A New and Unique Training Method is Here

[b said:
Quote[/b] (Sub7 @ Jan. 07 2006,3:38)]I am not sure how you have concluded that this method increases glycogen storage in the muscle...
From the human research that showed massive increases in muscle glycogen?
[b said:
Quote[/b] ]So do you mean that there is little evidence that any decent stuff showing muscle gains at all will work continually?
Most occlusion based research is very short term, in complete noobs. Two week research projects do not really show what is happening.
[b said:
Quote[/b] ]If so, I guess the implication of this conclusion would be to switch back and forth between methods, which is one suggestion I tried to bring up just a few posts ago...
Hunkar
THat is if utilizing ACIT is actually occluding the muscle, or occluding the muscle enough to achieve the 'potential' endpoint.
 
Yes one study did show that CSA drop, but, I'm sure if only one study showed a CSA gain we'd assume err on the researchers... why not on this too?

The main thing is, there is zero research showing whole muscle tension matters, only the effects of tension. Any study that assumed whole muscle tension mattered, didn't look at, or analyze recruitment levels, ATP turnover rates, fiber activity, etc.

It makes sense and fits the hypertrophic model for this type of training to work.
 
[b said:
Quote[/b] (Aaron_F @ Jan. 06 2006,5:53)]Muscle protein.
Glycogen and water changes within the tissue drop quickly after stopping training, which is why the 2 week Japanese research shows a drop in CSA on the off day. Did they lose muscle tissue? as they are no longer significantly larger than the non occlusion group
You can when using a good technique. 90% increases in glycogen are pretty significant. As above, why does the CSA decrease the day you stop training? muscle protein?
I saw you mention this before but I didn't see the same thing.
Are you referencing the study "Skeletal muscle size and circulating IGF-1 are increased after two weeks of twice daily “KAATSU” resistance training"?
Because as I see it on the 6th day of the study, the Kaatsu group was 7% above baseline, the non Kaatsu was at 2% above. After the day off the Kaatsu group was at 6% and the non Kaatsu was still around 2%. So even though the Kaatsu group dropped 1% they were still significantly higher than non Kaatsu.
 
I found this, 3.5% is a bit more than I thought for glycogen. Still not huge but not too bad. But the ceiling is reached pretty rapidly from what I remember. Also, I've never read anything about strength increases from glycogen. I suppose a bit of leverage from the water? Of course, extra hydration of muscle cells is supposed to also stimulate MPS...

[b said:
Quote[/b] ]Effect of glycogen loading on skeletal muscle cross-sectional area and T2 relaxation time
A. T. Nygren1, M. Karlsson2, B. Norman1 & L. Kaijser1
This study was performed to investigate if glycogen loading of skeletal muscles, by binding water, would effect the cross-sectional area (CSA) and if an altered water content would alter the transverse relaxation time (T2) measured by magnetic resonance imaging (MRI). Five healthy volunteers participated in a programme with 4 days of extremely carbohydrate-restricted meals followed by 4 days of extremely high carbohydrate intake. The CSA and T2 of thigh and calf muscles were related to the intramuscular glycogen content evaluated at days 4 and 8. An increase in glycogen content from 281 to 634 mmol kg1 dry wt increased the CSA of the vastus muscles by 3.5% from 78 ± 11 to 80 ± 12 cm2 and the thigh circumference by 2.5% from 146 ± 20 to 150 ± 23 cm2. Calf circumference increased non-significantly by 4% from 78 ± 15 to 82 ± 19 cm2. Mono-exponential T2 decreased in m tibialis anterior from 27.8 ± 1.2 to 26.9 ± 1.7 ms, did not change in m. vastus lateralis 26.5 ± 1.9 ms/26.6 ± 1.3 ms or in m. gastrocnemius 29.5 ± 1.0 ms/29.8 ± 1.9 ms. Glycogen loading increased the signal intensity mainly at different echo times (TE) 15 and 30 ms. The study shows that increased glycogen filling in the muscles increases muscle CSA and that this can be detected by MRI. The signal intensity increased the most at shorter TEs suggesting a more tight intracellular binding of water in glycogen loaded muscles.
 
