THE
EFFECTS ON ACUTE ATROPHIED MUSCLES IN SPINAL CORD INJURY BY THERAPEUTIC
ELECTRICAL STIMULATION
A.
Misawa, Y. Shimada, K. Sato, T. Matsunaga,
M.
Sato, S. Chida, K. Hatakeyama
Department
of Orthopedic Surgery,
ABSTRACT
Therapeutic electrical stimulation (TES)
has been performed to increase muscle force, and to prevent muscle
atrophy. In this study, we evaluated the
differences in the effects on acute atrophied muscles after stimulation at
different frequencies. The TA and EDL
muscles of paraplegic Wistar male rats were used. An electrode was unilaterally inserted
percutaneously in the vicinity of the peroneal nerve. The TA and EDL were
stimulated for 60 min / day, at either 20 or 100 Hz, for up to 1 week. The TA and EDL muscles from both legs were
surgically removed after stimulation.
Muscle fibers were identified with ATPase stain, and the lesser fiber
diameters were measured. A comparison
between stimulated muscle and non-stimulated muscle was done. In type 2A and 2B, the lesser diameters,
stimulated at 100 Hz, were significantly larger than those non-stimulated at
100 Hz on TA and EDL. In type 2B, the
lesser diameter of TA stimulated at 100 Hz was significantly larger than that
of TA stimulated at 20 Hz. These results
support that high frequency stimulation for acute atrophied muscles are useful
in reducing muscle atrophy.
Keywords: muscle atrophy, therapeutic
electrical stimulation, frequency
INTRODUCTION
Electrical activation of the
neuromuscular system produces therapeutic effects and is a useful method for
the restoration of lost or impaired motor function. With electrical stimulation it is possible to
increase muscle activity to influence their morphological, physiological and
biochemical properties. This results in
an improvement of muscle strength in healthy subjects or recovery of atrophied
muscle due to disuse caused by injury. In order to restore ambulatory function
in paralyzed lower limbs, the force of atrophied muscles must be increased.
Therapeutic electrical stimulation (TES) has been performed to prevent or
decrease these muscles from atrophying, and to increase the force of these
muscles. Clinically, we adopt the
application of low-frequency stimulation (20 Hz) for atrophied muscles, because
we have used this frequency in functional electrical stimulation (
METHODS
Thirty adult male Wistar ST rats average
body weight 448g (380 - 550 g) were used in experiments. We grouped the rats into those stimulated at
20 Hz (low frequency) and those stimulated at 100 Hz (high frequency); each
group had 15 rats. During operations
rats were deeply anaesthetized with an intraperitoneal injection of 40 mg per
kg body weight of pentobarbital sodium.
A percutaneous intramuscular electrode which has been used in human was
implanted unilaterally (in only the right leg) in the vicinity of the peroneal
nerve in order to stimulate the TA and EDL.
The percutaneous electrode was a helical coil wound from a Teflon-coated
19-strand stainless steel cable (SES114, Nippon Seisen, Japan) [1]. The electrode led under the skin towards the
back of the rat. After implanting the
electrode, the spinal cord was cut at the level of infra thoracic spine (Th 9 –
10); the lower limbs were then paralyzed.
TA and EDL was stimulated using the stimulator for 60 min / day, at
either 20 or 100 Hz, for up to 1 week.
In both frequencies, the pulses had square monophasic waveforms, pulse
width was 0.2 ms, and constant voltage was adjusted to give maximum contraction
force on palpation. The stimulation
cycle was 4 sec of stimulation for every 8 sec (on time / off time: 4 sec / 4
sec). This intermittent stimulation
lasted for 60 min. After stimulation the
TA and EDL muscles from both legs were surgically removed. Muscle samples were taken from the center of
each muscle in a 1 cm thick cross section.
