15's 10's 5's in one week

[Jester]

Quote[/b] (Aaron_F @ Aug. 23 2005,12:37)]Both programs will result in a chronic overloading of the tissue, one achieves this by linearly increasing over the period of training (12weeks in the above example), the other does it by a more zig zag approach.  Which if you have been around this forum for any length of time, is a well established modality of manipulating load to achieve the end result.  
Over the 12 weeks the increase in progressive load (in terms of end loads - starting load) was greater in the undulating, compared with the linear, so ultimately if the RBE is the final factor, the undulating keeps ahead of the curve better than linear.
So whats the final factor...  SD and thats independent of any program setup.

Questions for Aaron . . . does the degree of zigzag matter for the amount of hypertrophy over your chronic time periods (call it 2months/8weeks at a time ~ HST cycle length)...?

If I use my 12RM 6RM and then 1RM on Mon-Wed Fri, will that make a difference compared to the 8RM 6RM 4RM...?

I suppose this is a question related to RBE and I'm not phrasing it very well.

So long as my load progresses from the initial session/week to the final session/week, will I get the same amount of hypertrophy from lil zig-zag to big zig -zag..?

Would there be any benefit in doing flies - monday, incline - wed, dips on friday...as the amount of weight I handle is increased for each exercise..? Or is that just too fine details...

 

[leanlifter]

This has become a facinating topic.
The only reason I asked was because I enjoy doing the 5's and would rather do them every week instead of waiting till I get through the 15's and 10's.
I understand the undulating periodization however the way I'm currently doing HST (which I belive is the right way) involves increasing weight every workout not every 4 weeks. Granted my rep scheme changes every 2 weeks but I'm still increasing weight every workout just as the "zig-zag" style was but in a linear fashion.
Currently I am pushing more weight than I expected however my bodyweight and composition has not changes since I started.

 

[jvroig]

Hey

I have the same thing Jester asked in mind.

In the study cited, they used 8, 6, and 4RM. I don't know for sure right now, but that seems a whole different thing from something like 15, 10 and 5RM. 8RM is a weight that's not too shabby anymore (that is, it is starting to get really heavy), and by the time weights start getting heavy, there generally is far less difference between them compared to lighter weights (say, between 15RM and 10RM).

A "soft" estimate of RBE would be 4-6 weeks. Before that, naturally the muscles are still adapting, but the weights will still be effective until a month or a little after that (again, "soft" estimate, meaning there are a lot of other variables), but that's not saying the effectiveness is the same as the first workout, of course it isn't - we just can't put a number, say only 85% as effective as the first, because of so many other variables - and first of all, how can you measure how much the muscles have adapted to the load anyway? But what we know for a fact is: Microtrauma is rapidly reduced from workout to workout (Repeated bout effect) thereby limiting the effectiveness of any given load to induce further hypertrophy. Also, the lighter the load, the shorter the amount of time it will be able to induce muscle growth - one of the factors that affect the "soft" estimate of 4-6 weeks.

What I'm getting at is the cited study used RMs much closer to each other. Looking at it and comparing it to the linear progression outlined by Bryan, it's almost a different thing - taking into account only the difference in loads used. 8,6,4RMs are by far closer to each other than 15, 10 and 5RMs - unless of course, for bodybuilding beginners, where their RMs are close to each other no matter what.

But by the time you reach 150+ or 200+ pounds, your 15, 10 and 5RMs would be much farther from each other than your 8, 6 and 4RMs. Maybe you have around 140,170,220 for your 15, 10 and 5RM. Your 8,6 and 4RM would perhaps be 180, 195, 220, respectively. Just rough estimates, but i'm just trying to show the small point that the load ranges is far different.

That's important because dealing in loads closer to each other generally won't cause a big problem with RBE. But it's different when you use 15, 10 and 5 RMs, especially when they are really far from each other. I doubt using undulating loads in that setup would suffice. A better way would be to separate the whole range into two separte phases, something like 15,12,9RMs every week for 8 weeks (using load progresion of course), then using 8,6,4RMs for the next 8 weeks or so. That way, we are pretty sure we use undulating loads for loads that aren't so far from each other, to make sure all our workouts stay ahead of RBE. Of course, this is an issue only if we extend the phase longer than perhaps around 2-4 weeks. Again, just a soft estimate. Each individual weight is ok for 4-6 weeks, but since heavier weights are used with some lighter weights, we can't expect the muscles to discriminate between them because they are on separate workouts. As the muscles start adapting to heavier loads, the lighter loads will be less effective than if those same lighter loads were just repeated minus the heavier loads first (as in linear progression) - so RBE faster. But if in just a short amount of time, and keeping RMs closer to each other (like using perhaps 15,12,9, then when that's over 8,6,4), we can most probably stay ahead of RBE.

