The science of Hypertrophy Part1 (Prob the most Important Read about Training Ever)

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    The science of Hypertrophy Part1 (Prob the most Important Read about Training Ever)


    The Science of Hypertrophy
    Taking a new look at the “workout”

    Introduction: Hypertrophy, simply stated, is an increase in muscle. Muscle cells are not like regular circular cells. Muscle cells are long and complicated and have several nuclei (brains of the cell). They are elongated with a fibrous interior full of little bands of contractile proteins that pull against each other to make muscles contract.. There are several ways to achieve hypertrophy. One way is to add more contractile proteins so the muscle is bigger and has more to pull with, making it stronger; however, only so much protein can be added before the muscle runs out of nuclei to control all the contractile proteins. In this case, muscles must actually recruit more nuclei, cellular organelles and proteins etc. from satellite cells. Satellite cells are essentially dormant in the body, waiting to be recruited to become a functional cell. They have no function until they are signaled to become something else, such as joining with other muscle cells to make a single, larger cell out of two merging cells.

    Brief Physiology and Endocrinology
    Your body has many ways to accomplish the above to things. It can release IGF-I (insulin like growth factor) both systemically and locally which causes the satellite cells to replicate, as well as, the relocation of some satellite cells to existing muscle cells by fusing with them, making them larger, and giving the ability to take on more contractile protein. Testosterone and other androgens can also cause satellite cells to replicate and relocate. They work by signaling androgen receptors on the satellite cells signaling them to replicate and fuse with muscle cells. Androgen receptors are unique in that, unlike most other receptors, androgen receptors actually increase in number with stimulation, making testosterone more effective over time. These receptors will drop down after a prolonged period or exposure to high levels of testosterone though. Lactic Acid is created during workouts as a bi product of creating energy. This is usually the cause of the burn, or soreness that follows shortly after a workout. Lactic acid signals the muscle and connective tissues for repair and in doing so also directly corresponds to an increase in HGH (human growth hormone). HGH is the body's main growth hormone. It signals the release of many other growth factors and metabolic regulators, so while it may not be directly affecting the muscle in the way that some of these other hormones do, HGH indirectly increases things such as IGF. Studies have also shown that in the absence of HGH the muscles while still containing the same number of fibers have significantly reduced muscle fiber width. MGF (mechano growth factor) and IGF-IEa are locally produced growth factors that are produced by the muscle itself. MGF is the main growth factor in replicating the satellite cells, it is the most important and most effective thing produced for increasing muscle satellite cells. IGF-IEa is its counterpart and is most effective at causing the satellite cells to fuse with muscle cells. MGF and IGF-IEa are released by muscles in response to stress and stretch stimulation. They are released in stages, MGF first and IGF-IEa a few days later. This allows for a natural process of regeneration of satellite cells, ensuring the population is never depleted. Depletion of satellite cells makes replenishing them harder because there are fewer cells replicating. These two growth factors are splice variants of IGF-I, together they are more effective than IGF-I but they are limited in that they can not cause hypertrophy themselves. However, IGF-I can signal the process of both of these, but not as effectively. The other difference is MGF and IGF-IEa are produced locally and do not effect other parts of the body where as IGF-I is a systemic growth factor mainly produced by the liver that effects many other parts of the body. There are also things that our body does to limit hypertrophy and/or induce atrophy (muscle wasting). Some training methods, although they up-regulate several of the hypertrophy inducing factors, actually stimulate some of the limiting and atrophy inducing factors. One hot topic is Myostatin. Myostatin is a protein produced by the body that keeps the muscle stem cells from replicating. This counteracts the positive effects of growth factors like IGF and hormones like testosterone. Another way that the body can prevent hypertrophy is through a rapamycin. Rapamycin blocks the hypertrophy signaling that is brought about by the activation of the AKT pathway and down stream regulators that are up-regulated by IGF. So it prevents some effects of training and IGF.
    Angiotensin II is a factor that down regulates AKT, reduces circulating IGF levels and increases protein breakdown and programmed cell death in muscle tissue. Limiting any expression of this factor is extremely valuable. It seems that stimulation of IGF combats the effects of Angiotensin II as well.

    In vivo research studies
    The Basic Rep
    Each repetition of an exercise consist of two motions. The eccentric (lowering or un-contracting) and the concentric (raising or contracting). Studies have shown that performed individually concentric training yields a greater gain in muscle size, soreness, and creatine kinase activities. Eccentric training yields greater range of motion, and maximum isolation strength. The amount of tissue damage is significantly greater during the eccentric portion of the rep. Taken together in the proper ratio of emphasis using tempo lifts such as a 2 sec contraction and a 1 second eccentric motion for example can provide optimal increase in muscle size and strength. It is important to note that while the eccentric training may not yield immediate gains in mass, the damage induced repair will lead to increased muscle cell nuclei giving it a higher potential for further growth. This is because the stretch and stress will increase MGF and IGF-IEa in the muscles worked. So the importance of the negative portion of a rep can not be underestimated.

