NSCA Mechanical work theory-Preferential hypertrophy

[Dr James Daemon]

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"This could be the end of one factor theory!"

Concrete guidelines for increasing strength, and for hypertrophy have been laid down in, well, concrete for many years.

However, I have noticed a discrepancy when looking at a presentation of the protocol recently. It boils down to the application of one factor theory in bodybuilding training.

If we for a second split the training methods down into hypertrophy and strength. Strength, unless neurally mediated comes down to the contractile apparatus… This is essentially what hypertrophy should mean, but this is semantics.

So, due to cross sectional area, muscle must become stronger as it grows. However, this isn’t always a proportional increase, because the transfer of results from an endurance (hi rep hypertrophy) program do not transfer into strength, unless the ability (strength) is specifically cultivated. In short, lifting 100kg once means you will be able to lift 50kg twice. However, lifting 50kg ten times is no guarantee that you will be able to lift 100kg even once. Why..? Recruitment patterns.

Training produces specific results called adaptations and it must be realised that the adaptation of a high rep program is going to be the ability to do more reps, which doesn’t necessarily mean you must be bigger to do so. This can be an enzymatic adaptation, and does not technically, or in practice mean greater size.

Bodybuilders are not usually reputed to be strong proportionately, due to this simple principle. The sarcoplasmic bloat associated with elite bodybuilders is not down to an increased size of contractile apparatus, it can be down to Non contractile tissue, that doesn’t contribute toward force production aside from weighing down the lever arm more. Bodybuilding training is (if at all) is rarely used in arenas outside bodybuilding. This demonstrates the specific nature of the adaptations.

(NB-There are some misguided coaches imposing HIT training on athletes)

Zatsiorsky touched upon this idea when he mentioned that although the intensity of strength training is high, and the protein loss is concurrently, the reps are few, and thus the overall amount of protein loss is slight compared to hypertrophy training.


The protein loss from bodybuilding, apparently, is lower per rep, but stacks up over the course of a session.(Volume)

This notion of absolute volume fails to take into account the way in which the body performs work at different intensities.

This is where mathematics fails us.

The concept that if you add up the total work performed in a Hypertrophy session, contrast it with the total work done in Strength session, the higher number is the person whose muscles have shouldered the greatest load, and will be proportionately rewarded... Sound a little unrealistic now..? Good.

If this mathematical approach is to be used realistically, it needs to figure the greater effect on the desired fibres that working at maximal levels induces, or the end figures are just an abstract calculus. A similar phenomenon has overshadowed many countries athletic performance with the conventional style of periodisation- much of it pure mathematics.


So a major key in the separation of these two styles is the amount of mechanical work performed. Zatsiorsky proposed that the increased amount of protein loss (and the mechanical work preventing immediate replenishment) is what prompts the super compensation, and fibre size increase- I propose we go with that for the time being.

Fibres hypertrophy in response to a training stimulus, the training stimulus of course dictating the course of adaptations. Studies note that elite bodybuilders have a higher number, and greater size of type 1 fibres. The type one fibres are recruited first due to the size principle. This basically means that if maximum force isn't’t needed, the body uses the smaller motor units first.

This is why this style of training is useless in athletics, as type 2 fibres are usually called upon to do the required work as high force levels, and quickly for short periods. So the load in hypertrophy training does not stimulate type 2 fibres preferentially, because of the moderate load, the body reaches for a substantial amount of slow twitch fibres.
This is the compromise of training to failure. It is frequently noted that motor unit corridors are exploited fully only when trained till failure, and that failure training produces the most growth.

[Dr James Daemon]

I postulate this is because it is not until the slow twitch fibres are worked to fatigue, that the fast twitch ones shoulder the load. It may seem odd that you would only get 8 reps out with oxidative fibres, but the load is too high for them to cope with, and the idea of continued repetitions is to exhaust them.

My point is, if the idea is to recruit the fast twitch fibres, because they hypertrophy faster, and better -why wait until the end of the set..?

If we consider that training till failure without substantial pharmaceutical assistance is not an option to be employed every training session because of the demand on the nervous system. If we then compare the proportion of reps done roughly on the different fibres (the mathematical co-efficiant!), we could be looking at for instance 8 reps unassisted, and then 3 till concentric failure. This would theoretically and numerically mean that the growth of the type two fibres would be severely overshadowed by type 1.

Guess what..? In elite bodybuilders- they are.

If we explore this a stage further, eccentric failure is another selectively used system. It causes muscle damage on a large scale. It is often used for this reason, the proposed super compensation being desired, over the fact that it allows the muscles to get used to working with more force and current.



This leads us on to the specific goal of hypertrophy training- Size.