[b said:
Quote[/b] (Dood @ Jan. 06 2006,3:04)]
[b said:
Quote[/b] (Aaron_F @ Jan. 06 2006,5:53)]Muscle protein.  
Glycogen and water changes within the tissue drop quickly after stopping training, which is why the 2 week Japanese research shows a drop in CSA on the off day.  Did they lose muscle tissue? as they are no longer significantly larger than the non occlusion group
You can when using a good technique.  90% increases in glycogen are pretty significant.   As above, why does the CSA decrease the day you stop training? muscle protein?
I saw you mention this before but I didn't see the same thing.
Are you referencing the study "Skeletal muscle size and circulating IGF-1 are increased after two weeks of twice daily “KAATSU” resistance training"?
Because as I see it on the 6th day of the study, the Kaatsu group was 7% above baseline, the non Kaatsu was at 2% above.  After the day off the Kaatsu group was at 6% and the non Kaatsu was still around 2%.  So even though the Kaatsu group dropped 1% they were still significantly higher than non Kaatsu.
Good catch Dood, I just assumed they'd lost more and didn't bother to look, good job
 
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[b said:
Quote[/b] (Dood @ Jan. 07 2006,12
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4)]So even though the Kaatsu group dropped 1% they were still significantly higher than non Kaatsu.
Notice on figure 1. Where it points to Sunday
the lack of a # or * implies no statistically significant difference.
 
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[b said:
Quote[/b] (NWlifter @ Jan. 07 2006,12
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4)]Yes one study did show that CSA drop, but, I'm sure if only one study showed a CSA gain we'd assume err on the researchers... why not on this too?
Becuase most of the other research doesnt provide 1) the same information 2) using the same methodology so its hard to see the same picture out of other research.
THe group does have a case report of an extremely low number of subjects, but they do not provide the information in the same way.
[b said:
Quote[/b] ]The main thing is, there is zero research showing whole muscle tension matters, only the effects of tension
How do you get the effects of tension without tension?
 
How, ?

Occlusion is one way, but my main point is whole muscle tension is not the variable, it's 'per fiber tension' and 'fiber activity' that counts.

Some studies compare a 5RM to a 10RM, but they don't equalize recruitment and ATP turnover to elimate those and leave whole muscle tension as the only difference. So the results are skewed. The study Rennie points to is a more accurate way to look at it. Also, the TTI studies, ect.

We can try to discount much of this, but every study out there that has the subjects hit high levels of fiber activity, whether it be occlusion, heavy weights, light weights with short interset rp's, etc. all show size and strength. I find it darned near impossible to beleive that every one using less than 80% is getting non contractile CSA gains.

One thing that convinces me, is actually training with lighter weights and higher fatigue levels myself. I've tried superslow stuff, Gironda stuff, etc. I always keep the routine (exercises, ROM, frequency, etc) the same but just change the load. I'm not a beginner but do receive size and strength.
 
I will not be able to participate in the endless discussion about whether occlusion studies did or did not show trre sarcomere growth because I have neither the analytical knowledge nor the details about each of these studies to reach a definitive conclusion. However, please keep in mind that the researchers are not gods and they almost never investigate the best possible way to train. Just because they have used 20% of 1RM in some studies does not mean that we have to limit ourselves to the same load. Some people in the forums have actually tried to tie a band around their arms while training and if I am not mistaken, they found that they could use much more than 20% 1RM even when occluded. This thread is not intending to prove the value of occlusion, but is actually about ACIT, which is only related but not identical to occlusion.

As I am continuing to work with ACIT, I am finding that in some exercises I can lift as much as 80% while doing ACIT as I was able to lift in a conventional manner. As you will recall, in the beginning I had to reduce the load by 30% or more. This is of course natural as one will get better at a "handicapped" method of training with time and be able to reduce the impact of the handicap as time goes by. If you tried to bench press while simultaneously pushing up a heavy platform with your feet, you would have to reduce the weight on the bench a great deal at first. With time however, the amount by which you would have to reduce the weight would decline. The exact same will likely happen with ACIT and you will probably be able to lift a load that still qualifies as heavy after some time.

