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Electrical Stimulation In Muscular Dystrophy
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Tong K.Y. and Mak A.F. (2001)
Development of computer-based environment for simulating the voluntary
upper-limb movements of persons with disability. Med. Biol. Eng Comput.
39, 414-421.
Abstract: Upper-limb orthotic systems have been designed for restoring the
upper- limb functions of individuals with disabilities resulting from spinal
cord injury (SCI), stroke and muscular dystrophy. These systems employ either
functional electrical stimulation or external power. It is proposed that,
instead of time-consuming and complicated monitoring using sensors and motion
analysis, a software simulator with both angular displacement and acceleration
parameters can facilitate the design of a control strategy for an orthosis.
Reaching movements of three cervical SCI subjects are used to verify the
simulator. A motion analysis system is used to measure the range of motion and
joint angles during hand reaching. Results indicate that quaternion and spline
curve techniques are suitable for interpolation of the hand reaching movements.
The information needed for good simulation only compress the shoulder and elbow
joint angles in a few key postures. Stimulated acceleration signals on the
upper-arm segment have a high correlation coefficient (> 0.9) and a small root
mean squared error (< 0.11 g) with a real bi-axial accelerometer
Yang B., Verbavatz J.M., Song
Y., Vetrivel L., Manley G., Kao W.M., Ma T., and Verkman A.S. (2000) Skeletal
muscle function and water permeability in aquaporin-4 deficient mice. Am. J.
Physiol Cell Physiol 278, C1108-C1115.
Abstract: It has been proposed that aquaporin-4 (AQP4), a water channel
expressed at the plasmalemma of skeletal muscle cells, is important in normal
muscle physiology and in the pathophysiology of Duchenne's muscular dystrophy.
To test this hypothesis, muscle water permeability and function were compared in
wild-type and AQP4 knockout mice. Immunofluorescence and freeze-fracture
electron microscopy showed AQP4 protein expression in plasmalemma of fast-twitch
skeletal muscle fibers of wild-type mice. Osmotic water permeability was
measured in microdissected muscle fibers from the extensor digitorum longus (EDL)
and fractionated membrane vesicles from EDL homogenates. With the use of
spatial-filtering microscopy to measure osmotically induced volume changes in
EDL fibers, half times (t(1/2)) for osmotic equilibration (7.5-8.5 s) were not
affected by AQP4 deletion. Stopped-flow light- scattering measurements of
osmotically induced volume changes in plasmalemma vesicles also showed no
significant differences in water permeability. Similar water permeability, yet
approximately 90% decreased AQP4 protein expression was found in EDL from mdx
mice that lack dystrophin. Skeletal muscle function was measured by force
generation in isolated EDL, treadmill performance time, and in vivo muscle
swelling in response to water intoxication. No differences were found in EDL
force generation after electrical stimulation [42 +/- 2 (wild-type) vs. 41 +/- 2
(knockout) g/s], treadmill performance time (22 vs. 26 min; 29 m/min, 13 degrees
incline), or muscle swelling (2.8 vs. 2.9% increased water content at 90 min
after intraperitoneal water infusion). Together these results provide evidence
against a significant role of AQP4 in skeletal muscle physiology in mice
Goldspink G. (1999) Changes in
muscle mass and phenotype and the expression of autocrine and systemic growth
factors by muscle in response to stretch and overload. J. Anat. 194 ( Pt
3), 323-334.
Abstract: The study of the underlying mechanisms by which cells respond to
mechanical stimuli, i.e. the link between the mechanical stimulus and gene
expression, represents a new and important area in the morphological sciences.
Several cell types ('mechanocytes'), e.g. osteoblasts and fibroblasts as well as
smooth, cardiac and skeletal muscle cells are activated by mechanical strain and
there is now mounting evidence that this involves the cytoskeleton. Muscle
offers one of the best opportunities for studying this type of
mechanotransduction as the mechanical activity generated by and imposed upon
muscle tissue can be accurately controlled and measured in both in vitro and in
vivo systems. Muscle is highly responsive to changes in functional demands.