Subsequent samples were taken using a ninety-degree cut cross section of
this sample. The muscles were then
frozen in isopentane chilled with liquid nitrogen, and 10 µm thick serial
sections were made. Transverse serial
sections were stained by histochemical method ATPase with preincubation at pH
4.4. Type 1, type 2A and type 2B fibers
were identified according to the criteria of Brooke and Kaiser, and the lesser
fiber diameters of 300 fibers from each type muscle fiber were measured with a
NIH image. This measurement is designed
to overcome the distortion, which occurs when a muscle fiber is cut obliquely,
producing an oval appearance [2].
RESULTS
There was significant difference between
stimulated and non-stimulated type 2B muscle fiber at 20 Hz (p<0.05). There was no significant difference at any
frequency in type 1 muscle fiber. There
was significant difference in type 2B muscle fiber diameter between the two
frequencies used at TA (p<0.01). In
addition, there was significant difference in the size of muscle fiber diameter
between non-stimulated and stimulated muscles at 100 Hz in type 2A (p<0.05) and type 2B (p<0.01) (Fig. 1,
2).

Fig. 1 TA: There was significant difference in type 2B
muscle fiber diameter between the two frequencies used at TA (p<0.01). There was significant difference in the size
of muscle fiber diameter between non-stimulated and stimulated muscles at 100
Hz in type 2A and type 2B (p<0.01).

Fig. 2 EDL: There was significant difference in the size
of muscle fiber diameter between non-stimulated and stimulated muscles at 100
Hz in type 2A (p<0.05) and type 2B
(p<0.01).
DISCUSSION
In these results we assessed muscle
atrophy in each frequency group from the size of the muscle fiber. Our results indicate that intermittent high frequency
stimulation of acute atrophied muscles is more effective than low frequency
intermittent stimulation for reducing muscle atrophy. The muscle atrophy in
patients suffering from spinal cord injury has been demonstrated with a
progressive decrease in the fiber diameter and changes in the fiber type
distribution with predominant type 2 atrophy in the early stage and type 1
atrophy in the later stage of the cord transection [3]. In order to restore paralyzed muscles by FES,
an increase in muscle fiber diameter is required. It is important to maintain muscle power by
increasing the size of muscle fiber. If
muscle atrophy develops, recovery time is much longer so muscles must be
stimulated before muscle atrophy develops.
Physiologically, type 1 muscle fibers (slow muscle) were stimulated at
low frequency (10 - 20 Hz), and type 2 muscle fibers (fast muscle) were
stimulated at high frequency (30 - 60 Hz) by dominating the nerve [4]. In our results, there were significant
differences in the size of muscle fiber diameter between non-stimulated and
stimulated muscles at 100 Hz in type 2A and 2B.
While there is no significant difference at 20 Hz or 100 Hz in type 1
muscle we believe that high frequency stimulation, because of its positive
effects on type 2 muscle, should be used.
In the acute phase type 2 muscle fibers are smaller by slow
degrees. As a result, high frequency
stimlulation, due to it's positive effect on these particular muscle fibers, is
more beneficial. In this study, we
adopted intermittent stimulation as the stimulation cycle. During intermittent stimulation, muscle
fatigue was greater at lower frequencies than it was at higher
frequencies. This is opposite to results
obtained during continuous stimulation [5].
The mechanism of intermittent stimulation is unclear, however, the
condition of high and intermittent stimulation has a synergism. As a result of using intermittent high
frequency stimulation, type 2 muscle growth in the acute phase of spinal cord
injury outpaces fast muscle atrophy.
These results suggest that high frequency stimulation for acute
atrophied muscles are more effective in reducing muscle atrophy.
CONCLUSION
Intermittent high frequency stimulation
of acute atrophied muscles is more effective than low frequency intermittent
stimulation for reducing muscle atrophy.
REFERENCES
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percutaneous intramuscular electrodes for functional electrical stimulation.
Arch Phys Med Rehabil. 77: 1014-1018, 1996.
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morphology and distribution in paraplegic patients with traumatis cord lesion.
Acta. Neuropathol. 57: 243-248, 1982.
[4] Eccles JC. et al.: The action potentials
of the alpha motoneurones supplying fast and slow muscles. J. Physiol. 142:
275-296, 1958.
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Arch Phys Med Rehabil. 80: 48-53, 1999.