So if we are talking about a reduction of possibly as little as 20% in tension why split hairs about glycogen vs fibril growth in some occlusion studies where they used feather weights? No one is recommending feather weights here. Instead of all this talking, people should just pick up a weight, try the system and then share with us what they observed so we can refine the system.

Hunkar
 
[b said:
Quote[/b] (Aaron_F @ Jan. 06 2006,6:16)]
[b said:
Quote[/b] (Dood @ Jan. 07 2006,12<!--emo&amp;
wow.gif
)]So even though the Kaatsu group dropped 1% they were still significantly higher than non Kaatsu.
Notice on figure 1. Where it points to Sunday
the lack of a # or * implies no statistically significant difference.
I'm not going to pretend to know how to interpret a study better than you since I'm a layman, but I took it that there was no measurment done on Sunday, and on Monday, Kaatsu was at 6% above baseline, non Kaatsu was at 2%. How is that not signifcant?
Also, at post testing the Kaatsu group was at 8% and non Kaatsu was at 1%. I could not find what the time period was between the last workout and post testing
 
[b said:
Quote[/b] (Sub7 @ Jan. 07 2006,1:26)]I will not be able to participate in the endless discussion about whether occlusion studies did or did not show trre sarcomere growth because I have neither the analytical knowledge nor the details about each of these studies to reach a definitive conclusion.
So you have created a scientific based program on research you have no analytical knowledge or the actual research itself?

[b said:
Quote[/b] ]So if we are talking about a reduction of possibly as little as 20% in tension why split hairs about glycogen vs fibril growth in some occlusion studies where they used feather weights?
You understand that even if there is an apparent difference in CSA that the lack of a statistical significance indicates a much increased probability that the difference is just chance? THere is a major reason they use statistics in research.

And its a huge assumption that it will achieve different effects when using different loadings.
 
Sub- I myself see no doubt of it's effectiveness.
The study Dan found &quot;Effects of low-intensity...&quot; by Michiya Tanimoto,..ect is almost ACIT to a &quot;T&quot;.

Also, the following shows fatigue leads to high fiber activity and in every case was equal to, or superior to less 'fiber active' type training, reguardless of the load.

Check all these out....

[b said:
Quote[/b] ]Training leading to repetition failure enhances bench press strength gains in elite junior athletes.

Drinkwater EJ, Lawton TW, Lindsell RP, Pyne DB, Hunt PH, McKenna MJ.

Department of Physiology, Australian Institute of Sport, Canberra, ACT, Australia. [email protected]

The purpose of this study was to investigate the importance of training leading to repetition failure in the performance of 2 different tests: 6 repetition maximum (6RM) bench press strength and 40-kg bench throw power in elite junior athletes. Subjects were 26 elite junior male basketball players (n = 12; age = 18.6 +/- 0.3 years; height = 202.0 +/- 11.6 cm; mass = 97.0 +/- 12.9 kg; mean +/- SD) and soccer players (n = 14; age = 17.4 +/- 0.5 years; height = 179.0 +/- 7.0 cm; mass = 75.0 +/- 7.1 kg) with a history of greater than 6 months' strength training. Subjects were initially tested twice for 6RM bench press mass and 40-kg Smith machine bench throw power output (in watts) to establish retest reliability. Subjects then undertook bench press training with 3 sessions per week for 6 weeks, using equal volume programs (24 repetitions x 80-105% 6RM in 13 minutes 20 seconds). Subjects were assigned to one of two experimental groups designed either to elicit repetition failure with 4 sets of 6 repetitions every 260 seconds (RF(4 x 6)) or allow all repetitions to be completed with 8 sets of 3 repetitions every 113 seconds (NF(8 x 3)). The RF(4 x 6) treatment elicited substantial increases in strength (7.3 +/- 2.4 kg, +9.5%, p &lt; 0.001) and power (40.8 +/- 24.1 W, +10.6%, p &lt; 0.001), while the NF(8 x 3) group elicited 3.6 +/- 3.0 kg (+5.0%, p &lt; 0.005) and 25 +/- 19.0 W increases (+6.8%, p &lt; 0.001). The improvements in the RF(4 x 6) group were greater than those in the repetition rest group for both strength (p &lt; 0.005) and power (p &lt; 0.05). Bench press training that leads to repetition failure induces greater strength gains than nonfailure training in the bench press exercise for elite junior team sport athletes.

