I’ve heard about some hypothesis of muscle growth based on ATP depletion inside the muscle.
Like during the set ATP source of energy has depleted and therefor muscle fibers damaged more easily.
The question is there any studies that discrete this theory?
Thanks

That sounds a bit weird. Low ATP would activate AMPK, which isn’t associated with hypertrophy.

Any more details? Why would ATP depletion damage muscle cells?

I’m not sure why.
But in paper “INTENSITY OF STRENGTH TRAINING FACTS AND THEORY: RUSSIAN AND EASTERN EUROPEAN APPROACH” of Zatsiorsky written:

The ATP-debt theory is based on the assumption that ATP concentration
is decreased after heavy resistive exercise (about 15 repetitions in 20
seconds per set were recommended for training). However, recent
findings indicate that even in a completely exhausted muscle, the ATP
level does not change.

wonder what the “recent findings” are.

wonder what the “recent findings” are.

Me too?

Yeah, ATP levels don’t change much. There is a hypothesis that it might change in different “compartments” of the muscle, so that it won’t show up on a biopsy.

I should be able to find some references on this. I’ll see what I can do.

Also, let me correct myself. I earlier said low ATP would activate AMPK.. high AMP would activate AMPK, which would most likely happen if ATP decreased.

EDIT:
Seems I might have been wrong. Can’t find anything on resistance exercise specifically, but found an abstract
http://www.ncbi.nlm.nih.gov/pubmed/17255174

In type II muscle fibers.

This is what I wrote in a forum back in 2002 i guess:

The theory about microtrauma outlined in my previous post was hinted to me by Vlad Medeski. This theory was postulated by a Russian bodybuilder. I heard that Yuri Vershankov and Mel Siff were to translate it into English. This theory has been put forward by the scientific community but was more intended for exploring the microtrauma due to endurance events. Microtrauma caused by weight training is still not in the agenda of many researchers. The theory seems to be really interesting but I still have some doubts. I tried contacting Vlad, but he hasn’t got back yet.

In general, why weights greater than 15 RM are not effective for hypertrophy?

Muscle cells can produce ATP by one or combination of three pathways1) formation of creatine by PC breakdown 2) formation of ATP by glycolyisis termed as glycolyisis 3) oxidative formation. Short term intense exercises like sprinting 50 meters, high jumping uses the ATP-Pc energy system. Weight training uses both ATP-PC and Glycolyisis for ATP synthesis. However, during a 15 RM the PC store are depleted very slowly and before it gets completely depleted or depleted enough to cause microtrauma, failure sets in. That is, accumulation of metabolic products like hydrogen ions and especially lactic acid (since intensity is really high than common events like running, oxygen availability is compromised thereby lactic acid tends to be the byproduct ;anaerobic glycolyisis) tend to terminate the set even before CP depletion. On the contrary, when using a heavy weight like 5 RM, the CP stores are depleted rapidly and the muscle never gets the time to replete ATP levels, thereby causing the more cross bridges to rupture before failure due to metabolic products sets in. In an event where we use a weight more than 20 RM maximum, the energy system used will be oxidative and it is nearly impossible for the ATP levels to fatigue before the metabolic failure appears.

Why Type 2 fibers are prone to microtrauma more than Type 1 fibers?

According to this theory, as I mentioned, it is the depletion of ATP and PC that causes the cross bridges to go into rigor thereby causing its rupture. Type 2 fibers have more myosin ATPase. ATPase is the enzyme which speeds up the usage or breakdown of ATP and thereby releasing energy. The more the myosin ATPase the greater the ATP depletion. The very reason why Type 1 muscle fibers are 3 to 5 time slower than Type 2. Hence, the faster depletion of ATP in Type 2 muscles naturally results in greater microtrauma in Type 2 fibers.

Why eccentrics causes greater microtrauma than concentrics and why still there are conflicting opinions?

