It was not me that first made the assumption, it was the people that work in the field. There is an irony to both your question and staement.
The cheetah’s don’t rely on paper work timetables and maths - they rely on there instinct. Nobody has got time to grab a cheetah after it has cought an animal in the wild, and do the tests on it. The only cheetahs you can do tests on are ones in captivity which are not going to be doing an all out sprint. Don’t tell me that you expect data on c.n.s pool depletion of cheetahs to be able to realize the theory. The people that put forward the theory are the ones who sit in big jeeps all day, in the Serengety, studying, observing all day, the behaviour/activity/results, and they draw there conclusions. Ofcourse the cheetah has to worry about lins and hyeenas aswell as bodyheat and oxygen recovery after a big sprint, but why do you assume c.n.s awareness (freshness v general fatigue) would not be a factor with the cheetah?
Of course there was an irony…
My point being:how do we know what mechanisms really make Cheetah’s’ strategies efficient survival wise? And:even if we prove that after an presumed “all out” sprint Cheeta’s do need long days of rest (which does not really abides to the general rules set by evolution itself by the way),how do we know it is their “CNS” and not other organs to be so heavily taxed???
More than an irony mine was a veiled suggestion to reconsider possibly the so easily accepted,and never enough defined concept of “CNS Fatigue”,either in humans or eeven Cheetah’s!
Yes overtraining myopathy can lead to ischemia. Massage or certain types of massage increase blood flow. Peripheral blood flow increases with contrast showers. Supertraining has a section on the use of blood pressure to monitor recovery.
"Eur J Appl Physiol. 2004 Apr ;91:382-91
New aspects of the hormone and cytokine response to training.
Jürgen M Steinacker, Werner Lormes, Susanne Reissnecker, Yuefei Liu
Exercise training is associated with peripheral-cellular and central-cerebral processes, hormonal-neuronal regulation and transmission mechanisms. During the acute training response, peripheral cellular mechanisms are mainly metabolostatic to achieve energy supply and involve associated cytokine and hormonal reactions. Glycogen deficiency is associated with increased expression of local cytokines (interleukin-6, IL-6), decreased expression of glucose transporters, increased cortisol and decreased insulin secretion and beta-adrenergic stimulation. A nutrient-sensing signal of adipose tissue may be represented by leptin which, as for insulin, IL-6 and insulin-like growth-factor I (IGF-I), has profound effects on the hypothalamus and is involved in the metabolic hormonal regulation of exercise and training. Muscle damage and repair processes may involve the expression of inflammatory cytokines (e.g. tumour necrosis factor-alpha, TNF-alpha) and of stress proteins (e.g. heat shock protein 72). During overreaching and overtraining, a myopathy-like state is observed in skeletal muscle with depressed turnover of contractile proteins (e.g. in fast-type glycolytic fibres with a concomitant increase in slow type myosins). These alterations are influenced by exercise-induced hypercortisolism, and by decreased somatotropic hormones (e.g. IGF-I). The hypothalamus integrates various error signals (metabolic, hormonal, sensory afferents and central stimuli) and therefore pituitary releasing hormones represent the functional status of an athlete and long-term hypothalamic hormonal and sympathoadrenal downregulation are some of the prominent hormonal signs of prolonged overtraining and performance incompetence syndrome."
Any chance you could expand on that? I remember in previous threads that you mentioned that the idea of CNS fatigue was fallicious. What occurances in the body/possibly mind do you believe we are actually observing when we experience what we call ‘CNS fatigue’. I believe it was you and James in another thread that described CNS fatigue as inhibition. Any idea on why this inhibition takes place? And also, any idea on the real world applications of ‘inhibition rather than true fatigue’ in the planning of training?
To get back to the original intent of this topic (not that the other discussions that have arisen don’t have merit)…
Yes, RFD and speed-strength can experience the delayed training effect.
Whether or not a concentrated loading block is more effective than a distributed loading block depends on the level of the athlete. If acceptable results are being seen from distributed loading, then there is no need to incorporate concentrated loading. Concentrated loading blocks were developed for the purpose of increasing traits in those athletes who no longer respond to distributed loading.
Verkhoshansky discusses the specifics of concentrated loading in his training manual “Special Strength Training,” with the caveat that it is only for advanced athletes.
Why this may happen in the first place though? Thanks!
The organization of the load is a specific stressor to which the athlete can adapt.
Just as long-term exposure to any stressor (a particular exercise, set or rep scheme, etc.) will render it of insignificant strength to induce adaptation, so too can the long-term use of a particular loading structure.
Concentrated loading gives the athlete a new stressor to adapt to. It is not the only way to elicit positive adaptations in an athlete who is no longer responding to “typical” training protocols, but another tool that can be utilized.
very interesting. Thanks for the reply
A brief summary:
1: Those who are likliest to need concentrated loading are also those who are least likely to have a problem with it.
2: The duration of the concentrated load varies by event demand. For example RFD (shorter) vs Absolute Strength (longer), even though none is very long overall, even though absolute str events are usually to the left of RFD events.
3: The likeliest candidates have events concentrated to the left of the F/T curve, moving from Left to Right. For example, a 100m man will be more likely to need and thrive on concentrated loading than a 400m man.
4: Concentrated loading can be done in ANY of the High Intensity elements of the program, not just weights, and, if it is done in one place, it should be avoided in others during that period, with the exception of slight overlaps in events to the far Left.
Due to the effects of fatigue (+residual) during the block is this type of training realistic. A 100m man times are going to be very poor and there is more chance of injury. Is it worth the risk? Clearly many have succeeded without resorting to the concentrated approach.
what if it goes the other way? IE the 100man competes 3 x per week for 5 to 6 meets? That could be considered a concentrated load also. The weight load concentration is likeliest to occur early in an SPP in an S-to-L program, if done, when short accel can be emphasized and speed limited.
It’s worth the risk if the athlete is not responding to other loading parameters. And as Charlie said, those who need concentrated loading are also those who are best prepared to handle its effects.
Of course the times will be poor during this block, but as Charlie said this type of training block is to be used during the SPP, not the competitive phase. This will allow the delayed training effect to be realized during the competitive period.
This is one advantage to concentrated loading for speed-strength athletes, as their strength will be high during the competitive phase without the detrimental effects of heavy loading on the CNS. Another modality some have suggested to elicit this same effect is EMS during the competitive phase to maintain strength without stressing the CNS.
Charlie, what are your thoughts on this use of EMS?
The good side of the EMS is the lack of CNS conflict but there are coordination issues which lead me to prefer to use it earlier in the SPP as you’ve seen illustrated unless there is an injury issue.
Charlie, was Maximum Strength along with EMS the only concentrated loading phase/component you used? Thanks!
Charlie I have been rereading the forum review and CFTS and I am still confused how you mix max strength in the SPP.
You say no max strength in GPP, hypertrophy and AA weights.
Max strength w/ EMS during the first 7 weeks of SPP,
BUT
You need to be in a maintenance phase to really increase max speed and max strgth is to be done when accel is focused (which I would have believed was GPP).
Can you clarify this issue?
You are still working accel first in the SPP and for higher level athletes, where this is mostly required, the GPP tends to be short in phase one, very short in phase two, and mostly active rest in phase three. Even when the runs are longer, they can be controlled by the distance over which you accelerate. The level of stress to be tolerated in other componants varies with the athlete. AND the level of gain sought in the concentration phase is constantly being reduced in ALL elements.
That explains why I have sub optimal speed sessions when I introduce EMS into my training. It definitely feels like a coordination issue because it is definitely not overtraining/cns exhaustion.