[b said:
Quote[/b] ]Regulation of mTOR by amino acids and resistance exercise in skeletal muscle.

Deldicque L, Theisen D, Francaux M.

Institut d'Education Physique et de Readaptation, Universite catholique de Louvain, Place Pierre de Coubertin 1, Louvain-la-Neuve, Belgium, [email protected].

Resistance exercise disturbs skeletal muscle homeostasis leading to activation of catabolic and anabolic processes within the muscle cell. A current challenge of exercise biology is to describe the molecular mechanisms of regulation by which contractile activity stimulates net protein breakdown during exercise and net protein synthesis during recovery. Muscle growth is optimized by combining exercise and appropriate nutritional strategies, such as amino acid (AA) and carbohydrate ingestion. The effects are integrated at the level of one central regulatory protein, mTOR (mammalian target of rapamycin). mTOR is a complex protein integrating signals of the energetic status of the cell and environmental stimuli to control protein synthesis, protein breakdown and therefore cell growth. mTOR is known to be activated by insulin, and the mechanisms involved are well documented. The ways by which exercise and AA lead to mTOR activation remain partially unclear. Exercise and AA use different signalling pathways upstream of mTOR. Exercise seems to recruit partially the same pathway as insulin, whereas AA could act more directly on mTOR. During resistance exercise, the activity of mTOR could be acutely blunted by AMP-activated protein kinase (AMPK), thus inhibiting protein synthesis and enhancing AA availability for energy metabolism. During recovery, the inhibition of mTOR by AMPK is suppressed, and its activation is maximized by the presence of AA. There appears to be a requirement for a minimal concentration of plasma insulin to stimulate muscle protein synthesis in response to resistance exercise and AA ingestion.

[b said:
Quote[/b] ]The role of metabolites in strength training. I. A comparison of eccentric and concentric contractions.

Smith RC, Rutherford OM.

Department of Physiology, St. Mary's Hospital Medical School, London, UK.

This study examined the role of high forces versus metabolic cost in the adaptations following strength training. Ten young, healthy male and female subjects trained one leg using concentric (CL) and the other using eccentric (EL) contractions of the quadriceps muscle for 20 weeks. EL used weights which were 35% higher than those used for CL. Isometric strength, and the length:tension and force:velocity relationship of the muscle were measured before and after training. Muscle cross-sectional area (CSA) was measured near the knee and hip using computed tomography. Increases in isometric strength were greater for CL compared to EL, the difference being significant with the knee at 1.57 rad (90 degrees) [mean (SD), 43.7 (19.6)% vs 22.9 (9.8)%, respectively; P = 0.01]. Increases in isokinetic strength tended to be larger for EL, although the differences were not significant. Significant increases in CSA occurred near the hip for both EL and CL. These results suggest that metabolic cost, and not high forces alone, are involved in the stimuli for muscle hypertrophy and strength gains following high-resistance training.

[b said:
Quote[/b] ]The role of metabolites in strength training. II. Short versus long isometric contractions.

Schott J, McCully K, Rutherford OM.

Department of Physiology, St. Mary's Hospital Medical School, London, UK.