    How Many Sets?
    Studies show that when comparing a single max effort set of 10 reps after warm up compared to that of a set of 6 reps yielded very different results. Androgen receptors were up-regulated greater in the single set group, in fact there was a 46% drop in androgen receptor content at 1 hour post exercise in the 6 rep group. However the 6 rep group showed a 12-23% increase in testosterone levels post exercise. Thus further research has shown that between these extremes in the 2-3 rep range with proper intensity you can up-regulate both testosterone levels and the androgen receptors with less muscle damage creating a much more anabolic environment. In addition to testosterone studies have shown that when comparing 2 vs 4 sets of an exercise, the 4 sets resulting in increased cortisol levels and HGH levels after muscle hypertrophy (1-RM), 3-min rest) and MH (10 reps at 75% of 1-RM, 2-min rest) and strength endurance training(15 reps at 60% of 1-RM, 1-min rest). There were no differences between muscular strength or testosterone levels between these two groups. Further research would suggest that because of the time length and repeated isolation of the same muscles only cortisol levels began to increase accordingly. By reducing either the time frame or number of sets the HGH./cortisol level may have been more favorable. Spending 12-18 minutes on one exercise is not a good idea. GTP utilizes a method of reps and sets to achieve the HGH stimulation without causing a cortisol increase as seen here.
    In addition one must consider the effects of exercise induced damage in high set workouts. It does not take a lot to achieve enough muscle damage to signal repair. Research shows that a few skeletal muscle adaptation can be brought about by a single bout of relatively few eccentric muscle contractions. Increasing the number of eccentric muscle repetitions did not result in an increased prophylactic effect on skeletal muscle. Furthermore adaptation to eccentric exercise can occur in the absence of significant muscle damage. Exposure to a small number of non-damaging eccentric contractions can significantly improve recovery after a subsequent damaging eccentric bout. However this adaptation appears to be mode-specific and not applicable to concentric contractions.
    In conclusion the cellular response for growth from muscle damage is directly related to creatine kinase levels which do not increase with further muscle damage by repeated eccentric sets.

    How often/ training frequency
    Training frequency has been discussed among athletes for quite some time. Research shows that while everyday training actually increases anti-hypertrophy factors and increase in myostatin levels, 48 hours in between sessions provides a steady anabolic environment. Serum testosterone levels, the free androgen index, Androgen receptor mRNA and protein were significantly increased. No negative factors were found to be increased in this study. With more than 48 hours between exercise sessions these levels begin to decline fast. This study used 3 sets of the exercise, and took data after 3 sessions each 48 hours apart.

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    Rating the Other Workout Routines

    HST Hypertrophy Specific Training
    Benefits: Utilizes optimum training frequency, fairly good stimulation of testosterone and androgen receptors and protein turn over. Low chance of increasing cortisol levels, does not cause unnecessary muscle damage. Moderate IGF-I stimulation.
    Flaws: Fails to utilize HGH and lactic acid induced hypertrophy, limited MGF/IGF-IEa stimulation.

    DC Training
    Benefits: Utilizes HGH and lactic acid pathways to hypertrophy very well. Good at increasing testosterone. Stimulates MGF and IGF-IEa pathways. Burns a lot of calories.
    Flaws: High likelihood of increased cortisol. Detrimental to androgen receptor content. Significant muscle damage can occur achieving your goal leading to increased risk of injury and limits in strength. Fails to keep the body in an anabolic state with time through training frequency.

    Traditional Upper/ Lower Body Split (M T TH F routines)

    Benefits: Generally utilizes HGH and lactic acid, provides stimulation for MGF and IGF-IEa somewhere between HST and DC. Better frequency than DC training, resulting in a more steady anabolic state but not as good as HST. Moderate to good testosterone stimulation.
    Flaws: Slightly less likely to increase cortisol than DC, and prone to decreased androgen receptor content. In between Dc and HST on muscle damage.

    The Once Per Week for Each Body part Routine
    Benefits: Good testosterone stimulation and HGH/lactic acid stimulation. Muscle damage is likely but optimal time for repair if muscle damage is moderate. Good MGF stimulation.
    Flaws: Very short term anabolic state for growth to occur. What stimulation there is, is short lived. Often times has high cortisol levels and decreased androgen receptors associated. While there may be optimal time for muscle repair, connective tissue damage may not be able to repair at a rate that is safe.

    HIT High Intensity Training
    Benefits: No muscle Damage issue. Not time consuming. No increase in cortisol levels. No negative effect on androgen receptor content.
    Flaws: Poor increase in testosterone and practically no increase in HGH or lactic acid levels. Limited MGF stimulation.

    GTP Games Training Protocol
    Benefits: Almost equal stimulation of HGH and lactic acid hypertrophy pathways without increasing muscle damage or cortisol levels. Significantly increased testosterone and androgen receptor content. Very good stimulation of MGF and IGF-IEa.
    Flaws: Workout is demanding and intense.
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    Interesting read, but is this nothing more than a thinly veiled advertisement for the games training protocol?
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    Quote Originally Posted by max silver
    Interesting read, but is this nothing more than a thinly veiled advertisement for the games training protocol?
    Thanks for seeing it that way.
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    I'm sorry but that's how it comes across. It shows the information about exercise and body hormone responses, and at the end posts information about different exercise programs. Of note is the GTP program, where the pros and cons are mysteriously highlighted, whereas they are not with any of the other programs. It states that it is optimal compared to the other programs, with the only con being the fact that the workouts are demanding. If this isn't written to specifically interest the reader in the GTP program, when what is it's purpose?
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    Quote Originally Posted by max silver
    I'm sorry but that's how it comes across. It shows the information about exercise and body hormone responses, and at the end posts information about different exercise programs. Of note is the GTP program, where the pros and cons are mysteriously highlighted, whereas they are not with any of the other programs. It states that it is optimal compared to the other programs, with the only con being the fact that the workouts are demanding. If this isn't written to specifically interest the reader in the GTP program, when what is it's purpose?
    Well actually it is written to interest the reader in GTP b/c of those very facts. I am not taking away from other programs, I researched them all extesnsively to be able to come up with GTP.

    If bobo lets me I'll link the log of GTP's testing. But i have made a few vairations and am gonna take testers from all boards soon so I want to get it out there. Its an amazing program, It kicks my butt still. I used to live by HST, but I wanted more cuz going fomr wsbb and DC and HST depedning on where I was with football I would always seem to go backwards in some areas with each program.
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    Can you provide any actual information about the program? I'm sure plenty of people (myself included) Would be interested in some concrete information about what makes the plan work.
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    Quote Originally Posted by max silver
    Can you provide any actual information about the program? I'm sure plenty of people (myself included) Would be interested in some concrete information about what makes the plan work.
    Thats coming in part 2. I dont have it finished and I am having it protected. so it will be linked here when I get it done
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    Quote Originally Posted by TheGame46
    Thats coming in part 2. I dont have it finished and I am having it protected. so it will be linked here when I get it done
    I'll wait for that. Should be interesting. Good luck.
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    Same advice here as I gave you elsewhere...