According to the theory, both eccentrics and concentrics cause muscle damage. Eccentrics due to the inherent stretch in its action causes cross bridges to be overstretched than in the concentrics. So both Con and ECC are effective, ECC more effective due to the forced mechanical breakdown of cross bridges. Also, due to less metabolic fatigue in ECC.

So what is the RBE?

The RBE is the increased accumulation of CP and increased activity and number of enzymes like Phosphofructokinase, creatine kinase etc. I assume this is the reason why there are both one set protocols and multi set protocols. One set protocol causes damage in the first set, but the more number of sets also causes the body to respond or adapt by increasing the reserves of CP and the foretold enzymes, thereby making it tougher to cause microtrauma in the next workout. It has always been a mystery why Type 2B (greatest ATPase activity) muscles convert to Type 2A (moderate ATPase activity) and more muscle fibers as a result of weight training. I guess this theory gives a convincing explanation for this common conversion of fibers.

I know there are some pitfalls in the theory, but it seems to be pretty close to an optimal theory for microtrauma in muscle fibers.

On a side note, I felt it was pretty funny to see so many people in another thread named “Approaches to knowledge in hypertrophy” where people arguing all over the place to convinve someone how science can answer all questions. At the same time, there is hardly very few people to discuss the science of microtrauma in this thread in the very same forum. Cheers to all those geniuine people who contributed to this thread.

As I mentioned, Vlad only gave me a few clues about the theory. I had to fill in the blanks on my own. This was a year back. Bcos of my class work and stuff, I never tried to contact him until a few days back. Vlad seems to have pretty much grasped it.

So what you’re saying basically is that it is the ATP depletion which causes microtrauma. If that’s true, more microtrauma would be done at the end of a set, and going to failure would be a legitimate. Right?

My reasoning follows.

Yes and no. ATP depletion is the mechanism by which cross bridges goes into rigor and causes its breakage. But ATP in muscle is “always” maintained a “constant” through out the set by breaking down CP stores. ATP levels can be maintained for long time from the oxidative metabolism. But it doesn’t happen. Why? Since the weight is so heavy (large number of cross bridges) that the rate of CP depletion is much faster than its production. So microtrauma is almost the same at the beginning and at the end of the set. I would say microtrauma is more at the beginning of the set since all the metabolic by products lowers the Ph in the muscle thereby inactivating or inhibiting the enzymes required for CP and ATP production (Mi

I was familiar with the works on muscle damage by Richard Lieber and Friden even before I talked to the Russian guy. And I had also mentioned in my post regarding how the theory was proposed more so to explain damage associated with endurance than resistance training protocols. The theory put forward by Lieber hypothesizes that muscle damage exclusively to fast fibers can be explained due to the lesser oxidative capacity of fast fibers compared to slow twitch fibers. The theory based on the muscles oxidative potential never even considered the ATP-PC system (Phosphagen system) or the related enzymes like ATPase. Their interest in the oxidative metabolism is understqndable considering the energy demands of endurance activites are mainly aerobic in nature.They proposed that the well known “protective effect” of endurance training is due to the typically observed conversion of fast fibers to fast oxidative glycolytic fibers (FOG), wherby the oxidative capacity is enhanced. The theory was promising, but was soon discarded because they found exclusive fast fiber damage even after experimentally converting F fibers to FOG fibers. I really don’t know why they couldn’t find any slow muscle fiber damage, though endurance training mainly stresses slow twitch fibers. What I feel is that the damage will always be present and will be more for fast twitch fibers, but will be decreasing over subsequent bouts.

The CP depletion theory cannot fully explain as you said is true. As you might know, eccentric contraction is unique in many regards. Even the well- accepted sliding flilament theory fails to explain the strength increases in eccentric contractions. Lieber himself has written that there is number of unexplained mechanical phenomena associated with eccebntric contractions. It is so rightly termed as the “black sheep” by exercise physiologists. Until we discover the precise mechanism of eccentric contraction, none of the theories can “fully” explain injutires associated with eccentric contraction. There can no be fool proof theory to explain ecc exercise indued injury when the eccentric contraction is itself a mystery. But we do know that extremely high forces are generated in the individual cross bridges due to eccentric contractions. In addition, the passive stretch of the series elastic components results in added stress. Both these mechanisms are attributed and should be considered when talking about the increased potential of ecc contarction induced injuries.Eccentric contractions are very peculiar in these regards compared to other contractions. I agree there is a Z disc thickness difference in Type 2 and Type 1, but these structuraldiffernces are only affected if the muscle is activated in the first place, which is in turn dependent on the energy stores.

