The basics of HST

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Short summary

In order of importance:

1) Satellite cells must be activated, differentiated, and fuse with existing fibers, donating their nuclei.

2) Mechanical stress must be transmitted to the sarcolemma (mechanotransduction) and contractile protein structures within the sarcomeres. This will trigger focal adhesion kinases (FAK) that in turn initiate the downstream signaling events leading to an increase in the contractile and cytoskeletal protein expression/synthesis.

3) pH and oxidative stress must be acutely increased within the muscle fiber.

Focusing just on the workout, this pretty much sums it up. If #1 doesn’t happen, you will not grow…ever. If number two doesn’t happen, you will grow a little, but you will soon reach the limits of the sarcoplasmic/nuclear ratio and growth will stop. If #3 doesn’t happen, you will still grow quite significantly, but the rate of growth might be enhanced or facilitated if #3 is achieved.

#1 is achieved when a certain level of microtrauma is experienced by the fibers. This is brought about by load, eccentric contractions, and to a much lesser extent, hypoxia (A.K.A. #3) When load, eccentric contractions and #3 occur, each fiber will produce and release muscle specific-IGF-1 (sometimes called mechano-growth factor) The IGF-1 in turn seeps out of leaky sarcolemmas and acts on nescient satellite cells to initiate #1. Microtrauma is rapidly reduced from workout to workout (Repeated bout effect) thereby limiting the effectiveness of any given load to induce further hypertrophy.

#2 is achieved by loading a muscle that is actively contracting.

#3 is achieved by contracting a muscle (doing reps) until you create an oxygen deficit and subsequent hypoxic byproducts (e.g. lactate and oxygen radicals).

The afore mentioned physiological principles of muscle growth are what we follow in order to ensure that 1,2 and 3 happen.

 

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What are satellite cells?

Satellite cells are myogenic stem cells, or pre-muscle cells, that serve to assist regeneration of adult skeletal muscle. Following proliferation (when the satellite cells reproduce) and subsequent differentiation (when the nucleus changes to become a specific type of cell, in this case, a muscle cell), satellite cells will fuse with one another or with the adjacent damaged muscle fiber, thereby increasing the number of myonuclei for fiber growth and repair. Proliferation of satellite cells is necessary in order to meet the needs of thousands of muscle cells all potentially requiring additional nuclei. Differentiation is necessary in order for the new nucleus to behave as a nucleus of muscle origin. The number of myonuclei directly determines the capacity of a muscle cell to manufacture proteins, including androgen receptors.

In order to better understand what is physically happening between satellite cells and muscle cells, try to picture 2 oil droplets floating on water. The two droplets represent a muscle cell and a satellite cell. Because the lipid bilayer of cells are hydrophobic just like common oil droplets, when brought into proximity to one another in an aqueous environment, they will come into contact for a moment and then fuse together to form one larger oil droplet. Now whatever was dissolved within one droplet (i.e. nuclei) will then mix with the contents of the other droplet. This is a simplified model of how satellite cells donate nuclei, and thus protein-synthesizing capacity, to existing muscle cells.

There appears to be a finite limit placed on the cytoplasmic/nuclear ratio (Rosenblatt,1994). Whenever a muscle grows in response to functional overload there is a positive correlation between the increase in the number of myonuclei and the increase in fiber cross sectional area (CSA). When satellite cells are prohibited from donating viable nuclei, overloaded muscle will not grow (Rosenblatt,1992; Phelan,1997). It is not a stretch to say that satellite cell activity is a required step, or prerequisite, in compensatory muscle hypertrophy, for without it, a muscle simply cannot significantly increase total protein content nor CSA.

So, in short, the number of nuclei determine how big a muscle cell can get. Satellite cells are the source for more nuclei.

 

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But why is HST organized into 2 week blocks and the 15/10/5 rep ranges - I don't understand it...

Keep in mind that you have to consider the tensile strength of the tissue itself. Lifting weights to induce hypertrophy is a very much a mechanical process. You are causing physical stress to the protein structures of the muscle tissue. A given amount of load is going to be required regardless of the number of repetitions, to induce hypertrophy.