    You're in someone else's house and are here as a guest. Respect the house rules and when you are trying to work a business then it pays to talk to the owners to make sure you:

    1. Get persmission
    2. Get any special considerations
    3. Say thanks.

    When the board members see this as a way to promote your business what do you think the board owners think who you are spamming. Most of us frequent the same circle of boards. I hope you end up making a great new way to get big but don't do it by stepping on the necks of those who facilitated it for you.
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    Hypertrophy and Load Part II by Anoop T. Balachandran

    What's different about it over Balachandran's?
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    Quote Originally Posted by max silver
    Can you provide any actual information about the program? I'm sure plenty of people (myself included) Would be interested in some concrete information about what makes the plan work.
    Me too. I'll be waiting for part II. I don't think any specific program is the end all be all of training, but all the well designed programs add something to the whole, and at the very least give you a new approach to use when you're bored with your current routine or change your goals.
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    Quote Originally Posted by Jayhawkk
    Same advice here as I gave you elsewhere...


    You're in someone else's house and are here as a guest. Respect the house rules and when you are trying to work a business then it pays to talk to the owners to make sure you:

    1. Get persmission
    2. Get any special considerations
    3. Say thanks.

    When the board members see this as a way to promote your business what do you think the board owners think who you are spamming. Most of us frequent the same circle of boards. I hope you end up making a great new way to get big but don't do it by stepping on the necks of those who facilitated it for you.

    I emailed bobo bro
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    Quote Originally Posted by Jayhawkk
    Hypertrophy and Load Part II by Anoop T. Balachandran

    What's different about it over Balachandran's?
    That was a good read.
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    Quote Originally Posted by Jayhawkk
    Hypertrophy and Load Part II by Anoop T. Balachandran

    What's different about it over Balachandran's?
    That barely covers IGF and the HGH IGF axis, and has no mention of MGF or IGF-IEa and those factors. The research I'm using is much newer, more in depth and pracically applied. Part too will be the meaty science part.
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    Quote Originally Posted by DragonRider
    That was a good read.
    Its very outdated though
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    Cool deal.
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    Actually this is the full article (part I) and it specifically mentions MGF.


    Hypertrophy and Load
    by
    Anoop T. Balachandran

    Needless to say, resistance training induced hypertrophy is inextricably linked to its participating variables, such as frequency, load, rest intervals, and the number of sets. As is true for adaptations like endurance and strength, the severity of the response is dependent on the manipulation of these variables. Although the role of these variables has been extensively studied and well documented, the optimum ”value” of these variables for maximum hypertrophy is still under considerate debate.

    Among these variables, load seems to be the most dominant variable dictating these muscular adaptations, and hence will assume the lead role in this article. Load, typically advertised in terms of repetition maximum (RM), can be equated to the number of repetitions performed in a set. The generally accepted repetition bracket for hypertrophy is 67 – 85% 1RM, which can be equated to 6–12 repetitions, and 85-100% 1RM (1-6 repetition) for strength (7, 21).

    Though the load recommendations for strength and hypertrophy seem to differ, except for existential evidence, there is hardly any scientific data to support this differential rep continuum. Interestingly, in contrast to the above said guidelines, the couple of studies which directly compared low rep and high rep protocols demonstrated similar hypertrophic responses (10, 29). Influenced by the above said discrepancies, this article will look into the factors implicated in skeletal muscle hypertrophy and examine how they are impacted by the manipulation of load.

    Before we continue, I will give an introduction to the well orchestrated events leading to skeletal muscle hypertrophy. Studies, both in vivo and in vitro have repeatedly demonstrated the involvement of two fundamental events in the hypertrophy of muscle fibers. The first and foremost is an increase in protein synthesis, mainly attributed to increased mRNA activity (translational capacity). The unstable relationship between protein synthesis and protein degradation represents the basis for hypertrophy. Muscle growth follows when a positive protein balance is established and maintained by an increase in protein synthesis that exceeds the rate of protein breakdown (24).

    The second facet of hypertrophy involves an increase in mRNA abundance (transcriptional capacity) via differentiation and proliferation of satellite cells, which is critical for donating additional myonuclei to the enlarging myofibers. Unlike most other cells, mammalian skeletal muscle is multinucleated. Each and every nucleus is responsible for a particular volume of the cell, known as a nuclear domain (16). This domain is tightly regulated and any increase in the fiber cross-sectional area requires a concomitant increase in the number of myonuclei (6). Conversely, if the cell experiences serious atrophy as seen in immobilization, space flight, malnutrition, or tenotomy, the number of myonuclei decreases by a process of programmed cell death (20, 26). This indicates that the tight regulation of the domain is preserved in either direction.

    The concept of a finite relationship between fiber size and myonuclei number predicts that the hypertrophying fibers must increase their myonuclear number proportionally. However, shortly after birth, mammalian myofibers are permanently differentiated, and thus cannot undergo mitotic division or directly increase their myonuclear number by means of the usual myonuclear division process (11). Therefore, hypertrophying fibers require an external source of new nuclei to maintain a relatively constant nucleus-to-fiber size ratio. A significant body of evidence blames satellite (stem) cells as the probable source of the new myonuclei (8, 28).The role of satellite cells in hypertrophy has been further corroborated by studies using radiation to prevent satellite cell activity, thereby negating any potential hypertrophic response (5, 25).

    In short, with utter disregard for the set tone, satellite cell activity is required for you to get big while protein synthesis is necessary for you to stay big. Frankly, at first, I thought of painting a scientific tone to the article, but soon realized that the complexity of the topic at hand would undermine the message. Perhaps, ignoring my mom’s words, there was never a scientist in me to begin with. Without further delay and resuming a laid back tone, let us cruise towards our next topic: how satellite cells are triggered and how load can have any bearing on this.



