A New and Unique Training Method is Here

[NWlifter]

Just so people see my train of thought on some of this...

Exercise
Heavy - tension may cause leaks allowing calcium to rush in to the cell
Lighter with high activity - high intracellular calcium from tetanic contractions

DOMS - Pain from the immune system in response to high intracellular calcium

Quote[/b] ]From Neuromechanics of Human Movement, by Roger M. Enoka

The sensation of tenderness appears to be triggered by the loss of cellular calcium homeostasis (Clarkson, Cyrnes, McCarmick, Turcotte, & White, 1986; Friden & Lieber, 1997' Jackson, Jones, & Edwards, 1984) due to the activity-induced disruption of sarcomeres. A high intracellular calcium concentration activates proteolytic and lipolytic systems that initiate the degradation of cellular structures (Armstrong, 1990). Because this inflamatory process has a time course smilar to that of the heightened tenderness (Lieber, Schimtz, et al., 1994) and there is an appropriate activation of the immune system (Malm, Lenkel, & Sjodin, 1999), the sensation of soreness is usually attributed to the inflammatory response.

DOMS - See Yu study. Most likely a remodeling rather than damage.

So far- High activity and/or tension lead to a remodeling

Tension & Tetany - will still increase intracellular calcium even if DOMS is not felt.

High activity - Kicks off the mTOR pathway. ATP turnover related to p70sk, p70sk almost linear with MPS.

Final - Tension and high activity start the chain of events that lead to MPS.

Both/either/or work. Both can be a variable. Drop the tension and increase the activity and come out the same.

 

[Dood]

Quote[/b] (Sub7 @ Dec. 28 2005,8:46)]Anyone want to take a stab at what the implications of these findings are for ACIT?
Any suggestions on how one can better occlude muscles in training, for example?

Well just looking at the abstract and reading the conclusion, I'd say it has no application for ACIT or occlusion. That study is looking at the effects of muscle stretching, which isn't really applicable to occlusion or ACIT, since without an external occlusion method the muscle will lose occlusion when fully extended/stretched.

 

[Sub7]

Quote[/b] (Dood @ Dec. 28 2005,10:07)]

Quote[/b] (Sub7 @ Dec. 28 2005,8:46)]Anyone want to take a stab at what the implications of these findings are for ACIT?
Any suggestions on how one can better occlude muscles in training, for example?

Well just looking at the abstract and reading the conclusion, I'd say it has no application for ACIT or occlusion. That study is looking at the effects of muscle stretching, which isn't really applicable to occlusion or ACIT, since without an external occlusion method the muscle will lose occlusion when fully extended/stretched.

The paper talks about eccentrics in great detail and I think it has some relevance. Though whether it has any practical implications that we can ise actual training; I don't know about that.

BTW, here is an interesting quote from the paper, read the second to last sentence:

" An important step in determining the mechanism of this damage is to find which parameters of the stretch are important in determining its extent. There is general agreement that longer stretches cause more damage (7, 36). In contrast, shortening over the same range of lengths does not cause any damage (45). Stretches in relaxed fibers generally cause no detectable damage (32, 54). A cumulative effect of extra eccentric contractions is also common, although the effect is usually nonlinear, with further increases in the number of eccentric contractions causing smaller increases in damage (46, 64). Similarly, there is general agreement that velocity is not a major determinant (46, 66). In situations where tension has been varied other than by changing length, there is general agreement that greater tension produces greater damage (46)."

Velocity is irrelvant in determining the damage induced by eccentrics? I thought faster negatives were known to cause more damage?