Overload leads to hypertrophy, whilst decreased load force generation and
immobilisation with the muscle in the shortened position leads to atrophy. For
instance it has been shown that stretch is an important mechanical signal for
the production of more actin and myosin filaments and the addition of new
sarcomeres in series and in parallel. This is preceded by upregulation of
transcription of the appropriate genes some of which such as the myosin isoforms
markedly change the muscle phenotype. Indeed, the switch in the expression
induced by mechanical activity of myosin heavy chain genes which encode
different molecular motors is a means via which the tissue adapts to a given
type of physical activity. As far as increase in mass is concerned, our group
have cloned the cDNA of a splice variant of IGF-1 that is produced by active
muscle that appears to be the factor that controls local tissue repair,
maintenance and remodelling. From its sequence it can be seen that it is derived
from the IGF-1 gene by alternative splicing but it has different exons to the
liver isoforms. It has a 52 base insert in the E domain which alters the reading
frame of the 3' end. Therefore, this splice variant of IGF-1 is likely to bind
to a different binding protein which exists in the interstitial tissue spaces of
muscle, neuronal tissue and bone. This would be expected to localise its action
as it would be unstable in the unbound form which is important as its production
would not disturb the glucose homeostasis unduly. This new growth factor has
been called mechano growth factor (MGF) to distinguish it from the liver IGFs
which have a systemic mode of action. Although the liver is usually thought of
as the source of circulating IGF-1, it has recently been shown that during
exercise skeletal muscle not only produces much of the circulating IGF-1 but
active musculature also utilises most of the IGF-I produced. We have cloned both
an autocrine and endocrine IGF- 1, both of which are upregulated in cardiac as
well as skeletal muscle when subjected to overload. It has been shown that, in
contrast to normal muscle, MGF is not detectable in dystrophic mdx muscles even
when subjected to stretch and stretch combined with electrical stimulation. This
is true for muscular dystrophies that are due to the lack of dystrophin
(X-linked) and due to a laminin deficiency (autosomal), thus indicating that the
dystrophin cytoskeletal complex may be involved in the mechanotransduction
mechanism. When this complex is defective the necessary systemic as well as
autocrine IGF-1 growth factors required for local repair are not produced and
the ensuing cell death results in progressive loss of muscle mass. The discovery
of the locally produced IGF-1 appears to provide the link between the mechanical
stimulus and the activation of gene expression
Rodriguez R.H., Cruz C.F.,
Iturralde T.P., de Micheli A., and Gonzalez Hermosillo J.A. (1997) [Persistent
atrial paralysis: reported of 2 cases]. Arch. Inst. Cardiol. Mex. 67,
498-502.
Abstract: Persistent atrial standstill is an uncommon clinical finding, this
condition has no atrial electrical activity and do not respond to electrical
stimulation. Electrophysiologic mapping of the heart, demonstrates two types of
standstill: total and partial. There are three types of patients with this
condition: patients with chronic cardiopathy, patients with muscular dystrophy
and the third idiopathic group. In this article, we present two clinical cases,
the fist one with dilated cardiomiopathy, in which we demonstrated total atrial
standstill. The second patient with rheumatic heart disease, in which we
demonstrated partial standstill that included the apical portion of the rigth
atrium. We discuss the clinical and electrophysiological finding of both cases
and we review the literature
Yoshida M., Matsuzaki T., Date
M., and Wada K. (1997) Skeletal muscle fiber degeneration in mdx mice induced by
electrical stimulation. Muscle Nerve 20, 1422-1432.
Abstract: We present an in vitro model in which mouse skeletal muscle fibers
undergo degeneration by increasing the current strength of tetanic stimulation.
To understand the mechanisms of muscle fiber necrosis in Duchenne muscular
dystrophy patients, the process of fiber degeneration was compared between mdx
and control mice. The process consisted of four steps, beginning with muscle
fiber contraction and extending to onset of myofibril disruption. The four
processes were not observed in fibers in Krebs-HEPES (-Ca2+) buffer, nor in the
presence of L-type Ca2+ channel blockers. These results suggest that this
degenerative phenomenon is regulated by intracellular Ca2+, which moved into
fibers mainly through voltage-dependent L-type Ca2+ channels. With the exception
of myofibril disruption, mdx mice also exhibited the three other steps, but at a
significantly lower current strength than in the fibers in the control mice. We
postulate that excess Ca2+ flux occurs in fibers, mainly through abnormal L-type
Ca2+ channels, and that the excessively accumulated calcium results in premature
degeneration of the fibers by tetanic contraction. This study would provide a
clue to investigate and prevent the degeneration processes in Duchenne muscular
dystrophy
Zupan A., Gregoric M., Valencic
V., and Vandot S. (1993) Effects of electrical stimulation on muscles of
children with Duchenne and Becker muscular dystrophy. Neuropediatrics 24,
189-192.
