This is where it becomes interesting becuase the body appears to be able to optimse the NS to perform as the athlete gets more efficient but the athlete must take longer to recover.
Which leads to James commnets in other threads of ‘by-passing’ or manipulating the NS using other training approaches.
It also brings in the whole area of CNS recovery, where I’m starting to revise my previous ideas on CNS regeneration too!
Good point - but how do we determine what to draw from the information or perofmances then?
Yes (and no) IMO … Is part of the solution or answer not in HOW the perofmrances (training) are being elicited? - i.e. using the SSC, Isometrics and Dynamics?
Are these a less demanding stress-type on the CNS?
I think this is what I am trying to get to … and I think Pakewi has put it far more eloqunetly than I could - Is it the nature of the disturbance that affects the CNS stress?
We know with High intensity & volume obviosuly has an affect - but is there a critical point under which Hi-intensity work can be conducted or hi-intensity neural training can be conducted - that permits faster CNS regeneration?
However, if we can find methods to ‘reset’ the CNS inhibitions, what implications does this have for the recovery of other tissues within the body? Can we continue to perform high intensity work without creating further maladaptive damage within those tissues?
And at what happens when neural pathways have been optomized for the force/power producing capacities of the musculoskeltetal system? Are we not getting back into a regular accumulate/intensify type of periodization scheme?
Even theortically, how is this practically applied?
That opens a whole other line of reasoning:
1: You are working to increase forces (amplitude of the stimulus wave)
2: A higher wave has a longer period so top athletes must, in their High Intensity work, intersperce Maximal work with Sub-Maximal sessions. The period between Maximal sessions will therefore become ever longer (think of a world record holder and how often he can express this level)
3: A closer proximity of Maximal speed sessions will increase the likelyhood of Tendon and Bone maladaptions as performance reaches ever higher levels. (this is already reflected by the lengthening taper periods for higher level athletes.)
Recognizing the points above, you can see why the ONLY goal must be the heightening of the Maximal stimulus sessions over the long haul by providing the variability, active and passive recovery, and safety required to make that happen.
Everything is built around this.
i have noticed a few individuals using the term “reset” when reffering to some of my comments on the CNS. in reference to my beliefs on inhibtion this term would be misplaced. its not the CNS that resets but inhibtion that breaks down and allows for continues output of the CNS.
i would also like to comment on adapatation. first lets consider it not a single component such as adaptation of the CNS but a aggragate of factors which upon summation do not equal their parts. so we speak of supercompensation as a whole or simply adaptation of the organism.
now lets consider an alternate series of event which leads to eventual adaptation. the normal scheme is a stressor is induced the organisms functional state declines and eventually supercompensation occures. but what if we incude a stressor and throughout a period of time maintain that stress on an even (or close to even) level. the longer this level is maintained the larger the subsequent supercompensatory effect upon recovery.
You’re right about an aggrigate of factors. My point is to pick the critical one that MUST adavance for you to achieve your objective and adjust all other factors to support the advancement. Clearly, the faster a favorable response to stimulus occurs, the greater the likelyhood of an advance when that element is stressed again within a range of stimulus periods.
Now let’s look at the timing of the stressor at Max. Let’s say you have 5 races in 12 days on the GP circuit. you can view these as One Single major stressor to the entire organism and when you allow supercompensation from that overall stressor (10 day tapers on BOTH SIDES of this block), that’s when the World Record comes- see Speed Trap and CFTS and refer to the detailed chart of Ben’s 1987 training plan in the Vanc 2004 download.
I think I feel another Graph comming on because the issue becomes confusing without better visualization as the major stressor is becomming higher and higher and farther apart, even though the final pre- key performance grouping could make it seem the other way.
Which ties in with your explanation on structuring Powell’s GL season
think of the groups of races as single units of work divided by a short recovery of up to one week, a training block, and a taper (I’d use the 10 day taper from CFTS, of course). That leaves around a two week window for normal training.
There are two issues running concurently here - and I see a distinction between competition and training.
In competition I do not see how the image that Charlie paints can be bypassed as the organism is stressed as a total … training can be arranged differently though.