But then again: "The tragedy of science is the slaying of a beutiful hypothesis by an ugly fact"
Thomas Huxley

(this was for Ron)

 

[mikeynov]

Quote[/b] (NWlifter @ Dec. 28 2005,9:47)]Just so people see my train of thought on some of this...
Exercise
Heavy - tension may cause leaks allowing calcium to rush in to the cell
Lighter with high activity - high intracellular calcium from tetanic contractions
DOMS - Pain from the immune system in response to high intracellular calcium

Quote[/b] ]From Neuromechanics of Human Movement, by Roger M. Enoka
The sensation of tenderness appears to be triggered by the loss of cellular calcium homeostasis (Clarkson, Cyrnes, McCarmick, Turcotte, & White, 1986; Friden & Lieber, 1997' Jackson, Jones, & Edwards, 1984) due to the activity-induced disruption of sarcomeres. A high intracellular calcium concentration activates proteolytic and lipolytic systems that initiate the degradation of cellular structures (Armstrong, 1990). Because this inflamatory process has a time course smilar to that of the heightened tenderness (Lieber, Schimtz, et al., 1994) and there is an appropriate activation of the immune system (Malm, Lenkel, & Sjodin, 1999), the sensation of soreness is usually attributed to the inflammatory response.

DOMS - See Yu study. Most likely a remodeling rather than damage.
So far- High activity and/or tension lead to a remodeling
Tension & Tetany - will still increase intracellular calcium even if DOMS is not felt.
High activity - Kicks off the mTOR pathway. ATP turnover related to p70sk, p70sk almost linear with MPS.
Final - Tension and high activity start the chain of events that lead to MPS.
Both/either/or work. Both can be a variable. Drop the tension and increase the activity and come out the same.

Yes, but as far as I can tell, tension still rules because it's the one thing you will have to consistently increase over time, regardless of the means of training, to get bigger and/or stronger.

So, sure, go the higher reps/fatigue route, and that can get you big like many other rep ranges. But how will it make you big over time?

You still have to be lifting heavier stuff in that context.

No way around it.

 

[Sub7]

This may soud like a totally redundant post, but may be we should seperate two kinds of trainees and look them seperately:

a) Proponents of Heavy training
b) Proponents of Heavier training

Group A says that the tension on the muscle is possibly the most important thing. If you are not moving a weight that is close to the heaviest posible weight that you are capable of moving, you won't grow well

Group B says: No, the above satement is not neccesarily right. I can use other approaches such as 5X5s ACIT, travel to Japan, enter Ishii's torture chamber and have my arms occluded with pressure cuffs, whatever... and still grow with weights that are much lower than my 80-90% 1RM that you guys worship. But as I grow, I must also increase the challenge because bigger muscles need bigger challenges to grow. The easiest way would be to add weight. I may be going from 30% of my 1RM to 40% but yes even then I know I have to increase weight, that I can see and agree with.


I think almost all of us are in category B and do agree that to keep growing, you have to trainer heaveir than you used to. But that is quite different from using weights that are >75-80% of your 1Rm all the time. That is what people in group A say. If we clarify what we mean in the future -in this and all threads- we'd communicate better I think

Does this makes sense at all?

 

[Dood]

Quote[/b] (mikeynov @ Dec. 29 2005,12:21)]Yes, but as far as I can tell, tension still rules because it's the one thing you will have to consistently increase over time, regardless of the means of training, to get bigger and/or stronger.

But, the occlusion studies show growth with little tension. The occlusion gets the muscle to react as if it is being hit with higher tension even though that tension is not present. So maybe we need to look at what high tension does, which is effectively occlude the muscle.

Relating this to Sub's last question, if using occlusion eliminates high tension, will RBE still be a factor? If RBE is a response to tension on the muscle, but tension remains low, will weight progression be necessary?

 

[mikeynov]

Quote[/b] (Dood @ Dec. 29 2005,8:55)]

Quote[/b] (mikeynov @ Dec. 29 2005,12:21)]Yes, but as far as I can tell, tension still rules because it's the one thing you will have to consistently increase over time, regardless of the means of training, to get bigger and/or stronger.

But, the occlusion studies show growth with little tension. The occlusion gets the muscle to react as if it is being hit with higher tension even though that tension is not present. So maybe we need to look at what high tension does, which is effectively occlude the muscle.
Relating this to Sub's last question, if using occlusion eliminates high tension, will RBE still be a factor? If RBE is a response to tension on the muscle, but tension remains low, will weight progression be necessary?

