The Doorway to Muscle Contraction
Pathology Perspectives

By Kalyani Premkumar

Originally published in Massage Bodywork magazine, February/March 2005.
Copyright 2005. Associated Bodywork and Massage Professionals. All rights reserved.

What is common between Botox, trigger points, myasthenia gravis, and muscle relaxants? They all affect skeletal muscle: Botox causes muscle paralysis; trigger points produce pain; myasthenia gravis and muscle relaxants result in weakness. But what is truly common is that all affect the myoneural junction -- the doorway to muscle contraction.

Let's explore the structure of the myoneural junction, the process of communication between nerve and
muscle, and how the above factors effectively disrupt communication.

Communication Patterns

Figure 1 -- A Motor Unit.
In order for skeletal muscle cells (muscle fibers) to contract, it is imperative they have communication with a motor neuron. A motor neuron is a nerve cell whose cell body is located in the spinal cord or brain. The axon of the nerve cell meanders toward the muscle it supplies. As it reaches the muscle, it branches: each branch going to a muscle fiber. The motor neuron, its axon branches, and all the muscle fibers it supplies is known as a motor unit and each muscle consists of numerous motor units (See Figure 1). When a motor neuron is stimulated, all the muscle fibers it innervates contract. On an average, a motor neuron innervates about 150 muscle fibers; however, in muscles that require precise control, a neuron may innervate only two or three fibers. By stimulating few or many motor units in a muscle, we are able to alter the force of contraction to pick up a pen or lift a table. In order to do this, the nerve has to communicate our intentions to the muscle fiber. This is where the myoneural junction comes into play.

The junction between a neuron and the muscle fiber it communicates with is known as the myoneural or neuromuscular junction (See Figure 2). Interestingly, there is no direct communication between the two. A space -- the synaptic cleft -- separates the two structures. Where they (the muscle cell memb

Figure 2 -- Structure of a Myoneural Junction.
rane and nerve ending) come close to each other, the nerve ending is modified to form a bulge -- the synaptic knob. Inside the synaptic knob are vesicles containing acetyl choline (ACh). The muscle cell membrane beneath the nerve ending (motor end plate) is also modified. It contains specialized proteins -- receptors that have an attachment site for ACh.

When the nerve is stimulated, a series of events quickly follow. First, the inside of the nerve ending becomes more positive (depolarized) than its resting state. This triggers calcium channels on the nerve cell membrane to open. Calcium ions flow rapidly into the nerve cytoplasm along its concentration gradient. The increase in calcium levels inside the nerve cytoplasm serves as the trigger for the synaptic vesicles to fuse with the nerve cell membrane and release the ACh into the synaptic cleft.

The ACh gets attached to the receptor proteins located in the motor end plate. The receptors are actually ligand-gated channels -- i.e. channels that are manipulated by chemicals. When ACh gets attached to the receptors, the channels open and sodium ions rush into the muscle cytoplasm (also known as sarcoplasm) along its concentration gradient. Since sodium ions carry positive charge, this results in the inside of the sarcoplasm becoming more positive as compared to its surrounding. The change in potential inside the muscle fiber is the trigger for sliding of the myofilaments actin and myosin with resultant shortening of the muscle fiber-muscle contraction.

The ACh, attached to the receptors as well as that in the synaptic cleft, is quickly removed by an enzyme known as acetyl cholinesterase. When ACh is no longer attached to the receptor, the ion channels close and no more sodium enters the muscle. The sodium ions that have already entered are removed by the sodium-potassium pump located on the sarcolemma. When sodium levels decrease in the sarcoplasm, the trigger for muscle contraction is removed and the muscle relaxes, ready to be stimulated again. If the stimuli arrive repeatedly and quickly, a sustained contraction of the muscle is produced. The above description,1 though simplified, gives an overview of how the nerve ending communicates with the muscle fiber.

