In the article "Muscle Weakness, Paralysis, and Atrophy after Human Cervical Spinal Cord Injury" (Thomas et alii, 1997) it is reported that "Severe muscle atrophy was revealed which might reflect disuse," and, "Thus, the weak voluntary strength of these partially paralyzed muscles is not due to submaximal excitation of higher CNS centers, but results mainly from reduction of this input to triceps motoneurons." The reduction of this input reflects the diminution of the power amplification of the nerve impulse across the synapse. Below this reduction of amplification of the power of the nerve impulse will be shown to be the result of the disuse atrophy of the muscle. This sort of myopathy, motor weakness and paralysis is the same sort of myopathy that is found in those exposed to microgravity and long term bedrest.
All spinal and head injuries, no matter how severe, are followed by disuse atrophy from at least the level of injury, and, in most cases, over the entire body as the acute phase is prolonged and the patient is immobilized either mechanically or by failure of the neurons in the cord to fire because of the presence of blood, as in a stroke or concussion. There is an implication that a great deal of chronic paralysis subsequent to such neural trauma may be due to muscle atrophy and not to enduring and irreversible neuropathy. During the acute phase of injury the blood/brain barrier must be reestablished, and pressure, as from swelling or slight vertebral displacement, must be relieved. This takes easily many weeks. While blood is still present in the nervous tissue and until it is absorbed the horn cells will not fire. This phase of recovery easily takes another two or three months more. The severity of muscle atrophy that advances during this time is far greater than that which routinely leaves astronauts too
weak to stand up upon return to earth after only a few weeks in space and still using their muscles, only minimally.
Disuse muscle atrophy is routinely described as the loss of muscle fiber cross-sectional area. In "Hemiplegic Amyotrophy" (Chokroverty, 1976) the author states that these fibers are the type II fibers also known as the transverse tubule or t-tubule. In "Muscles - Effectors of the Motor System," (Ghez, 1991) the author writes: "Contraction is set off by the depolarization of the muscle fiber. When an action potential in a motor axon reaches the neuromuscular junction it generates an endplate potential, which in turn triggers an action potential in the muscle fiber. This action potential is propagated rapidly over the surface of the fiber and conducted into the muscle fiber by means of the system of T-tubules. The T-tubule system insures that the contraction that follows a single action potential, termed a 'twitch', spreads throughout the entire fiber."
The t-tubules grow from the post-synaptic motoneurons, arborizing throughout the muscle, but maintain the cytoplasmic continuity characteristic of the electrical synapse, a device which the t-tubule forms as it contacts the sacrcomere, a reservoir of interstitial fluid. To understand how loss of cross-sectional area of the t-tubule might effect the power of muscle contraction it is only necessary to consider the motor unit as an electrochemical circuit, and to remember the amplifying characteristic of the peripheral, chemical synapse at the neuromuscular junction.
An excitatory, CNS impulse descends the axon. Arriving at the synapse/motor endplate region the negative charge draws calcium ions [positively charged molecules] across the cleft to break vesicles of acetylcholine. This neurotransmitter triggers the creation of another action potential postsynapticaly. An action potential is a voltage. A voltage is an electrical pressure. What is being pressured is the movement of negative electrical charge along the t-tubule to the electrical synapse at the sarcomere where calcium ions are again drawn by the arriving negative electrical charge from the fluid in the sarcomere to initiate the splitting of ATP and the energizing of the type I muscle fiber contraction.
The reason for the increase in power of the CNS nerve impulse across the chemical synapse is best described by the equations for electrical power, and for the inverse, exponential relationship of conductor cross-sectional area and resistance to flow. That is, if power = voltage x current flow[ p=vi], then to amplify power one must either increase voltage or current flow. The power of the nerve impulse is amplified by increased current flow made possible by a muscle’s transverse tubule that is larger than the microtubule which bears the nervous impulse. The t-tubule grows out from the motorneurons which were galvanized by the release of acetylcholine. To increase i or current flow along it, r or resistance must be decreased. Because r = 1/a2 where a is the cross-sectional area of the conductor, to reduce r the cross-sectional area of the conductor must be increased. On muscle this is done by causing the t-tubule to grow thicker. A t-tubule that is twice the cross sectional area of a microtubule passes four
times the power at the same voltage. It is possible then that the CNS excitatory impulse not being sufficiently amplified to result in usable muscle contraction because of disuse atrophy may be the reason for residual and chronic paralysis in those who have suffered concussive but not destructive spinal and cerebral injury. And this is in accordance with the findings of Thomas et alii mentioned at the start of this essay.
