbones, such as the bone inyour forehead, can still in-crease in thickness, however. People whoabuse growth hormone experience thiscondition, known as acromegaly.Thyroid Hormone: Thyroid hormoneis present in two forms, known as T3 andT4. Most of the circulating hormone is inthe form of T4 which is converted to themore active T3 form inside target cells.Thyroidectomy (removal of the thyroidgland) has nearly as devastating an effecton growth as does hypophysectomy (re-moval of the pituitary gland — the body’ssource of GH). Restoration of T3 and T4promptly reinitiates growth. T3 and T4have little if any growth promoting effectin the absence of GH however. T3 acts topromote the actions of GH at three levels:GH synthesis, GH secretion and GH ac-tion. Plasma concentrations of GH arevery low in the absence of T3 or T4. This action is independent of GHRH (growthhormone releasing hormone) and appearsto be exerted directly at the level of genetranscription. In addition to its permissiveeffects on GH synthesis, T3 maintainsnormal responsiveness of somatotropes(the cells that make GH) to GHRH. Fail-ure of growth in thyroid deficient indi-viduals is largely due to GH deficiency.However, even large amounts of GH can-not sustain normal growth in thyroidec-tomized animals unless thyroid hormoneis also given. Thyroxin decreases theamount of GH needed to stimulate growth(increases sensitivity) and exaggerates themagnitude of the response (increases ef-ficacy). T3 and T4 seem to potentiate theeffects of GH on long bones and to in-crease its effects on protein synthesis inmuscle and liver.In summary, GH interacts withinsulin, the sex steroids and thyroidhormones directly to stimulategrowth. These actions are not onlycrucial to growth during childhoodbut are also at the very core of theadaptations which occur in responseto exercise.

Thyroid hormone is re-quired for optimal GH release andfunction. Glucocorticoids (cortisol)are also required in normal levels toplay a supporting role. Cortisol en-sures that the metabolic enzymes arepresent in sufficient amounts so thatGH, insulin and testosterone can ex-ert their effects. If cortisol is too low,optimal growth cannot occur be-cause enzyme levels are too low, and ifcortisol is too high you will actually losemass because high cortisol levels are cata-bolic and promote protein breakdown.Epinephrine is released during exercise andis the most potent stimulus for fat break-down. It is the interplay of these hormonesin the proper balance that makes a greatbodybuilder. These hormones controlmuscle and fat metabolism, and the strat-egy behind a bodybuilding diet and train-ing is to control them to produce a lean,muscular body.7. What exactly is the molecularstructure of human growth hormone?GH is a protein. Ninety percent of GHproduced by somatotropes (cells of thepituitary gland where growth hormone ismade) is comprised of 191 amino acidsand has a molecular weight (MW) of about22,000 daltons (6). The other 10% has aMW of 20,000 and lacks 15 amino acidscorresponding to residues 32 to 46 of the22,000 MW form. Both forms are prod-ucts of the same gene and arise from dif-ferential RNA splicing. Both forms aresecreted and have similar growth-promot-ing activity, although the metabolic effectsof the 20K form are reduced. GH is storedin the anterior pituitary and is the mostabundant of the anterior pituitary hor-mones. As much as half of the GH inplasma protein and a substantial fractionis in the form of dimers or oligomerswhich are inactive. hGH used for therapytoday is produced in bacteria from thecloned gene.8. Describe the major effects ofGH on growth (linear and mass) andmetabolism of carbohydrate, proteinand fat.Linear growth: Linear growth is aconsequence of elongation of the skeleton,especially the spine and leg bones. Prolif-eration of chondrocytes (cartilage cells)at the epiphyseal border of the growthplate is balanced by cellular degenerationat the diaphyseal end, so in the normallygrowing individual the thickness of thegrowth plate remains constant as the asthe epiphyses are pushed farther apart bythe elongating shaft of the bone (6). Inthe absence of GH there is severe atro-phy of the epiphyseal plates, which be-come narrower as proliferation of carti-lage progenitor cells slows markedly. Con-versely, after GH is given to a hypopitu-itary subject, resumption of cellular pro-liferation causes columns of chondrocytesto elongate and the epiphyseal plates towiden. Bone growth is also accompaniedby an increase in diameter, which involvesbone remodeling. Treatment with GH of-ten induces a transient increase in urinecalcium and phosphorus excretion, re-flecting stimulation bone remodeling.Mass: GH increases lean body massby stimulating protein synthesis and in-creasing nitrogen retention.