Abstract: Twelve children with progressive muscular dystrophy (10 Duchenne and 2
Becker type) were included in a low-frequency electrical stimulation (LFES)
program of the right tibialis anterior (TA) muscle for three months. Muscle
strength was estimated by measuring torques in the ankle during short attempts
of maximal voluntary isometric contraction (MVIC) in the direction of dorsal
flexion of the foot. Muscle fatigue was assessed by the decrease of force during
sustained (1-minute) voluntary contraction. The measurements were carried out
before the beginning of the stimulation program and immediately after its
conclusion. At the end of the stimulation program there were higher torques in
10 out of 12 children in the stimulated leg. The increase in torques in the
stimulated leg was statistically significant (p < 0.01). Regarding the fatigue
of the stimulated muscle there was no change after the conclusion of stimulation
Zupan A. (1992) Long-term
electrical stimulation of muscles in children with Duchenne and Becker muscular
dystrophy. Muscle Nerve 15, 362-367.
Abstract: Nine children suffering from progressive muscular dystrophy (7
Duchenne and 2 Becker) were included in a program of low-frequency electrical
stimulation (LFES) of the right tibialis anterior (TA) muscle. Muscle strength
and muscle fatigue were estimated by measuring torques in the ankle during
attempts of maximal voluntary contraction (MVC) in the direction of dorsal
flexion of the foot and during electrically evoked contractions (EEC). No
important increase in the strength of the stimulated muscles was noticed in 4
boys whose muscles were stimulated for 3 months. The muscles of 5 boys who were
subjected to electrical stimulation for 9 months showed an improvement; 6
measurements made during the stimulation program revealed that changes of
torques in the ankle of the right stimulated extremity were significantly
different (P less than 0.001) from the changes of torques in the ankle of the
left nonstimulated extremity
McCully K., Giger U., Argov
Z., Valentine B., Cooper B., Chance B., and Bank W. (1991) Canine X-linked
muscular dystrophy studied with in vivo phosphorus magnetic resonance
spectroscopy. Muscle Nerve 14, 1091-1098.
Abstract: Duchenne muscular dystrophy (DMD) is an X-linked disease characterized
by progressive muscle weakness and degeneration. Dystrophin is the product of
the missing gene in this disorder. However, the cause of the dystrophic process
is not understood. Transient muscle injury is normally seen after muscle
exercise, and may be a necessary process in muscle growth and preservation. We,
therefore, chose to evaluate the role of exercise in Duchenne dystrophy by
studying the canine X-linked animal model (CXMD). These dogs also lack
dystrophin and have clinical signs similar to humans. Exercise was initiated by
electrical stimulation, and muscle metabolism was monitored with phosphorus
magnetic resonance spectroscopy (P-MRS). Dogs with CXMD had abnormal muscle
pathology and markedly elevated serum CK. The inorganic phosphate (Pi) to
phosphocreatine (PCr) ratio was increased in CXMD dogs at rest compared with
normal dogs (Pi/(Pi + PCr) = 0.166 +/- 0.054 for CXMD and 0.073 +/- 0.017 for
normals, mean +/- SE). No changes in resting ATP, pH, phosphomonoesters (PME),
and phosphodiesters (PDE) were seen. The mean Pi/(Pi + PCr) and pH values during
stimulation were normal in the CXMD dogs. Two to three days after electrical
stimulation, resting Pi/(Pi + PCr) ratios were significantly increased in the
CXMD dogs (0.127 +/- 0.029 compared with 0.172 +/- 0.054, mean +/- SD). Normal
dogs showed no increase in Pi/(Pi + PCr) following stimulation. There was a
50-fold greater increase in serum CK in CXMD compared with normal dogs following
exercise. These results indicate greater muscle injury in CXMD muscle, and
suggest that in the absence of dystrophin, exercise-induced muscle injury may
play a role in the dystrophic process
Mihelin M., Trontelj J.V., and
Stalberg E. (1991) Muscle fiber recovery functions studied with double pulse
stimulation. Muscle Nerve 14, 739-747.
