Study: 1 set vs 3

The Dt/dt conclusions seem to corroborate with the conclusion rep speed doesn't really contribute to eccentric contractions, besides that of influencing the TTI through a stretch.

[b said:
Quote[/b] ]In proliferating myoblasts, the ERK pathway represses myogenic transcription and contributes to the maintenance of the undifferentiated phenotype. The reduction of ERK activity upon serum removal can therefore relieve that repression and allow p38-mediated muscle-specific transcription.

Ahh, that was what I'm interested in . . .

[b said:
Quote[/b] ]Once the activation of the myogenic program is initiated, ERK activation is no longer repressive and cooperates with p38 in promoting postmitotic responses in differentiated myotubes

Can this be interpreted as saying, create your significant mechanical strain first, then throw in your metabolic stress?

cheers,
Jules
 
[b said:
Quote[/b] (vicious @ May 19 2005,3:27)]Can this be interpreted as saying, create your significant mechanical strain first, then throw in your metabolic stress?
cheers,
Jules
Even though I make that assumption I might be way way wrong. It's hard to say since must of the studies Wu is discussing are not studies in humans.

We would have to ask the Oracle ;)
 
This topic is really interesting to me right now, because I'm experimenting with using a combination of clustering and (declining, as opposed to escalating) density training as a strain optimization technique.

Basically, you use the cluster miniset as your minimal TTI to elicit p38 signaling. Then, with very brief rest periods, each minimal TTI integral (better MU recruitment, moderate rise in contraction frequency) will have either a constant or positive delta for the p38 signal. Then you moderate the erk pathway by increasing these rest periods.

And this strategy might be used during 15s (the burn would still be pretty high) and 10s if one were to do multiple sets per exercise. I know the validity of it is shaky, but at worst, you'll still get the reps in. :)

cheers,
Jules
 
[b said:
Quote[/b] (vicious @ May 19 2005,4:02)]This topic is really interesting to me right now, because I'm experimenting with using a combination of clustering and (declining, as opposed to escalating) density training as a strain optimization technique.  
Basically, you use the cluster miniset as your minimal TTI to elicit p38 signaling.  Then, with very brief rest periods, each minimal TTI integral (better MU recruitment, moderate rise in contraction frequency) will have either a constant or positive delta for the p38 signal.  Then you moderate the erk pathway by increasing these rest periods.
And this strategy might be used during 15s (the burn would still be pretty high) and 10s if one were to do multiple sets per exercise.  I know the validity of it is shaky, but at worst, you'll still get the reps in.  :)
cheers,
Jules
Well to help you in your endeavor, once I put my finger on it, i'll send you an email with a study relating the MAPK response in time, IE how long each lasts. This should give you a idea of the needed rest periods, so not to have interfering signals, if they are truly interfering.

One very tricky question on your assumptions, is how would you be able to measure the delta (I prefer variance, just because of a President I reported too who loved using the term Delta, delta this, Dan what's the Delta of that, drove me friggin nuts) without a lab. Lastly what are you basing the increase in ERK on and it raising with decreased rest, I haven't seen anything that substantiates that, do you have something in that realm?
 
[b said:
Quote[/b] (vicious @ May 19 2005,2:27)]
Hello Gentlemen! (and ladies if you’re reading) Great thread!

[b said:
Quote[/b] ]The Dt/dt conclusions seem to corroborate with the conclusion rep speed doesn't really contribute to eccentric contractions, besides that of influencing the TTI through a stretch.

I don't know if I'm misunderstanding something here but there are a couple studies demonstrating that eccentric rep speed does influence subsequent hypertrophy. Basically they show that slower is not necessarily better for hypertrophy...within a reasonable range of movement speeds.

[b said:
Quote[/b] ]Once the activation of the myogenic program is initiated, ERK activation is no longer repressive and cooperates with p38 in promoting post-mitotic responses in differentiated myotubes
[b said:
Quote[/b] ]Can this be interpreted as saying, create your significant mechanical strain first, then throw in your metabolic stress?