So, please try to think outside of reps and sets. The purpose of every workout is simply to apply an effective stimulus by providing an incremental increase in tension from the last workout. Just arbitrarily picking a certain number of workouts before you change isn’t going to ensure you are applying an effective stimulus. That’s more akin to periodization, rather than hypertrophy-specific progressions.

Muscle tissue does not distinguish between rep ranges. There is not a special number of contractions that "triggers" a hypertrophic response. The only thing that triggers hypertrophy is sarcolemma distortion and subsequent microtrauma and to a MUCH lesser extent, metabolic activity. Metabolic activity is more anticatabolic, then anabolic. These pathways of mechanotransduction have been mapped and are not in question. Yes, there are always more details to be ironed out, but the pathways are now established that go from mechanical load to muscle cell growth.

In order to adhere to the principles of training induced muscle hypertrophy we must have progressive load. Progressive load sufficient to cause hypertrophy will limit the number of times the muscle can successfully contract against the resistance. There are several old studies that narrowed it down to a range of perhaps 20 reps (if the muscle is deconditioned) all the way up to 120% of your 1RM. So, depending on how conditioned the muscle is, you can use any rep range between 20 reps and negatives.

While using HST, your reps decrease over time simply because the load is constantly increasing. It's that simple. There is no magic number, though others might have you believe there is.

Why 6 workouts in 2 week blocks? Because it takes about that long using decent increments to reach your specified RM.

The whole purpose of HST’s organization is to give you some idea of what that stimulus needs to be on that day’s workout.
SD is kind of like a reset button. It gives you some place to start, where you are pretty sure about the condition of the tissue when you begin. Because you can’t see what is actually happening inside the microscopic world of your muscles, you can only get an idea of what kind of stimulus is required by knowing what the tissue has recently undergone. Even then, all you really know is that the tension applied has to be either greater in amplitude, duration, or some combination of the two, with amplitude being the most effective of the two.

All of this methodology (for lack of a better word) is based on tangible yet invisible things like heat shock proteins, microscopically thin connective tissue, kinase-type signaling proteins, and all the protein synthetic machinery and all the genes that regulate them.

Now, it isn’t necessary to become an expert on the details of each of these cellular components, but it does become necessary to have a basic understanding of “what it all means” if you really want to understand HST.

Without this understanding, HST will appear to be no better or worse than any other routine. This is the trap that many experienced lifters fall into. They been around the block, they’ve seen it all before, but they fail to understand that there is an underlying truth about how muscle works that the previous routines weren’t able to pattern themselves after. They were in the general vicinity, through trial an error, but there just wasn’t enough research available to reduce the uncertainty that drives the endless variation in strategy and method.

So you aren't going to understand HST by studying its sets, reps, and workouts. You can only understand HST by studying how muscle tissue works. I can't emphasize this enough. HST is not about sets and reps, it is about getting people to change the way they think about training for size. It is about introducing demonstrable physiological concepts into a culture dominated by marketing hype, tradition and regurgitation of every single BB myth ever known.

 

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The more advanced insights

First let me clarify that HST is based on physiologically sound principles not numbers. In short, they are:

• Progressive load
• Training volume
• Training frequency
• Conditioning (Repeated Bout effect)/Strategic Deconditioning

So we are dealing with 4 basic issues, Load, Volume, Frequency and Conditioning. Within these basic factors we have reps, sets, and rest. HST differs from previous training methods in many aspects, but particularly in how it incorporates knowledge of how the “cell” physiologically responds to the training stimulus in its methodology. Previous methods focus on effort (A.K.A Intensity), current voluntary strength, and psychological factors such as fatigue and variety.

• The number of Reps is determined by the minimum effective load (this changes over time based on Conditioning)
• The number of Sets is determined by the minimum effective volume (this changes over time according to current load and Conditioning.)
• The Rest between sets is determined by the amount of time required to regain sufficient strength to successfully achieve the minimum effective Volume.
• The Frequency (rest between workouts) is determined by the ability of the CNS to recover sufficiently to maintain baseline “health” indicators. It is also determined by the time course of genetic expression resultant from the previous workout.
• The interval of Strategic Deconditioning (SD) is determined by the time course of adaptation to the individuals maximum weight loads. In other words, SD is required to reset growth potential after plateauing. The duration of SD is determined by the level of conditioning attained during the training cycle.