The thing that worries me is that in determining what is optimal, I'm not sure we're looking at this over a long enough period of time.

Even in the occlusion studies, my question is: "what happens over, say, YEARS of performing exercise like that?"

Do you really think you could use static load X and continually grow, even in a state of occlusion, indefinitely? That makes no sense to me at all.

That was my point - "tension" rules insofar as "progressive tension overload" is necessary in ANY context - occlusion vs. non-occlusion vs. 85% 1 RM vs. 70% 1 RM. However you implement your training, what will have to go up over time is the amount of weight/tension you are placing on your muscles, preferrably in some not-retarded context (i.e. reasonable volume/frequency/intensity).

"So maybe we need to look at what high tension does, which is effectively occlude the muscle."

As to this comment, I do agree, it is critical to understanding why the occlusion studies imply what they do. Another way of putting it, though, is what commonalities are shared between the occlusion studies and higher tension scenarios?

And I think Ron/Dan already answered this - "fiber activity." The "work per unit time" being performed by a given muscle's fibers, including higher threshold motor units. When you force the occlusion of a muscle, higher threshold motor units are recruited much more quickly and the activity of your muscle fibers within that set start to resemble what happen under much heavier scenarios.

So that's "why" occlusion works so well. But as above, even in that context, in terms of what we can realistically alter over time, it all seems to point back towards "progressive tension overload."

Incidentally, I really wish Bryan would comment on some of this stuff. Particularly in that the model being put forward by some researchers in the past couple of years seems to contradict of some of the ideas behind HST - namely that hypertrophy is primarily a mechanical phenomenon that's a result of physical strain on muscle tissue.

 

[xahrx]

I'm with Dan overall. Tension and work seem to be the best approach. I guess a lot of us get stuck in a one or the other kidn of mindset. I think ACIT might make a good addition to high intensity programs if it is indeed easier on the CNS and PNS. If so it migh be possible to achieve a higher frequency of workouts in the context of high intensity strength programs without frying yourself. That in and of itself could be usefull.

Also I don't think progressive overload is an issue as everyone seems to agree that whatever the context of the workout an increase in load over time would be necessary.

 

[imported_dkm1987]

I don't think what has been presented lately contradicts what Bryan has put forth. Bryan has always mentioned that TUT is a factor, now what Ron and I have beeen discussing is how this relates to the tension in a given amount of time. Tension is also impacted by metabolic constituents and again how does changing the metabolic environment change the response to a given tension in a given time frame, obviously it does and is showing some pretty dramatic results as far as growth.

I agree with Mikey on the progression aspect at some point tension must be increased even with occlusion. There is one study in particluar and I would need to review it again to see the jist of it, but I do remember something to the effect of them increasing the cuff pressure gradually, so would increasing the occlusion over time be one way to increase the response? Don't know? But even still at some point you would totally restrict flow and therefore could not continually increase the occlusion.

I guess what I am getting at is if occlusion amplifies the response to lower tension then PERHAPS using an occlusion type of stimulus would allow using lighter weights but still get the benefit.

Secondarily to that comes the question of, Does constant tension mimic true occlusion? Honestly I haven't gotten as deep into it as Ron but I am sure eventually I will begin to wade through it. So for now I am unsure.

 

[NWlifter]

Hey Dan- I would also like to get a bit deeper into the 'pressure tension occlusion' stuff. The studies I found showed the approx percentage of MVC where muscle pressure becomes high enough to almost or completely occlude blood flow. It seems to be pretty solid about it. BUT, I think the tricky part is keeping it occluded.

Example: With an isometric isolation exercise, I'm postive we could keep the tension on and occlude blood flow. But with a compound, especially with movement, it becomes trickier. It would be VERY hard to use a part of the ROM where several muscles just happened to be under 'greater than minimum occlusion tension'.

Quote[/b] ]Yes, but as far as I can tell, tension still rules because it's the one thing you will have to consistently increase over time, regardless of the means of training, to get bigger and/or stronger.