The role of intramuscular metabolite changes in the adaptations following isometric strength training was examined by comparing the effect of short, intermittent contractions (IC) and longer, continuous (CC) contractions. In a parallel study, the changes in phosphate metabolites and pH were examined during the two protocols using whole-body nuclear magnetic resonance spectroscopy (NMRS). Seven subjects trained three time per week for 14 weeks. The right leg was trained using four sets of ten contractions, each lasting 3 s with a 2-s rest period between each contraction and 2 min between each set. The left leg was trained using four 30-s contractions with a 1-min rest period between each. Both protocols involved isometric contractions at 70% of a maximum voluntary isometric contraction (MVC). The MVC, length:tension and force:velocity relationships and cross-sectional area (CSA) of each leg were measured before and after training. The increase in isometric strength was significantly greater (P = 0.041) for the CC leg (median 54.7%; P = 0.022) than for IC (31.5%; P = 0.022). There were no significant differences between the two protocols for changes in the length:tension or force:velocity relationships. There were significant increases in muscle CSA for the CC leg only. NMRS demonstrated that the changes in phosphate metabolites and pH were greater for the CC protocol. These findings suggest that factors related to the greater metabolite changes during CC training results in greater increases in isometric strength and muscle CSA.

[b said:
Quote[/b] ]Fatigue contributes to the strength training stimulus.

Rooney KJ, Herbert RD, Balnave RJ.

School of Physiotherapy, University of Sydney, Australia.

To investigate the role of fatigue in strength training, strength increases produced by a training protocol in which subjects rested between contractions were compared with those produced when subjects did not rest. Forty-two healthy subjects were randomly allocated to either a no-rest group, a rest group, or a control group. Subjects in the two training groups trained their elbow flexor muscles by lifting a 6RM weight 6-10 times on 3 d each week for 6 wk. Subjects in the no-rest group performed repeated lifts without resting, whereas subjects in the rest group rested for 30 s between lifts. Both training groups performed the same number of lifts at the same relative intensity. The control group did not train. Subjects who trained without rests experienced significantly greater mean increases in dynamic strength (56.3% +/- 6.8% (SD)) than subjects who trained with rests (41.2% +/- 6.6%), and both training groups experienced significantly greater mean increases in dynamic strength than the control group (19.7% +/- 6.6%). It was concluded that greater short-term strength increases are achieved when subjects are required to lift training weights without resting. These findings suggest that processes associated with fatigue contribute to the strength training stimulus.

[b said:
Quote[/b] ]Effects of low-intensity resistance exercise with short interset rest period on muscular function in middle-aged women.

Takarada Y, Ishii N.

Department of Life Science, College of Arts and Science, University of Tokyo, Tokyo 153-8902, Japan. [email protected].

We investigated the effect of low-intensity resistance exercise training on muscular size and strength where the interset rest period was shortened so as to reduce the metabolite clearance. Female subjects (aged 45.4 +/- 9.5 years, n = 10) performed bilateral knee extension exercises in a seated position on an isotonic leg extension machine. The exercise sessions consisted of 3 sets of exercise at a mean intensity of approximately 50% 1RM with an interset rest period of 30 seconds and was performed twice a week for a period of 12 weeks. The strength and the cross-sectional area (CSA) of the knee extensors and flexors were examined with an isokinetic dynamometer and magnetic resonance imaging (MRI), respectively. The CSAs of the knee extensors and flexors increased by 7.1 +/- 1.6% (p &lt; 0.01, Wilcoxon signed rank test) and 2.5 +/- 1.4% (not significant), respectively. Isometric and isokinetic strengths increased significantly (p &lt; 0.01) at all velocities examined, whereas no significant change was observed in those of knee flexors. These results indicate that a low-intensity resistance exercise with a short interset rest period is substantially effective in inducing muscular hypertrophy and concomitant increase in strength.

[b said:
Quote[/b] ]Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans.

Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, Ishii N.

Physiology Division, Yokohama City Sports Medical Center, Japan.