Mechanical tension on the protein structures of the muscle cells is the primary stimulus for hypertrophy. This tension can elicit anabolic processes with or without damaged to the cell membrane. However, some damage to the cell membrane seems to be critical for the action of autocrine and paracrine growth factors (FGF, IGF-1, etc). Without the activity of these growth factors outside the cell there will be no increase in myonuclei, and thus no significant increase the the volume and/or number of the cells.

Some improvements in muscle cell function do occur even if the number of myonuclei remains the same. These won't lead to significant hypertrophy though. These improvements in muscle cell functional capacity involve ERK1/2. This is the pathway activated most when you get an intense burn and/or train to failure.

Muscle "activity" such as the typical repetition, and the metabolic byproducts and change in the internal millieu of the cell also "contribute" to hypertrophy, but only indirectly. Reps, and fatigue activate signaling proteins and transcription factors that increase protein synthesis. This increase in protein synthesis allows an increase in crucial enzymes, receptors (yes even androgen receptors), membrane and structural proteins. Remember that protein breakdown is also accelerated so the net effect is most often merely a maintenance of muscle protein levels. This is what goes on after each workout when plateauing after years of training.

As mentioned, without the activity of IGF-1 and FGF outside of the cell, satellite cells will not contribute significantly to hypertrophy. The process is dependant on microtrauma at some degree.

Studies have shown that the ability of a given amount of tension to elicit hypertrophy decreases over time in a given muscle. This is because the same adaptive process that leads to muscle growth, also leads to resistance to the stimulus of muscle growth. It has a lot to do with the principle of homeostasis, in other words, the body will always fight further change as it’s changing.

Studies have shown too much microtrauma is a bad thing. The rapid infiltration of immune factors (the primary cause of DOMS) actually causes significant breakdown of muscle proteins and the death of some cells.

Now, the ability of mechanical tension to cause microtrauma to the cell membrane is dependant on the condition of the extracellular matrix. If it is robust as a result of chronic strain, is will take an unaccustomed load to induce any trauma. Your ability to apply this load is dependant on your voluntary strength. Your body is able to protect your muscle cells from microtrauma even when using max loads. It isn't always able to protect tendons.

Anytime you do a set and it burns like crazy (painful burn) you are creating the same conditions of the occlusion studies. In other words, its not that the effects seen in this study don't happen without cutting off the blood supply, they do depending on the type of set. I would guess the vascular occlusion is increasing phosphorylation of MAPKerk1/2. erk1/2 appears to be more sensitive to acidosis, and oxygen radicals, both of which would be increased by lack of blood flow. Although less of a contributor than p38, erk1/2 does appear to contribute to hypertrophy.

Keep in mind that as a muscle contracts, it squeezes the blood out from the blood vessels around it. That is why your blood pressure goes up as large muscle groups contract (even clenching your fists actually raises blood pressure). This is also why pilots learn to contract their musculature to keep from passing out during high G-forces.

Contracting and relaxing a muscle acts like a blood-pump and plays a role in proper function of the cardiovascular system during exercise.

As was mentioned earlier, if you can increase the level of metabolic byproducts, decrease the pH and increase the level of oxygen radicals you will "help" to stimulate hypertrophy. However, this is not sufficient to elicit significant hypertrophy in the absence of progressive loading. In other words, flexing your muscles until they really burn won't really make you grow all that well. But combine it with progressive load and you will facilitate growth.

