PRACTICAL
SIGNIFICANCE
Soleus
spinal
stretch
reflex (SSR)
latency
and
amplitude
were not
affected
by
varying
levels
of
triceps
surae
(TS)
stiffness.
Low
levels
of
muscle
stiffness
require
greater
neural
drive to
the
muscle
spindle
to reach
these
set
points,
while
high
levels
of
muscle
stiffness
require
less
neural
drive to
the
muscle
spindle.
These
results
may
suggest
that
rehabilitation
programs
aimed at
improving
dynamic
joint
stability
should
incorporate
increases
in
muscle
stiffness.
STUDY
BACKGROUND
Muscle
stiffness
provided
by the
series
elastic
element
potentially
contributes
to joint
stability
from
both
mechanical
and
neuromuscular
perspectives.
The
spinal
stretch
reflex (SSR)
is a
component
of
neuromuscular
control,
which
contributes
to joint
stability.
Sensitivity
of the
spinal
stretch
reflex
operates
on a
set-point
basis,
whereby
the
latency
and
amplitude
responses
of a
muscle
are
functions
of its
stiffness
and
neuromotor
drive.
Increased
muscle
stiffness
may
heighten
SSR
sensitivity
via
enhancement
of the
mechanical
coupling
of the
muscle
spindle
and the
stretch
reflex
stimulus.
A
reflexive
response
of
greater
magnitude
in a
timelier
manner
following
the
onset of
joint
perturbation
may
allow
for
enhanced
dynamic
joint
stabilization.
OBJECTIVE
To
determine
if
higher
series
elastic
muscle
stiffness
would
shorten
soleus
spinal
stretch
reflex
latency,
while
increasing
its
amplitude
during a
mechanical
perturbation.
DESIGN
AND
SETTING
Triceps
surae
(TS)
muscle
group
stiffness,
the
soleus
Hoffmann
reflex
(H-reflex),
and the
soleus
SSR
responses
were
compared
between
males
and
female.
All
testing
was
performed
in the
Sports
Medicine
Research
Laboratory
at the
University
of North
Carolina
at
Chapel
Hill.
SUBJECTS
Twenty
males
(ht =
1.81±0.06
m, mass
=
81.83±12.21
kg, age
=22±3
yrs) and
20
females
(ht
=1.67±0.07
m, mass
=
63.55±9.84
kg, age
= 22±3
yrs)
participated.
MEASUREMENTS
TS
stiffness,
the
soleus
H-reflex,
and the
soleus
SSR were
compared
across
sex. TS
stiffness
was
estimated
from the
damped
frequency
of
oscillation
of the
shank
about
the
ankle
following
perturbation.
The
soleus
Hreflex
was
elicited
by
electrically
stimulating
the
tibial
nerve,
providing
an
indication
of total
motorneuron
pool
excitability.
The
soleus
SSR was
evoked
via
mechanical
ankle
dorsiflexion
perturbation.
For each
assessment,
subjects
were
seated
with the
soleus
active
to
~15%MVC.
RESULTS
TS
stiffness
was
significantly
greater
in males
than in
females
(t38 =
6.160, P
<
0.001),
thus
verifying
high
(males)
and low
(females)
stiffness
groups.
Soleus
H-reflex
latency
(F1,37
=0.030,
P =
0.862;
ANCOVA,
covariate
= leg
length)
and
amplitude
(t38 =
0.412, p
=
0.683),
and SSR
latency
(F1,37 =
0.026, P
= 0.872;
ANCOVA,
covariate
= leg
length)
and
amplitude
(t38 =
0.755, P
=0.455)
were not
significantly
different
between
stiffness
groups.
Similarly,
the
respective
relationships
between
TS
stiffness
and
soleus
SSR
latency
(r =
0.072, P
= 0.659)
and
amplitude
(r =
0.047, P
= 0.772)
were not
significant.
CONCLUSIONS
Similarity
of SSR
latency
and
amplitude
across
varying
levels
of
muscle
stiffness
was due
to the
combined
effects
of
series
elastic
stiffness
and
neural
drive to
the
muscle
spindle
to
achieve
set-point
values
for SSR
latency
and
amplitude
for
standardized
testing
conditions.
Given
the
limited
sample
variability
in SSR
latency
and
amplitude
and the
relationship
between
muscle
stiffness
and
neural
drive to
the
muscle
spindle
suggested
by
previous
literature,
these
results
indicate
that low
levels
of
muscle
stiffness
require
more
neural
drive to
the
muscle
spindle
to
attain
SSR
latency
and
amplitude
set
points
compared
to high
levels
of
stiffness.
Publication
and
Presentation
List:
-
NATA
Annual
Meeting,
Baltimore,
MD,
June
15-19,
2004
|
J. Troy Blackburn, PhD, ATC
Principal Investigator
|
Troy Blackburn received a B.A. in Exercise and Sport Science (Athletic Training Concentration) from the University of North Carolina at Chapel Hill (1998), a M.S. in Sports Medicine from the University of Pittsburgh (2000), and a Ph.D. in Human Movement Science (Biomechanics Concentration) from the University of North Carolina at Chapel Hill (2004). He joined the Department of Exercise and Sport Science as an assistant professor in the fall of 2006. He currently serves as the director of the Motor Control Laboratory, and teaches courses in Research in Exercise and Sport Science and Neuromuscular Control and Learning |
|
J. Troy Blackburn, PhD, ATC
Sports Medicine Research Laboratory
The University of North Carolina
CB# 8700, Fetzer Gymnasium South Road
Chapel Hill, NC 27599
Phone:: 919.962.7187
Fax:
919.962.0489
Email:
troyb@email.unc.edu
|
|
This Grant Information Summary may be downloaded in a 2-page pdf file from http://www.natafoundation.org/refgrants/Blackburn.pdf. |
Back to
November 28, 2006
eBlast
Newsletter
Send e-mail
to johno@nata.org with questions
or
comments
about this web site. |