Abstract: Direct electrical stimulation with paired pulses at varied intervals
was used to study the propagation velocity and action potential amplitude
recovery functions (VRF and ARF) of single muscle fibers. Following a subnormal
period with slowed conduction, most of the muscle fibers tested in healthy
subjects showed a period of supernormal propagation velocity starting at 3 to 12
ms, with a peak between about 5 and 15 ms, a mean increase of 7%, and an
approximately logarithmic decay toward 1 second. The onset of supernormality was
earlier in muscle fibers from patients with muscular dystrophy and significantly
delayed in those from denervated muscles. Denervated muscle fibers also had a
significantly longer refractory period
Scott O.M., Hyde S.A., Vrbova
G., and Dubowitz V. (1990) Therapeutic possibilities of chronic low frequency
electrical stimulation in children with Duchenne muscular dystrophy. J.
Neurol. Sci. 95, 171-182.
Abstract: To evaluate the therapeutic possibilities of chronic electrical
stimulation, muscle function studies and quantitative tests of physical
assessment were used to monitor the response of quadriceps femoris to prolonged
low frequency stimulation. Comparative studies of the maximum voluntary and
electrically elicited responses of muscles of young ambulant children with
Duchenne muscular dystrophy, when compared to those of normal children's
muscles, revealed lower values of maximum voluntary contraction, significant
slowing (P less than 0.001) of mean relaxation times and a higher resistance to
fatigue testing. Intermittent chronic low frequency stimulation resulted in a
significant (P less than 0.01) increase in mean maximum voluntary contraction of
the stimulated muscles compared with the mean force exerted by the unstimulated
control muscles. There are clear therapeutic possibilities for the use of
chronic low frequency stimulation in these children
Dangain J. and Vrbova G. (1989)
Long term effect of low frequency chronic electrical stimulation on the fast
hind limb muscles of dystrophic mice. J. Neurol. Neurosurg. Psychiatry
52, 1382-1389.
Abstract: Low frequency chronic electrical stimulation can have a beneficial
effect on dystrophic muscles. The present study was undertaken to assess the
long term effect of such stimulation on the fast hind limb muscles of dystrophic
mice. The relationship between the changes induced by stimulation and the
initial condition of the dystrophic muscles, as well as other factors which
might contribute to this relationship, were examined. The stimulation induced an
increase in the force output of weak dystrophic muscles and a speeding of their
time course of contraction and relaxation, as well as an increase in their
fatigue resistance. In relatively strong dystrophic muscles, the stimulation
induced similar changes in contractile speed and fatigue characteristics, but it
led to a slight decrease in force output. Our results suggest that the
stimulation promotes the growth and differentiation of the small regenerating
fibres known to be present in the diseased muscles and, in addition, induces an
increase in the mitochondrial content of the muscle fibres. Our results indicate
that these effects are not permanent
Dangain J. and Vrbova G. (1988)
Response of dystrophic muscles to reduced load. J. Neurol. Sci. 88,
277-285.
Abstract: We have previously reported that, in dystrophic mice, functional
overload has a damaging effect on the tibialis anterior (TA) muscle. In the
present study, we have examined the effect of a load reduction on the TA and
extensor digitorum longus (EDL) muscles. Our results show that reducing the
passive load to which these muscles are subjected in dystrophic mice by
resecting the Achilles tendon has a beneficial effect. The force output of the
"released" EDL muscle improved, while the time course of contraction and
relaxation of the "released" TA muscle became faster. Also in this muscle,
resistance to fatigue became significantly greater. Low frequency electrical
stimulation of the "released" muscles via implanted electrodes had little effect
on their force output. It led, however, to a relative speeding of their time
course of contraction and relaxation and to a further increase in their
resistance to fatigue. Taken together, our results suggest that the beneficial
effect of low frequency electrical stimulation on the force output of weak
dystrophic muscles, described in the preceding paper, might be conditioned by
the load to which these muscles are subjected
Backman E. (1988) Methods for
measurement of muscle function. Methodological aspects, reference values for
children, and clinical applications. Scand. J. Rehabil. Med. Suppl 20,
9-95.
Abstract: In children isometric muscle force can be measured with acceptable
reproducibility by using a simple hand-held dynamometer. Reference values for 10
different muscle groups are given for children aged 3.5- 15 years. If age and
weight are known, the force can be predicted. The most pronounced differences
between the dominant and the non-dominant side were found in the elbow flexors,
3 of the 6 age groups showing greater force on the dominant side, and in the
wrist extensors, the 2 oldest age groups being stronger on the dominant side.