HST assumes this to be true. The whole idea of using Drop-sets is based on the assumption that once the strain in the tissue has been "registered" in the strain-sensing pathways (i.e. activation of mechanoreceptors), metabolic stimuli can then be added without compromising the hypertrophic response to the bout as a whole.

I probably need to add that this assumes that the metabolic stimuli (e.g. drop set) won't be too aerobic in nature but instead intensely anaerobic.
 
[b said:
Quote[/b] (Bryan Haycock @ May 19 2005,6:04)]I don't know if I'm misunderstanding something here but there are a couple studies demonstrating that eccentric rep speed does influence subsequent hypertrophy. Basically they show that slower is not necessarily better for hypertrophy...within a reasonable range of movement speeds.

once the strain in the tissue has been "registered" in the strain-sensing pathways (i.e. activation of mechanoreceptors), metabolic stimuli can then be added without compromising the hypertrophic response to the bout as a whole.
Hey Bryan, how's it going?

2 questions then.

What studies are you referring to about the eccentric speed?

Do you happen to remember the study or Author that showed the MAPK activation time, I think it was somewhere in the realm of minutes ??, I remember it but can't find it in my papers.
 
[b said:
Quote[/b] (Captain Crunch @ May 19 2005,8:23)]HST.COM
We all seem to rely on this site for research and training and it is a DOT COM.
True, but many references to the actual journal origins are made, where you can look the research up yourself, and aren't made to blindly believe that "Dr. so and so" did this and discovered that.
 
[b said:
Quote[/b] (Rovi @ May 20 2005,12:50)]
[b said:
Quote[/b] (Captain Crunch @ May 19 2005,8:23)]HST.COM
We all seem to rely on this site for research and training and it is a DOT COM.
True, but many references to the actual journal origins are made, where you can look the research up yourself, and aren't made to blindly believe that "Dr. so and so" did this and discovered that.
That's why this forum and HST is so unique, Bryan took years to develop his ideas but instead of blatantly saying this is how it is "beleive it", he simply says "here is what I have found and why I put it together this way, read it and if you do not agree let's discuss what you don't agree with."

It makes a world of difference when you can research it yourself, in time as you piece it all together you begin to see a formula, strain/no strain = response, Frequency of strain/no strain = response, Metabolic stress/no stress = response, nutrition/lack of nutrition = response. All these responses can and do change based on application and adaptation, so nothing is completely linear, actually nothing is hardly ever linear :), but no matter how it's applied, correctly or incorrectly you will see a response, therefore the principles are true. ;)
 
Bryan, thanks for the Farthing study, looking at it and looking at Paddon-Jones, both show a 3.14 radian/sec eccentric to create the most hypertrophy. Now that's 180 degree's per second, is this because of the "braking" involved at the end of the movement. Also do you remember seeing the intensity they used because neither of the abstracts say?
 
This IS a great thread, it's my great interest also :D

[b said:
Quote[/b] ] I don't know if I'm misunderstanding something here but there are a couple studies demonstrating that eccentric rep speed does influence subsequent hypertrophy. Basically they show that slower is not necessarily better for hypertrophy...within a reasonable range of movement speeds.

I remember reading that too, also, in one of my physiology books, the author speaks of how a faster eccentric actually causes more strain as with slower eccentrics, the cross bridges can 'keep up'.

[b said:
Quote[/b] ]I probably need to add that this assumes that the metabolic stimuli (e.g. drop set) won't be too aerobic in nature but instead intensely anaerobic.

I agree

[b said:
Quote[/b] ]But since you mentioned it here's a snippet from
p38 and Extracellular Signal-Regulated Kinases Regulate the Myogenic Program at Multiple Steps
MOLECULAR AND CELLULAR BIOLOGY,
June 2000, p. 3951–3964 Vol. 20, No. 11

Hey that was great DKM! Glad you posted that :)

This stuff really interests me, especially after reading the latest 'occlusion study' (the one I emailed you Dan), it's really becoming clear that tension and chemical changes are either synergystic or permissive in reguards to the upregulation of protein synthesis. We can find proof that tension stimulates myofibrillar hypertrophy and also the occlusion studies show myofibrillar hypertrophy with very low tension and no damage, but only increases in IGF1 and high metabolites.