So, sure, go the higher reps/fatigue route, and that can get you big like many other rep ranges. But how will it make you big over time?

You still have to be lifting heavier stuff in that context.

No way around it.

True, but two things,

1) Do we only have to raise the tension so we keep above the minimum? (since were increasing strength our MVC is raising)

2) I'm very sure the fatigue stuff can make you big over time, if a person sticks with it. I know a couple people I've emailed with for quite a while, they train 'Gironda Style' and use relatively light weights, they've grown quite a bit. (One guy recently went from I think 16.75 arms to over 17 in a few weeks using high volume, light weights and training his arms 4-5 days per week. Clean no 'supplements&#39

Again, it seems tension is a means to an end, and that 'end' being high fiber activity.

 

[mikeynov]

Quote[/b] (dkm1987 @ Dec. 29 2005,10:29)]I don't think what has been presented lately contradicts what Bryan has put forth. Bryan has always mentioned that TUT is a factor, now what Ron and I have beeen discussing is how this relates to the tension in a given amount of time. Tension is also impacted by metabolic constituents and again how does changing the metabolic environment change the response to a given tension in a given time frame, obviously it does and is showing some pretty dramatic results as far as growth.

Well, let's look at this as a reasonable summary of Bryan's perspective on hypertrophy.

This section is the most relevent:

Quote[/b] ]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.

To me, what Bryan seems to be saying here is that for growth to be sustained over time, microtrauma to muscle fibers is a necessary prerequisite. If researchers are calling into question 'damage before hypertrophy,' I would think this is exactly what they're challenging.

So, using this as a launching point (because I'm trying to play catch up to you and Ron who seem to have eclipsed my understanding of skeletal muscle hypertrophy in the past couple of years absence geometrically), I'm curious how accurate you feel this assessment is, and where you would disagree with Bryan's conclusions.

For starters, do you feel that #1 is necessary to long-term growth? If so, do you feel this can occur in the absence of microtrauma to a given muscle fiber?

 

[mikeynov]

Quote[/b] (NWlifter @ Dec. 29 2005,10:58)]2) I'm very sure the fatigue stuff can make you big over time, if a person sticks with it. I know a couple people I've emailed with for quite a while, they train 'Gironda Style' and use relatively light weights, they've grown quite a bit. (One guy recently went from I think 16.75 arms to over 17 in a few weeks using high volume, light weights and training his arms 4-5 days per week. Clean no 'supplements&#39
Again, it seems tension is a means to an end, and that 'end' being high fiber activity.

Quote[/b] ]1) Do we only have to raise the tension so we keep above the minimum? (since were increasing strength our MVC is raising)

This is sort of what I'm wondering. Would the only reason that we have to raise tension over time is due to increasing strength and what this implies about fiber activity? Ie as your get stronger 'work per unit time' of a given muscle fiber at a fixed load would decrease, no?

Quote[/b] ]2) I'm very sure the fatigue stuff can make you big over time, if a person sticks with it. I know a couple people I've emailed with for quite a while, they train 'Gironda Style' and use relatively light weights, they've grown quite a bit. (One guy recently went from I think 16.75 arms to over 17 in a few weeks using high volume, light weights and training his arms 4-5 days per week. Clean no 'supplements&#39

I still see this as misleading in a way, though, because I know for a fact that Gironda style stuff still emphasis progressive weights. "Fatigue" in the abstract will make you grow acutely, but over time, what has to happen? Weights have to go up.

Volume/fatigue approaches certainly work, but even in that context, in any long run scenario, what can you affect to keep up growth (in respect to the training side of the equation, at least)? How much you're lifting.

 

[Sub7]

I would like to clarify just one thing:
Nowhere in the ACIT site are we rejecting progressive overload. As you are getting stronger with ACIT, of course you should increase the weight. In fact you are going to have to. As Ron clearly pointed out: to occlude the blood, the contraction must be above a % of the MVC. So when MVC goes up as you are growing new muscle, naturally the weight has to go up to be able to occlude the muscle. I may be oversimplifying this but I don't know why anyone may have thought ACIT and progressive overload were contradictory.