Acute and long-term effects of resistance exercise combined with vascular occlusion on muscular function were investigated. Changes in integrated electromyogram with respect to time (iEMG), vascular resistive index, and plasma lactate concentration were measured in five men either during or after elbow flexion exercises with the proximal end of the arm occluded at 0-100 mmHg. The mean iEMG, postexercise hyperemia, and plasma lactate concentration were all elevated with the increase in occlusion pressure at a low-intensity exercise, whereas they were unchanged with the increase in occlusion pressure at high-intensity exercise. To investigate the long-term effects of low-intensity exercise with occlusion, older women (n = 24) were subjected to a 16-wk exercise training for elbow flexor muscles, in which low-intensity [ approximately 50-30% one repetition maximum (1 RM)] exercise with occlusion at approximately 110 mmHg (LIO), low-intensity exercise without occlusion (LI), and high- to medium-intensity ( approximately 80-50% 1 RM) exercise without occlusion (HI) were performed. Percent increases in both cross-sectional area and isokinetic strength of elbow flexor muscles after LIO were larger than those after LI (P &lt; 0.05) and similar to those after HI. The results suggest that resistance exercise at an intensity even lower than 50% 1 RM is effective in inducing muscular hypertrophy and concomitant increase in strength when combined with vascular occlusion.

[b said:
Quote[/b] ]The effects of acute passive stretch on muscle protein synthesis in humans.

Fowles JR, MacDougall JD, Tarnopolsky MA, Sale DG, Roy BD, Yarasheski KE.

Department of Kinesiology, McMaster University, Hamilton, Ontario.

We examined the effect of an isolated bout of maximal tolerated passive stretch on fractional muscle protein synthetic rate in human soleus muscle. Eight healthy males performed two separate trials with the same leg: one session of passive stretch and one of intermittent active isometric contraction at a force equivalent to that which occurred during the passive stretch trial. This force was approximately 40% of maximum voluntary contraction force and produced volitional fatigue in approximately 27 min. Intermittent passive stretch, for the same duration, elicited a 6.1 degrees increase in joint angle (P&lt;.0005) with silent electromyography. Fractional protein synthetic rate from experimental and control soleus in each trial was assessed from biopsy samples over the period 10-22 hr postexercise by the incorporation rate of L-[1-13C] leucine into muscle. Protein synthesis was elevated in the soleus of the exercised leg following the active contraction trial by 49% (P&lt;.05) but not following the passive stretch trial. Results indicate that a single bout of maximal passive stretch does not significantly elevate fractional muscle protein synthetic rate in humans and thus suggests that muscle stretch per se is not the stimulus for the muscle hypertrophy that occurs with resistance training.
 
[b said:
Quote[/b] (Sub7 @ Jan. 06 2006,7:26)]Instead of all this talking, people should just pick up a weight, try the system and then share with us what they observed so we can refine the system.
Hunkar
While I'm all for real world testing, I understand how many, (including myself), wish to understand the science behind something before they undertake it. You came up with this system, (which I think is quite interesting), and you used occlusion science to back it up. When that science is called into question it also calls your system into question.
My interpretation of the science leads me to believe that IF ACIT creates constant occlusion THEN it has the potential to create hypertrophy with less weight. If you have to use as much or almost as much weight as you would in regular training, then what is the benefit of ACIT? Occlusion stops blood flow, and using ACIT is the same as occlusion using 70% RM which is the same occlusion as using an external cuff. You can't create more occlusion.
 
[b said:
Quote[/b] (NWlifter @ Jan. 06 2006,7:43)]Sub- I myself see no doubt of it's effectiveness.
The study Dan found &quot;Effects of low-intensity...&quot; by Michiya Tanimoto,..ect is almost ACIT to a &quot;T&quot;.
Agree, but of course they were untrained individuals, which is always the fly in the ointment so to speak.
 
True...

But, so many studies use untrained that I think we can kinda compare those studies. And it is hard for untrained to add csa, so if untrained added, that 'might' mean it's pretty effective?

