A New and Unique Training Method is Here

[imported_dkm1987]

BTW, Mikey, where's that stuff you were going to send my way?

 

[xahrx]

This is the best thread in a long, long time.

 

 

Here's a question though: Would the occlusion method of ACIT confer any advantage over techniques already used for metabolic work? For example, during the 10s and fives of an HST cycle, instead of doing high rep work after work sets would ACIT be a good replacement, or more to the point a better way of getting metabolic work in?

 

[imported_dkm1987]

Strictly metabolicaly speaking probably not, but that isn't the real fascination with occlusion type training. It is really how occlusion causes maximum recruitment without having to utilize extremely heavy weight.

 

[colby2152]

Quote[/b] ]It is really how occlusion causes maximum recruitment without having to utilize extremely heavy weight.

The basis being to prevent injuries? I still have to read this ACIT website. Maybe, I should quit commenting on this thread until I read it.

 

[Dood]

I would also suggest heading over to Dan's site and reading up on occlusion and it's mechanisms. Check out the forums and search "occlusion" and "Kaatsu". Enjoy

 

[NWlifter]

Quote[/b] ]sounds like some Pete Sisco stuff

Eek, I hope not! :O

Quote[/b] ]Here's a question though: Would the occlusion method of ACIT confer any advantage over techniques already used for metabolic work? For example, during the 10s and fives of an HST cycle, instead of doing high rep work after work sets would ACIT be a good replacement, or more to the point a better way of getting metabolic work in?

First, what is metabolic work? Somehow stimulation adaptations in the mitochondria and blood vessels minus any hypertrophy? I don't think one can do that with heavier sets (ie 15RM or heavier).

Quote[/b] ]Strictly metabolicaly speaking probably not, but that isn't the real fascination with occlusion type training. It is really how occlusion causes maximum recruitment without having to utilize extremely heavy weight.

Dats the ticket!

Read these...(if ya want )

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.

My article from Hypertrophy research on energetics

Quote[/b] ]Energetics


Introduction
There are several paths that lead to upregulated protein synthesis in resistance training. It would be naive to focus completely on any one, or to neglect the aspects of any one of the various signaling factors. Many times, a means is thought of as the actual stimulation. Or more simply, a method of applying a stimulation is deemed as an actual path of stimulation. An important marker for the hypertrophic stimulus, lies in the energetic cost of the set, usually in reference to the time span per amount of energy consumed. This is the energetic theory.

Definition
The energetic theory is one in which the energetic cost of the contractions, or sum of contractions, is used as a measurement tool for the upregulation of protein synthesis.(14) Many debate this, usually from a lack of understanding. An opposing point might be, that running or aerobics burn ample energy but are not a good stimulus for hypertrophy. This is true, but is wrongly applied to this theory. The energetic cost is more related to the time factor.(5,9,14,21) ie ATP turnover per time period. A muscle fiber uses ATP to break the contraction bonds, and burns it in proportion to the rate at which the sarcomeres are crossbridging.(5) This rate is determined by the neurological input frequency. (rate coding) Exercise which is of low intensity, calls for slower contractions of the motor unit pools. Thus, total energy for the exercise session might be high, but the rate at which ATP is turned over, is low.

The science of the energetic theory is based upon the action of mTOR (mammalian target of rapamycin). mTOR is a regulator of protein synthesis in a muscle cell, simply, it monitors and adjusts protein metabolism (synthesis/degradation) in response to energy requirements. mTOR is very sensitive to amino acids and insulin. How the process appears to work, is AMP-activated protein kinase (AMPK) blunts mTOR during contraction. By mTOR slowing protein synthesis, more ATP is available for use during the contractions. When contractions cease, mTOR rebounds to a higher level, increasing protein synthesis to a greater than resting levels. The presences of amino acids at this time also seem to be required. It's possible that a high ATP turnover, such as found during heavy or high intensity contractions, blunts mTOR to a maximum or close to maximum level, causing the highest level of rebound afterwards. The rebound level may or may not be proportion, or somehow related to the rate of ATP turnover and/or the time it is blunted. (5,14)

Explanations
The reason aerobics or endurance activities do not cause this effect, is due to the lower levels of tension. High rates of ATP turnover require high frequency contractions (rate coding).(9) The way in which the CNS manipulates activity is by the level of required effort. First order is to increase recruitment levels, once recruitment becomes full, then, and only then, will firing frequencies be increased. Depending in the muscle or muscle group in question, full recruitment will occur anywhere from approximately 40% (for smaller muscles such as those of the hand) to possibly 95% (upper thigh musculature) of maximum momentary MVC. Other muscles of the torso usually fall somewhere inbetween, such as biceps at approx. 70-80% of momentary maximum MVC. (16,17,18,22)

Note: The reason "momentary" maximum MVC is stressed, is to emphasize that the resistance does not have to be that particular percentage of fresh maximum force (percent of 1RM), but that anytime that level of effort is required, recruitment follows these patterns. For example, if your biceps reach full recruitment at 80% of 1RM, and your 1RM is 100lbs, a single rep with 80 pounds will induce full recruitment, as will the last several reps of a set with your 10RM, where fatigue has limited your strength. Anytime your CNS is putting out a "greater than the minimum" level of effort for full recruitment, rate coding is employed afterwards for further force requirements.