GH-deficientindividuals have a relatively high propor-tion of body fat. Treatment with GHcauses a decrease in body fat accompa-nied by an increase in body protein,mostly muscle.Carbohydrate Metabolism:Sometimes, particularly after a pe-riod of glucose deprivation, GH hasan insulin-like effect in increasingglucose uptake and utilization. Thisanomalous effect disappears quicklyand its physiological significance isa mystery. After about two hours,glucose metabolism is inhibited inmuscle and adipose tissue. There isa decrease in glucose uptake andmuscle glycogen stores are pre-served.Fat Metabolism: In adipose tis-sue GH promotes breakdown ofstored triglyceride (body fat) whichincreases plasma free fatty acids(FFA). Since glucose uptake is sup-pressed by GH, fat synthesis is also sup-pressed. These effects, combined resultis a net loss of body fat.Protein Metabolism: As already dis-cussed, GH promotes nitrogen retentionand increases protein synthesis, mainly asmuscle. Part of this effect may be due toGH’s role in transport of certain aminoacids inside cells (5). Immediately afterGH injection, plasma amino acid concen-trations decrease as a result of rapid up-take and conversion of protein.The thing to remember is GH de-creases glucose uptake and utilization andspares glycogen, it increases use of fatfor energy by mobilizing fat stores and it increases protein synthesis. The net ef-fect is to make the body leaner and moremuscular. Many of the effects of exer-cise in making the body leaner and moremuscular are mediated by an exercise-in-duced increase in growth hormone (1,2).9. How do bones grow and how doesGH affect this process? Growth of long bones occurs by aprocess of called endochondrial ossifica-tion, in which proliferating cartilage is re-placed by bone. Proliferation ofchondrocytes (cartilage cells) occurs atthe epiphyseal plate — the ends of thebones where growth occurs. Frequent di-vision of small cells in the germinal zoneat the distal end of the growth plate pro-vides for continual elongation of the col-umns of chondrocytes. GH stimulatesproliferation of chondrocytes, and thusbone elongation. GH also stimulates os-teoblastic progenitor cells to proliferatecausing bone remodeling and an in-crease in bone diameter. Lack of GHgreatly retards bone growth, and with-out GH normal height cannot beachieved.10. How are the effects of GHmediated at the cellular level? Whatis the “somatomedin hypothesis”and the “dual effector hypothesis?”The SOMATOMEDIN HYPOTH-ESIS explains the observation that GHalone is not sufficient to stimulate pro-liferation of cartilage progenitor cells,or protein synthesis by cartilage cells,in vitro.