The question then arises, how is a muscle strengthened if it cannot be used, that is, how can muscle power be increased if the muscle cannot be exercised? Even more, if only a muscle that is used powerfully [‘overloaded’, as they say] can be built up, anabolized, then the strengthening of weak muscles must be an exceedingly difficult task since the ability of a muscle to be used powerfully is dependent upon the preexisting good health of that muscle where good health is taken as lack of amyotrophy or atrophy. The electrical equation for power, p=vi, provides an answer to the question of muscle strengthening of unusable muscles. What must be provided to a muscle that cannot be used is a simulation of the nerve impulse, the wave of depolarization/polarization, that causes the twitch, but that simulation must be of greater power than the nervous system is capable of. By introducing an electrochemical impulse to the neuromuscular junction that is of greater voltage and current flow one is able to overload the
muscle as if the nervous system had done so. The transverse tubule will grow in response so that the energy of contraction of the type I fiber will increase.
The field of electrotherapy is severely riddled with misunderstanding about what is happening when electrodes send impulses into the body transcutaneously. This misunderstanding is most evident in the failure to appreciate the importance of amperage and its role in electrochemistry. It is apparent too in the mistaken notion that what is important for muscle strengthening is muscle contraction, and that the way to achieve this most harmlessly is to increase electrical power to the muscle by increasing voltage only while de-emphasizing amperage. Amperage is given so little attention that in the attempts to avoid it those using DC stimulation to cause muscle to contract use voltages ten times higher than necessary so that minuscule amperages can be spurted in microsecond bursts. Amperage is a rate of current flow; it has a time factor in it. Voltage is nearly instantaneous while amperes passed depend upon a time factor. Microsecond pulses are too short to let much current pass.
Worse still are those who make muscle contract using AC or biphasic current that in effect passes no amperage at all. The contractions triggered by biphasic current are triggered as a result of voltage transmission, and do not involve any sort of biochemical change. In addition electrotherapists who rely upon AC or biphasic current do not seem to grasp that the stimulus must also be provided to the neuromuscular junction [motor endplate region] and not to the surface of the muscle in general. Traditional electrotherapeutic approaches to building muscle fail to consider that what is happening on the muscle is that electrons are being driven by an action potential originating in the post-synaptic motor neurons, that these electrons are traveling on the t-tubule to the sarcomere, and that the more of these electrons that arrive at the sarcomere the more powerful the muscle contraction. The failure to grasp this distinction is the reason why traditional electrotherapy has never been able to affect the building of muscle, and why it is not used by any athletes or NASA to prevent muscle wasting or to build muscle. It places emphasis on muscle contraction triggered by voltage transission using AC as if the contraction and not how it was triggered is what is important. Emphasis should be instead on increasing amperage to increase electrical power to a muscle, not voltage, since this is more like the action potential itself. And this is done by stimulating at the endplate region with the anode of the DC or monophasic current, thereby triggering anabolism, the building of tissue through the energizing of the synthesis of proteins. It is the anode that delivers electrons, it is the cathode that carries them off. This is the key to understanding electrochemistry and the functioning of a battery.
Electrochemistry involves oxidation/reduction reactions. These are reactions that involve the movement of an electron from the catabolic, oxidizing reaction to the anabolic, reduction reaction. This implies then two chemical reactions which are separated by a barrier, like a cell wall, and across which a voltage may be measured. A voltage is an electrical pressure, that is, a pressure which tends to drive electrons to where they are lacked. The movement of electrons is the flow of chemical energy. Reduction reactions necessary for the building of carbon/hydrogen bonds like those of all organic molecules, need to be energized, need electrons. These electrons are harvested by the cell and the multicellular organism through oxidative, catabolic, corrosive reactions like those in which stomach acids breakdown organic molecules. These reactions are seen in mitochondrial respiration in the cell, and in the breathing and gastrulation [digestion] of the multicellular organism. Every chemical reaction either takes
energy to happen, or gives off energy as it happens. Chemical energy is electrons, once known as cathode rays, and presently known as beta radiation. This sort of energy is like that which is given off by a battery. A battery is powered by chemical reactions which take place inside of it. These reactions are catabolic, corrosive or oxidative reactions, and are those kinds of reactions which give off energy, cathode rays, rather than requiring it. The cell is likened to a battery because it can give off energy as a result of oxidation through the breakdown of ATP taking place inside of it
The energy gotten from a battery can be used to power those reactions that take energy rather than giving it off. In 1800 Alessandro Volta announced his new invention to the Royal Society, the battery. Chemists started to play with it immediately because by using it the energy could be provided which would cause chemicals to break down into their constituent elements, and the chemists wanted to find out what these were. The classical example was the putting of a battery’s electrodes into water and turning it on, causing hydrogen to form at one pole and oxygen at the other as the water broke down in what came to be known as hydrolysis, the general process for all chemicals being described as electrolysis.
Electrochemists then spoke of oxidation-reduction reactions, which were reactions which involved the movement of electrons, as in direct current. Reduction is, in organic chemistry, the combination of carbon and hydrogen, a process which takes energy rather than liberates it. All biological molecules are based upon carbon and hydrogen bonds. What the electrochemists were speaking of by oxidation-reduction reactions were two reactions involving the movement of electrons from one to the other, the one an oxidative or catabolic one which liberated electrons, and the other a reduction reaction which needed electrons.
