Surface EMG (SEMG) biofeedback is arguably the most widely used biofeedback modality due to its diverse applications ranging from neuromuscular to psychophysiological disorders. The electromyograph measures the electrical changes in the muscle fiber membrane that precede contraction, and not muscle contraction itself. However, the SEMG does linearly correlate with isotonic muscle contraction over a range of contraction force.
This unit discusses Descriptions of most commonly employed biofeedback modalities: SEMG (III-A 1-2) and Muscle anatomy and physiology; antagonistic and synergistic muscle groups (IV-A).
Students completing this unit will be able to discuss:
The human body contains three types of muscles: skeletal, smooth, and cardiac.
Skeletal muscles are striated (striped) due to alternating light (I) and dark (A) bands. They are called skeletal muscles because most of them move the bones that comprise the skeleton. We control skeletal muscles voluntarily and involuntarily.
We can voluntarily control skeletal muscles through the somatic division of the peripheral nervous system because their contraction produces proprioceptive feedback. Contract a skeletal muscle like the biceps brachii and the arm flexes. This limb movement provides the information needed to adjust arm movement.
Most muscles are also controlled involuntarily. We are often unaware of the rhythmic movement of the diaphragm and the intercostal muscles that allow us to breathe. The monosynaptic stretch reflex, that maintains postural muscle tone and stabilizes limb position, also operates unconsciously.
Smooth muscles appear nonstriated under a microscope.
There are two kinds of smooth muscle: single-unit and multiunit smooth muscle.
Single-unit smooth muscle comprises part of the walls of small arteries and veins, and the stomach, intestines, uterus, and urinary bladder
Multiunit smooth muscle is found in the walls of large arteries, airways to the lungs, the arrector pili muscles that move hair follicles, the muscle rings of the iris, and the ciliary body that focuses the lens.
Compared with skeletal muscles, smooth muscle contraction starts more gradually and persists longer. Smooth muscles can shorten and stretch more than other kinds of muscles (Tortora & Derrickson, 2006). Smooth muscles usually operate involuntarily and some tissues have an intrinsic rhythm (autorhythmicity). They are jointly controlled by the autonomic branch of the peripheral nervous system and the endocrine system.
Before biofeedback training, most patients cannot voluntarily control smooth muscles since their contraction does not provide sufficient feedback. For example, blood vessel dilation or constriction in the fingers produces such "faint" feedback that we are ordinarily unaware of these changes. Biofeedback converts smooth muscle activity into a digital display, colored bar, or tone that a patient can use to voluntarily warm or cool the fingers.
Temperature biofeedback illustrates a crucial concept. We can teach patients to control "involuntary" processes by supplementing inadequate natural feedback.
Cardiac muscle comprises most of the heart wall. Cardiac muscle has crossed striations that allow the heart to pump. Cardiac muscle fibers contain the same actin and myosin myofilaments, bands, zones, and Z discs as skeletal muscles.
Cardiac muscle striations (bands) cross like X’s, which allows cardiac muscle to perform a pumping action. This action ejects blood from the four chambers of the heart. Adjacent cardiac muscle fibers attach to each other via intercalated discs (transverse thickened regions of the sarcolemma) that conduct muscle action potentials via gap junctions.
Cardiac muscle contraction lasts 10-15 times longer than skeletal muscle contraction due the gradual movement of calcium ions into the sarcoplasm (muscle fiber cytoplasm).
While skeletal muscle contraction only occurs when a motor neuron releases acetylcholine, the heart rhythm is generated by pacemaker cells located at the sinoatrial and atrioventricular nodes of the heart. The autonomic branch of the peripheral nervous system and the endocrine system jointly adjust heart rate by acting on these pacemakers (Tortora & Derrickson, 2006).
As with smooth muscle, most patients cannot voluntarily control the heart rhythm before biofeedback training. Biofeedback supplements cardiac muscle feedback to teach patients to slow their heart rate or reduce the frequency of abnormal rhythms like premature ventricular contractions (PVCs) when they are distressed.
The skeletal muscle system consists of extrafusal muscle fibers and connective tissue. Extrafusal fibers are striated (striped) due to alternating light and dark bands. These fibers run from 10-100 mm in diameter and up to 30 cm in length. The sarcolemma, a plasma membrane, encloses individual fibers.
Each extrafusal muscle fiber is composed of cylindrical myofibrils (hundreds to thousands) built from smaller myofilaments (thin and thick). Thin myofilaments are mainly composed of the protein, actin, and produce light-colored bands. Thick myofilaments are mainly composed of myosin and produce dark-colored bands. Myofilaments are shorter than a muscle fiber and are stacked in compartments called sarcomeres (separated by dense zones called Z discs).
