[Histological changes, muscle force and fatigability after electrical stimulation to experimentally paralyzed muscles].
In order to use functional electrical stimulation effectively in paralyzed muscle treatment, changes in the maximal muscle force, muscle fatigue, and histological changes were evaluated in electrically stimulated muscles. Study 1. Tissue damage by percutaneous intramuscular electrodes implanted into the quadriceps muscle was examined in rat. Stimulation was conducted at various output voltages, and for various durations of time, in order to assess the histological changes in the muscle around the electrodes. Study 2. Electrodes were implanted into the bilateral quadriceps and gastrocnemius muscles of adult cat, and the unilateral muscles were then stimulated from 3 weeks following the transection of the spinal cord at the T9 level. Stimulus parameters were divided into two groups; as "A" stimulation: at -8V for 15min twice/week, and as "B" stimulation: at -16V for 30 min 4 times/week. The histological changes were examined using the myofibrillar ATPase method to determine the diameters and occupation ratios for each muscle fiber type. RESULTS. Study 1. Significant tissue damage began to occur when the voltage output created the maximum muscle contraction force. Until that critical voltage point was reached, tissue damage was not significant, regardless of the duration of the stimulation. Study 2. The maximum muscle force decreased until 4 weeks after the transection, then increased regardless of the presence of electrical stimulation. The muscle fatigability of the non-stimulated muscle was greater than that of the stimulated muscle. High voltage, long duration, and frequent stimulation was effective in controlling fatigue. The ratio of type I fibers was higher in the stimulated muscle. There was no evidence, however, of suppressing muscle fiber atrophy after electrical stimulation. These results suggested that electrically stimulating paralyzed muscles was effective for suppressing muscle fatigue, and for reducing the ratio of type I fibers. In clinical use, the output voltage should be kept below the voltage that induces the maximum muscle contraction to prevent tissue damage.
Department of Orthopedic Surgery, Akita University School of Medicine, Japan.
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D000818:Animals; D001696:Biomechanical Phenomena; D002415:Cats; D004599:Electric Stimulation Therapy; D004567:Electrodes, Implanted; D008297:Male; D018763:Muscle Fatigue; D018482:Muscle, Skeletal / Q000473:pathology / Q000503:physiopathology*; D010243:Paralysis / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D051381:Rats; D017208:Rats, Wistar