    Mechanical Factors

    Staying true to the principle of specificity, the cellular level changes discussed above are specific to the muscle that is experiencing functional changes. That is, the factors that confine for example almost exclusively the growth of the biceps when the biceps are exercised alone are largely mediated by things that are intrinsic or local to the exercised muscle (19). As it turns out, mounting evidence has revealed growth factors to be responsible for these localized changes.


    Among these growth factors, insulin like growth factor (IGF-1) is known to stimulate satellite cell activity as well as protein synthesis, and has received increasing attention in the studies of hypertrophy. This increasing attention to IGF-1 is understandable, given its ability to stimulate both proliferation and differentiation, making it unique within the ranks of growth factors. Lest you get confused, this locally expressed IGF-1 acts independently of any change in the serum growth hormone or the serum IGF-1.


    More importantly, IGF-1 is sensitive to mechanical load, as observed in a number of in vivo activity models, such as increased loading, stretch, and eccentric contraction (recently discovered, a specific isoform of IGF-1 called mechano growth factor is exclusively regulated by mechanical loading and/stretch) (1, 2, 3). To further seal IGF-1’s fate, infusion of local IGF-1 directly to skeletal muscles has shown increased muscle mass (4). Looking at all the studies (and the studies which I have omitted for the fear of turning this article into an IGF-1 review paper), I cannot help but conclude that locally expressed IGF-1 is the CHIEF player in mediating muscle growth.


    Just when you thought it was over, I’d like to share what Bamman and his crew discovered when investigating IGF-1’s role in resistance training (9). Not surprisingly, they found that eccentric exercise showed the greatest muscle damage and muscle soreness. As suspected, they found significant increases in IGF-1 mRNA concentration for eccentric than concentric exercises (p<0.05). Based on the soreness and the creatine kinase (CK) data, the researchers concluded myofibrillar disruption and/or sarcolemma damage most likely to play a role in activating the IGF-1 system, and in turn activating the satellite cells.


    The conclusion is in accord with the results observed in vitro, suggesting that the release of other growth factors like hepatocyte growth factor and fibroblast growth factor are also injury-mediated, and their expression is proportional to the degree of injury (13, 27). Another study of note also revealed that the magnitude of protein synthesis was shown to depend on the extent of muscle damage (14). And, as you know very well, muscle damage has been consistently observed in resistance training studies (21).


    As an example of the infamous Repeated Bout Effect (RBE), it was shown using electron microscope that untrained subjects suffered 35% more myofibrillar disruption than strength trained individuals after a typical weight training session, and 40% of fibers of the untrained group displayed severe disruption compared to 3% of the strength trained participants (I guess that’s one more study for Bryan to stack in his HST archives) (17, 18). Now you tell me why you think you stopped growing? Connecting the dots, we get the picture of IGF-1 expression being injury-mediated, with its expression being dependent on the severity of the injury.


    It can be clearly inferred from the previous passages that as the load goes up, the magnitude of the injury should go up too. And this is precisely what Nosake, Newton and Saka concluded after their study (23). They found that the group performing 12 maximal eccentric elbow flexion exercises compared to the group who performed 3600 elbow flexion showed significantly greater muscle damage as tested from B-mode ultrasound and creatine kinase (p<0.05).


    In their second study, Nosake, Newton and Saka concluded that though the magnitude of damage was similar for maximal and submaximal eccentric loading (50% RM), the secondary damage was less after the submaximal loading (22). Though low load activities like endurance training and downhill protocols are said to cause marked muscle damage, the damage appears to be relatively low compared to maximal eccentric exercise of the elbow flexors (12). As an attempt to link hypertrophy and load, an extensive review of weight training studies illustrated greater hypertrophic responses associated with greater load in both Type 1 and Type 2 fibers (16) (29).

    Taken together, all these studies has given me enough confidence to state that the extent of muscle damage is dependent primarily on load, and the degree of damage traces a linear relationship with load.


    So the moral of the story is that microtrauma is mandatory for continued hypertrophy, and the extent of hypertrophy is dictated largely by the load on the bar. The endocrine and metabolic factors implicated in hypertrophy and how load affects those factors will be explored in the next article. Until then, happy loading.
    For answers to board issues, read the Suggestion and News forum at the bottom of the main page.
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    Part II:


    The last article we discussed microtrauma and why it is essential for hypertrophy, as well as how load is linearly related to microtrauma. In this concluding part, we will look into the endocrine and metabolic factors that are often used to determine load guidelines for optimal hypertrophy.


    Endocrine Factors

    As the name connotes, growth hormone (GH) is anabolic in nature. The loss of strength and muscle mass characteristic of GH deficient folks, and the reversal in these performance indices upon GH supplementation, clearly reveals its anabolic role (1,2,3). This information, coupled with the presence of greater GH secretion following resistance training, leads to a barrage of GH studies which are worth discussing.



    Interestingly, common to all these studies is a greater growth hormone response following moderate loads using shorter rest periods when compared with high loads using longer rest periods (4,5,6). Kraemer et al., for instance, showed that performing a 10 RM with 1 minute rest between sets showed greater GH response than performing a 5 RM with 5 minute rest periods (4). Another study reported that performance of 20 sets of 1RM produced a slight increase in GH, whereas a substantial increase in GH was observed following 10 sets of 10 repetitions with 70% of 1RM (5). Call it coincidence if you like, but the protocol that shows the greatest GH release appears to be that of a typical bodybuilding routine, while the program which showed the least GH response mirrored what we typically consider a powerlifting program.



    Although researchers couldn’t find any causal evidence, this GH hypothesis was evidence enough to establish the current load and rest time guidelines for hypertrophy.