Cautions
A first thought is usually, "Why not just train to failure?". As far as energetics are concerned, yes, going to failure, and even beyond would cause a high sustained ATP turnover. However, there is a price to pay. Both short term, and long term. For short term, failure training and sustained high frequency type contractions may cause failure in the EC (excitation contraction) systems. Failure may lie in the local propagation of the neural signals.(23) And, it may cause a lengthy recovery period.(24) What this means, is your muscles may be long recovered and ready to go before your local neural system is up to performing those types of contractions with any meaningful intensity again. For long term, the mental toll of such taxing training can cause an overtraining of the CNS and systemic factors. Symptoms such as those found with depression may become evident. Loss of appetite, loss of desire, etc. Annecdotally, many find that with regular high effort training, long recovery periods are required before strength returns or even the desire to put oneself through another torturous affair of the like. Many trainees turn to stimulants, such as amphetimines or high doses of caffine to reach the needed level of mental effort for a productive session. These drugs work by increasing neuro-transmitters, ie. they 'wire up' the CNS. This itself, is evidence the CNS is the lacking component in continous training of this sort. (11,12)

A Better Application
Multiple sets are a safer and less taxing method for the neural systems. It is true there are many studies showing that single sets can be as effective for short term gains, but again, this involves the trainee making sure that the single set used, is maximized. A turn around could be said that all the studies show mutliple sets are as effective, or more effective than single sets.(1) A good way to think of this, is why kill yourself with one "do or die, all out, torturous" set, when a few, or at most, several more enjoyable sets could be performed? Anyone who has done both will know that the time factor is not of that much concern. After a killer single set, most end up on the floor "seeing stars" for several minutes before the next exercise can be performed. Instead, several 'less intense' sets could have also been performed in that time. And, with much less discomfort or ill effects.

We are not saying people should avoid training hard, and avoid pushing themselves. Progress is not easy and you will hit failure by accident now and again if your working hard. But, to work yourself to this point regularly, may not be the quickest means of progress.(11,12,24)

Assurance
How do we know that energetics are even a viable marker? First, studies using occlusion have found rapid increases in size and strength, with very low resistance.(6,7) The fatigue induced from the lack of blood flow, causes the muscles to reach full recruitment and high levels of rate coding with very low whole muscle tension. Damage, or micro-trauma is low to non-existant but marked hypertrophy is still evident. Further, what was once thought to be damage, is now seen to be more of the remodeling process.(13) The smeared Z lines found in exercised muscle cells, are much more evident several days after exercise. If damage from the contractions were causing this, they would be seen immediately. Since their prominence is greater days afterwards, it shows the process of recovery has caused this rather than the acute effects of exercise. Why is this important? This effect (smeared Z lines) is sometimes, but not always, in accordance with DOMS. One of the best explanations of DOMS, describes the effects stemming from high intra-cellular calcium concentrations initiating the process, and the time course of the immune system following the time course of the soreness.(15) High peak tension, eccentrics, and many other aspects of training, including high frequency contractions, can increase intra-cellular calcium concentrations through various means.(3) We've all experienced increased levels of DOMS with higher levels of intensity and/or the volume of exercise. Obviously, both of these applications (intensity and volume) are increasing the stimulation of the remodeling process.

Also, a measurement variable, termed TTI (Tension Time Integral), where the average true tension is computated, (4,5) is directly proportional to the energetic cost of a contraction. Even tension signaling factors, such as P70 (70-kDa ribosomal S6 kinase, an important marker for hypertrophy) (9,10) can be tracked by calculating the TTI of the contractions. One can then extrapolate, that ATP turnover (the energetic cost/time) is proportional to the stimulation induced by resistance based contractions. (5,6,7,8,21)

Means To an End
What your seeking, is protein upregulation. Your means is through an application of external resistance that will induce full recruitment and higher levels of rate coding.