Sex differences were present as early as 9.5-11 years of age, boys being
stronger than girls. Isokinetic muscle torque of the dorsiflexors of the ankle
increased with age. Reference values are given for peak torque in children 6, 9,
12, and 15 years of age. The most intense force development occurs between 12
and 15 years of age in boys, and earlier in girls. Sex differences appear in
early puberty. In young children the dominant leg was the stronger at the
highest velocities. In the older children the non-dominant leg was the stronger
at low velocities. Isokinetic measurements are time-consuming and require
experience, and should be regarded as complementary to isometric testing. In
muscle groups that are too weak to overcome gravity isometric and isokinetic
methods cannot be used. Functional tests of motor ability are especially useful
in patients with severely impaired muscle function when other test methods are
inadequate or difficult to evaluate. The natural course of Duchenne muscular
dystrophy was followed in 16 boys by means of functional tests, isometric tests,
isokinetic tests of concentric muscle contraction, and manual tests. Of these
only the isokinetic method proved unreliable, possibly because of difficulty in
activating the muscles at different speeds. The function of adductor pollicis
was studied by supramaximal electrical stimulation of the ulnar nerve.
Force-frequency curves and reference values for relaxation rate and half
contraction time to tetanus for children aged 9, 12, and 15 years are presented.
The half contraction time to tetanus was briefer in the older children than in
the younger. The relative force developed at a stimulation of 10 Hz increased
with age. Apart for the increase in muscle force with increasing age, no other
differences emerged between the different age groups. No sex differences were
found. The electrical stimulation test is rather painful, and only about 60% of
the children persevered to the end of the test.(ABSTRACT TRUNCATED AT 400 WORDS)
Dubowitz V. (1988) Responses of
diseased muscle to electrical and mechanical intervention. Ciba Found. Symp.
138, 240-255.
Abstract: It is well established that the properties of muscle fibres are
influenced by their neurons and that this is at least in part mediated by the
pattern of activity. Application of this knowledge has led to the experimental
trial of electrical stimulation in diseased muscle, both in the dystrophic mouse
and in children with Duchenne muscular dystrophy. This has shown a beneficial
effect of slow frequency stimulation. Another route through which muscle
properties can be influenced is by changing the load by procedures such as
tenotomy. This has been studied by complete tenotomy in normal animals and
recently by selective partial procedures in human disease. Y. Rideau has shown
that release of early shortening (contractures) of several muscles, a consistent
feature in Duchenne muscular dystrophy, has a beneficial effect on muscle
function. From personal observations on a number of Rideau's patients who have
undergone this procedure the improvement in function seems disproportionate to
what could be explained on simple biomechanical grounds alone and suggests some
more fundamental change in the contractile properties of the muscle
Edwards R.H., Chapman S.J.,
Newham D.J., and Jones D.A. (1987) Practical analysis of variability of muscle
function measurements in Duchenne muscular dystrophy. Muscle Nerve 10,
6-14.
Abstract: To determine the possible sources of variation in performance
indicators used in therapeutic trials, electrical stimulation techniques were
used to measure contractile properties of the adductor pollicis and quadriceps
muscles in boys with Duchenne muscular dystrophy. As no therapeutic effects were
observed, longitudinal data obtained are taken to indicate changes in disease
progress. Variance in voluntary contractions was found to be similar to that
with electrically stimulated contractions; thus, variation could not be
attributed to motivational changes, but rather to physiologic changes.
Dystrophic muscle was slower to relax and less fatiguable than normal. However,
such changes are of less significance to the overall disability compared to the
loss of muscle bulk (cross-sectional area). Important variations in the function
of individual muscles essential to complex performance, such as walking or
getting up from the floor, could be masked by combining results from several
muscle groups
Scott O.M., Vrbova G., Hyde S.A.,
and Dubowitz V. (1986) Responses of muscles of patients with Duchenne muscular
dystrophy to chronic electrical stimulation. J. Neurol. Neurosurg. Psychiatry
49, 1427-1434.
Abstract: The effect of chronic low frequency stimulation on the tibialis
anterior muscle of children with Duchenne muscular dystrophy was investigated.