There is an excellent issue of The Journal of Pysiology that ties in the participation of mechanical strain vs Metabolic strain to muscle hypertrophy. In the issue you will get good explanations of mechanotransduction and how it relates to genetic expression leading to muscular hypertrophy. Its a must read for anybody into the science of contraction induced hypertrophy. J Phys Vol 535 No.1

Here is a model from the article showing in general terms how mechanical strain, and metabolic strain both contribute to hypertrophy, but to differing degrees. p38 leading more specifically to muscle size, while erk1/2 leads more towards improvements in muscle function or capacity. However, there is some overlap:

There are studies showing passive stretch eliciting a greater influence on erk1/2, and less so on p38.

Passive stretch puts the strain of the load on “structural” proteins (both collagenous and otherwise) and the cell membranes. When the fibers contract, it shifts the load to the contractile proteins (myosin, actin, z-discs, etc). This appears to be crucial for activation of p38, which of course leads to significant fiber hypertrophy.

I still like the loaded stretching. I do it where I can, shrugs, incline curls, chins, etc. But not all movements lend themselves to this kind of stretching.

Whether actual detrimental disruption of the structural proteins is required for growth or not is a good question. But what is not in question, is that mechanical (as opposed to metabolic) strain is required. The load must be transfered through mechanotransduction to the cell membrane and contractile structures.

I have used "muscle damage", "microtrauma" and "tissue strain" interchangeably...just easier to grasp I guess.

I would have to argue with the concept of the need for inflammation. With the release (autocrine & paracrine) of intracellular IGF-1 and subsequent activation of satellite cells, inflammation per say isn't required at all...

So, erk1/2 is phosphorylated in response to a drop in pH (lactic acid) and increase oxygen radicals. These are the two primary effects of metabolic activity. Thus, the cell will respond by increasing its metabolic and oxidative capacity in response to increases in erk1/2 and its associated transcriptional factors.

p38 on the other hand is not really effected by either pH or oxygen radicals. It is phosphorylated in respnse to strain on the contractile proteins in a muscle cell. This is why moderate "passive" stretch has little effect on muscle cells in-vitro.

In-vivo is a different situation using stretch. Animal models using stretch are not true stretch conditions because the animal will contract the muscles being stretched. The stretch is like holding onto a set of dumbells for days at a time. You will naturally contract against the pull of the weight by contracting the traps, even if it isn't hard enough to actually shrug the shoulders, you will hold a static contraction as long as you can. Make sense?

This is why in animal stretch studies you see significant hypertrophy associated with both erk1/2 and p38 activity.

 

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Hyperplasia

"Title: Effects of anabolic steroids on the muscle cells of strength-trained athletes.

Researchers: Kadi F, Eriksson A, Holmner S, Thornell LE Department of Integrative Medical Biology, Umea University, Sweden.

Source: Med Sci Sports Exerc 1999 Nov;31(11):1528-34

Summary:

Athletes who use anabolic steroids get larger and stronger muscles. How this is reflected at the level of the muscle fibers has not yet been established and was the topic of this investigation. METHODS: Muscle biopsies were obtained from the trapezius muscles of high-level power lifters who have reported the use of anabolic steroids in high doses for several years and from high-level power lifters who have never used these drugs. Enzyme-immunohistochemical investigation was performed to assess muscle fiber types, fiber area, myonuclear number, frequency of satellite cells, and fibers expressing developmental protein isoforms.

RESULTS: The overall muscle fiber composition was the same in both groups. The mean area for each fiber type in the reported steroid users was larger than that in the nonsteroid users (P < 0.05). The number of myonuclei and the proportion of central nuclei were also significantly higher in the reported steroid users (P < 0.05). Likewise, the frequency of fibers expressing developmental protein isoforms was significantly higher in the reported steroid users group (P < 0.05). [these researchers found embryonic fiber development in the nonsteroid using group as well...just not as much as in the group using.]

CONCLUSION: Intake of anabolic steroids and strength-training induce an increase in muscle size by both hypertrophy and the formation of new muscle fibers (hyperplasia). We propose that activation of satellite cells is a key process and is enhanced by the steroid use. The incorporation of the satellite cells into preexisting fibers to maintain a constant nuclear to cytoplasmic ratio seems to be a fundamental mechanism for muscle fiber growth. Although all the subjects in this study have the same level of performance, the possibility of genetic differences between the two groups cannot be completely excluded."