    But is the evidence really enough? Let's see: one of the early processes involved in the secretions of GH is the accumulation of metabolic products like lactate (La) and proton (H) in the muscle. The acidic environment in the muscle stimulates sympathetic nerve activity through chemoreceptors, which may send signals to the hypothalamus-pituitary system, and in turn trigger the secretion of GH (6,7). Apparently, the changes in GH seen in most of the studies were in phase with changes in the lactate concentration (4,5). This suggests that metabolic accumulation during exercise is the primary stimulus influencing GH release. For example, Takarada showed a low intensity (20 RM) exercise to cause a 290-fold increase in the concentration of GH when the blood flow was blocked by occlusion (8). This magnitude of increase, even larger than that reported using heavier loads, reveals metabolic accumulation due to occlusion to be primarily responsible for GH release.



    Activities that stress the metabolic pathways like hyperventilation, breath holding, hypoxia and even nicotinic acid ingestion have been shown to profoundly influence growth hormone release (9,10). The high correlation of GH and metabolic products is further supported by the decreased GH response following induced alkalosis during cycling (11). And, keep in mind that all these changes in GH are transient: the resting concentration of GH has never been altered by any sort of resistance training (12,13,14).



    Researchers began to suspect that raising the resting concentration of GH through supplementation might be the key to inducing hypertrophy. After all, GH is a common ingredient in any bodybuilder's drug list. As expected, this let lose another flurry of GH supplementation studies. Surprisingly the majority of the studies, whether in young men, older men or athletes, showed little change in muscle fiber size or strength after GH supplementation (15,16,17). The inability of even supraphysiological doses to elicit a hypertrophic response clearly undermines the role these training-induced tiny spikes of GH play in hypertrophy.



    The discovery of local growth factors and their central role in hypertrophy was the final blow which shifted the foundation of the growth hormone hypothesis. Studies showed muscle growth even after the depression of circulating GH and IGF-1 levels (19). Worse yet, substantial increase in muscle mass was observed even after the GH axis was surgically interrupted (20,21).



    Ironically, after all these counter evidences the repetition bracket of 8-12 is still hailed as the optimum range for hypertrophy- and the same old GH hypothesis is still being quoted in its defense.


    Metabolic Factors

    Though mechanical factors are essential to resistance training adaptations, metabolic factors have also been shown to play a role in hypertrophy.



    The feeling of "pump" or “burn” is associated with the build up of these metabolic products (H, La, P, Cr, and K) in the muscle; the higher the number of reps in a set, the greater their accumulation and effect. Traditionally, studies have used three methods to understand the influence of metabolites on hypertrophy and strength. And, all three methods have revealed conflicting roles for metabolites in hypertrophy.



    Eccentric contractions recruit fewer fibers than concentric contractions when using the same load. This distinct metabolic characteristic of contractions is often exploited to examine the importance of high force stress versus metabolic stress on hypertrophy (1,2). The second method involves the manipulation of rest intervals between sets: shorter rest intervals are metabolically more taxing than longer rest intervals (3,4). The occlusion method uses a pressurized cuff to occlude or clog the blood flow to the exercising muscle and in turn also increases the metabolic fatigue (5,6).



    Now let's delve deeper and look at the possible mechanisms by which the metabolic milieu can impact hypertrophy. One possibility is that the ischemic condition and/or the metabolic changes in the muscle could lead to a greater recruitment of the fast twitch muscle fibers (Type 2). This is quite evident from the greater EMG activity recorded in the occlusion studies. For instance, Moore and his team specifically investigated the neuromuscular activity accompanying occlusion and showed that there is an early activation of Type 2 fibers for the occlusive group compared to the non-occlusive group (5). Another study showed the EMG activity in the low intensity exercise (40% 1RM) with occlusion to be almost equal to that in the high intensity exercise (80% 1RM) without occlusion (6).



    This, along with the greater vulnerability of Type 2 fibers to injury and subsequent hypertrophy might very well be responsible for the greater hypertrophy and strength observed in some of the occlusion and rest interval studies using lighter loads.



    Muscular hypertrophy is a combination of both sarcoplasmic and sarcomeric hypertrophy. In contrast to the actual growth of muscle fibers as in sarcomeric hypertrophy, sarcoplasmic hypertrophy involves the "swelling" of the muscle mainly via increase in water and glycogen accumulation without any change in strength. As evident from the occlusion studies, this increase is prompted largely by the accumulation of metabolites. For instance, exercise in the occluded group showed greater glycogen accumulation than in the non-occluded group (7). Additionally, studies showed glucose uptake to be enhanced in response to hypoxic conditions (8,9).



    The increase in sarcoplasmic volume certainly contributes to overall hypertrophy and might partly explain the increase in muscle mass observed with higher rep training. And it is likely that comparison between repetition studies is distorted, since the current methods for measuring fiber size are incapable of identifying the contribution of sarcoplasmic hypertrophy to the overall muscle size.



    Another mechanism which seems to suggest a role for metabolites in hypertrophy is the production of free radicals. It has been shown that muscular xanthase activity is elevated in hypoxic conditions and produces ROS (free radicals) during subsequent reperfusions. These free radicals via ischemic/reperfusion injuries have been shown to promote growth in smooth and cardiac muscles (11). The periodic application of occlusive stimulus, without any exercise stimulus, attenuates the disuse atrophy of leg muscles. This is possibly due to the direct effect free radicals have on muscle protein synthesis (10).



    All said, hypertrophy through metabolic accumulation almost always occurred in conjunction with some sort of load training. Further, the importance of load is clearly revealed by the greater need for heavier loads in the strength continuum as opposed to the endurance continuum. Hypertrophy credits only a secondary role to metabolic fatigue.


    Practical Considerations

    It is well established that load is the primary stimulus for strength. And if you cared to notice, I've been trying to convey how load is the primary stimulus for hypertrophy too. The greater the load, the greater your strength and muscle gains. Simply put, you can expect greater gains in strength and hypertrophy by using your 1RM for 10 reps than using your 10RM for 10 reps.