My fundamental query keeps coming back to this -
“Can the body’s ability to absorb and generate force be improved by improving the neural effciency of the athlete thru the use of exercises, or combination of exercises (bench press, squat), performed in a manner (slow eccentrics, balistics, isometrics etc.) that by-pass the CNS or do not impact on the CNS to same degree or the same manner as conventional eccentric-concentric training, and thus allow the body to be trained to a greater level of force generation?”
As regards the tissue adaptation - this must be prepared for - and I think this is one of the uses or aims of the slower eccentric work… and as I understand, it also results in an increased rate of firing.
The importance of this Iso and Eccentric work rises as the body readapts to the stresses on it and the forces it can handle.
(Also eccentric and isometric work are essentially one in the same thing - or at least very similar.)
From what I understand, these are some of the issues raised:
-a system adaptation (James), which IMO may lead to “brain” rather than only NS resetting, which makes you consider how parts of the system may cope (svass).
-the solution provided by Charlie is mainly via “a higher wave” (and its “peaks”) that deal with both maximal and sub-maximal work for progress to be made, which also takes care of svass’ concerns. James proposes an extension of this wave, which by definition will contain sub-maximal stressors (example is provided by Charlie with GP races leading to a WR performance).
If the two can ever come together, I want to know how this efficiency is reached… pakewi!
With this in mind what no23 is saying, i.e., the how or nature of the stressor -although important for sure- becomes a “secondary” issue. That is, I would look into that at a later stage, since it could be resolved by the “efficiency”, a la pakewi, itself (no23, I hope you get what I mean, these are interelated anyway).
What I am finding hard to comphrehend is how the capacity of the athlete affects the length of ‘peak’ or grouping of stresses or indeed the supercompensation or even when to decide the athlete’s length of peak has been reached … I guess this is down to both experience, level of performance (efficiency) and athlete trg age?
i attempted to explain this before in this thread but when i did people screamed for cookie cutter programs. but anyway you have to stop viewing the CNS as a pool of resources which can be drained (via intensive physical work) and filled (via rest and recuperation). nothing i have found scientifically supports this and it is excepted i believe because on outward appearance people believe this is what is happening to them. “i just maxed yesterday, im spent”. now think of the CNS as it truly is (IMO) a complex network which transfers impulses and in its complexity has the ability to inhibit its own output in order to preserve the systems healthy status. like i said before, in this thread, the only way around this is through reflexive action. why cant we voluntarily recruit all of our motor units yet we have heard stories of grandmothers lifting a car off their grandchildren. we inhibit ourselves and only fight or flight situations and reflexes allow us to fully recruit our motor pool. no matter how tired u are, fatigues whatever reflexes will remain reflexes (in actuality reflex can be trained but thats not important to the discussion). so what do we do with this, we train the reflex forcing the body to continually send powerful impulses to the system. there are other considerations but that is pretty much it. you train the reflex reteaching the body that it is able to recruit maximally over and over.
But even if we view the CNS as a protective mechanism is there is NO physiological adaptation to the new effciency at all?
Surely there is some physiological response or adptation?
… And to progress that to the question that many were asking earlier - program design - any training program to elicit these advances the muscluature must be trained to absorb the loading imposed therefore specific training must be used to strengthen both muscles and the tendons (in tension) to be used.
Group members - please excuse me as I go off on a physiology rant.
James,
Herein lies my main problem with any of your arguments. While it is easy to throw in tons of scientific terms and fool people that don’t have any physiological background (wasn’t this one of the things on Siff’s How to Spot a Quack/Guru checklist) - it did nothing but demostrate your limited knowledge of what goes on within the human body during training.
This description of the stretch reflex is what I would expect from a 100 level student looking at a picture in a text, and does not descibe what is actually happening during the high velocity/high intensity movements that you are describing.
First, in reactive/high power movements, the anatgonists are not inhibited. Conversely, in the moevements you are describing anatgonist recruitment is actually increased. The high forces and torques that are put on the joint requires increased anatagonist involvement to stabalize the joint (protection) and allow for proper tracking of the joint during the movement. At this time, there is no concensus in the literature as to whether the CNS will optomize the interaction between agonist/anagonists for either power production or joint stability. Regardless, this point is not that important.