Which fibres are proven to hypertrophy faster (when stimulated), and are bigger..? Type 2.


Why bother training type 1 in this system…? The theory is hardly expedient.

Muscles are composed of both type 1 and type 2 fibres. It would make sense to train both, in a given muscle, for an optimal size increase. Ok, this means varied training, but still.


Again, to refer back to the biopsy results, elite bodybuilders have more type one fibres- what would happen to their overall dimensions if the existing type 2’s were added..? Size.

A small motor unit is exactly that- small. Making a small thing grow past the size of a big thing takes a lot of effort, and after a while it may still not even be as big as the big one was untrained.

Here is some of the information that made me wonder:

“Training performed with near maximal loads increases the cross sectional area of the exercised muscles with type 2 fibre areas increasing more readily and at a faster rate than type 1 fibres. The degree and rate of hypertrophy of type 2 fibres demonstrate their greater recruitment during strength training than during other modes of exercise- This is the desired response since type 2 motor units produce a greater force output and contract with greater velocity than type 1 motor units. Additionally, an initial dominance of type 2 fibres is an advantage to increasing muscular strength, because their growth results in an increase in lean body mass….."

Furthermore:


"….Bodybuilders exhibit a larger absolute amount of collagen and other non contractile connective tissue that also contributes to increases in overall muscle size. Other cross sectional studies revealed a lower percentage of type 2 fibres in bodybuilders than found in other anaerobic athletes and a larger number and size of type 1 fibres. Note that some of these characteristics are similar to those found in other aerobic endurance athletes”

I note the comparison between bodybuilding and endurance, and consider the relevance of the next passage:

“Aerobic endurance training reduces the concentration of glycolitic enzymes and can reduce the overall muscle mass of the hypertrophied (and non hypertrophied) type 2 fibres. Conversely there is selective hypertrophy of type 1 muscle fibres due to increased recruitment during aerobic endurance activities, although the resulting cross sectional diameter is not as great as those seen in type 2 fibre adaptations to resistance exercised. Also, the change is smaller than the hypertrophy of type 1 fibres from a bodybuilding style of resistance program.."




It strikes me as odd that this book then goes on to give guidelines for hypertrophy as "Moderate loads, high volume, short to moderate rest periods."

I have also looked at one definition of aerobic exercise being less than 20 seconds rest. Strength training is often described as being intermittent because the rest intervals are so long. Many disagree with the pre exhaustion system of training, but will stick religiously to a short Rest interval… One presupposes the other.

Gradual exhaustion is a result of volume, and a fatigued state is not the best state to inflict damage on the muscles, as by the time you are worn out, you are worn out!

The nervous system will often start to fail before the muscle. Unless were talking about serious contusion, muscle damage in the bodybuilding arena is a culiminative result of volume, caused by working type 2 until failure repeatedly.

Over training in hypertrophy training only occurs over a given period.

In strength training, one can do too many sets in a session, if the correct rest intervals are observed. So, over training results from volume. Think about it...

Why can you do more on stimulants like clen and ephedrine…? Nervous stimulation.


To give an anecdotal account, think about last time you trained on a stimulant such as ephedrine or clenbuterol. Its highly likely that on the first day you took it (before you attenuated) that you overdid it, and hurt like hell for the next few days. This stimulation, overcomes certain inhibitory nueral responses, and will allow you to perform more reps, with the ephedrine reinforcing the nervous component that usually drops off.

Think about bio-energetics, and recall that you cannot expend maximum force bilaterally… A nervous stimulant will allow you to reinflcit damage at a greater (real, not just perceived) level until fatigue. Overcoming nervous inhibition means more power can be applied to the muscles, and thus more damage can be inflicted.

Ephedrine thus increases maximal strength (as b2 stimulants increase the force of skeletal muscle contraction) and the extra amounts of adren/noradren circulating will allow more sets to be performed.

Muscle will obviously become damaged with heavy loads, and the only variable to be adjusted for hypertrophic results is volume, which can be done quite simply by increasing set number, but maintaining a long rest interval. The only defence to conventional hypertrophy training can be that the thing that may separate two bodybuilders could be if both had large, well developed type two motor units, that the one who addressed the weak link, the type 1’s, would be bigger (all else being equal).


However, as studies prove- type 2’s are the weak link, and remain unaddressed. It is not a huge leap of logic to propose that the bodybuilder who develops both types will be larger. The last straw may be overall culminative training volume being lowered due to the inclusion and therefore exclusion, of one style of training. I don’t have a definitive answer to this, but I would like to see this approach adopted and tried. It may cost you six weeks of growth if its wrong- is it worth a try..?



Can you think of a reason why you wouldn’t like large type 2 fibres in addition to what you have already..?