Where are these Doorways of Muscle?
Research has shown that myoneural junctions tend to be concentrated in the belly of muscles with parallel arrangement of fibers.2 In muscles such as the gastrocnemius, deltoid, flexors, and extensors of the forearm, that have more complicated muscle fiber arrangements, the innervation zones seem to be more widely distributed. Similarly, in muscles such as gracilis and sartorius, where the muscle fibers are of varying length, the myoneural junctions are scattered throughout.3

What is Botox and How Does it Work?
Botox is a potent neurotoxin produced by the anaerobic bacteria Clostridium botulinum. This bacterium is found in soil and water. Botulinum toxin is the most poisonous substance known and ironically, it is the first biological toxin to be licensed for treatment in human disease.4 It is responsible for botulism -- a paralytic disease seen in some types of wound infection and food contamination.

Following ingestion of food containing the toxin or contamination of wound, the neurotoxin is absorbed into the blood which in turn transports it to the myoneural junction and other peripheral locations where acetyl choline is the neurotransmitter. At the myoneural junction, the toxin enters the nerve ending and irreversibly prevents the fusion of the synaptic vesicles with the nerve cell membrane -- an event needed to release ACh into the synaptic cleft. The outcome is flaccid paralysis of muscle until the nerve endings sprout again anew.5

Realizing the potential of this toxin to reduce muscle tone, physicians routinely inject it into hypertonic muscles. In the last decade, botulinum toxin is increasingly used to treat a variety of ailments causing muscle hypertonicity such as cervical torticollis, strabismus, blepharospasm, stroke, spinal cord injuries, multiple sclerosis, cerebral palsy, and cervical dystonia, among many others.6,7,8 Equally popular is its cosmetic use to reduce wrinkles.

Botox injection is expensive -- more than $400 for 100 units (approximate dosage used in one session). The general consensus for maximum dose is about 400 to 600 units per session. The effect of the toxin decreases with time and the injections have to be repeated every 3 to 5 months.9 In addition, if the dosage is too high, it may not only reduce the tone, but also cause paralysis of muscle. In December, an outbreak of botulism in Florida was attributed to the use of Botox injections for concealing wrinkles.10 Another problem, relating to repeated use of the toxin, is the development of antibodies against the toxin.

Implication for Bodyworkers. Bodyworkers need to be aware that this toxin causes only motor loss and has no effects on the sensations. Massage or early manipulation of the injection site can speed up absorption and spread of toxin leading to paralysis of the injected as well as adjacent muscles.

Trigger Points and Myoneural Junction

Figure 3 -- Integrated Hypothesis for Origin of Myofascial Trigger Points.
Trigger points (TrPs) are defined as localized spots of tenderness in a nodule or a palpable taut band of muscle fibers.11 TrPs are believed to be caused by dysfunction of the motor end plate. According to the integrated hypothesis for the origin of myofascial trigger points,12 there is an abnormal increase in production and release of ACh in some myoneural junctions even when the muscle is at rest. This results in localized, sustained contraction of the muscle fiber (taut band). The shortening of muscle fiber compresses local blood vessels, reducing the nutrient and oxygen availability (See Figure 3). This, in turn, causes release of substances that sensitize pain receptors and pain ensues.

Implication for Bodyworkers. TrPs are responsive to stretch therapy used in massage. Stretch therapy, by lengthening the sarcomeres and reducing overlap between actin and myosin molecules, reduces energy consumption of the local tissue. Blood flow to the muscle fibers is also restored when the muscles are relaxed by stretch. When more blood flows through this region, nutrients and oxygen are made available and substances that cause pain are washed away.13

Myasthenia Gravis and Myoneural Junction
Myasthenia gravis is a chronic autoimmune disease characterized by muscle weakness and easy fatigability of muscle. It is seen in people of all ages, with higher incidence in women between 20 to 30 years and men between 50 and 60 years of age.14,15 Drooping of the eyelids, difficulty in swallowing, and abnormal speech are some of the common symptoms. In this disease, the immune system attacks muscle cells at the neuromuscular junction, with resultant decrease in ACh receptors. When a motor nerve is stimulated, despite release of normal amounts of ACh, there are fewer receptors to bind to ACh. This in turn results in fewer sodium channels opening in the motor end plate and smaller potential changes inside the muscle.

The outcome? Weak or no contractions of muscle. The disorder is treated by drugs that reduce anticholinesterase (an enzyme that destroys ACh) activity; suppression of immunity, (e.g., use of steroids); removal of the thymus; and procedures to remove the antibodies that target ACh, among others.