What is more important is what you state in the first post I quoted:
During fatigue situations, you are right in stating that the reflex still remains. And not only does the reflex remain - it gets stronger! This thought to occur because of an accumulation of metabolites which induce acidosis surrounding the 1a afferent terminals. This increased stertch reflex response reponse is thought to occur as a reaction of the CNS to try to change the stiffness regulation of the musculotendinous unit. However, the important thing you are overlooking is the ‘peripheral factors.’ You addressed this in your initial thread as lack of ATP production by the muscle fibre. However, lack of ATP is not a factor in muscle fatigue!!!
You are overlooking the true peripheral factors that include: neuromuscular transmission and propagation down the sarcolemma, dysfunction within the sarcoplasmic reticulum involving calcium release and uptake, availability of metabolic substrates and accumulation of metabolites, and actin-myosin cross bridge interactions.
Bottom line: Although the stretch reflex not only remains but is also enhanced (along with increased rate coding and motor unit recruitment) - muscle fatigue still occurs, contact times increase as do the times for both the concentric and eccentric muscle contractions during the SSC, and force absorption ability STILL decreases.
I have a hard time buying your training beliefs that are scientifically based when you say - “nothing i have found scientifically supports this” and IMO (in my opinion) when you show that you do not understand the science. Please correct my physiology if I am wrong.
you are wrong, first off I wasn’t trying to describe the physiology of the stretch reflex, you jumped to that conclusion. I was simply presenting an argument for neurological motor learning. also the stretch reflex DOES inhibit the antagonist muscle group its basic ballistic feed-forward muscle control. maybe you should go back and reread.
You’ve made a lot of assertions and assumption like im trying to prove something via my knowledge of physiology. before you call someone a quack maybe you should do a little more reading. I never said the stretch reflex allows for intense fast or whatever contractions. what I did say is that I believe that repeatedly recruiting the reflex can break down the barriers of inhibition.
im so tired of this bull shit you and some other make arguments against what I say by making assumption about what i am trying to communicate. its obvious you don’t understand what I’ve been posting as you responses are like that of someone who was reading something else.
why the flying fuck during a ballistic action would the human body recruit the antagonist muscle group if it hoped to produce any type of efficient movement. do me a favor find anything written my Enoka and look up the alpha gamma loop, inter-neurons, reflexes, for Christ sake anything.
im not debating that reflexes are enhanced but now your saying that ATP has nothing to do with fatigue, unless your talking about the work of AV hill (which I mentioned in an earlier post) your muscle needs ATP to contract. That’s fucking basic. NO ATP NO CONTRACTION, and ummmm isn’t a fatigued state one in which the functional state of a tissue is inhibited hmm sound like it cant contract or at least contract optimally.
im not forgetting anything just cause you spit out the physiology of nerve transmission doesn’t change or go against anything I’ve stated.
you make a big assumption at then end that I stated that training the stretch reflex will make it so force doesn’t decrease, that contact times wont increase etc. I never fucking said that. I simply stated the effect it had on inhibition of the CNS. your so far off base that you cant even see dry land.
GUESS WHAT ASSUMPTIONS MAKE AN ASS OUT OF YOU AND ME… WELL IN THIS CASE JUST YOU.
James, you offer nothing really new, Professor Gunter Tidow and Dietmar Schmidtbliecher, world renouned researchers have demonstrated that inhibition of the stretch reflex and CNS as a whole decreases with training, using H-reflex as a measure…we know that. We also know that through training over time, inhibition decreases allowing more muscle fibers to be recruited and used in a sporting action thats the ultimate aim of strength training. This can be and has been demonstrated by Maximal Voluntary Contractions that remove inhibition of the CNS for lower and upper extremeties but with a marked difference between the two body parts (upper body usually has much higher muscle fiber percentages and so the effect is greater).
Its been demonstrated that inhibition of the CNS decreases with training…this is nothing new.
ok im gunna say this slowly. I AM NOT DISPUTING THIS. and i in no way said i came up with this shit. again you guys are assuming i was only commenting on the subject. are we reading the same posts? seriously what going on here? is this a joke or something?
i read ur post again, your talking about motor unit inhibtion and reflex inhibtion (and i agree with everything your talking about) im talking about CNS inhibtion or fatigue. we arent even on the same page…