I found one study which showed a significant increase in creatine phosphate stores. But the rest of the studies I looked at seemed to show either no increase or slight increase in the CP stores. I believe the depletion rate is manipulated by changes in enzymatic activity than by substrate storage mechanisms. I guess it is similar to how body fat is regulated; body tries preserve or minimize its usage by both increasing the enzymatic activity associated with fat storage and decreasing the rate of uytilization.

I perfectly understand that this theory is still arguable. But it appears much more convincing than the other theories out there when youconsider the RBE and detrainin adapatations.This is an excerpt from the same HST thread.

According to the RBE research, a muscular adaptation may occur as early as 24 after the initial bout. These observations lead to the exclusion of two theories; the connective tissue theory and cellular adaptation theory (Morgan’s sarcomeres popping theory). Both of these theories suggested the structural change in muscle as the onset of the RBE. But the time required for structural remodeling discredits these theories bcos RBE is observed within a time frame of 24 hours. The neural adaptation theory was excluded after observation of RBE with electrical stimulation. Likewise, the dissipation of RBE if it were for structural components would take much longer. I has been observed though that an reduction in tendon compliance to be occurring following training. The reaserchers doubt this to be due to the strengthening of the cross bridges. I wont disagree considering this theory.

Bryan believes that RBE is a structural phenomena , like the sarcolemma getting tougher. But as you can see the RBE is is observed with 24 hrs or maybe even less time. There is not enough time for structural adaptation to appear nor even if it appears to cause any significant change in muscle function. I am assuming the 24 hrs is enough for enzymatic changes to appaear and therby cause the RBE. Not sure though. Structural adaptations do happen, but that can be classified as a chronic adaptation. Muscle getting decondtioned in very litlle time compared to the time it takes to get conditioned shows that the changes are more chemical than mechanical.

I have trouble believing that parts of the muscle will actually go into rigor during exercise.. This needs to be confirmed experimentally.

“According to the RBE research, a muscular adaptation may occur as early as 24 after the initial bout”
What muscular adaptation are you talking about here? And how does it exclude the two other theories?
Are you talking about an adaptation making the muscles stronger? If it’s enzymatic adaptation, that wouldn’t exclude the popping sarcomere hypothesis.. as that doesn’t have anything to do with enzymatic changes, but with changes in sarcomeres in series after a bout of eccentric exercise.

And I’ve never seen any large enzymatic adaptations to resistance exercise. ATPase activity can change, but glycolytic enzymes probably don’t change much.

Anoop, as I understand from above, you think it’s quite solid theory that can explain muscle growth?

If you remember we have a thread about V.Protasenko work
He use this theory and define how the ultimate training must be programmed.
It must include hard sessions once a while (once in 2 weeks) separated by easy sessions for keeping MPS high but without microtravma. Does this setup reminds you something very familiar?

I had never heard of V.Protasenko before, but I currently do something similar to what you describe: I lift 3 days per week alternating two different workouts, and I peak on one workout once every three weeks.  Every other workout is sub-maximal using 80-92.5% of the best effort (though I am strongly considering dropping down even into the 70-80% range for some workouts).  The result is that I go for new PRs in each workout once every six weeks (alternating workout A and B, of course).  This has been working really well for me for the past several months.

Anyway, I did look this guy up, and I couldn’t find much, but here is what I did find (in case anyone else is curious):

The author of this website says his workout theories are based on V. Protasenko.

A forum post outlining some of Protasenko’s concepts in short.