That's why it seems the "ultimate set" would have both, a good peak tension for max recruitment and high activity, and a duration long enough to increase intracellular metabolites and calcium.

Cheers!
Ron
 
[b said:
Quote[/b] (dkm1987 @ May 20 2005,6:11)]Now that's 180 degree's per second, is this because of the "braking" involved at the end of the movement.
That's exactly what I've been thinking with regards to eccentric rep speed. A faster speed, if stopped at the end of ROM by your muscles and not joint max or bouncing off your body, puts extreme loading in a stretched position, basically a loaded stretched pulse.
 
[b said:
Quote[/b] ]That's exactly what I've been thinking with regards to eccentric rep speed.  A faster speed, if stopped at the end of ROM by your muscles and not joint max or bouncing off your body, puts extreme loading in a stretched position, basically a loaded stretched pulse.
Now what I read was that 'during' the eccentric contraction, if the rep speed is faster, since the cross bridges release 'out of sync' with each other, you will incurr lateral strain between the sarcomeres.
You couldn't increase 'per fiber' tension by 'braking suddenly', the fibers can only display their maximum tension no matter what the action so in effect, the braking is just a higher recruitment/synchronization of the fibers displaying their tension at once which if is enough, will stop the lengthening of the muscle and transfer the tension to the connective tissues, like the tendons.
Ron
 
[b said:
Quote[/b] (NWlifter @ May 20 2005,6:50)]you will incurr lateral strain between the sarcomeres.
Ah ha, that's cool because the Ingber studies show a different cascade between lateral and axial strain. Thanks Ron that's puts another thought in my head, dang IT.
 
[b said:
Quote[/b] (Dood @ May 20 2005,6:44)]
[b said:
Quote[/b] (dkm1987 @ May 20 2005,6:11)]Now that's 180 degree's per second, is this because of the "braking" involved at the end of the movement.
That's exactly what I've been thinking with regards to eccentric rep speed.  A faster speed, if stopped at the end of ROM by your muscles and not joint max or bouncing off your body, puts extreme loading in a stretched position, basically a loaded stretched pulse.
Fits with what VIcious was saying about the myotatic reflex, I just wonder if it's necessary to invoke the relfex, it seems so especially with 180 degree per second that's a fast eccentric.
 
I'm wary with many rep speed studies because they've used isokinetic dynamometers.  But, yes, a 180-degrees/s spin should hitch the reflex.  

[b said:
Quote[/b] ]That's why it seems the "ultimate set" would have both, a good peak tension for max recruitment and high activity, and a duration long enough to increase intracellular metabolites and calcium.

Yeah, that's the direction I'm going with this point.  Basically I'm using a combination of cluster minisets and low-level density training a la Gironda / 20-rep.  The feedback seems favorable so far (earlier DOMS through earlier part of HST), but I'm having problems actually establishing a proper model whereby this would actually work.  IF it works, somebody could stimulate significant growth through the 15s, and it's fairly easy to implement.

cheers,
Jules
 
Touching back on the original topic I've come across these links dealing with the single vs. multiple sets debate. If these are redundant please forgive, but I found them interesting and amusing, especially the first. The author of the first quotes Arthur Jones: "Dr. Berger’s published statements literally force me to assume that the man is an outright idiot”
LOL, the beauty of rational scientific discourse.
laugh.gif


http://72.14.207.104/search?....e&hl=en

http://bjsm.bmjjournals.com/cgi/content/full/38/2/240-a

http://bjsm.bmjjournals.com/cgi....0aef3be
 
[b said:
Quote[/b] ]Yeah, that's the direction I'm going with this point. Basically I'm using a combination of cluster minisets and low-level density training a la Gironda / 20-rep. The feedback seems favorable so far (earlier DOMS through earlier part of HST), but I'm having problems actually establishing a proper model whereby this would actually work. IF it works, somebody could stimulate significant growth through the 15s, and it's fairly easy to implement.