Baseline data from 16 boys established low values of maximum voluntary
contraction which did not improve with age. Studies of the contractile
properties revealed significant slowing (p less than 0.001) of mean relaxation
time compared to that of normal children's muscles. There was no loss of force
during fatigue testing, as in normal children, but in contrast to normal
children, there was no potentiation at lower frequencies of stimulation.
Intermittent chronic low frequency stimulation of muscles in six young ambulant
children with Duchenne muscular dystrophy resulted in a significant increase (p
less than 0.05) in mean maximum voluntary contraction compared with the mean
forces exerted by the unstimulated control muscles of the contralateral leg
Barnard E.A., Barnard P.J.,
Jarvis J.C., and Lai J. (1986) Low frequency chronic electrical stimulation of
normal and dystrophic chicken muscle. J. Physiol 376, 377-409.
Abstract: The fast-twitch posterior latissimus dorsi muscle of normal and
genetically dystrophic chickens was subjected to continuous indirect electrical
stimulation at 10 Hz for periods of 4-8 weeks. To sustain this in vivo nerve
stimulation an internally implantable miniature stimulator device was designed.
This regime of stimulation caused complete fatigue of the normal muscle within 5
min of its initiation. The dystrophic muscles maintained a very small degree of
contractile activity during this initial phase. Tangible twitching of the muscle
returned in 5 week birds between 3 and 5 days and in 10 week birds between 11
and 16 days after implantation. After 4 weeks of stimulation, no significant
change was measured in the time-to-peak of the isometric twitch response, nor in
the half-relaxation time. The resistance to fatigue was significantly increased
in the stimulated muscles when tested with a series of tetani at 40 Hz. The mean
fibre area was decreased, in all muscles stimulated for longer than 3 weeks, in
comparison to their contralateral controls, except where fibre splitting in
dystrophic birds abnormally reduced the control value. The majority fibre type
of the muscle was changed from type IIB to IIA. The histochemical reactions for
both NADH-linked oxidation and phosphorylase were distinctly increased in the
stimulated muscles. In normal muscle, stimulation increased somewhat the number
of nuclei per unit area and changed their intracellular distribution, so that a
greater proportion was found adjacent to the sarcolemma. The normal posterior
latissimus dorsi muscle responded to chronic stimulation with increases of
3-6-fold in its acetylcholinesterase (AChE) activity. The maximum change in AChE
occurred after 2 weeks stimulation; a steady level, 3 times that of the control
unstimulated muscle, persisted at later times. Chronic stimulation suppressed
the over-production of AChE that is characteristic of dystrophic chicken
fast-twitch muscle, to attain a level comparable to the AChE activity in a
stimulated normal muscle. Stimulation exerted a strong normalizing influence on
dystrophic muscle, as assessed morphologically. The characteristic fibre
rounding, fibre hypertrophy and myonuclear proliferation were reduced. This
influence was most marked where the stimulation was initiated before the major
pathological changes had occurred, but was also significant when commenced in
strongly affected birds of 10-11 weeks
Dangain J. and Vrbova G. (1983)
Effect of chronic electrical stimulation at low frequency on the passive
membrane properties of muscle fibers from dystrophic mice. Exp. Neurol.
79, 630-640.
Abstract: It has been reported that chronic electrical stimulation at low
frequency applied to dystrophic muscles has a beneficial effect. In this study,
the effect of this treatment on the passive membrane properties of muscle fibers
from dystrophic mice was followed. Cable properties were assessed by the
two-microelectrodes DC method and spacial decay analysis. Earlier results
showing a decrease in resting potential, an increase in input resistance and in
specific membrane resistance in muscle fibers from dystrophic mice were
confirmed. In addition, the specific membrane capacitance of these muscle fibers
was found to be lower than normal. This suggests that the membrane properties of
fibers from dystrophic muscles are similar to those of immature muscle fibers.
Muscle fibers from dystrophic animals that were stimulated for 2 to 4 weeks had
membrane properties similar to those from normal muscles. This indicates that
electrical stimulation at low frequency for 2 to 4 weeks restores membrane
properties of dystrophic muscle fibers to normal and we suggest that an
appropriate pattern of stimulation induces the maturation of dystrophic muscle
fibers
Watanabe K., Uramoto I., and
Totsuka T. (1982) Different time courses of reduction in muscular potentials to
moderate frequency stimulation in dystrophic and normal mice. Nippon
Seirigaku Zasshi 44, 99-102.