Multicellular organisms with nervous systems use those nervous systems to direct the flow of chemical energy liberated by respiration and digestion, catabolic reactions. This flow is directed to the organs and muscles of the organism so that it can continue in the search for more energy sources. This energy is delivered by the nerves to the synapses which cause both anabolism, the building of tissue, and motor functioning necessary for escape and search. Anabolism and anode are related words. The anode is the source of electrons from a battery. Just as the cell is compared to a battery, so the organism made up of cells is like a battery. Direct or galvanic current in pulses from the anode delivered by transcutaneouis electrodes to points in the body where there are clusters of synapses [ganglia and motor endplate regions], simulates the nerve impulse and stimulates the building of tissue just as would follow from exercise. And that is electrochemistry and its application to the body.
The reason for the preference of AC or biphasic current in electrotherapy over DC or monophasic current has its origins in the middle of the 19th century. AC was preferred over DC because the former would make the muscle contract strongly no matter where the electrode was placed on the muscle, no matter how badly atrophic the muscle was, and for as long as the current ran. The latter would make the muscle contract strongly only if the muscle were already healthy, only if the stimulus were provided at the endplate region, and only with the initiation of current flow. The muscle would relax after each pulse even if the current were allowed to continue. The current had to be stopped and restarted for each new contraction. But more important still was a phenomenon given little attention by traditional electrotherapists who sought to avoid it by minimizing amperage passed. This phenomenon was the ionization of the skin which showed up as blistering at the anode and pitting at the cathode. So the preference of AC
to DC for electrotherapy was driven by the desire to avoid skin damage and by the ease of use of AC in causing strong muscle contractions even on weak muscles without having to repeatedly stop and start current flow.
When a muscle is exercised over a period of time using the anode of the DC to bombard the synapses at the motor endplate region with electrons, it will be seen that at first, if the muscle is weak, the contractions triggered will also be weak. If the muscle is exercised regularly and for an extended period of time, the muscle’s contractions will be seen to grow stronger, the muscle will have more bulk, and whereas its contraction formerly caused only the movement of tissue, after numerous sessions of electrochemical stimulation the muscle’s contractions will start tomove a limb.. The muscle may be made to twitch 2000 times per second. At this rate it takes only one second to exercise the muscle, to overload it with depolarizing pulses of electrons that trigger the building of the transverse tubule, and thereby the strengthening of the muscle. At rates higher than this the muscle does not contract as strongly since it does not have the time to re-polarize fully before the next pulse. Current strengths can be
as low as 5 to 15 milliamperes, and voltages as low as 20 to 60 volts. Pulse widths can be .25 milliseconds, with time in between pulses being the same. To let the pulses be delivered for longer than a few seconds per motor endplate region at the rate of 2000 herz causes a longer reddening of the skin which may, if the stimulus is prolonged beyond a point results in the blistering of the skin. Although the cathode used, being greater in surface area than the stimulating electrode, can be allowed to remain in one place far longer than the stimulating electrode, it too needs to be moved from time to time to prevent pitting of the skin beneath it. The dispersive, cathodic electrode is between 9 and 16 square inches while the stimulating electrode is round with a diameter of 12 to 15 millimeters.
Because with the use of DC what is involved is the delivery of electrons or chemical energy to the body, it is important that the number of electrons delivered by the anode be more than the number of electrons carried off by the cathode. To insure this it is important that the cathode be made of what is called a sacrificial metal, and that is a metal which corrodes, oxidizes or rusts as its electrons are drawn from the metal rather than from the body. These electrons are then delivered to the body by the anode for a net increase in chemical energy to the body delivered in a way simulating the body’s own nervous, delivery system, i.e., the electrons are delivered to the peripheral chemical synapses found in all motor endplate regions and ganglia of the body.
There are 1,152 motor endplate regions and ganglia in the body. Spending one second on each with the stimulating electrode every 2 or 3 days maximizes the rate at which the muscle can be built given the limitations on the muscle resulting from the state of health of the body’s other subsystems like the vascular system. In other words a healthy young person will build muscle more quickly that an older, disabled person. But as that older person builds muscle and restores the body the rate of recovery will increase. The problem of disuse atrophy, whether in the astronaut, the bed-ridden patient, or the spinal cord or brain injured patient, can only be ameliorated through the use of DC stimulation, through the provision of negative electrical charge at the site of the motor endplate region using the anode. It is only through electrochemical intervention and not voltage transmission that the t-tubule can be made to grow.
Dr. Sudhansu Chokroverty et alii (1976) Archives of Neurology, vol.23, no.6, February
Dr. Claude Ghez (1991), Principles of Neural Science , 3rd ed., Kandel, Jessell, Schwartz, Appleton and Lange, Norwalk, Connecticutt, 1991, p.549.
Dr. C.K.Thomas et alii (1997), Experimental Neurology, vol.148, no.2, December.