And the below from this blog post:

About a year ago I came across a book by Vadim Protasenko written in Russian on the same subject. His goal was to verify Mentzer’s claims with published research. He started from the very beginning, what causes muscular failure on the physiological level. Next – what makes muscle tissue grow and so on. His conclusion was similar to Mentzer’s, that long recovery intervals are beneficial for training. However, the premise behind it was different. Mentzer claimed that the improved result is due to recovery. According to Protasenko, allowing long intervals between training session leads to some degree of detraining and increases the sensitivity of the muscle to training stimuli. Never mind the actual reason behind it, both authors claimed that long intervals between training sessions are good. Protasenko, however, instead of complete rest, rather favored infrequent heavy sessions with light sessions in between. Cycling loads leads exactly to this way of training: the load increases from session to session, and as soon as you hit a new high you start the cycle with much lower all over again, thus working maximally only once every two weeks or so.

This blog post is kind of interesting because it is primarily about rationalizing the superiority of low-frequency training via the discussion of some Russian research conducted in the ‘70s.  Sadly, the research is entirely about rowing performance, not about muscle hypertrophy or strength.

This is google translation his most known work:
http://translate.google.com/translate?js=y&prev=_t&hl=en&ie=UTF-8&layout=1&eotf=1&u=http://bodybilding.info/books/text/protasenko.html/0.html&sl=ru&tl=en

Anoop, as I understand from above, you think it’s quite solid theory that can explain muscle growth?

That post was from 2002. I don’t know even remember most of the stuff I wrote and never really kept up with it.

Even if there is something i it, I am not sure how you can apply it practically.

Creatine phosphate depletion causes a decline in the rate at which ATP can be generated, in effect depleting ATP for whatever load you go to concentric failure with.  If you do some eccentric muscle actions with the same weight immediatly after you reach con. failure then you will increase microtrauma because ATP is needed to cause the myosin heads to release the actin filaments.  When there is not enough ATP available at the time of the eccentric action to allow the myosin heads to release the actin then you will forcibly break the connections thus causing microtrauma.  This is why eccentric are so effective for recruiting satellite cells and causing hypertrophy. 

So, effective eccentrics can be done with less than 1RM weights provided the target muscle is depleted for CP first with concentric failure and the eccentrics follow immedately.  If you like a lot of good pain then these kinds of sets are what the doctor ordered.  I only do one set like this for each exercise.  I do around a 10RM with continuous tension and then do 20 negatives.  They kind of go rest pause because the lactic acid burns so.  If I can get 10 con. reps then I increase the weight.  The exercises I do this with are high bar back squats, pullups, one leg deadlifts, 3 chair pushups, one arm DB curls, one arm french presses,  barefoot heel raises, and incline side delt raises.  I am 220lbs at a height of 6’3” and a bf% less than 10. 

Just my two cents that I gleaned from a few A&P textbooks and various articles about muscle physiology and energetics and how I apply them.

Hi Paul,

Welcome to Exercise biology!

Good first post.

I think part of the problem with the theory is that ATP never gets really depleted in a set. I don’t think it gets depleted more than 50% from what I can remember. Also, eccentric contractions cause damage due to the unique type of contraction ( stretch and contraction). Eccentric contractions use very little ATP than concentrics and yet has more damage!

Anoop, 

In this review

Sports Med. 2001;31(10):725-41.
Energy system interaction and relative contribution during maximal exercise.

Gastin PB.

