Electrical muscle stimulation

ADRENAL MEDULLA HORMONES. Adrenaline (epinephrine) and its immediate biological precursor noradrenaline (norepinephrine, levartei-nol) are the principal hormones of the adult adrenal medulla. See Fig.l. Some of the physiological effects produced by adrenaline arc contraction of the dilator muscle of the pupil of the eye (mydriasis), relaxation of the smooth muscle of the bronchi constriction of most small blood vessels dilation of some blood vessels, notably those in skeletal muscle increase in heart rate and force of ventricular conlraction relaxation of the smooth muscle of the intestinal tract and either contraction or relaxation, or both, of uterine smooth muscle. Electrical stimulation of appropriate sympathetic (adrenergic) nerves can produce all the aforementioned effects with exception of vasodilation in skeletal muscle. 

Cardiomyopathy. The best available solution to cardiomyopathy may be one that is less sophisticated than transplant surgery or the artificial heart. The cardiomyoplasty-assist system combines eariier electrical stimulation technology with a new surgical technique of utilizing muscle from another part of the body to assist the heart. 

The myocytes of smooth muscle are approximately 100 to 500 p,m in length and only 2 to 6 p,m in diameter. Smooth muscle contains very few t-tubules and much less SR than skeletal muscle. The Ca that stimulates contraction in smooth muscle cells is predominantly extracellular in origin. This Ca enters the cell through Ca channels in the sarcolemmal membrane that can be opened by electrical stimulation, or by the binding of hormones or drugs. The contraction response time of smooth muscle cells is very slow compared with that of skeletal and cardiac muscle. 

Figure 3. Top panel Whole muscle force (x) and single fiber PCr (a, a) and ATP ( , ) concentrations at rest and after 10 and 20 sec of intermittent electrical stimulation at 50 Hz. Open symbols denote type I fibers closed symbols denote type II fibers. Bottom panel Glycogenolytic rates in type I and II fibers during the 20 sec stimulation period. The open bar denotes type I fibers the closed bar denotes type II fibers.

This section examined small muscle preparations stimulated electrically or skinned muscle fibers maintained in superfused baths with different substance concentrations. The electrical stimulation was either continuous or intermittent for relatively short durations. 

Bergstrom, M. Hultman. E. (1990). Contraction characteristics of the human quardriceps muscle during percutaneous electrical stimulation. Pflugers Arch. 417, 136-141. 

Hultman, E. Sjoholm, H. (1983b). Electromyogram, force and relaxation time during and after continuous electrical stimulation of human skeletal muscle in situ. J. Physiol. 339, 33-40. 

Hultman, E. Spriet, L.L. (1986). Skeletal muscle metabolism, contraction force and glycogen utilization during prolonged electrical stimulation in humans. J. Physiol. 374,493-501. 

Spriet, L.L., Soderlund, K., Bergstrom, M., Hultman, E. (1987a). Anaerobic energy release in skeletal muscle during electrical stimulation in men. J. Appl. Physiol. 62, 611-615. 

The presence of toxins in C. geographus venom which block the response of vertebrate skeletal muscle to direct electrical stimulation was first detected by Endean et al. (14). A toxic component which reversibly blocked the generation of action... 

However, there are a significant number of cases, sometimes estimated as 19% of fractures, where repair does not occur in a reasonable amount of time. The problems are associated primarily with severe injury, infection, arthritis, or biochemical abnormalities. A very common cause, known as the compartment syndrome, is related to severe swelling pressure on the blood vessels that limits blood access to the muscles. In many of these cases, electrical stimulation has been shown to be effective in accelerating repair. 

Fatigue of muscles is found post-exercise and in some patients with disorders of limb or respiratory muscles. Peripheral muscle fatigue is generally characterized by the changes in force frequency relationships that occur. The process is traditionally divided into a failure of force production at either low or high frequencies of electrical stimulation. 

Figure 11.2 Loss of glutathione from isolated rat soleus muscles subjected to either repetitive, electrically stimulated, contractile activity ( a ), treated with the mitochondrial inhibitor 2,4-dinitrophenoi ( ) or untreated ( ). Vaiues significantly different to resting controi muscles, P < 0.05 P < 0.01. Redrawn from Jackson et al. (1991).

Quantal analysis defines the mechanism of release as exocytosis. Stimulation of the motor neuron causes a large depolarization of the motor end plate. In 1952, Fatt and Katz [11] observed that spontaneous potentials of approximately 1 mV occur at the motor endplate. Each individual potential change has a time course similar to the much larger evoked response of the muscle membrane that results from electrical stimulation of the motor nerve. These small spontaneous potentials were therefore called... 

Measuring muscle-evoked responses to repetitive motor nerve electrical stimulation permits detection of presyn-aptic neuromuscular junction dysfunction. In botulism and the Lambert-Eaton syndrome, repetitive stimulation elicits a smaller than normal skeletal muscle response at the beginning of the stimulus train, due to impaired initial release of acetylcholine-containing vesicles from presyn-aptic terminals of motor neurons followed by a normal or accentuated incremental muscle response during repeated stimulation. This incremental response to repetitive stimulation in presynaptic neuromuscular disorders can be distinguished from the decremental response that characterizes autoimmune myasthenia gravis, which affects the postsynaptic component of neuromuscular junctions. 

Botulinum exotoxin impedes release of neurotransmitter vesicles from cholinergic terminals at neuromuscular junctions. Botulinum exotoxin is ingested with food or, in infants, synthesized in situ by anaerobic bacteria that colonize the gut. A characteristic feature of botulinum paralysis is that the maximal force of muscle contraction increases when motor nerve electrical stimulation is repeated at low frequency, a phenomenon attributable to the recruitment of additional cholinergic vesicles with repetitive depolarization of neuromuscular presynaptic terminals. Local administration of Clostridium botulinum exotoxin is now in vogue for its cosmetic effects and is used for relief of spasticity in dystonia and cerebral palsy [21]. 

Nonpharmacologic methods improve venous blood flow by mechanical means and include early ambulation, electrical stimulation of calf muscles during prolonged surgery, graduated compression stockings, intermittent pneumatic compression devices, and inferior vena cava filters. 

Electrically stimulated longitudinal muscle/myenteric plexus preparations from guinea-pig ileum (LMMP-GPI)... 

Action potentials of the small muscles of the hands were recorded. The muscles were fatigued by electrical stimulation of the nerves, and the effects of D.F.P. and of neostigmine,... 

Figure 13.22 The decrease in phosphocreatine concentration in the muscle during stimulation. Electrical stimulation of muscle in the laboratory is used to mimic sprinting activity in the muscle. Data from Hultman Sjoholm (1983). The units for the concentration of phosphocreatine are pmole per gram dry weight of muscle taken by biopsy. Note apparent differences in concentration when data are presented as wet or dry weight.

Electrical stimulation of muscle to mimic sprinting (Eigure 13.22). 

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