All I know, is I'm using low RM stuff right now, so soon I will know beyond a shadow of a doubt if low Rm/high fatigue works in trained people ;)
 
[b said:
Quote[/b] (Dood @ Jan. 06 2006,8<!--emo&amp;
wow.gif
)]If you have to use as much or almost as much weight as you would in regular training, then what is the benefit of ACIT? Occlusion stops blood flow, and using ACIT is the same as occlusion using 70% RM which is the same occlusion as using an external cuff. You can't create more occlusion.
Gentlemen,
Let us not get lost here. Please everyone take a step back and see the sunset in this beautiful forest instead of measuring the height and width of every tree around. In Japan, Kaatsu is advertised as a way of getting the elderly stronger and presents its ability to use very low weights during this process as a virtue. Nowhere in the ACIT web site did I claim that one would be able to grow with as little weight using ACIT as was utilized in Kaatsu studies. Therefore, ACIT is similar but not identical to Kaatsu. I think we all agree on that. Yes, I indeed presented Kaatsu as encouraging evidence that occlusion has beneficial effects, but even if we can prove that Kaatsu definitely and certainly works, this does not constitute proof that ACIT works equally well. They are derivations of each other but do require their seperate proofs and as of now, ACIT remains a thoroughly discussed hypothesis based on a great deal of interesting evidence. It is not yet a theory....
Coming to your question: What good is ACIT if you still have to lift heavy? Well, I would look at it the other way and ask &quot;Isn't it great if you can occlude the muscles and still utilize a heavy load at the same time? Would you not get a lot of the hypertropic benefits of both pathways? I personally want to get stonger and bigger and don't care if I am using a 20% 1RM or 99% 1Rm in the process as long as it is safe and effective.
Little discalimer here: Some may look at what i posted above and say &quot;aaaha, now you're backtracking. so you do think that the load matters and you now do agree that the heavier the weight on the bar, the better... what happened brota?&quot;
My answer to that would be: I completely agree with Ron that the weight on the bar is a means to an end (and the studies posted above very strongly suggest so, wouldn't yo say???). If you use light weights (let's say for argument's sake &lt;70% 1RM) you have to do something additional to elicit growth, i.e. you have to work harder to reach that end. This something can be very short rest periods -like 5X5- occlusion, ACIT.... You have to do something to force maximal rate coding and recruitment, which if you simply lifted the weight in a conventional manner would not occur with that light load. Now, the lighter the weight, the more radical of a solution you need to find to ensure max rate coding/recruitment. Maybe one day someone will come up with a drug that will give us max rate coding/recruitment with a 10% 1RM weight. But obviously the intervention and inventiveness that one needs to use is less if a higher weight is used. Example:
20% 1 RM ==&gt; one must a hard core occlusion with a cuff, pretty dramatic measure
50% 1 RM ==&gt; one can use 5X5s, less radical more realistic
~60% 1 RM (for arguments sake) ==&gt; one can use ACIT, again less radical pretty doable, probably safer than do-it-yourself occlusion.
If one masters ACIT and can use ACIT with an even higher weight (say 70% 1RM) even better, because ACIT then has a smaller gap to fill since max rate coding and recruitment would almost be occuring on its own with that kind of weight ,plus you get a lot of metabolic work on top.
.....................................................................................
BTW Captain RON: Thank you very much Sir for taking the time to post all of those studies. This is now a very good thread for future reference whenever people discuss metabolic work vs tension. I don't think all those studies were in one place in any other thread until now. As always, Grazie Millie Con Tutto Il Cuore....

Hunkar
 
[b said:
Quote[/b] (Sub7 @ Jan. 07 2006,4:19)]Gentlemen,
Let us not get lost here. Please everyone take a step back and see the sunset in this beautiful forest instead of measuring the height and width of every tree around. In Japan, Kaatsu is advertised as a way of getting the elderly stronger and presents its ability to use very low weights during this process as a virtue.

Whether it is promoted for anything is besides the point. I can advertise anything for any purpose I feel like, it does not mean there is any evidence for it working in those roles.

Which is what we are discussing.

Occlusion may be the most magical thing in the known universe, but the evidence base is minimal, but increasing.
 
[b said:
Quote[/b] (NWlifter @ Jan. 07 2006,3:40)]True...
But, so many studies use untrained that I think we can kinda compare those studies. And it is hard for untrained to add csa, so if untrained added, that 'might' mean it's pretty effective?
All I know, is I'm using low RM stuff right now, so soon I will know beyond a shadow of a doubt if low Rm/high fatigue works in trained people ;)
Hard for untrained to add CSA?
 