Victorian Institute of Sport, Melbourne, Australia. .(JavaScript must be enabled to view this email address)

He writes

Power Output, Fatigue and Anaerobic Energy Supply

Rate of energy release is critical to success in sports that require the development and short term maintenance of high power outputs. Lamb[41] has estimated that world-class weightlifters can produce power outputs that are 10 to 20 times that required to elicit the maximal rate of aerobic energy supply [maximal oxygen uptake (V-dot2max)]. Such power outputs are almost instantaneous. Sprinters may be able to achieve 3 to 5 times the power output that elicits V-dot2max yet cannot sustain such high power outputs.[41] Ward-Smith,[42] using mathematical modelling techniques on running performances of elite male athletes, has estimated that the ratio between maximal anaerobic power to maximum sustainable aerobic power is in the range of 2.0 to 2.6, a value consistent with the 2 to 4 range suggested by Spriet.[43] During the acceleration phase of the sprint, the average power output over a complete running stride may exceed 1000W, with values of over 3kW being reported during the propulsive phase of the stride.[44]

The rate of anaerobic provision of ATP is critical to the development of high power output. Peak rates for ATP synthesis from both the degradation of PCr and glycolysis during various modes of exercise lasting 10 seconds or less appear to be in the range of 6 to 9 mmol ATP · kg dry mass-1 · sec-1.[43] Together, these 2 energy pathways may combine to provide approximately 15 mmol ATP · kg dry mass-1 · sec-1 over the first 6 seconds of sprint exercise, with some 50% of the ATP being supplied from the degradation of PCr.[44] The rate of PCr degradation is at its maximum immediately after the initiation of contraction and begins to decline after only 1.3 seconds.[45] ATP production from glycolysis, on the other hand, does not reach its maximal rate until after 5 seconds and is maintained at this rate for several seconds.[45]

The decreasing force generation during brief, intense exercise is the result of either a reduced rate of ATP resynthesis or a decreasing rate of ATP utilisation by the contractile apparatus.[46,47] The resting levels of ATP and PCr in skeletal muscle are in the range of 25 and 70 to 80 mmol · kg dry mass-1,[43,45] respectively, and appear to be relatively unaffected by the state of training.[48] A total depletion of ATP does not occur even in extreme exercise conditions, although a 30 to 40% decrease in muscle ATP has been reported.[18,49] In contrast, almost complete depletion of PCr stores is possible.[47,50,51] Energy derived from the stores of ATP and PCr, considered the alactic component, have been estimated to contribute between 20 to 30% of the anaerobic energy release during intense exhaustive exercise of 2 to 3 minutes in duration.[17,18,28]

I say that once creatine phosphate is depleted, then the rate of ATP resynthesis drops off which causes a drop off in peak power output.  The drop off in power output allows anaerobic glycolysis to step up and be the primary ATP resynthesizer for a short while longer.  Then when lactic acid accumulates to a high enough concentration the power output drops off again so that aerobic glycolysis can take over the prime role. 

Anyway, when momentary concentric failure is attained, the rate of ATP resynthesis for more concentric reps with the given load is insufficient.  As a result there is not enough ATP available, in real time, to enable the lifting of the load, but the load can be lowered because, as you rightly state, eccentrics require less ATP than concentrics.  But still,  after doing enough eccentric work immediately following concentric failure, the amount of ATP needed for crossbridge detachment becomes greater than what is available at any given moment.  When that happens, no matter how much you try to resist the descent of the weight, it continues to go down, and when the weight gets to the bottom of the range of motion, it is impossible to lift it.  When I get to this point, I hypothesize that microtrauma is happening because of the forcing apart of the crossbridges that do not have ATP. 

So, when I do an extended set, I go to concentric failure and then do negative reps immediately after, and at the end of each negative, I try to lift the weight for a second or two.  This amounts to a static hold in the loaded stretch position for the full range of motion exercises (like doggcrapp’s extreme stretching). 

I rest as little as possible between negatives.  If I can do a concentric after a negative, then I know I have rested too long between reps.  I chose 20 negative reps, as a follow up for the 8-10 concentric RM, so that the exposure to the load would be long enough (TUT) to cause some serious burning and that the negative work would be high enough to cause some DOMS.  Again, I only do one work set per exercise (like the doggcrapp protocol). 

So, I agree that ATP is never depleted, but the rate of its resynthesis is definitely diminished during exhaustive exercise.  That is the key for my hypothesis of “generate fatigue with concentric failure to better induce microtrauma with eccentrics”. 

Happy training,
Paul