OK, so your using Gironda type fatigue training for the higher rep stuff?
When I used 6x6 almost a year ago, I incurred more DOMS than anything I've ever tried and I was using a LIGHT weight.
MASSIVE calcium accumulation!
butbut.gif
 
[b said:
Quote[/b] (NWlifter @ May 20 2005,4:50)]
[b said:
Quote[/b] ]That's exactly what I've been thinking with regards to eccentric rep speed.  A faster speed, if stopped at the end of ROM by your muscles and not joint max or bouncing off your body, puts extreme loading in a stretched position, basically a loaded stretched pulse.
Now what I read was that 'during' the eccentric contraction, if the rep speed is faster, since the cross bridges release 'out of sync' with each other, you will incurr lateral strain between the sarcomeres.
You couldn't increase 'per fiber' tension by 'braking suddenly', the fibers can only display their maximum tension no matter what the action so in effect, the braking is just a higher recruitment/synchronization of the fibers displaying their tension at once which if is enough, will stop the lengthening of the muscle and transfer the tension to the connective tissues, like the tendons.
Ron
Heres some stuff you guys might enjoy, it's on sarcomeres and non-uniform lengthening


Single muscle fiber contraction is dictated by inter-sarcomere dynamics.

Denoth J, Stussi E, Csucs G, Danuser G.

Laboratory for Biomechanics, Department of Materials, Swiss Federal Institute of Technology (ETH), Wagistrasse 4, CH-8952 Schlieren, Switzerland. denoth@biomech.mat.ethz.ch

This paper presents first results from a study where we developed a generic framework for analysing inter-sarcomere dynamics. Our objective is to find an accurate description of a muscle as a linear motor composed of parallel and series coupled subunits. The quality of theoretical models can be tested through their ability to predict experimental observations. With the current method we have found rigorous mathematical explanations for mechanisms such as sarcomere popping, extra tension and homogenization. These phenomena have been observed for many years in single fibers experiments, yet have never been completely understood in terms of a mechanical model. Now they can be explained on a theoretical basis. Interestingly, rather simplistic descriptions of each of the various molecular components in the sarcomere (actin-myosin cross-bridges, titin and contributions from passive elastic components) are sufficient to predict these behaviors. The complexity of a real muscle fiber is addressed through rigorous coupling of the single component models in a system of differential equations. We examine the properties of the differential equations, based on a down-stripped model, which permits the derivation of analytical solutions. They suggest that the contraction characteristics of inter-connected sarcomeres are essentially dictated by the initial distribution of the sarcomeres on the force-length curve and their starting velocities. The complete model is applied to show the complexity of inter-sarcomere dynamics of activated fibers in stretch-release experiments with either external force or length control. Seemingly contradictory and unexpected observations from single fiber experiments, which have hitherto been discussed with the argument of uncontrollable biological variability, turn out to be a consistent set of possible fiber responses. They result from a convolution of multiple relatively simple rules each of them defining a certain characteristics of the single sarcomere. Copyright 2002 Elsevier Science Ltd. All rights reserved.

Characteristics of isometric and dynamic strength loss following eccentric exercise-induced muscle damage.

Byrne C, Eston RG, Edwards RH.

School of Sport, Health and Exercise Sciences, University of Wales, Bangor, Gwynedd, UK.

Angle-specific isometric strength and angular velocity-specific concentric strength of the knee extensors were studied in eight subjects (5 males and 3 females) following a bout of muscular damaging exercise. One hundred maximal voluntary eccentric contractions of the knee extensors were performed in the prone position through a range of motion from 40 degrees to 140 degrees (0 degrees = full extension) at 1.57 rads(-1). Isometric peak torque was measured whilst seated at 10 degrees and 80 degrees knee flexion, corresponding to short and optimal muscle length, respectively. Isokinetic concentric peak torque was measured at 0.52 and 3.14 rad x s(-1). Plasma creatine kinase (CK) activity was also measured from a fingertip blood sample. These measures were taken before, immediately after and on days 1, 2, 4, and 7 following the eccentric exercise. The eccentric exercise protocol resuited in a greater relative loss of strength (P< 0.05) at short muscle length (76.3 +/- 2.5% of pre-exercise values) compared to optimal length (82.1 +/- 2.7%). There were no differences in the relative strength loss between isometric strength at optimal length and isokinetic concentric strength at 0.52 and 3.14 rad x s(-1). CK activity was significantly elevated above baseline at days 4 (P < 0.01) and 7 (P < 0.01). The greater relative strength loss at short muscle length appeared to persist throughout the seven-day testing period and provides indirect evidence of a shift in the angle-torque relationship towards longer muscle lengths. The results lend partial support to the popping sarcomere hypothesis of muscle damage, but could also be explained by an impairment of activation at short muscle lengths.