Also as far as keeping the muscles occluded, especially on compounds: Yes it is difficult, but I personally found that chest presses and leg presses -despite being textbook examples of multi-joint compound exercises- are the most suited moves for ACIT, in my highly scientific sample of n=me, myself and Hunkar at least. By squeezing the muscles actively on the way down and only slightly shortening the ROM, I feel that I get a better occlusion effect in these moves than anywhere else. Here is a little something from the ACIT web site:


"A little homework
An excellent practice that will give you a better feel and appreciation for ACIT as well as greater muscle control, especially on your legs, is the Tabata Protocol. The Tabata protocol has been developed in order to enhance general fitness in as short a time as possible and works nicely if you are feeling adventurous and are up for a challenge. While the basic idea can be applied in a number of ways, Dr. Tabata’s method is based on very intense 20 second sprints separated by 10 second rest periods (each such 30 second block constitutes one set). The idea is to set up a stationary bike or other similar device at such a resistance that you can only perform 6 to 8 such sets but no more. So if you aim for 7 sets, you should really be spent and more or less unable to cycle any more by the end of set 7. If you try this experiment, you will see that by set 3 or 4, your legs will burn like hell. The interesting thing is that this “fire” so to speak, will be sort of trapped while you are cycling and will start to dissipate as soon as you stop cycling –or even slowing down. You will be able to literally feel something acidic start to travel through your veins as soon as you slow down or take a break. The sensation is amazing and outright spooky, so try it sometime (though, like with any new method, this may take a while to master, so don’t despair if the protocol doesn’t feel as I have described right away).

You will also notice that one really must cycle as hard as possible to reap the desired benefits as the dissipation of lactic acid and new blood rushing into the muscle will give the whole area a big rest and boost of energy as soon as the tension on the muscles is relieved –even slightly. What is happening during the Tabata protocol is very similar to ACIT. As you are cycling very hard, the acid and other waste products are building up inside the muscles and the circulatory system is unable to clear them up because the tension of the quads is restricting blood flow. As soon as you relax the tension, the blood that has been "waiting at the gates" takes the opportunity to rush in and you feel the acidic blood travel through your veins. As this exercise shows, it really is crucial to keep the tension on the muscles as high as possible during an ACIT-style set because even a second or two of relaxation will bring fresh blood into the area and negate the effect you are looking for. Now all of this being said, do not let this little experiment discourage you either. It may sound too difficult to keep the muscles under constant-tension throughout an entire set, but, as you will see after some practice, this is entirely possible. Keep in mind that learning to ride a bicycle or jump up and down on one leg require a tremendous amount of neural skill and are far harder than squeezing a muscle at all times. If you can master those things, you will certainly be able to master ACIT after some practice."

 

[imported_dkm1987]

Quote[/b] (mikeynov @ Dec. 29 2005,10:28)]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.

Remodeling yes, damage no. First what must be recognized is as stated earlier, that many earlier researches looking at damage may have been a little off, as far as to what extent, and even what markers and when these are seen. So in a nutshell yes, microtrauma is needed.

Load has shown to be ONE way of causing leakage and disruption, Over abundance of calcium is another. Over abundance of calcium can be initiated via long duration contractions of relatively less load and also via heavier loads.

Moving on, satellite cells are activated via a ton of pathways and not only IGF-1 (MGF). But absolutely I agree that for continued growth sat cells must donate their nuclei. But I am incline to believe this is more of a response to training status than training modality (at least in humans).

Now don't get me wrong, all I am saying is hypertrophy will occur with or without the damage caused by eccentrics, and secondly when most humans work out they utilize both aspects of isotonic movements. To say eccentrics cause more hypertrophy hasn't been truly identified, IMO.

An interesting study I've held on too for some time and unfortunately I still haven't seen any follow up done by the researches questioned this idea about 5 years ago.