So, there is really no argument anymore among groups uptodate on their muscle physiology...that includes people into HST.

 

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Effects of exercise on GH

I don't know if you will find any studies showing that "blood" lactate levels stimulate GH release, but the available research does demonstrate that lactate production within muscle cells is associated with the stimulus for GH release during exercise. And an increase in lactate production doesn't cause a decrease in fatty acid oxidation. On the contrary, a decrease in fatty acid oxidation will necessarily increase glycolytic pathways and thus lactate production (see nicotinic acid studies below).

Anything that puts an acute demand on the anaerobic metabolic pathways will stimulate GH release. One of the early processes involved in the stimulation of GH and gonadotropic hormones is the intramuscular accumulation of metabolic subproducts such as lactate and proton (1,2). The elevated concentration of metabolites and associated acidification within the muscles stimulate chemoreceptors (3), which then send afferent signals to the hypothalamic-pituitary system through group III and IV nerve fibers (4).

Anything that will increase the metabolic demand on the muscles themselves will increase GH release, including vascular occlusion (cutting off the blood supply). In a study of vascular occlusion they were able to demonstrate a doubling of lactate levels and, as you might expect, significant GH release, even with loads as low as 20% of their 1RM. (5)

Not only does vascular occlusion increase GH release, but so does anything that is more metabolically demanding, such as concentric reps vs. eccentric reps. Concentric reps cause a greater increase in GH than Eccentric reps (6)…why? Because concentric reps activate the anaerobic pathways more than eccentric reps.

Nicotinic acid (NA) ingestion prevents fatty acid levels from rising above resting values when giving before exercise. (7) In a study looking at the effects of using NA to blunt the rise in fatty acid levels, the NA ingestion was associated with a 3- to 6-fold increase in concentrations of growth hormone throughout exercise. (8) This occurs for at least 2 reasons, fatty acids can act as negative feedback control on the hypothalamus, and the prevention of fatty acid metabolism puts more pressure on the anaerobic pathways, because the uptake of fatty acids into muscle during exercise is proportional to their levels in the serum.

1. Kraemer, W. J., S. E. Gordon, S. J. Fleck, L. J. Marchitelli, R. Mello, J. E. Dziados, K. Friedl, E. Harman, C. Maresh, and A. C. Fry. Endogenous anabolic hormonal and growth factor responses to heavy resistance exercise in males and females. Int. J. Sports Med. 12: 228-235, 1991

2. Sutton, J. R. Effect of acute hypoxia on the hormonal response to exercise. J. Appl. Physiol. 42: 587-592, 1977

3. Victor, R. G., and D. R. Seals. Reflex stimulation of sympathetic outflow during rhythmic exercise in humans. Am. J. Physiol. Heart Circ. Physiol. 257: H2017-H2024, 1989

4. Gosselink, K. L., R. E. Grindeland, R. R. Roy, H. Zhong, A. J. Bigbee, E. J. Grossman, and V. R. Edgerton. Skeletal muscle afferent regulation of bioassayable growth hormone in the rat pituitary. J. Appl. Physiol. 84: 1425-1430, 1998

5. Takarada Y, Nakamura Y, Aruga S, Onda T, Miyazaki S, Ishii N. Rapid increase in plasma growth hormone after low-intensity resistance exercise with vascular occlusion.
J Appl Physiol. 2000 Jan;88(1):61-5.

6. Kraemer WJ, Dudley GA, Tesch PA, Gordon SE, Hather BM, Volek JS, Ratamess
NA. The influence of muscle action on the acute growth hormone response to resistance exercise and short-term detraining. Growth Horm IGF Res. 2001 Apr;11(2):75-83.

7. Norris B, Schade DS, Eaton RP. Effects of altered free fatty acid mobilization on the metabolic response to exercise. J Clin Endocrinol Metab. 1978 Feb;46(2):254-9.

8. Murray R, Bartoli WP, Eddy DE, Horn MK. Physiological and performance responses to nicotinic-acid ingestion during exercise. Med Sci Sports Exerc. 1995 Jul;27(7):1057-62.