    So a fair question would be: are strength increases a good measure of muscle growth? I would say that strength is a yard stick for muscle growth, as well as the BEST indicator of progress one has in a hypertrophy routine. This might seem in stark contrast to those funky neural adaptation programs claiming to selectively target hypertrophy and leave out strength or vice versa.
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    The expression of strength is a blend of neural and muscular adaptations. Neural adaptations are in the form of increased activation, enhanced supraspinal output, intermuscular and intramuscular coordination, antagonist co-activation and so on (1,2). Muscular adaptations can not only show up in the form of increased muscle mass but also in the form of subtle architectural changes in pennation angle, muscle fascicle length and specific tension (3,4). However, most of us have missed that all these neural and architectural adaptations can only contribute so much so far, and beyond those “optimizations” muscle size becomes the leading and indeed the only adaptation that will allow continued gains in strength.

    According to the scheme proposed by D. G Sale--a pioneer in field of neural adaptations--neural mechanisms largely contribute to strength gains during the early phase of training, after which muscular adaptations dominate (1). The same can be inferred from his recent remarks: “After years of training, I suspect that there is little or no neural adaptation that can increase strength further, apart from a change in technique. Strength in the highly trained state is almost entirely a function of muscle mass. This would explain why athletes ultimately resort to anabolic steroids - increasing muscle mass is the only way to increase strength further (Personal Communication).”

    The prevailing belief that powerlifters target the nervous system more so than the muscles by using low reps is yet to be proved by science. It is clear that heavy load around the 1RM causes higher fatigue and requires longer recovery periods than a lighter load. The high fatigue experienced is not just due to nervous system fatigue alone; disruptions in the contractile system are equally responsible (5,6). Powerlifting, often seen as a "little-to-do-with-muscle-event", has been shown to indeed be a function of muscle mass, and lifting performance has been shown to be limited by the ability to accumulate muscle mass (3). And once these elite lifters hit their genetic limits with regard to muscle mass, strength increases are marginal at best (7).


    Even the CNS fatigue which seems to be the buzz word these days is not just a neural phenomenon as it sounds. Overtraining as most of us might have experienced hits in the form of generalized fatigue, depression, muscle and joint pain, loss of appetite, decreased performance, decreased muscular strength and so forth. These signs/symptoms of overtraining are often blamed as a neural phenomenon. But according to the cytokine hypothesis of overtraining, repetitive trauma to the musculoskeletal system due to high intensity/volume training is the predominant cause of overtraining (8,9). That is, the many physiological and behavioral signs associated with overtraining syndrome are basically triggered by a musculoskeletal injury.


    But the question remains: If strength is highly correlated with muscle size, what about those bodybuilders who are big yet not strong?


    First and foremost, elite class bodybuilders are dipped in drugs. And drugs lie right to your face. Testosterone and GH administration have shown to increase retention of fluid (water/salt) within the muscle that would cause an enlargement of the muscle fibers with little strength change (15,16). Second, testosterone is shown to cause changes in strength by altering the muscle architecture in the absence of any major increase in muscle mass (4,14). And when on test you can always compromise on load unlike the natural trainees. It is now becoming increasingly clear that testosterone promotes its anabolic effects primarily through an increase in satellite cell proliferation and myonuclear number (10,4). Sadly for natural trainees the only viable option to activate satellite cell is through load mediated injury.


    More important, direct comparison with highly trained athletes can be misleading because the neural patterns have probably matured in these individuals. Thus without major neural changes, the force per cross sectional area remains the same or decreased compared to less trained individuals. Further, some of the incongruity surrounding strength with enlarging muscle can be accounted by changes within the muscle cells like enlarged interstitial space, and decreased protein concentration (11). So, don’t let appearances lead your conclusions.


    Whether you hit a muscle group thrice a week or once a week, whether you perform 1 set or 6 sets, high rep or low rep, if strength is climbing, stick with it. The tenets of typical bodybuilding routines like repetitions of 8-12, sets to failure, changing exercises often, and short rest intervals were all laid on the faulty premise that not load but fatigue is the primary stimulant for hypertrophy.


    Opt for a periodized routine (cycling of loads to manage fatigue) built on a few basic and a few auxiliary exercises with adequate rest between sets. Additionally, stick to around 5 reps per set, and terminate each set 1 or 2 reps short of failure. A drop set of 15-20 reps right after your last work set would work well to create metabolic fatigue without sacrificing load.


    Anyhow, to make a long story short, the ultimate hypertrophy routine will be the ultimate strength routine.


    Good luck.
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    .
    I think he has 1 source at 2003, and one at 2002 and the rest are 80's and 90's

    Like I said that is good, never seen it before today, but its outdated, and there are some areas that need changing and expanding but overall good. Wish I had this before lol
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    This is not Part I of that Part II, those studies are way outdated.
    I think he has 1 source at 2003, and one at 2002 and the rest are 80's and 90's

    Like I said that is good, never seen it before today, but its outdated, and there are some ares that need changing and expanding
    Excuse me?

    Part I was printed 12/03/2004

    Part II was printed 3/11/2005

    both in Mind and Muscle Magazine.
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    what does printed have to do with the date of the references?
    I did find one reference to 2004 I guess but thats still the newest on there

    5) Moore, D. R, Burgomaster, K. A, Schofield, L. M, Gibala, J. M, Sale, D. G, and Phillips, S. M. (2004). Neuromuscular adapataions in human muscle following low intensity resistance training with vascular occlusion. European Journal of Applied Physiology, 92, 399-406.

    7) Burgomaster, K. A, Moore, D. R., Schofield LM, Phillips SM, Sale DG, Gibala MJ.(2003).Resistance training with vascular occlusion: metabolic adaptations in human muscle. 35(7),1203-8.

