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D Ferris
02-06-1997, 01:07 PM
Here is the summary of replies concerning the role of Golgi tendon
organ inhibition during maximum voluntary contractions. Thanks to all
those who replied.

df

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ORIGINAL POSTING:

A topic of recent interest has been the difference between the
maximum force generating capacity of a muscle group and the measure of a
maximum voluntary contraction (MVC). Enoka and Fuglevand (1992) discuss
several lines of evidence which support a difference, including neural
adaptations with training, neural insufficiency, and neural
supplementation. More recently, Winter (1996) states that "because of the
inhibitory feedback from the Golgi tendon organs it is virtually impossible
to recruit all motor units at their maximum firing rates."

My question is this, have there been any studies directly examining
the role of Golgi tendon organ inhibition on either muscle activation or
force production during an MVC? I have tried database searches and
reference searches from reviews (Jami, 1992) without much luck.

References

Enoka, R.M. and A.J. Fuglevand (1992) Neuromuscular basis of the maximum
voluntary force capacity of muscle. In: Current Issues in Biomechanics
(ed. Mark Grabiner), pp. 215-235.

Jami, L. (1992) Golgi tendon organs in mammalian skeletal muscle:
functional properties and central actions. Physiol. Rev. 72:623-666.

Winter, D. (1996) EMG interpretation. In: Electromyography in Ergonomics
(ed. S Kumar and A. Mital), pp. 109-125.



Thanks for your help.

df

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Daniel P. Ferris
UC Berkeley Locomotion Laboratory
3060 Valley Life Sciences Building
University of California
Berkeley, CA 94720-3140

dferris@uclink2.berkeley.edu
http://garnet.berkeley.edu/~hbbiomxl/dferris/

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REPLIES:

Several people suggested I read the Crossbridges posting by T. Richard
Nichols on the Neuromuscular Control Web Site:

http://www.activemed.com/neuromus

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>From Brian Bergemann :


I did a dissertation at Penn State University in 1975. I had 21
subjects and I was looking at the maximum rate of tension development in the
quadriceps femoris muscle group. There was an anomalie in the laboratory
with very rapid force development phases in isometric contractions,
resulting in an oscillation of the force time curve during the rise phase.
I thought that it might be due to autogenic inhibition. There were four
testing sessions per subject with a 48 hour period between sessions. Each
session consisted of a 2 second contraction followed by 58 seconds of rest.
The computer controlled the timing, the 5 second warning light and the
buzzer that signalled the subject to contract maximally and as rapidly as
possible. The MVIC force time curves were electronically recorded on reel
to reel 8 track scientific recording tape. A channel was devoted to the
first derivative of the FT curve, two channels were devoted to the agonist
muscles (rectus femoris and vastus lateralis) and two antagonist muscles
(semimembranosis and short head of biceps femoris). I hypothesized that if
there was autogenic inhibition there would be a silent period preceding the
oscillation. A secondary hypothesis was that the oscillation could have
been due to a reciprocal innervation from a rapid slight stretch of the
hamstrings during the isometric extension attempt.

In processing the data, the first derivative of the forcetime curve was very
revealing. The oscillations in the FT curve produced very prominent maximum
and minimum values in the first derivative. These max and min values
constituted the changes in the rate of tension development and served as the
key variables. The first max value was the max rate of tension development,
the first min value was the drop in the rate of tension development. This
sometimes was negative, because the rate actually dropped. It sometimes
stayed positive, when the rate changed slightly, but did not decrease. The
correlation between the max dF/dt and the drop from max dF/dt to min dF/dt
was .95. The higher the max dF/dt the greater the drop. That was a
remarkable finding. However, when I compared this with the IEMGs from the
electromyograms there were no significant drops in IEMG during the period
just prior to the drop in dF/dt. There also were no bursts of IEMG just
prior to the drop in dF/dt in the antagonist muscles. If golgi tendon organ
response would have been inhibiting the MVIC at the point of greatest dF/dt
it would have shown up in the IEMGs of the agonists and antagonists.
Similar dips in the isometric force time curves were apparent in the works
of Kaneko from Japan and Wartenweiler from Switzerland. I contacted Kaneko
and he believed these dips to be related to the elastic recoil of the
quadriceps muscle.

I hope this sheds some light on your inquiry. My dissertation is in
microfiche from University of Oregon or available through interlibrary loan.
The date of the dissertation was 1977, and the title was the "Effects of
Practice and Pretension on the Rate of Tension Development in Muscle."

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>From Charles T Leonard :


We are currently examining indirectly the role of short and long latency
relfex pathways, including Ibs during voluntary contractions.
Unfortuantely technically not possible to examine MVC. Max we have been
able to do is 50% MVC. Try doing a medline search using electrical
stimulation as your key words. I know there is some work out there e.g.
athletes can volutarily perform MVC, disabled cannot etc.

Chuck Leonard PT,PhD
Director, Motor Control Research Laboratory
The University of Montana
Missoula, MT 59812 USA
Phone (406) 243-2710
FAX (406) 243-2795
Email LEONARD@SELWAY.UMT.EDU

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>From T. Richard Nichols :

GTO's don't always lead to
inhibition. There are excitatory pathways at work also. Second,
even in the presence of inhibition, one should be able to reach
maximum with a larger driving signal. This extra excitation is
simply the price one pays for having the force loop intact. I
suspect a more central location for the constraint on maximum force
production. See references by Bigland Ritchie on this topic. Also,
see my article in Crossbridges for more details and references on
tendon organs.

Sincerely,
Richard Nichols

T. Richard Nichols
Department of Physiology
Emory University
Atlanta, GA 30322
(404)727-7406
(404)727-2648 FAX
trn@physio.emory.edu

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Daniel P. Ferris
UC Berkeley Locomotion Laboratory
3060 Valley Life Sciences Building
University of California
Berkeley, CA 94720-3140

dferris@uclink2.berkeley.edu
http://garnet.berkeley.edu/~hbbiomxl/dferris/

Tel (510) 642-8662
Fax (510) 643-6264
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