To study the cellular effects ofGH, cartilage cells are isolated andgrown in culture dishes. When normalblood plasma was added to the mixture,or plasma from a hypophysectomizedrat which had been treated with GH, therewas a sharp increase in protein synthesis,DNA synthesis and bone matrix forma-tion. These effects could not be stimu-lated by adding plasma from a hypophy-sectomized rat which was not treated withGH. These experiments demonstrate thatGH requires a factor from plasma to beactive, and this factor itself is induced byGH. Thus, GH may not directly promotegrowth itself, but rather stimulates the liverto produce and intermediate blood-bornesubstance that stimulates chondrogenesisand perhaps other processes as well. Thissubstance was originally called somatome-din C (somatotropin mediator C). Its in-sulin-like effects on glucose and its mo-lecular resemblance to proinsulin gave riseto the name insulin-like growth factor(IGF). Now, two IGFs are known: IGF-I (somatomedin C) and IGF-II. IGF-I isa small peptide (MW 7500) produced pri-marily by the liver. It is tightly bound tospecific carrier proteins in the plasma.IGF-I can cause hypophysectomized ratsto grow in the absence of GH, indicatingmany of the actions of GH are mediatedby IGF-I.The DUAL EFFECTOR HYPOTH-ESIS explains the observation that injec-tion of GH into epiphyseal cartilage of oneleg of a hypophysectomized rat producesgrowth in only that leg. This means thatthings are a little more complicated thanexplained by the original somatomedinhypothesis. Studies with cultured fibro-blasts which can differentiate intoadipocytes in a manner which is absolutelywhich is absolutely dependent on GH mayact directly on precursor cells to initiatedifferentiation. According to the dual ef-fector hypothesis, cartilage progenitor cellsin the epiphyseal plates differentiate in re-sponse to GH and then undergo clonalexpansion (cell division) in response toIGF-I, whose production is also triggeredby GH. Chondrocytes and other cells cansynthesize and secrete GH when stimu-lated by GH. IGF-I may then act as anautocrine to stimulate cell division. Thuswe have two effectors, one to stimulatedifferentiation (GH), and one to stimulatecell division (IGF-I). IGF-I may act lo-cally in processes such as wound healingand compensatory growth.Apparently eccentric (lowering) mus-cular contractions result in tearing of myo-fibrils (muscle fibers) and this in someway causes local release of IGF-I whichacts as a paracrine to stimulate differ-entiation of satellite cells into newmyocytes (muscle cells). Exercise is re-quired to induce a GH response (whichin turn induces hepatic IGF-I produc-tion) and to produce the micro-traumawhich serves as the stimulus for tissueremodeling.11. How is GH secretion regulatedin humans?GH secretion is stimulated by sleep,stress, low blood glucose, an increasein certain amino acids (especially argin-ine, leucine, valine and ornithine) andexercise. Normally GH is secreted in anepisodic fashion with maximal secretionoccurring during deep sleep. GH is syn-thesized and stored in the anterior pitu-itary, and its plasma level is controlledvia its rate of secretion. Its rate of se-cretion is controlled by two hormonesin the hypothalamus: GHRH (growthhormone releasing hormone) and soma-tostatin (which inhibits GH release). GHsecretion is thus under minute-by-minutecontrol by the nervous system. GH se-cretion is also controlled by negative feed-back, mediated by IGF-I. IGF-I appearsto increase release of somatostatin by thehypothalamus and to reduce the respon-siveness of the pituitary to GHRH. In ad-dition to direct regulation by the hypothala-mus, GH release is indirectly regulated bythyroid hormone. T3 stimulates GH re-lease by maintaining sensitivity tosomatotropes to GHRH.

T3 enhancesGH’s actions by decreasing the amount of GH needed to stimulate growth (in-creases sensitivity) and exaggerating themagnitude of the response (increases ef-ficacy). T3 and T4 seem to potentiate theeffects of GH on long bones and to in-crease its effects on protein synthesis inmuscle and liver.12. How does the integrated GHconcentration change with age?GH secretion is most active duringthe adolescent growth spurt and persiststhroughout life, long after the epiphyseshave closed. GH secretion gradually de-creases in both men and women betweenages 20-40.13. What are the effects of excessGH in humans before and after the endof adolescent growth?Overproduction of GH in childrenproduces giantism — and adult height ofover eight feet may be achieved. Over-production of GH in adulthood resultingfrom a pituitary tumor, or abuse of GH,produces acromegaly. This condition ischaracterized by thickening of the craniumand mandible and enlargement of the bonesof the hands and feet. There is also ab-normal growth of the ribs, liver and spleenand thickening of the skin. You never haveto worry about acromegaly resulting fromnaturally increasing your body’s own pro-duction of GH. You can naturally increaseGH enough to dramatically increasemuscle mass and decrease body fat, butnot enough to experience the side effectsof acromegaly. Acromegaly only resultsfrom pituitary disease or abuse of exog-enous GH.14. What are the effects of diet andexercise on GH?What should I do to naturally increaseGH levels? There are several things youcan do as a bodybuilder to naturally in-crease your GH levels (9). First, eat anadequate diet containing at least one gramof protein per pound of body weight. Ahigh protein meal increases GH release.Also remember our previous bulletin aboutdialing in your protein to carbohydrateratio to optimize insulin and glucagon lev-els. Second, supplement your diet withMax GH Formula containing the most ef-fective combination of amino acids for GHrelease ever produced (10). Use Max GHFormula before bed and before training.Always take it on an empty stomach. Gly-cine is also a potent GH stimulator (3) andthis may explain the well-known anaboliceffects of glycine. Parrillo PerformanceHi-Protein Powder and Pro-Carb Formulaare fortified with significant amounts ofglycine. This combination of supplements,along with the right diet, has proven overthe years to be incredibly anabolic. Third,make sure you get enough sleep. Maxi-mal GH release occurs during deep sleep.Take a nap during the afternoon if pos-sible. Fourth, train smart.

