This thread is open for comments on postings on EMS Theory. More installments will follow.
why dont you just write up a article and have rupert post it?
I prefer doing it this way.
Charlie thinkd differently:
EMS reverses the natural recruitment order, as its nonspecific current flows more easily through the bigger neuron of the white fiber (less resistance) forcing red and intermediate fibers to shorten their recruitment rates in response to white fiber recruitment, which now precedes rather than follows in the contraction.
thoughts?
You and Charlie are correct about the fact that EMS disrupts the voluntary recruitment order. That particular paragraph posted in EMS theory refers to voluntary contractions not to EMS. I will modify the paragraph to clarify it.
I appreciate your feedback. It helps me refine my script. I may have mentioned that the thread on EMS theory is a digest of an Italian book exclusively on EMS. In an effort to be concise some paragraph have been orphaned of parts of their context.
It will be explained in future installments that rather than reversing voluntary recruitment, EMS is indiscriminate in activating neurons. What discriminates between the different types of fibers is frequency.
OK! It wasn’t clear.
Have you anymore evidence relating to the myosin HC expression change. Literature regarding heavy weight training suggest adaptions are IIB -> IIA. You quoted some literature relating to this phenomenon in EMS… can you expand.
BTW Charlie’s system uses 2 week EMS blocks, I imagine these blocks are to short for this type of adaption, which may not happen at all with all the high int’ sprint work performed.
Yeah, Charlie discusses this in the latest EMS podcast. The strength gains are very quick and there is likely insufficient time for significant structural adaptation. Charlie ties strength gains in with EMS’s ability to modify muscle tone.
Is there a link to this Podcast, was it free?
Hello UKcheetah,
For a study on muscle plasticity showing a fiber type shift 2b -> 2a (it seems that researchers are replacing the notation 2x for 2b), see: Maffiuletti et al., Neuromuscular Adaptations to Electrostimulation Resistance Training, 2006 American Journal of Physical Medicine & Rehabilitation; the study employed EMS at 75 Hz.
For a study showing the opposite change, fiber type 2a -> 1, see Nuhr et al., Functional and biochemical properties of chronically stimulated human skeletal muscle, 2003 European Journal of Applied Physiology; the study employed 15 Hz EMS.
The first study was conducted over 4-8 weeks, and its author suggested that previous studies limiting EMS to 4 weeks were not able to produce significant results.
Best regards,
Giovanni Ciriani
There is tone change almost immediately but also fibre shift based on the plasticity suggested here BUT I suspect the shift from IIa to IIx can occur more quickly than initially imagined because there are multiple means to this end, and picture EMS playing the role of a catalyst in this overall interaction.
The podcast on EMS will be released very shortly.
The podcasts sound a great idea - keep up the good work!
Charlie,
the study I quoted measured experimentally on the subject a shift 2x to 2a at 75 Hz. You suspect the opposite shift 2a to 2x; at what frequency?
Giovanni Ciriani
I am referring to the complimentary interplay between EMS and the other high intensity stimulae in this conversion from 2a to 2x.
Sorry for any misunderstanding- I used a freq of 120 where possible
As a novice in EMS, what is the difference between EMS and a TENS unit? Could a TENS be used in place of EMS?
The main difference is the pulse width. TENS is not supposed to contract muscles, and employs lower widths. EMS contracts muscles and employs longer pulse widths.
The theory thread explains the role of pulse widths, and how it relates to the chronaxie of the muscle. Generally TENS goes up to 200 microseconds, whereas EMS needs to go up to 450 microseconds. TENS only need to excite pain nerves (nociceptive neurons). EMS need to excite motor nerves. There are also other differences, like on/off (work/rest) cycles, but in general TENS, given their goal to mask pain, and because they do not contract muscles, can stay on continuously. There are other secondary effects, but the above are the main ones.
This post is superseded by a later post by Dan Partelly. It has been preserved for thread history integrity. Click on the link to go directly to his post. Giovanni Ciriani.
I may be incorrect, but I think we should distinguish between muscle plasticity and muscle adaptation.
Muscle adaptation is the faster change in muscle fiber strength, which starts occurring within two weeks from the beginning of training. I think this is what Charlie was referring to in a previous post in this thread. In muscle adaptation, the number of fibers remain the same. Their cross section increases, which explains the strength increase and the bulk increase.
Muscle plasticity is different from muscle adaptation; it’s a longer-term change in muscle composition, which probably takes at least 6 weeks (according to research). It involves a change of muscle fiber numbers, as well as their size (cross section). This causes a much larger increase in muscle strength.
It was greatly debated in the past, whether healthy muscles were capable or not of plasticity. Most practitioners and researchers believed that muscles were not plastic. That is, they believed an athlete’s muscle endowment was genetically determined, and would not change with training. In other words, the number of muscle fibers would remain the same, and the athlete would only be able to increase the size of individual cells. According to this belief, an endurance athlete would never become a sprinter, and vice versa.
However, research performed during the current decade has shown positive proof that slow-twitch fibers can be transformed into fast-twitch fibers and vice versa. Although a marathon runner would not be able to become a sprinter, being able to transform a percentage of slow-twitch fibers into fast-twitch fibers makes a difference at professional level.
Changing muscle composition, takes a longer training course, and it requires an exact understanding of what the goal is. That’s why it’s important that we use the right terminology, so that we are not misunderstood.
The pad placement pictures Colour of the leads are confusing.
With my machine, the Ends of the leads are colour coded so as not to get confused - ie red for active and black for neutral.
Here we have blue n yellow but blue is neither positive nor neutral?? How do you tell?
Each color is for a different muscle group: both yellow go on the same muscle group and both blue go on a different muscle group. Active or inactive electrode depends on its position on the muscle, but it doesn’t matter whether the electrode is marked + or -. This is explained in the section.
As a consequence, if your electrostimulator has a symmetrical waveform, you can swap the red lead with the black lead and nothing would change.
I hope this responds to your question.
Giovanni Ciriani
Thanks man for the speedy reply
Very important to use right terminology, I agree. Therefore:
Altered gene expression (in effect to certain training loads) results in variations (increase / decrease) in the amount of specific proteins in muscle (an adaptive change).
The capacity for adaptive change of the skeletal muscle is termed myoplasticity.
Please note that its an adaptive phenomena.
The definitions you use are wrong. Faster of slower changes in muscle are both adaptations.
Capacity for such adaptations is plasticity.
Research showing transition from type I to type II is not conclusive yet. It appears that
voluntary effort (hence usual training loads)does not cause such shifts.
However, cross-innervation and cross-transplantation experiments , and direct stimulation with various frequencies show that its possible to alter MHC expression.
EMS is a very good candidate for this.