Thanks to all who made contributions. Along with the original query, they
are listed below.
Original query:
Dear Subscribers,
There have been two articles in the literature (Rose et al., J. Orth. Res.
12 758-68 and Ito et al., Brain and Development 18: 299-303) suggesting that
there is a predominance of type-I fibres in gastrocnemius muscle of children
with spastic cerebral palsy, possibly due to the altererd patterns of
stimulation that these muscles receive. Because of the slower dynamic
qualities of these muscles it is possible that they exacerbate the poor
motor abilities that these children possess.
It has been suggested to me that transformation of type-I to type II fibres
may occur with high intensity exercise or high intensity electrical
stimulation. It makes soem sense, but does anybody know of reported data to
support this view?
I'd be grateful for any help.

Adam Shortland PhD
One Small Step Gait Laboratory

Take a look at:

Skeletal muscle adaptation to chronic low-frequency motor nerve stimulation.
AUTHORS: Kraus WE, Torgan CE, Taylor DA
SOURCE: Exerc Sport Sci Rev. 1994;22:313-60. Review

It is an excellent review and should get you going.

James C. Martin
Assistant Professor
Department of Exercise and Sport Science
University of Utah
Check Astrand and Rodahl Textbook of work physiology. I'm not sure, but it
may be there.
Beverly Burke RN CMA CIE
I know of no evidence to support the inference that ES will assist in a
transfer of Type I to Type II.

The evidence would suggest that long term training may slow muscle
characteristics down (suggesting a response to the stimulus which
parallels the suggested Type II - I change). The possible reason for this
is that during submaximal stimulation the fast twitch fibres tend to be
activated. (loosely following the principle of reverse recruitment order),
with long-term low grade activations the metabolic charactertistic of the
muscle tend to be more endurance orientated. - hence a "shift to slow".

other points for consideration.

1. I'm not sure of the reason why High intensity would tend to speed up the
fibre twitches - There is a suggestion that the recruitment of fibre type
is reversed with ES. Increasing the intensity would just target more Slow
twitch fibres.

2. Using frequency to modulate the "intensity" may have a slightly
different effect by altering when certain fibres contract tetanically -
obviously this has an upper limit and increased frequency may increase the
chance of "cramp" and / or frequency dependent fatigue. ("calcium washout"
I think is partially the mechanism?). This type of ES would not be
considered 'functiona;" and would probably mean to target a specific
neurological response or to strengthen the muscle.

3. the relative responses of muscle in a training situation are relative to
the stimulus it receives in the process of normal activity. For example in
individuals with SCI the decreased activation of muscles with an UMNL is
relatively low and 8 hours a day of ES represents a signficiant training
stimulus resulting in a relatively large training response. Therefore, one
would have to be concerned as to the relative training stimulus an ES
program would have on a child with CP who is functionally active (or may
have a high level of tone even at rest) and has normal sensation and
compliance :-).

4. The differences in the rate of torque production of the gastrocnemius in
a "predominantly slow twitch" vs. a gastrocnemius with a "predominantly
fast twitch" is clinically insignficiant in the functional outcome of gait.
In the circumstance where there is a limitation to the ability to
co-ordinate agonists and antagonists during a ballistic action (or some
degree of velocity sensitivity to muscle length changes - spastcity) then
the rate of force production as determined by twicth fibre type in my
opinion can not be clinically significant for an activity like walking.

5. The sensory impact of high intensity ES in CP child may have more effect
on the central mechanisms than the peripheral (muscle fibres). For example,
synergies of the motor patterns for gait may be altered. In some
circunstances it may improve the gait by creating muscle fatigue in a
muscle which is inapprorpiately active, it may facilitate voluntary
activation of the muscle or it's synergists or indeed it may create a
inhibitory effect of the antagonistic that may or may not be a problem.

In summary, I'm not sure the predominance of fibre type in the gastroc. has
a significant impact on the function of CP gait over and above the central
motor control dysfunction. The fibre type is probably a reflection of the
stimulus the muscle receives. ES may have an impact but not for the reason
of muscle fibre transformations.

Just my opinion and 2 cents worth.

Garry T Allison (A/Professor of Physiotherapy)
The Centre for Musculoskeletal Studies
Department of Surgery, The University of Western Australia.

Dear Dr. Shortland,
I received you query second hand, thus the delay. I imagine you have had
a wealth of response. I seem to recall one paper, probably back in the
1970's, that reported changing muscle fibers from slow to fast. The paper
was never substantiated, and I don't recall the authors, so they probably
didn't publish a lot more, further casting doubt on their work. Most of
the literature on fiber type conversion (true conversion for one class to
the other) says that ES as it is conventionally used shifts fibers toward
being slow. The little bit of human work and most of the animal work
definately demonstrates the shift from fast to slow when adequate levels of
stimulation are used.
The one other thought I had is that Dr. Daniel Kernell had some
preliminary work attempting to maintain muscle power during prolonged
inactivity. He was using a hybrid stimulation program of high intensity,
short duration (presumibly challinging the largest, fastest fibers) along
with the more common long duration stimulation. I don't recall that he did
any fiber typing. The paper I reference for this was in J Neurophys
58:598-613, 1987. I looked for anything more recent about a year ago, but
I haven't checked for anything in the last several months.
It is my understanding that voluntary exercise, no matter the intensiy,
really doesn't cause fiber type shift from slow or fast. There are changes
within the fast fiber type, but no clear cut shift to slow. I have seen
nothing that would indicate slow fibers shifting to fast ones under
voluntary exercise conditions.

Lucinda L. Baker PT PhD
Department Biokinesiology & Physical Therapy
University of Southern California

In response to your query, there is a review article from 1991 (Roy, Baldwin
and Edgerton, 1991. The plasticity of skeletal muscle: Effects of
neuromuscular activity, Exercise and Sport Sciences Reviews, 19, 269-312)
which goes into detail as to myosin heavy chain changes found in various
animals e.g. cats and rats, when subjected to various protocols, from
suspended limb inactivity to neuromuscular electrical stimulation.

There is also a recent article that goes towards fibre type changes after a
period of bed rest, although these changes were only found at the gene
level, not at the protein level. Therefore it could be proposed that a
longer period of bed rest may elicit more demonstratable changes from type 1
to type 2 fibres.

A study that has demonstrated the changes in fibre types is:
{PRIVATE}Andersen and Aagaard (2000). ,Myosin heavy chain IIX overshoot in
human skeletal muscle. Muscle Nerve; 23(7):1095- 104. Apparently JL Andersen
from the muscle research group in Copenhagen has done a fair amount of work
in this area, so I guess that he's your man.

I hope that these little suggestions are of assistance.

Chris Swann,
MSc Sport and Exercise Science (Biomechanics),
School of Sport Science,
University College Chichester,
College Lane,
West Sussex PO19 4PE,
United King dom.

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