    14) Storer TW, Magliano L, Woodhouse L, Lee ML, Dzekov C, Dzekov J, Casaburi R, Bhasin S.estosterone Dose-Dependently Increases Maximal Voluntary Strength and Leg Power, but Does Not Affect Fatigability or Specific Tension. Clin Endocrinol Metab. 2003 Apr;88(4):1478-85.
    Quote Originally Posted by Bobo
    Excuse me?

    Part I was printed 12/03/2004

    Part II was printed 3/11/2005

    both in Mind and Muscle Magazine.
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    Quote Originally Posted by TheGame46
    what does printed have to do with the date of the references?
    I did find one reference to 2004 I guess but thats still the newest on there

    5) Moore, D. R, Burgomaster, K. A, Schofield, L. M, Gibala, J. M, Sale, D. G, and Phillips, S. M. (2004). Neuromuscular adapataions in human muscle following low intensity resistance training with vascular occlusion. European Journal of Applied Physiology, 92, 399-406.

    7) Burgomaster, K. A, Moore, D. R., Schofield LM, Phillips SM, Sale DG, Gibala MJ.(2003).Resistance training with vascular occlusion: metabolic adaptations in human muscle. 35(7),1203-8.

    14) Storer TW, Magliano L, Woodhouse L, Lee ML, Dzekov C, Dzekov J, Casaburi R, Bhasin S.estosterone Dose-Dependently Increases Maximal Voluntary Strength and Leg Power, but Does Not Affect Fatigability or Specific Tension. Clin Endocrinol Metab. 2003 Apr;88(4):1478-85.

    I didn't say anything about his references.

    You said this:

    "This is not Part I of that Part II, those studies are way outdated."

    then edited it out of your post.


    I could care less about the date of his studies.


    Plus, here is his full list from Part I

    References

    1) Adams, G. (1998). Role of insulin-like growth factor-I in the regulation of skeletal muscle adaptation to increased loading. Exercise and Sports Sciences Reviews, 26, 31-60.

    2) Adams, G. R., & Haddad, F. (1996). The relationships between IGF-1, DNA content, and protein accumulation during skeletal muscle hypertrophy. Journal of Applied Physiology, 81, 2509-2516.

    3) Adams, G. R., Haddad, F., & Baldwin, K. M. (1999). Time course of changes in markers of myogenesis in overloaded rat skeletal muscles. Journal of Applied Physiology, 87, 1705-1712

    4) Adams, G. R., & McCue, S. A.(1998). Localized infusion of IGF-I results in skeletal muscle hypertrophy in rats. Journal of Applied Physiology, 84(5),1716-1722.

    5)Adams, G. R, Vincent, J. C., Fadia, H., & Kenneth, M. B.(2002). Cellular and molecular responses to increased skeletal muscle loading after irradiation. American Journal of Physiology, 283(4), 1182-1195.

    6) Allen, D. L., Yasui, T., Tanaka, Y., Ohira, S., Nagaoka, C., Sekiguchi, W. E., Hinds, R. R., Roy, & Edgerton. (1996). Myonuclear number and myosin heavy chain expression in rat soleus single muscle fibers after spaceflight. Journal of Applied Physiology, 81, 145-151.

    7) Baechle, T. R., & Earle, R. W. (2000). Essentials of strength and conditioning (2nd ed.). Champaign, IL: Human Kinetics.

    8) Barton-Davis, E. R., Shoturma, D. I., & Sweeney, H. L. (1999). Contribution of satellite cells to IGF-I induced hypertrophy of skeletal muscle. Acta Physiologica Scandinavica 167, 301-305.

    9) Bamman, M. M., Shipp, J. R., Jiang, J., Gower, B. A., Hunter, G. R., Goodman, A., McLafferty, C. L., & Urban, R. J. (2001). Mechanical load increases muscle IGF-I and androgen receptor mRNA concentrations in humans. American Journal Physiology and Endocrinology Metabolism, 280(3), E383-90.
    10) Campos, G. E., Leucke, T. J., Wendeln, H. K., Toma, K., Hagerman, F. C., Murray, T. F., Ratamess, N. A., Kramer, W. J., & Staron, R. S. (2002). Muscular adaptations in response to three different resistance-training regimens: specificity of repetition maximum training zones. European Journal of Applied Physiology, 88(1-2), 50-60.

    11) Chambers, R. L., & McDermott, J. C. (1996). Molecular basis of skeletal muscle regeneration. Canadian Journal of applied physiology, 21, 155-184.

    12) Clarkson, P. M. & Hubal, M. J.. (2002). Exercise-induced muscle damage in humans. American Journal of Physical Medicine and Rehabilitation, 81(11), S52-S69.

    13) Clarke, M. S., Khakee, R., & McNeil, P.L. (1993). Loss of cytoplasmic basic fibroblast growth factor from physiologically wounded myofibers of normal and dystrophic muscle. Journal of Cell Science, 106, 121-133.

    14) Dolezal, B. A., Potteiger, J. A., Jacobsen, D. J., & Benedict, S. H. (2000). Muscle damage and resting metabolic rate after acute resistance exercise with an eccentric overload. Medicine and science in sports and exercise, 32 (7), 1202–1207.

    15) Edgerton, V. R., & Roy, R. R. (1991). Regulation of skeletal muscle fiber size, shape and function. Journal of Biomechanics, 1, 123-133.

    16) Fry, A. C. (2004). The role of resistance exercise intensity on muscle fiber adaptations. Sports Medicine, 34(10), 663-679.

    17) Gibala, M. J., Interisano, S. A., Tarnopolsky, M. A., Roy, B. D., MacDonald, J. R., Yarasheski, K. E., & MacDougall, J, D. (2000). Myofibrillar disruption following acute concentric and eccentric resistance exercise in strength-trained men. Canadian Journal of Physiology and Pharmacology, 78(8), 656-661.
    18) Gibala, M. J., MacDougall, J. D., Tarnopolsky, M. A., Stauber, W. T., & Elorriaga, A. (1995). Changes in human skeletal muscle ultrastructure and force production after acute resistance exercise. Journal of Applied Physiology, 78(2),702-708.