Controlled lengthening or shortening contraction-induced damage is followed by fiber hypertrophy in rat skeletal muscle.
Int J Sports Med. 2000 Feb;21(2):107-12.

To study the hypothesis that more severe damage, caused by controlled lengthening (L) contractions, results in greater myofiber hypertrophy compared to increase in fiber size followed shortening (S) contractions, tibialis anterior muscles of anesthesized male Wistar rats were subjected to 240 either L or S contractions. The highest increase in muscle beta-glucuronidase activity, an indicator of muscle damage, was observed in L (7.1-fold) 4 days and in S (2.6-fold) 8 days postexercise. Dystrophin- and desmin-negative as well as fibronectin-positive fibers (signs of the early phase of damage) were observed immediately after exercise in the L group. At 4 days, massive myofiber injury was visible, and internally localized nuclei were present at 15-80 days after exercise in the L group. The shift towards more glycolytic fiber types (p<0.05 in L and S) and an increased mean cross-sectional area of type IIX/B fibers (p < 0.001 in L and S) at 80 days were observed in both groups. The observed minor damage with unchanged myofiber structures following S induced, however, an increase in myofiber cross-sectional area of nearly the same magnitude as that following L, which was more damaging. The results do not support the hypothesis that fiber hypertrophy depends on the extent of the myofiber damage upon the exercised muscles.

 

[Dood]

Quote[/b] (dkm1987 @ Dec. 29 2005,10:29)]There is one study in particluar and I would need to review it again to see the jist of it, but I do remember something to the effect of them increasing the cuff pressure gradually, so would increasing the occlusion over time be one way to increase the response? Don't know? But even still at some point you would totally restrict flow and therefore could not continually increase the occlusion.
I guess what I am getting at is if occlusion amplifies the response to lower tension then PERHAPS using an occlusion type of stimulus would allow using lighter weights but still get the benefit.

I believe in that study they "progressed" the amount of occlusion more as a means of seeing what was enough. Not surprisingly leg muscles need more pressure to be occluded than arm, and pressure needed varies to some degree from one person to another. I'm not aware of any "resistance" being built up to a certain level of occlusion pressure.
One benchmark I've seen mentioned, and the one I used on myself, is that occlusion is reached when the veins of the top of the foot, (for legs), or back of the hand, (for arms), protrude more. Too much pressure and you squeeze off the arteries as well, which does not allow the blood pressure to increase and the veins don't stand up. This may be more for safety than anything, as I would think both scenarios would stop blood flow and allow lactic acid to build up, but if you're squeezing hard enough to block an artery you might cause some damage.

 

[Sub7]

I have brought up this point before, but it is important not to attempt hard-core occlusion on your own with a cuff or elastic band. A quote form an earlier post of mine on another board:
From Mr Sato's paper -who was the first person to develop and use occlusion: (http://kaatsu.jp/pdf/0101/01Sato.pdf)
"A turning point in my personal training technique
came in 1967, when I was freshman in college.
Numbness in my leg due to my reckless KAATSU
Training routine became so severe that I was
hospitalized. Up to that point I had ignored the
numbness in my legs during KAATSU Training and
continued with my training despite the discomfort.
At one point, however I began experiencing an acute
attack of shortness of breath. I went to the
emergency room and was diagnosed with a
pulmonary embolism. Once the physician who was
treating me learned of my training methods he
warned me to immediately discontinue my KAATSU
Training." Kaatsu by the way is the name given to occlusion in Japan.
Hunkar

 

[NWlifter]

Hey Sub- Yes, that info. makes me never wanna really try occlusion training!

Quote[/b] ]

Quote[/b] ]
1) Do we only have to raise the tension so we keep above the minimum? (since were increasing strength our MVC is raising)

This is sort of what I'm wondering. Would the only reason that we have to raise tension over time is due to increasing strength and what this implies about fiber activity? Ie as your get stronger 'work per unit time' of a given muscle fiber at a fixed load would decrease, no?