Well, that's it. That's what I had in mind. Hopefully, somebody can sort this issue out. Like Jester, I'm really curious about the whole big zigzag vs lil zigzag issue.

Regards,

-JV

 

[imported_dkm1987]

Quote[/b] (Jester @ Aug. 23 2005,5:48)]

Quote[/b] (Aaron_F @ Aug. 23 2005,12:37)]Both programs will result in a chronic overloading of the tissue, one achieves this by linearly increasing over the period of training (12weeks in the above example), the other does it by a more zig zag approach.  Which if you have been around this forum for any length of time, is a well established modality of manipulating load to achieve the end result.  
Over the 12 weeks the increase in progressive load (in terms of end loads - starting load) was greater in the undulating, compared with the linear, so ultimately if the RBE is the final factor, the undulating keeps ahead of the curve better than linear.
So whats the final factor...  SD and thats independent of any program setup.

Questions for Aaron . . . does the degree of zigzag matter for the amount of hypertrophy over your chronic time periods (call it 2months/8weeks at a time ~ HST cycle length)...?
If I use my 12RM 6RM and then 1RM on Mon-Wed Fri, will that make a difference compared to the 8RM 6RM 4RM...?
I suppose this is a question related to RBE and I'm not phrasing it very well.
So long as my load progresses from the initial session/week to the final session/week, will I get the same amount of hypertrophy from lil zig-zag to big zig -zag..?
Would there be any benefit in doing flies - monday, incline - wed, dips on friday...as the amount of weight I handle is increased for each exercise..? Or is that just too fine details...

This is a partial repost of something I just posted today on my forum, even though it doesn't clarify anything here it does add to what Aaron is saying and introduces some interesting, to me at least ideas.

Quote[/b] ]One question that has begun to be looked at in terms of tension, is it truly whole muscle tension or more reliant upon tension time integral? For instance a recent work by Bowtell et al (Stimulation of human quadriceps protein synthesis after strenuous exercise: no effects of varying intensity between 60 and 90% of one repetition maximum (1RM). J Physiol 547.P, P16.) shows that even in the face of differing intensity PS elevated to roughly the same amounts as long as TTI was constant and recruitment was full. This study also points to the fact that once recruitment is high and tension is roughly about 65% further increases in tension do not produce changes in the FSR of proteins. Expanding further upon this brings to light other items dealing with the differences in Myofibrilar vs. Sarcoplasmic elevations in PS. Looking at this work and references show that both muscle proteins are elevated. There is a marked increase in myofibrilar vs. sarcoplasmic (~2-5 vs ~1-3 fold) no matter which intensity 60 or 90% as in the study cited above or even 75% as int he study by Louis et al 2003. Further making the argument that "Hypertrophy" training vs. "Strength" training is unwarranted in terms of PS.

Newer work by Rennie looking at myofibrilar, tendon and ECM protein and collagen turnover also shows a strong correlation to TTI rather than peak tension and calls into question as to whether or not damage is necessary (J Physiol. 2005 Jul 7; [Epub ahead of print]).

In a recent correspondence I had with Dr. Rennie I asked him about damage and it's impact, his response was that even though damage would upregulate PS, damage itself wasn't necessary to see similar increases and that he didn't absolutely agree with the damage BEFORE hypertrophy hypothesis.

So bottom line appears to be that TTI, time tension integral is beginning to look like a very key player.

As a side note I also asked him about RBE "repeated bout effect" and the currently seen timecourse as in the studies by Nosaka et al and McHugh et al. Although he do not greatly ellaborate on the issue he did mention that the time course of this phenomena needs to be re-evaluated. But that is a different discussion.
Dan

Bryan has mentioned on numerous occasions how TUT is a big factor, Bryan has also mentioned several times that during the 15's it may be useful to do 2 sets, during the lighter work of both the 10's and 5's also, reducing down to one set as the weight gets heavier. This seems to coincide very well with the work that I cited in that post. TTI is a key player in hypertrophic signaling and upregulating PS.