[b said:
Quote[/b] (Sub7 @ Jan. 06 2006,10:19)]Coming to your question: What good is ACIT if you still have to lift heavy? Well, I would look at it the other way and ask &quot;Isn't it great if you can occlude the muscles and still utilize a heavy load at the same time? Would you not get a lot of the hypertropic benefits of both pathways?
But that's just it, they are the same pathways.
The whole point of occlusion is to recreate the same environment in the muscle which occurs during high tension work: tetany and hypoxic environment. My understanding of ACIT is that it attempts to keep the muscle occluded without an external cuff. Since heavy weight already achieves this, (as long as lockout is avoided), what is the point of using ACIT with heavy weight?
Same situation with external occlusion, why use external occlusion with 80%RM when 80%RM already creates occlusion and it's effects?
The way I see it, the benefit of external occlusion or ACIT is that it allows you to use lighter weights under full tetany, which allows more reps to be done in a set, less CNS fatigue, more frequent training, and less chance of injury or strain.
 
[b said:
Quote[/b] (Dood @ Jan. 06 2006,11:43)]
[b said:
Quote[/b] (Sub7 @ Jan. 06 2006,10:19)]Coming to your question: What good is ACIT if you still have to lift heavy? Well, I would look at it the other way and ask &quot;Isn't it great if you can occlude the muscles and still utilize a heavy load at the same time? Would you not get a lot of the hypertropic benefits of both pathways?
But that's just it, they are the same pathways.
The whole point of occlusion is to recreate the same environment in the muscle which occurs during high tension work: tetany and hypoxic environment. My understanding of ACIT is that it attempts to keep the muscle occluded without an external cuff. Since heavy weight already achieves this, (as long as lockout is avoided), what is the point of using ACIT with heavy weight?
Same situation with external occlusion, why use external occlusion with 80%RM when 80%RM already creates occlusion and it's effects?
The way I see it, the benefit of external occlusion or ACIT is that it allows you to use lighter weights under full tetany, which allows more reps to be done in a set, less CNS fatigue, more frequent training, and less chance of injury or strain.
Oh, there is much much more than that going on during an ACIT set. If all ACIT did was accomplish the exact same thing that a heavier set does by using less weight, it would only be useful for people who have fragile joints or an injury, and this thread would not have even started.

Regular set with 8 RM weight to failure: The muscles are occluded only for 60-70% of the set. During relatively easy positions on the ROM and while lowering the weight -at least during the first few reps- there is insufficient effort to achieve occlusive effects. The PH level does not drop as radically, plus ATP gets regenrated while the level of effort declines during those easier points on the ROM and eccentrics.

A Set of ACIT: Our aim is to occlude the muscles from the first until the last second of the set with no break in between. This is why we are avoiding those easier points and squeezing the crap out of the muscle all the time. A very different experience, with a constant occlusion effect, lower PH in and around the fibers and great inhibition of ATP regeneration during the set. All those factors combine to produce an unusual effect. Just as importantly, contracting the exercised muscle requires you to also contract the antagonist as explained on the ACIT site, which also makes the eccentric portion of the exercise harder than a conventional set. This factor alone makes ACIT a totally different animal. It becomes almost like doing the concentrics with a regular weight but switching to a much heavier weight during eccentrics.

Here is a concrete example for you with numbers. When I do a set of leg presses ACIT style (to failure) and rest for 4 minutes, I can then get 10 reps on the calf raise with 540 lbs. Today, just for the heck of it, I did a regaular set of leg presses -not ACIT- and was wiped out by the time I had reached positive failure. After waiting for 4 minutes, however, I got out 12 reps with 540 lbs on calf raises. So one set of ACIT training for legs produces a greater level of exhaustion in my calves, which is totally consistent with my earlier epxerience in the other muscle groups as well as the idea around which ACIT revolves: The inroading is happening much much faster and is deeper. But the great thing is that while this is occuring without your body as a whole is less tired and less burnt-out.

To make a long story short: a lot is happening other than simply reaching tetany earlier...
 
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