I'm kinda thinking that.
Back a while ago I harped a lot on the 'tension per fiber' stuff. That no matter what load we use, once a fiber reaches tetany, it's putting out it's max tension. Rep 3 of a 3 RM is about the same as a rep with a 1RM.

So what does a heavier load do? It get's you to tetany sooner.

Quote[/b] ]

Quote[/b] ]
2) I'm very sure the fatigue stuff can make you big over time, if a person sticks with it. I know a couple people I've emailed with for quite a while, they train 'Gironda Style' and use relatively light weights, they've grown quite a bit. (One guy recently went from I think 16.75 arms to over 17 in a few weeks using high volume, light weights and training his arms 4-5 days per week. Clean no 'supplements'

I still see this as misleading in a way, though, because I know for a fact that Gironda style stuff still emphasis progressive weights. "Fatigue" in the abstract will make you grow acutely, but over time, what has to happen? Weights have to go up.

True, also, Gironda emphasizes progressive density. Many keep the same weights for quite a while, but shorten the interset rest periods. Then increase the load. So you might use the same load for 6 weeks before increasing it. Then a small increase, etc.

Charles Staley has some good info. on density training, it's about the same idea, just a different format.

Quote[/b] ]Volume/fatigue approaches certainly work, but even in that context, in any long run scenario, what can you affect to keep up growth (in respect to the training side of the equation, at least)? How much you're lifting.

But again, do we have to increase the RM or just increase the load to keep up with the greater strength that the hypertrophic adapations have induced?

 

[mikeynov]

Hey Dan, wanted one thing clarified:

"Remodeling yes, damage no. First what must be recognized is as stated earlier, that many earlier researches looking at damage may have been a little off, as far as to what extent, and even what markers and when these are seen. So in a nutshell yes, microtrauma is needed."

I'm confused here. Earlier in the thread I pointed out that you and Ron doubt the "damage before hypertrophy" assumption that's underlied a lot of hypertrophy research over the years. The "damage" I was talking about was precisely "microtrauma/microstrain to muscle fibers."

So on the one hand you (or was it Ron..maybe I'll just refer to you collectively as Danron, kind of like Enron, but won't cheat me out of my life savings...) said earlier that there was evidence that hypertrophy could occur just fine in the absence of "damage." On the other hand it seems suggested that microtrauma to muscle fibers is still a necessary pre-requisite.

I'm probably missing something, so are you saying:

Microtrauma can result from lots of different stuff, including heavy eccentrics, but also lighter, higher rep, longer lasting affairs?

Or that microtrauma to muscle fibers as a result of SOME exercise isn't necessary at all to activate satellite cells and kick off that whole cascade of events?

And to the other half of Danron (Ron), I'm curious of your thoughts on this too. If you do feel microtrauma is a prerequisite for growth (but, like above, feel that it's inducable via a variety of means, even with lighter loads), would you then characterize microtrauma as probably a result of "high work per unit time of a given muscle fiber?"

Not sure on your (Ron's) perspective on the necessity of satellite cells or microtrauma in this either.

 

[imported_dkm1987]

I thought I had made this clear but perhaps not.

My definition of microtrauma is the distortion of the structural components of the sarcomere. So to me microtrauma = remodeling, not damage per se. So yes to me this is necessary. Even shortening and isometrics cause this distortion just to a lesser degree but yet hypertrophy still occurs if it is applied in a chronic fashion. You would really need to read Yu's work on remodeling to see where I am coming from I guess.

Looking at satellite cell activity and fiber CSA increases we know that increases can be done two ways, either each myonucleus has to increase it's transciption rate of the genes or satellite cells have to donate nuclei to the parent fiber. It's also pretty clear that in humans our ability for transcription isn't nearly maximal. With that being the case increases in the sarcoplasmic domain can increase via upregulated transcription, therefore when starting out untrained donation is unlikely to occur as the domain size has not increased enough to warrant additional nuclei donation. As time passes and the domain reaches maximum size, reaching maximum transcription rate, more nuclei must be donated.