 

[jvroig]

Hey

Cool, more stuff to study.

Quote[/b] ]In a recent correspondence I had with Dr. Rennie I asked him about damage and it's impact, his response was that even though damage would upregulate PS, damage itself wasn't necessary to see similar increases and that he didn't absolutely agree with the damage BEFORE hypertrophy hypothesis.

Ok... so damage = microtrauma. That's saying microtrauma isn't absolutely necessary to see such increases? Damage not being necessary would pretty much explain why RBE would need to be re-evaluated since it's not the microtrauma that's the main factor, so even though the microtrauma is lessened due to the muscles' adaptation we are still growing. But really? Proving damage is not necessary would be really huge for bodybuilding. As far as I can remember, it was outlined as a core of HST that microtrauma is the point of lifting a weight. Satellite cells must be activated, differentiated, and fuse with existing fibers, donating their nuclei, and for this to happen, the fibers must experience a certain level of microtrauma. So this one can be proven to be not accurate at all? I mean, in the future it may be determined damage isn't the main factor to initiate the satellite cell activities necessary for hypertrophy?

-JV

 

[jvroig]

Oh, sorry, I just remembered.

Mechanical tension on the protein structures of the muscle cells is the primary stimulus for hypertrophy. Not damage (microtrauma). So yeah, "damage before hypertrophy" hypothesis should be challenged. But then again, it does seem that some damage is necessary. Ah, but who knows, maybe it will be discovered that it actually isn't necessary after all, and that mechanical tension is truly the key even in the absence of microtrauma.

Well, like I said before... cool, more stuff to study.

 

[imported_dkm1987]

Looking at the recent work of Miller et al (J Physiol. 2005 Jul 7; [Epub ahead of print]) this was exactly the hypothesis which they proved. Non damaging exercise, as seen on histological evaluation increased the fractional synthetic rates of all proteins at 6 h and rose rapidly to peak at 24 h post exercise (tendon collagen (0.077 %.h(-1)), muscle collagen (0.054 %.h(-1)), myofibrillar protein (0.121 %.h(-1)), and sarcoplasmic protein (0.134%. h(-1))). The rates decreased toward basal values by 72 h although rates of tendon collagen and myofibrillar protein synthesis remained elevated.

 

[jvroig]

Cool... so I don't have to bust my @$$ deadlifting heavy? I love deadlfiting now, but if I don't have to do it, then hey, why bother?

I just don't get it Dan... how can an exercise be non-damaging? How can we lift weights without inducing microtrauma?

What kinds of exercise did they do in the study, and how did they do it? Did they not lift weights at all? Or did they use those pink girly 5-pound dumbbells?

-JV

 

[imported_dkm1987]

Quote[/b] (jvroig @ Aug. 23 2005,12:28)]Mechanical tension on the protein structures of the muscle cells is the primary stimulus for hypertrophy.

Ah, but who knows, maybe it will be discovered that it actually isn't necessary after all, and that mechanical tension is truly the key even in the absence of microtrauma.

When I asked Dr. Rennie this question he said tension is definatley a key but he's been pondering more on integral tension rather than peak.

 

[imported_dkm1987]

Quote[/b] (jvroig @ Aug. 23 2005,12:52)]Cool... so I don't have to bust my @$$ deadlifting heavy? I love deadlfiting now, but if I don't have to do it, then hey, why bother?
I just don't get it Dan... how can an exercise be non-damaging? How can we lift weights without inducing microtrauma?
What kinds of exercise did they do in the study, and how did they do it? Did they not lift weights at all? Or did they use those pink girly 5-pound dumbbells?
-JV

In the Miller study they used one legged kicking exercise at about 67% Wmax.

In the Bowtell studies they used stimulation to represent the intesity.

Remember even in the relaxed state tesion is being produced in the contractile elements, IE passive Tension. So even lifting your arm creates increases in tension.

 

[jvroig]

Yes, of course, I know that. But just plain old lifting my arms (or anybody lifting their arms) never caused hypertrophy by itself.

So they basically used submaximal weights. How did they increase the tension there? I mean, if we go on to the direction of using less weights, more tension, do we lift each repetition longer? Just increase TUT? Make a progression on TUT? More reps?