Application
Keeping with a CNS and EC friendly method, a repeated application is probably superior to a single all out set. (as discussed above)

*Multiple hard, but not to failure, sets
*Density type programs. Work per time unit is a watched variable
*Heavy/Light setups. Work is equalized while the load is alternated
*Rapid progression programs. Work is equalized while load is increased
(1,2,3,19,20)

References

1) Human Skeletal Muscle Hypertrophy Jose Antonio, Ph.D.
2) Carey-Smith R, Rutherford OM: The role of metabolites in strength training. Eur J Appl Physiology
3) Calcineurin Is Required for Skeletal Muscle Hypertrophy* Shannon E. Dunn, Jennifer L. Burns, and Robin N. Michel 1999
4) Influence of tension time on muscle fiber sarcolemmal injury in rat diaphragm
Ercheng Zhu, Alain S. Comtois, Liwei Fang, Norman R. Comtois, and Alejandro E. Grassino
5) Tension-time index, fatigue, and energetics in isolated rat diaphragm: a new experimental model Paul F. Klawitter1 and Thomas L. Clanton2 2003
6) Skeletal muscle size and circulating IGF-1 are increased
after two weeks of twice daily “KAATSU” resistance
training T. Abe, T. Yasuda, T. Midorikawa, Y. Sato, C. F. Kearns, K. Inoue, K. Koizumi, N. Ishii 2005
7) 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.
8) CONTROL OF THE SIZE OF THE HUMAN MUSCLE MASS Michael J. Rennie,1,4 Henning Wackerhage,1 Espen E. Spangenburg,3 and Frank W. Booth 2 2004
9) Intracellular signaling specificity in skeletal muscle in response to different modes of exercise Gustavo A. Nader and Karyn A. Esser 2001
10) Phosphorylation of p70S6k correlates with increased skeletal muscle mass following resistance exercise Keith Baar1,2 and Karyn Esser2 1999
11) Resistance exercise overtraining and overreaching. Neuroendocrine responses.
12) Spinal and Supraspinal Factors in Human Muscle Fatigue
S. C. Gandevia Prince of Wales Medical Research Institute, Prince of Wales Hospital and University of New South Wales, Sydney, Australia
13) Evidence for myofibril remodeling as opposed to myofibril damage in human muscles with DOMS: an ultrastructural and immunoelectron microscopic study. Yu JG, Carlsson L, Thornell LE.
14) Regulation of mTOR by amino acids and resistance exercise in skeletal muscle. Deldicque L, Theisen D, Francaux M.
15) Enoka; Neuromechanics of Human Movement 3rd edition (Clarkson, Cyrnes, McCarmick, Turcotte, & White, 1986; Friden & Lieber, 1997' Jackson, Jones, & Edwards, 1984; Armstrong, 1990; Lieber, Schimtz, et al., 1994; Malm, Lenkel, & Sjodin, 1999)
16) Enoka; Neuromechanics of Human Movement 3rd edition (Deluca, LeFever, McCue & Xenakis, 1982a; Kukulka & Clamann, 1981; Van Cutsem et al,. 1997)
17) Intermuscle differences in activation. Behm DG, Whittle J, Button D, Power K.
18) Influence of exercise and training on motor unit activation. Sale DG.
19) Effects of low-intensity resistance exercise with short interset rest period on muscular function in middle-aged women. Takarada Y, Ishii N.
20) Fatigue contributes to the strength training stimulus. Rooney KJ, Herbert RD, Balnave RJ.
21) Mechanism of work-induced hypertrophy of skeletal muscle. Goldberg AL, Etlinger JD, Goldspink DF, Jablecki C.
22) Motor unit activity during long-lasting intermittent muscle contractions in humans. Christova P, Kossev A.
23) Behavior of motor units in human biceps brachii during a submaximal fatiguing contraction. Garland SJ, Enoka RM, Serrano LP, Robinson GA.
24) Neuromuscular disturbance outlasts other symptoms of exercise-induced muscle damage.Deschenes MR, Brewer RE, Bush JA, McCoy RW, Volek JS, Kraemer WJ.

 

[imported_dkm1987]

Quote[/b] (NWlifter @ Dec. 27 2005,5:43)]My article from Hypertrophy research on energetics

Which you need to repost Since the backup fiasco

 

[Sub7]

Dan, Ron, and Other Experts,

So do you think that the weight on the bar has other additional benefits over and above full recruitment and maximum rate coding.

Let me make this question more concrete and realistic:

I am now training exclusively with ACIT (except fr calves and one of my two lat exercises) and consequently using less weight than I would if I were doing a conventional style. Assuming that I am achieving as much TTI or IOW, all the necessary fibers are getting the recruitment and tetany they would be receiving from heavier weights, should I still try to use heavy weights (once in a while or regularly?)

Hunkar

 

[Dood]

Quote[/b] (dkm1987 @ Dec. 27 2005,7:58)]

Quote[/b] (NWlifter @ Dec. 27 2005,5:43)]My article from Hypertrophy research on energetics

Which you need to repost Since the backup fiasco

I just PM'd him about that

 

[imported_dkm1987]

Quote[/b] (Sub7 @ Dec. 27 2005,7:02)]Dan, Ron, and Other Experts,
So do you think that the weight on the bar has other additional benefits over and above full recruitment and maximum rate coding.