Now tying that to contraction mode, Kadi used an exercise protocol that from what I can tell did not use stricly eccentric exercise and even though they didn't note so I would bet some sort of trauma occured.

Quote[/b] ]The various exercises were essentially conducted in 4–5 sets of 6–15 repetitions (corresponding to a 6–15 RM loading). In general, in the first weeks (training sessions 0–5) exercises involved 10–15 RM loads, followed by 10 RM loads in early weeks (training sessions 6–15), heavier loads of 6–10 RM in the later weeks (training sessions 16–30), and very heavy loads of 6–8 RM in the final weeks (training sessions 31–38)

but yet induced some pretty good hypertrophy at 90 days,

Quote[/b] ]Significant hypertrophy was observed for type II fibers (16%) after resistance training, whereas no significant hypertrophy was observed for type I fibers.

In this study they found a large increase in the satellite pool but the mean number of myonuclei was unchanged over this period. Indicating that the human muscle can hypertrophy without the aid of donation and, at least to me, is also indicating that it is more of a matter of training state than modality (something I said earlier) or damage (trauma or whatever you want to call it).

Damage and is it necessary? Let's look at another angle. Resistance training increases protein sysnthesis, this is a given. Chronic resistance training should then increases synthesis over longer timeframes causing increased translational capacity which would therefore increase the domain size to a point where transcription becomes maximalized and then satellite cells would have to donate there nuclei to support further translational capacity. The Yu work now pretty much confirms what Grounds found out several years ago, resistance training's impact as far as damage goes, isn't nearly as important as once thought and resistance training does not cause the same extent of damage in humans as once thought.

What appears to be more important is the chronic stimulation of protein synthesis causing hypertrophy, therefore the damage BEFORE hypertrophy model may not be all it's cracked up to be.

Lastly let me make myself clear, we workout for the most part in a dynamic fashion, we lift, we lower, we lift again, we lower again. We use both concentric and eccentric so to say one mode increases size more than the other is to continually debate about nothing.

Sorry for the long post guys. I hope I did'nt put anyone to sleep.

Dan

 

[xahrx]

Had a thought on the weird fatigue ACIT seems to get in people. If ATP/ADP turnover is going at much higher rate in the muscles wouldn't that lead to an overall higher level of ceatine kinase? I'd say that's especially so if occlusion does bring the type IIs into the movement earlier than usual. Check this one out:

Is creatine kinase responsible for fatigue? Studies of isolated skeletal muscle deficient in creatine kinase.

Dahlstedt AJ, Katz A, Wieringa B, Westerblad H.

Department of Physiology and Pharmacology, Karolinska Institutet, S-171 77 Stockholm, Sweden.

Creatine kinase (CK) is a key enzyme for maintaining a constant ATP/ADP ratio during rapid energy turnover. To investigate the role of CK in skeletal muscle fatigue, we used isolated whole muscles and intact single fibers from CK-deficient mice (CK(-/-)). With high-intensity electrical stimulation, single fibers from CK(-/-) mice displayed a transient decrease in both tetanic free myoplasmic [Ca(2+)] ([Ca(2+)](i), measured with the fluorescent dye indo-1) and force that was not observed in wild-type fibers. With less intense, repeated tetanic stimulation single fibers and EDL muscles, both of which are fast-twitch, fatigued more slowly in CK(-/-) than in wild-type mice; on the other hand, the slow-twitch soleus muscle fatigued more rapidly in CK(-/-) mice. In single wild-type fibers, tetanic force decreased and [Ca(2+)](i) increased during the first 10 fatiguing tetani, but this was not observed in CK(-/-) fibers. Fatigue was not accompanied by phosphocreatine breakdown and accumulation of inorganic phosphate in CK(-/-) muscles. In conclusion, CK is important for avoiding fatigue at the onset of high-intensity stimulation. However, during more prolonged stimulation, CK may contribute to the fatigue process by increasing the myoplasmic concentration of inorganic phosphate.