More references on the relationship between FFAs and GH secretion:

Quabbe HJ, Bratzke HJ, Siegers U, et al. 1972 Studies on the relationship between plasma free fatty acids and growth hormone secretion in man. J Clin Invest. 51:2388–2398.

Pontiroli AE, Lanzi R, Monti LD, Pozza G. 1990 Effect of acipimox, a lipid lowering drug, on growth hormone (GH) response to GH-releasing hormone in normal subjects. J Endocrinol Invest. 13:539–542.

Pontiroli AE, Lanzi R, Monti LD, Sandoli E, Pozza G. 1991 Growth hormone (GH) autofeedback on GH response to GH-releasing hormone. Role of free fatty acids and somatostatin. J Clin Endocrinol Metab. 72:492–495.

Blackard WG, Hull EW, Lopez-S A. 1971 Effect of lipids on growth hormone secretion in humans. J Clin Invest. 50:1439–1443.

Casanueva F, Villanueva L, Penalva A, Vila T, Cabezas-Cerrato J. 1981 Free fatty acids inhibition of exercise-induced growth hormone secretion. Horm Metab Res. 13:348–350.

Imaki T, Shibasaki T, Shizume K, et al. 1985 The effect of free fatty acids on growth hormone (GH)-releasing hormone-mediated GH secretion in man. J Clin Endocrinol Metab. 60:290–293.

 

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<span style='color:black'>Advanced Protein Synthesis Insights

When talking about elevated protein synthetic rates.

The duration of this will depend on the effectiveness of that particular workout. If your workout is inadequate, elevated protein synthesis rates will not stay elevated even 48 hours.

The accrual of muscle mass over time is a function of the overall balance between protein synthesis and breakdown. You must have a net increase in synthesis rates in order to see more muscel mass over time. Under normal conditions the muscle is in balance between synthesis and breakdown with no net change (except for losses over time due to aging)

There are several things that increase protein synthesis including, prostaglandins, hormones, and elevated extracellular amino acid levels. Modulation of protein synthesis rates occurs at two levels, the short phase and the long phase. The short phase alteration in protein synthesis rates occurs by altering the activity of existing ribosomes and/or eukaryotic initiation factors (eIFs). This happens within minutes of the appropriate physiological trigger. The long phase modulation of protein synthesis happens by way of increasing the number of myonuclei. This mechanism involves hormones and growth factors such as testosterone, MGF, and IGF-1 bringing about the activation of myogenic stem cells. This can take several days to effect protein synthesis rates. This is a simplified view but for our purposes it is sufficient.

Initiation of translation (the binding of mRNA to the ribosomal pre-initiation complex) which is critical for the immediate response in protein synthesis, requires group 4 eukaryotic initiation factors (eIFs). These initiation factors interact with the mRNA in such a way that makes translation (the construction of new proteins from the mRNA strand) possible.

Two eIFs, called eIF4A and eIF4B, act in concert to unwind the mRNA strand. Another one called eIF4E binds to what is called the “cap region” and is important for controlling which mRNA strands are translated and also for stabilization of the mRNA strand. Finally, eIF4G is a large polypeptide that acts as a scaffold or framework around which all of these initiation factors and the mRNA and ribosome can be kept in place and proper orientation for translation.

Long term modulation of protein synthesis involves the activation of myogenic stem cells or satellite cells. This is how existing muscle cells increase the number of nuclei they contain. If you recall, when a muscle is stretched it not only produces mechano growth factor (MGF), but also PGF2α and PGE2. PGE2 is a potent inducer of satellite cell proliferation and fusion. This is important because in order for a muscle to grow rapidly, it must produce more mRNA. This is done in the nucleus of the muscle cell. The more nuclei you have, the more mRNA you can produce. Within the cell, prostaglandins may also be involved in regulating the number of ribosomes. This could have long term implications for hypertrophy. This helps shed light on the ability of prostaglandin inhibitors such as ibuprofen and other NSAIDs to prevent training induced muscle growth.</span>