Well as I posted at my site, the weight on the bar does have a part to play when speaking of occlusionary stimulus, IE the greater the weight, the more fibers are intitially recruited and during contraction the more fibers involved cause a difference in the blood flow.

On the other hand you will eventually receive the same changes with a lighter load as the contraction caused fatigue begins enhancing recruitment.

Just means to an end, IMO. Bottom line you will need to try it both ways for a duration of time and compare results.

 

[xahrx]

Quote[/b] (NWlifter @ Dec. 27 2005,6:43)]My article from Hypertrophy research on energetics.

That was an awesome read, thanks. Now I have a much better idea of where you and Sub7 are coming from on this.

 

[xahrx]

Quote[/b] (Sub7 @ Dec. 27 2005,8:02)]I am now training exclusively with ACIT (except fr calves and one of my two lat exercises)

I remembered you had mentioned this before. On my last workout, other than messing up my left trap which will likely keep me from working out for a week or so, I put my mind to this calf problem. Since you said they're growing anyway it might not be necessary, but I found if you put the pivot point for a calf raise closer to the middle of your foot than toward the toe end you can use your tibialis to maintain the kind of tension I think you're going for in ACIT. Use a shoe with a very rigid bottom for this, otherwise it's likely the pivot point will dig into your foot most uncomfortably.

 

[NWlifter]

xahrx- Thanks, glad you liked it

Dood/Dan- Thanks for letting me know, it's reposted! Yours are missing too Dan!

Tension: Whole muscle tension also has the benefit of increased conective tissue stimulation. Also, it has an effect on golgi & afferent muscle fibers. Lowering of these inhibitory sensors will 'allow' one to use more weight. It's most likely why you need to practice a 1RM before you can really see your 'true' 1RM.

 

[xahrx]

Just want to clarify. I think someone mentioned remodeling earlier. To my understanding remodeling of muscle is different than the type of action that's occurring when the muscle is damaged. Remodeling, as I understand it, is a change in myosin types in muscle fibers, essentially a change in type I fibers to be more like type II and/or the other way around. This is different than the myotrauma/satelite cell fusion we're usually talking about in HST, correct?

 

[imported_dkm1987]

The remodeling we are referring too is what is actually happening at the sarcomere level not the isoform shifts.

 

[xahrx]

Quote[/b] (dkm1987 @ Dec. 28 2005,12:28)]The remodeling we are referring too is what is actually happening at the sarcomere level not the isoform shifts.

So physical and metabolic stress causing wider but not longer muscle cells through increased protein synthesis, correct?

 

[xahrx]

Early events in stretch-induced muscle damage

Don't know if you guys have seen this one, but I know Sub and few others are discussing the way their muscles fail after ACIT training. Thought this might interest them, though I didn't get to read much more than the abstract.

 

[yshemesh]

this new bandwagon is very exciting and at the same time causing me deep dissonance !! i guess in my head there's an assimilated (grammer?) idea of lifting heavy.

good looks and keep it going.

also where is this taking us in terms of strength training ?

 

[Sub7]

Quote[/b] (xahrx @ Dec. 28 2005,2:09)]Early events in stretch-induced muscle damage
Don't know if you guys have seen this one, but I know Sub and few others are discussing the way their muscles fail after ACIT training. Thought this might interest them, though I didn't get to read much more than the abstract.

This is a very nicely written document but veeeeery exhaustive. More than half what is known about how muscles operate has been crammed in there (slight exxageration, but you get the idea). A lot of wonderful findings from dozens of stuides presented, but I am not advanced enough to move from this level of theory into practice. 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?

Hunkar

 

[imported_dkm1987]

Quote[/b] (xahrx @ Dec. 28 2005,12:54)]

Quote[/b] (dkm1987 @ Dec. 28 2005,12:28)]The remodeling we are referring too is what is actually happening at the sarcomere level not the isoform shifts.

So physical and metabolic stress causing wider but not longer muscle cells through increased protein synthesis, correct?

Well, kinda.

When disruption within the fiber happens, the body adapts by removing bad proteins and replacing them. Sometimes these disruptions occur in a single fiber (single or multiple sarcomeres in series) or in multiple adjacent fibers.

The remodeling effect is an idea that the clinical signs of what represented damage, desmin and actin staining alterations, fibronectin increases and others, may not be signs of damage or may not be seen at all with unaccustomed exercise (fibronectin increases). Damage is generally thought of occurring rapidly after injury, think of crush or tear, but Yu found that some of these clinical signs did not happen immediately after exercise that caused DOMS so therefore it wasn't damage per se but a remodeling (protein changes) response at the sarcomeric level.