Heavy, low-repwork is known to be effective in increas-ing strength. This is probably due to anincrease in testosterone levels and a train-ing effect on the nervous system. High-rep work with moderate weights is moreeffective in stimulating GH release (1,2,9).It’s a huge mistake to leave out the high-rep part of your training. While low-repwork is more effective in increasingmuscle strength, high-rep work is veryeffective in increasing muscle size. TheGH release resulting from high volumetraining also serves as a potent stimulusfor fat loss.Of course, you need both high-repand low-rep work to make continuingprogress. Don’t get the idea that youdon’t have to lift heavy weights any-more. If you want to get biggermuscles, you will always have to liftheavy weights — but you also have toincorporate high-rep work for maximumdevelopment. There are several strate-gies for doing this. You can incorporateboth heavy and light work into the sametraining session using a pyramid tech-nique. Start with one or two warm upsets around 15 reps. Use a light weightwhen warming up and do not go to fail-ure. Then pick a weight you can handlein good form for ten reps. Continue in-creasing the weight and do sets of eight,six and four reps. Take all working setsto positive failure. Then decrease theweight and do a set of 20 reps to fail-ure. This helps pump the blood into themuscle and stimulates GH release.Lower the weight slowly, emphasizingthe eccentric part of the contraction.This is especially important at the endof a set when ATP is the muscle is de-pleted. ATP is required for muscle re-laxation as well as muscle contraction.When a muscle runs out of ATP it “locksup” in the contracted state and cannotrelax properly. This state is known as“ischemic rigor.” When the muscle isin rigor and your are lowering a weightfrom the contracted position, the fiberscannot relax and literally get torn as themuscle elongates. If this sounds pain-ful, it is. Most people stop a set just asthis starts to happen because the paingets unbearable. The ones who fightthrough the pain and crank out a fewmore reps are the ones who get bigmuscles. Sorry, but that’s the way it is.Another way to incorporate high repwork is to train in the four-to-eight reprange one week and the 12-to-20 reprange the next week. Finally, somepeople do a “powerlifting cycle” involv-ing heavy, low-rep work for four-to-sixweeks followed by a “bodybuildingcycle” with moderate weights and higherreps for the next four-to-six weeks.Most advanced bodybuilders have ex-perimented with all three strategies atsome point. The key is to find whatworks best for you. If you’re at a pla-teau, it’s probably time for a change.To break out of a plateau, increasecalories and try training less frequentlyby with heavier weights. If you haven’tbeen doing any high-rep work, doingsome will probably stimulate a growthspurt. Of course, there are many rea-sons for reaching a training plateau, butthey usually relate to over-training, un-der-training, under-nutrition or notenough rest. Constant fatigue, loss oflibido and failure to recover from work-outs are signs of over-training and notenough rest. If you neglect any part ofthe program — high-rep training, low-rep training, aerobics, stretching rest,nutrition, or supplementation — your re-sults will definitely suffer. The ParrilloProgram is a balanced approach cover-ing every facet of bodybuilding. Yousupply the hard work, consistency anddedication, and we’ll supply the winningstrategy.  

References

1. Kraemer WJ. Influence of the en-docrine system on resistance training ad-aptations. Nat’l Strength and Condition-ing J. 14: 47-54, 1992.

2. Kraemer RR, Kilgore JL, KraemerGR and Castracane VD. Growth hor-mone, IGF-I and testosterone responsesto resistive exercise. Med. Sci. SportsExerc. 24: 1346-1352, 1992.

3. Colgan M. Optimum Sports Nutri-tion. Advanced Research Press, NewYork, 1993.

4. Rudman D, et al. Effects of Hu-man Growth Hormone in Men over sixtyyears old. N Engl. J. Med. 323: 1, 1990.

5. Guyton AC. Textbook of MedicalPhysiology. W.B. Saunders, 1991.

6. Johnson, LR. Essential MedicalPhysiology. Raven Press, New York,1992.

7. de Castro JM, Paullin SK, andDeLugas GM. Insulin and glucagon asdeterminants of body weight set point andmicroregulation in rats. J. Comp. Physiol.Psychol. 92: 571-579, 1978.

8. Remington DW, Fisher AG, andParent EA. How to Lower your Fat Ther-mostat. Vitality House International,Provo, 1983.

9. Crist DM. Growth Hormone Syn-ergism. DMC Health Sciences, Albuquer-que, 1991.

10. Isidori A, Lo Monaco A, andCappa M. A study of growth hormonerelease in man after oral administration ofamino acids. Current Medical Researchand Opinion. 7: 475-481, 1981.

2018-03-13T11:10:38-04:00 May 13th, 2009|Technical Supplement Bulletins|

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