In conclusion then, if we want to preferentially recruit type 2 fibres, we have to increase the load.

If we want to present a sufficient stimulus for hypertrophy, we have to increase the mechanical work. These two concepts do not go hand in hand.

If we work at 93% of 1RM, we may be getting 3 reps before failure, but as we are stimulating the correct fibres initially, failure becomes overtraining, irrelevant.

In order to cause more protein loss, we need to do more work, the work cannot be performed in 3 sets, so what is the solution…? Increase the number of sets.

10 sets of 3 at 90% is enough to cause substantial muscle damage, even with correct technique.

If we follow this notion up a little further- almost into the partial rep range, we could speculate that even max lift attempts will recruit fast twicth fibres in the chosen muscle group, OK, granted(!) without the ability to cause sufficiant movement around the joint to give a full ROM, but a large amount of motor units, possibly even more than normal lifting at a 3RM may. It means that not enough force is being produced to overcome the weight concentrically- but we have taken that as a given in the design phase, as its a supra maximal load (relative to the lifter at that time) but will this carryover into increasing a plateau'd 1RM... I think so, just like eccentric work, a 1RM would be a psychological, and neurological step down- seems worth trying next time your stuck!

What is then essentially the difference between a partial rep as is usually performed, and a 1RM max lift attempt..? (designed to fail-and force hyperplasia)

Basically-Load. One is sub maximal, and one is maximal/supra maximal.

Most people do several partial reps (which places it firmly into the sub maximal category)-furthermore, many complete a normal 8 reps with partial reps to failure (but again, working the part they are strongest in, no body does partial reps in the ROM they've just hit failure in, its the peak contraction principle)

As the load in a partial rep is sub maximal, its not going to stimulate the cascade of neural events that culminates in maximal recruitment, and thus greatest hypertrophy.

So we come back to isometric, or quasi isometric work. Are we recruiting motor units only pertinent to the joint angle..?

Conventional theory would say yes. But conventional theory (joint angle specificity) also holds that there is a carryover of 20 degrees from isometric work, so a protractor and possibly having the weight just beyond your eccentric capacities could be a rapid and damaging prospect.

However, If there is the slightest concentric movement of the weight, it ceases to be isometric work, and we can assume that type 2 fibres throughout the muscle group (not just to maintain a static position) are belong stimulated, it is just that they are physically incapable of contracting with enough force to pull the weight through its concentric ROM.

If the body is in a position of maximal, or near maximal recruitment (depending on the athletes status) the relevant fibres will be stimulated but incapable. What's the athletic carryover of this...? Very little I suspect- but, this is an article about preferential hypertrophy!

Im sure we've all strained at some point against a weight we couldnt shift, and have felt pain at the time, and afterwards- I thought Id torn a pec once deadlifting, within a day it was fine...so of what nature was the damage....?

Repairable...?

Certainly.

A shock to the system..?

Definatley.

Indicative of an adaptation forming...?

Speculativley.

Or just the result of an isometric contraction..?

The latter I dispensed with because I was moving at the time of the pain.

Again, the number of sets would have to be adjusted- and it would be worthwhile running similar exercises concurrently with a full range of movement in the micro cycle, but if the max lift attempt is close enough to being feasible, it must be recruiting fast twitch fibres.

That much is indisputable, the rest remains to be seen. It should be noting againthat it is maximal work for the portion that you move, and supra maximal isometric work for the portion that it doesn't- it could bridge the gap between conventional isometric training and concentric/eccentric work.

When giving this consideration, I have been drawn to the nature of adaptations elicited by different styles of training (hypertrophy/strength) and although the following concept is grossly oversimplified, I am starting to believe that hyperplasia stands more chance of occurring if the body is confronted by loads on a systematic basis it thinks it has little or no chance of moving. Whereas with loads it knows it can move through a full rom, that primary adaptations will be hypertrophy, or enzymatic in nature. I traced this loosely back to the belief amongst strength coaches worldwide that power lifting stimulates hyperplasia, and that body building stimulates hypertrophy. It makes sense that the purpose of an adaptation is to allow the body to adapt and to cope with new situations- and growing more muscle fibres seems to be its way of coping with getting maximally stronger....

And again, don't rule out the medulla oblongata in all of this!

Finally, a question: Do type 1 fibres show a greater tendency toward hyperplasia in normal subjects- or is it just in elite bodybuilders known for their usage of HGH/IGF-1..?

Please refer to Baechle and Earle's monolithic text "Essentials of Strength Training and Conditioning" to join the fray! Quotions in the main body of text lifted directly from the second edition.

0.45 27/5/06 Dr. J. S. Daemon