 

[Jester]

Quote[/b] (dkm1987 @ Aug. 23 2005,1:42)]Looking at the recent work of Miller et al (J Physiol. 2005 Jul 7; [Epub ahead of print]) this was exactly the hypothesis which they proved. Non damaging exercise, as seen on histological evaluation increased the fractional synthetic rates of all proteins at 6 h and rose rapidly to peak at 24 h post exercise (tendon collagen (0.077 %.h(-1)), muscle collagen (0.054 %.h(-1)), myofibrillar protein (0.121 %.h(-1)), and sarcoplasmic protein (0.134%. h(-1))). The rates decreased toward basal values by 72 h although rates of tendon collagen and myofibrillar protein synthesis remained elevated.

So increasing TUT using a sub-maximal (less heavy weight)...? So if I hold 15kgs dumbells at incline stretch for say...5mins will that do more than if I pump out 30kg reps of incline curls..?

Does concentric vs. eccentric matter?

 

[navigator]

Hmmm...

We know that progressive weights with a constant volume causes growth. But now I wonder: would progressive volume with a constant, sufficiently heavy weight lead to growth, as well?

 

[imported_dkm1987]

Nav, one thing I think we have to come back to in all of this is;

There is a difference between a weight light enough to cause a more aerobic response than anaerobic. So you hit the nail on the head, it has to be sufficiently heavy.

My reasoning for posting this wasn't to have anyone start rearranging their workout to a more volumistic approach. It was to aid in the discussion on how recruitment impacts PS and why gains are seen in both Undulating Periodized Progression and Linear Progression.

In other work by Atherton et al, they show that there is a switching mechanism (TSC2) upstream of mTOR that eithers turns on or off mTOR through the type of workout that is performed.

 

[imported_dkm1987]

JV,

1. Understand what DAMAGE is and it's difference from myoTRAUMA.
2. Strain is absolutley necessary, but strain doesn't necessarily inflict DAMAGE.
3. Many branches of the signaling path initiate translation, some dependant on cellular strain some not.

Since I know you love learning, read the stuff from Ingber on Integrin signaling.

 

[navigator]

Sure, I know that we're supposed to be talking about gains with undulating periodization.

But still, the abstract you posted leads me to wonder if progressing one's volume with weights less than one's 5RMs might be a legitimate technique for keeping gains coming during the cycle. If so, using a lighter weight with ramping volume could be one way to keep the effective volume from plummeting towards the end of the cycle without having to resort to cluster techniques.

 

[imported_dkm1987]

Nav,

IMHO, yes but only to an extent. At some point by only adding in volume the MPS elevations would stagnate.

 

[jvroig]

Ah, well then, that's what got me confused.

Sorry, I always thought that "damage" always referred to "microtrauma", at least in the context of bodybuilding only, not in "real" life (I'm not about to tell someone who rear-ended my car, "Hey, jerk, you caused microtrauma on my car!!!"

)

Well, then, if it's not microtrauma they are talking about, so just what is "damage" in that context?

 

[jvroig]

What confuses me is, for example when Bryan explains advacned insights about HST, he uses "microtrauma" and "damage" interchangeably, so I always thought those two are the same. If microtrauma doesn't mean damage, then please explain the difference., because I'm lost. Before our conversation here, I never heard (or at least undestood) damage to refer to anything but microtrauma.

I know that mechanical tension is the primary stimulus for hypertrophy, and it can elicit anabolic processes with or without damage to cell membranes. That damage to cell membranes is what I understand to be "microtrauma", simply the scientific and more accurate term for it. Some degree of microtrauma - that is, damage to the cell membranes - seem to be necessary for the paracrine and autocrine growth factors like FGF and IGF-1. This is important because without the activity of these growth factors outside the cell, satellite cells will not contribute significantly to hypertrophy - and again, the activity of these growth factors is dependent on microtrauma - damage to cell membranes.

Now I realize that some execises don't necessarily cause damage, since tension doesn't automatically cause microtrauma. I'm sorry I forgot that when I blurted out "how can an exercise be non-damaging? How can we lift weights without inducing microtrauma? . It doesn't seem impossible to grow without damage, since tension does elicit anabolic processes regardless of damage, but again, my understanding of "damage" and "microtrauma" is that they are the same thing!

I'm totally lost on this whole "Damage != Microtrauma"... I always thought "Damage == Microtrauma".

 

[Jester]

Damage to protein structure/s within the cell without 'leakage'...?

Just guessing on where else damage could occcur