Quantitative analysis of sarcomere non-uniformities in active muscle following a stretch.

Talbot JA, Morgan DL.

Department of Physiology, Monash University Clayton, Victoria, Australia.

Electron microscopy of toad (Bufo marinus) muscle fixed without relaxing after a single eccentric contraction at muscle lengths greater than optimum showed over-stretched half-sarcomeres in sufficient numbers to account for more than half of the imposed stretch. Such sarcomeres were absent in another muscle fixed without relaxing after an isometric contraction at the same length and largely absent in a third muscle that underwent eccentric contraction at muscle lengths less than optimum. This provides direct evidence in support of the hypothesis that lengthening of muscles at long length involves lengthening of a few half sarcomeres to beyond filament overlap, while most half sarcomeres are extended much less than in proportion to muscle extension.

Effects of repeated eccentric contractions on structure and mechanical properties of toad sartorius muscle.

Wood SA, Morgan DL, Proske U.

Department of Physiology, Monash University, Clayton, Victoria, Australia.

It has been proposed that lengthening of active muscle at long lengths is nonuniformly distributed between sarcomeres, with a few being stretched beyond overlap and most hardly being stretched at all. A small fraction of the overstretched sarcomeres may fail to reinterdigitate on subsequent relaxation, leading to progressive changes in the muscle's mechanical properties. Sartorius muscles of the toad Bufo marinus were subjected to repeated lengthening (eccentric) contractions at long lengths, while controls were passively stretched and then contracted isometrically or stretched at short lengths. The muscles undergoing eccentric contractions showed a progressive shift to the right of the length-tension curve, a fall in the yield point during stretch, an increase in slope of the tension response during stretch, and a fall in isometric tension. In control muscles, changes, if any, were significantly less. In electron micrographs, muscle fibers that had been subjected to a series of eccentric contractions showed sarcomeres with A bands displaced toward one half-sarcomere, leaving no overlap in the other half. Adjacent regions often looked normal. These results are all in agreement with the predictions of the nonuniform stretch of sarcomeres hypothesis.

Muscle damage is not a function of muscle force but active muscle strain.

Lieber RL, Friden J.

Department of Orthopedics, University of California, San Diego.

Contractile properties of rabbit tibialis anterior muscles were measured after eccentric contraction to investigate the mechanism of muscle injury. In the first experiment, two groups of muscles were strained 25% of the muscle fiber length at identical rates. However, because the timing of the imposed length change relative to muscle activation was different, the groups experienced dramatically different muscle forces. Because muscle maximum tetanic tension and other contractile parameters measured after 30 min of cyclic activity with either strain timing pattern were identical (P > 0.4), we concluded that muscle damage was equivalent despite very different imposed forces. This result was supported by a second experiment in which the same protocol was performed at one-half the strain (12.5% muscle fiber length). Again, there was no difference in maximum tetanic tension after cyclic 12.5% strain with either strain timing. Data from both experiments were analyzed by two-way analysis of variance, which revealed a highly significant effect of strain magnitude (P < 0.001) but no significant effect of stretch timing (P > 0.7). We interpret these data to signify that it is not high force per se that causes muscle damage after eccentric contraction but the magnitude of the active strain (i.e., strain during active lengthening). This conclusion was supported by morphometric analysis showing equivalent area fractions of damaged muscle fibers that were observed throughout the muscle cross section. The active strain hypothesis is described in terms of the interaction between the myofibrillar cytoskeleton, the sarcomere, and the sarcolemma.
 
It's a less intense version of the Gironda scheme. Then as you go heavier, it eventually devolves into 20-rep-ish, then a rest-pause style scheme. Again, not as intense but it seems to generate DOMS out of proportion to the actual # of reps.

cheers,
Jules
 
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