    19) Goldberg, A. L. (1967). Work induced growth of skeletal muscle in normal and hypophsectomized rats. American journal of applied physiology, 213, 1193-1198.

    20) Grounds, M. D. (1998). Muscle regeneration: Molecular aspects and therapeutic implications. Current Opinion in Neurology, 12, 535-543.

    21) Kraemer, W. J., Ratamess, N. A., & Duncan, N. F. (2002). Resistance training for health and performance. Current Sports Medicine Reports, 1, 165-171.

    22) Nosaka, K., & Newton, M. (2002). Difference in the magnitude of muscle damage between maximal and submaximal eccentric loading. Journal of Strength and Conditioning Research, 16(2), 202-208.

    23) Nosaka, K., Newton, M., & Sacco, P. (2002). Muscle damage and soreness after endurance exercise of the elbow flexors. Medicine and science in sports and exercise, 34(6), 920-927.

    24) Pitkanen, H.T., Mykanen, T., Knuutinen, J., Lahti, K., Keinanen, O., Alen, M., Komi, P.V., & Mero, A. A. (2003). Free amino acid pool and muscle protein balance after resistance exercise. Medicine and science in sports and exercise, 35(5), 784-792.

    25)Phelan, J. N., & Gonyea, W. J. (1997). Effect of radiation on satellite cell activity and protein. Anatomical Records, 247(2), 179-188.

    26) Schultz, E. (1989). Satellite cell behavior during skeletal muscle growth and regeneration. Medicine and science in sports and exercise, 21, 181-186.

    27) Sheehan, S. M., Tatsumi, R., Temm-Grove, C.J., & Allen, R. E. (2000). HGF is an autocrine growth factor for skeletal muscle satellite cells in vitro. Muscle Nerve, 23, 239-245.

    28) Sinha-Hikim, S. M., Roth, M. I., Lee, H., & Bhasin, S. (2003). Testosterone-induced muscle hypertrophy is associated with an increase in satellite cell number in healthy, young men. American Journal Physiology and Endocrinology Metabolism, 285(1), E197 – 205.

    29) Florini, J. R., Ewton, D. Z., & Coolican, S. A. (2002). I knew that you were gonna fall for it. Don’t worry, I wont tell anybody.

    30) Weiss. W., Coney, H. D., & Clark, F. C. (2000). Gross measures of exercised induced muscular hypertrophy. Journal of orthopedic and sports physical Therapy, 30, 143-148.
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    Quote Originally Posted by Bobo
    I didn't say anything about his references.

    You said this:

    "This is not Part I of that Part II, those studies are way outdated."

    then edited it out of your post.


    I could care less about the date of his studies.
    at first I just saw the part II and thought u were posting that as if it was part II of mine. I wanted to avoid that confusion, but then I saw that u put part I on here too.

    And those references are even old than the one I posed from pat II
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    Quote Originally Posted by TheGame46
    at first I just saw the part II and thought u were posting that as if it was part II of mine. I wanted to avoid that confusion, but then I saw that u put part I on here too.

    And those references are even old than the one I posed from pat II
    So what? There hasn't been anything new stated in this thread at all.
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    Quote Originally Posted by TheGame46
    That barely covers IGF and the HGH IGF axis, and has no mention of MGF or IGF-IEa and those factors. The research I'm using is much newer, more in depth and pracically applied. Part too will be the meaty science part.
    I'm guessing he's referring to this earlier in the thread, and that his part II will have more up to date stuff, post 2004 references.
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    Quote Originally Posted by CDB
    I'm guessing he's referring to this earlier in the thread, and that his part II will have more up to date stuff, post 2004 references.
    Who knows. Nothing groundbreaking that I've seen and I subscribe to the JAP.

    ...but interpreations are often amusing at times.
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    Quote Originally Posted by CDB
    I'm guessing he's referring to this earlier in the thread, and that his part II will have more up to date stuff, post 2004 references.
    Exactly!!!! Finally someone else understand me lol
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    Quote Originally Posted by Bobo
    Who knows. Nothing groundbreaking that I've seen and I subscribe to the JAP.

    ...but interpreations are often amusing at times.
    See this is were you, gavin and I and a few of the other big guys could make some ground is by diggin into the new stuff like I have and putting the little things together to get something groundbreaking. Its not like the studies are focused on bodybuilding so you gotta peice things together for our purposes most of the time
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    I'll email you the tester results on GTP bobo
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    Quote Originally Posted by TheGame46
    See this is were you, gavin and I and a few of the other big guys could make some ground is by diggin into the new stuff like I have and putting the little things together to get something groundbreaking. Its not like the studies are focused on bodybuilding so you gotta peice things together for our purposes most of the time

    Huh?
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    I look forward to part two, sounds interesting,
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    Part 2 of what?
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    Intresting thread.. (subscribe)
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    Quote Originally Posted by Bobo
    Part 2 of what?
    LOL the Part 1 I just posted...
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    you have pictures of yourself to prove this "most important read about training ever"???
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    Quote Originally Posted by guyfromkop2
    you have pictures of yourself to prove this "most important read about training ever"???
    My testers are just finishing up and should be giving me final numbers and pics within the next week or 2, but they have been posting updats as they go. Sorry I have not taken any pics yet but plan on doing so theis next run.
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    Quote Originally Posted by TheGame46
    My testers are just finishing up and should be giving me final numbers and pics within the next week or 2, but they have been posting updats as they go. Sorry I have not taken any pics yet but plan on doing so theis next run.

    what about pictures of yourself?
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    Quote Originally Posted by TheGame46
    LOL the Part 1 I just posted...
    You mean another summary?

    Oh ok...
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