Implications for Bodyworkers. Bodywork such as massage may be helpful in reducing the fatigue in the muscles by increasing circulation and lymph drainage. Stimulatory massage may help improve weakness. If the client is on steroids, he/she may exhibit the side effects of the drug, such as lowering of immunity and increased susceptibility to infections. Suitable precautions need to be taken.16

Some Chemicals Affecting the Myoneural Junction
Botox, trigger points, and myasthenia gravis are not the only problems that affect the myoneural junction. Many chemicals such as pesticides and muscle relaxants also have an effect here. For example, the muscle relaxant curare (originally, a poison used in arrow heads by indigenous tribes), causes paralysis by blocking ACh receptors and preventing depolarization of the sarcolemma. Most antihypertensive drugs cause relaxation of smooth muscle in the walls of blood vessels by affecting the myoneural junction. Many antiasthmatics work the same way -- only they affect the smooth muscle in the walls of bronchi and bronchioles.

Myoneural Junction and Research
One of the concerns raised in relation to botulinum toxin is its use in bioterrorism.17 It is estimated that a single gram of crystallized botulinum toxin could kill more than 1 million people.18 Further research is underway in relation to antitoxins and the characteristics of the seven different types of botulinum toxins that have been identified.

Failure of myoneural junction activity has been implicated as one of the causes of the condition known as post polio syndrome.19 The polio virus injures and destroys motor neurons. During recovery, the axons of surviving motor neurons sprout to reach the orphaned muscle fibers. In the process, not all muscle fibers regain their innervation, leading to overuse of those that do get innervated. Studies indicate drugs that help improve transmission across the myoneural junction could be beneficial for these conditions.

The location of myoneural junctions in any given muscle is of importance in order to determine the injection site (for treatment of hypertonic muscles) and for the placement of electrodes in electromyogram studies.20.,21

Myoneural junctions are complex structures that help transmit messages from nerve to muscle. The solution to a number of disorders resulting in muscle paralysis still lies hidden in this mystifying doorway to every skeletal muscle fiber. Further research is needed to unravel this marvelous mystery.

Kalyani Premkumar, M.D., Ph.D., a physician and certified massage therapist, is an adjunct assistant professor, Faculty of Medicine, University of Calgary; an instructor at the Center for Complementary Health Education, Mount Royal College, Calgary, Canada; and tutor at Athabasca University, Canada. She is the author of The Massage Connection -- Anatomy and Physiology, Pathology A to Z -- A Handbook for Massage Therapists, and Medical Terminology, A Beginner's Guide.

1 Premkumar, K. The Massage Connection -- Anatomy and Physiology. Baltimore, MD: Lippincott Williams Wilkins; 2004.
2 Childers, M.K. Targeting the neuromuscular junction in skeletal muscles. American Journal of Physical Medicine Rehabilitation 2004;83(10):S38-S44.
3 Ibid.
4 Aaron, SS, et al. Botulinum toxin as a biological weapon. Journal of the American Medical Association 2001;285(8): 1059-1070. Also available at:
5 Abrutyn, E. Botulism. In: Fauci, A.S., et al. Editors. Harrison's Principles of Internal Medicine. 14th Ed. New York, NY: McGraw Hill; 1998. 904-905.
6 Childers, S38-S44.
7 Aaron,1059-1070.
8 Francisco, G.E. Botulinum toxin: dosing and dilution. American Journal of Physical Medicine Rehabilitation 2004;83(10):S30-S37.
9 Ibid.
10 Botox suspected in four botulism cases. Available at: botox/index.html Accessed Dec. 6, 2004.
11 Mense, S, Simons, D.G. Russell, I.J. Muscle Pain, understanding its nature, diagnosis, and treatment. Baltimore, MD: Lippincott Williams Wilkins; 2001.
12 Ibid.
13 Ibid.
14 Abrutyn, 904-905.
15 Premkumar, K. Pathology A to Z -- A handbook for massage therapists. 2nd Ed. Calgary, Alb: VanPub Books; 1999.
16 Ibid.
17 Aaron,1059-1070.
18 Ibid.
19 Post polio research update. Polio Outreach of Washington. Available at: index.html. Accessed Dec. 6, 2004.
20 Childers, S38-S44.
21 Francisco, S30-S37.

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