Abstract: Muscular potentials were evoked by electrical stimulation of sciatic
nerves and recorded from gastrocnemius muscles in dystrophic and normal mice.
When frequency of stimulation was accelerated from 0.5 to 5 per sec and
continued, the potentials were depressed to a notable extent in normal mice,
whereas only a slight decrease or even an increase in them was observed in
dystrophic mice. Thus, a simple method has been developed to differentiate pre-
and/or postjunctional properties for impulse transmission in dystrophic mice
from those in normal mice
Polinski W.J. and Rall J.A.
(1982) Mechanics and energetics of muscle contraction in normal and dystrophic
chickens. Am. J. Physiol 242, C19-C24.
Abstract: Energy liberation and isometric force generation were compared at 25
degrees C in isolated normal (n = 15) and dystrophic (n = 18) posterior
latissimus dorsi muscles (PLD) from 16- to 33-day-old chickens. Twitch- energy
liberation in dystrophic muscle decreased by 27 +/- 6%, and force per
cross-sectional area decreased by 26 +/- 11%. Tetanic energy liberation in
dystrophic PLD was depressed by 32 +/- 10% compared with a 22 +/- 9% reduction
in peak force per cross-sectional area plus a 26 +/- 3% reduction in ability to
maintain force. Normalizing results using the force-time integral demonstrates
an unaltered force generation per unit energy liberation in dystrophic PLD (7
+/- 11% difference from normal). Kinetic properties of the mechanical responses
were not significantly different in normal compared with dystrophic PLD.
Dystrophic PLD demonstrated hyperexcitability to nerve transection and
electrical stimulation. Although force-generating capacity is reduced in
dystrophic PLD, coupling of force production to energy utilization appears
unaltered
Vrbova G. and Ward K. (1981)
Observations on the effects of low frequency electrical stimulation on fast
muscles of dystrophic mice. J. Neurol. Neurosurg. Psychiatry 44,
1002-1006.
Abstract: The deterioration of tibialis anterior (TA) and extensor digitorum
longus (EDL) muscles in dystrophic mice (C 57 BL dy/dy) was compared. The
effects of chronic electrical stimulation on various characteristic properties
of these muscles were also studied. The results indicate that EDL muscles are
less affected by the disease than TA. This "selectivity" is difficult to explain
since both muscles have similar fibre type composition. TA and EDL muscles that
were stimulated for 10- 28 days developed greater tetanic tensions than the
contralateral muscles, but this effect was apparent only when the muscles were
severely affected by the disease, that is the contralateral TA or EDL muscles
developed less than 50% of the tension produced by muscles from normal animals.
In all EDL muscles, stimulation increased the fatigue resistance. The time
course of contraction and relaxation of dystrophic muscles is usually slower
than that of normal muscles. The stimulation reduced this slowing effect, so
that the stimulated muscles became similar to homologous muscles from normal
littermates
Reichmann H., Pette D., and
Vrbova G. (1981) Effects of low frequency electrical stimulation on enzyme and
isozyme patterns of dystrophic mouse muscle. FEBS Lett. 128, 55-58.
Luthert P., Vrbova G., and Ward
K.M. (1980) Effects of slow frequency electrical stimulation on muscles of
dystrophic mice. J. Neurol. Neurosurg. Psychiatry 43, 803-809.
Abstract: The hind leg muscles of dystrophic mice (C57 BL dy2J/dy2J) wer
chronically stimulated at 10 Hz for 30 minutes six times a day. After 14 days of
such activity a clinical improvement in the use of the stimulated leg was
noticed. The twitch and tetanic tensions developed by the stimulated tibialis
anterior and extensor digitorum longus muscles were higher than those developed
by the control, unstimulated muscles on the contralateral side. Histochemically
visualised activity of the oxidative enzyme succinic dehydrogenase was greater
in fibres of the stimulated muscles. The stimulated muscles contained more
muscle fibres than unstimulated controls. It is concluded that slow frequency
activity has a beneficial effect on muscles of dystrophic mice
Luthert P., Vrbova G., and Ward
K.M. (1979) Functional improvement of skeletal muscles of dystrophic mice
following electrical stimulation [proceedings]. J. Physiol 291, 31P.
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