Actin myofilaments are actually attached to Z discs. Muscle fibers generate force by pulling Z discs together, which shortens the sarcomeres. This force, called active tension, produces movement at joints and resists active stretching due to external forces like gravity.
Connective tissue packages muscle fibers together and connects muscle fibers to bone (and skin, muscle, and deep fascia). Fascia, fibrous connective tissue, divides muscles into functional groups. Muscle fiber bundles are called fascicles. Tendons are dense fascia that connect muscles to other structures. Connective tissue provides the skeletal muscle system's elasticity. Connective tissue elasticity produces passive tension which allows muscle fibers to produce, sum, and transmit force (Tortora & Derrickson, 2006).
Skeletal muscle fibers are organized into motor units that consist of an alpha motor neuron and the muscle fibers it controls. In the diagram below, a motor neuron's axon branches in order to simultaneously innervate five extrafusal muscle fibers. This motor unit is designed for precise control instead of generation of force.
An alpha motor neuron's cell body lies in the anterior horns of the spinal cord. The axon may extend three feet until it synapses with the middle of a muscle fiber. Muscles that perform several actions may be innervated by separate motor neurons.
Alpha motor neurons, which conduct messages from the central nervous system to skeletal muscles, are called efferent nerves because they leave the central nervous system.
A motor unit contains an average of 150 muscle fibers that contract completely or not at all (Tortora & Derrickson, 2006). All motor unit muscle fibers share the same composition. Smaller motor units are used for precise movement like the extraocular muscles which have an average of 33 muscle fibers. Larger motor units are designed to deliver power like the gastrocnemius whose motor units contain from 100 to 2,000 muscle fibers (Fox, 2006).
In SEMG biofeedback, we use an electromyograph to monitor the total electrical output in microvolts (millionths of a volt) from all the motor units that are firing near our surface electrodes. Contraction strength and SEMG signal voltage are proportional to the number of recruited motor units.
The muscles comprising each motor unit are protected against exhaustion by a refractory period of about 5 msec during which they lose their excitability. Cardiac muscle has a 300-ms refractory period (Tortora & Derrickson, 2006). Motor units control adjoining bundles of fibers to produce coordinated muscle contraction.
A skeletal muscle contains motor units that differ in both number and size of fibers. Motor unit firing is rotated to prevent fatigue and produce smooth movement. Motor units are recruited in order of size. Smaller units, which are highly excitable, are recruited first since they build up tension in gradual steps. These units provide the precise motor control required in tasks like writing. Larger motor units are normally recruited last as additional force is required, as in performing a bench press (Tortora & Derrickson, 2006). In life-threatening emergencies, many motor units may be recruited at once as part of the fight-or-flight response.
An alpha motor neuron divides into terminal branches that penetrate the muscle fiber membrane. The muscle fiber beneath a terminal branch is called a motor end plate. Both the terminal branch and motor end plate comprise the neuromuscular junction. When an action potential reaches the terminal branches, calcium ions flow inside and vesicles containing the neurotransmitter acetylcholine (ACh) expel their contents into the neuromuscular junction.
An alpha motor neuron's release of acetylcholine depolarizes skeletal muscles (producing the SEMG signal) and initiates skeletal muscle contraction.
When two ACh molecules bind to a nicotinic ACh receptor on the motor end plate, a sodium channel opens allowing sodium ions to enter the muscle fiber and then potassium ions to leave the fiber's interior. The inflow of positive sodium ions shifts the end plate's internal voltage from -80 to -90 mV to +50 to +75 mV producing a muscle action potential (MAP). This skeletal muscle fiber depolarization (positive shift in membrane potential) triggers muscle contraction (Guyton & Hall, 2006).
Below is a BioGraph ® Infiniti SEMG display.
The enzyme acetylcholine esterase (AChE) deactivates ACh to allow muscle fiber relaxation. The sodium-potassium pump restores the muscle fiber to a resting negative voltage so that it can be depolarized, again, resulting in new contraction (Tortora & Derrickson, 2006).
Skeletal muscle fibers vary in structure and function. Three fiber categories have been identified: slow oxidative, fast oxidative, and fast glycolytic. Skeletal muscles are composed of different proportions of these fibers depending on muscle action. However, the motor units that make up a muscle contain the same kind of fiber.
Slow oxidative (SO) fibers are also called slow twitch fibers. These red fibers are rich in myoglobin, mitochondria, and capillaries. Their capacity to produce ATP through oxidative metabolism is high. Since SO fibers split ATP at a slow rate, contraction velocity is slow and these fibers are highly resistant to fatigue. Postural muscles contain a high proportion of SO fibers. This allows continuous isometric contraction to resist gravity.
Fast oxidative-glycolytic (FOG) fibers are also called fast twitch A fibers. These red fibers are rich in myoglobin, mitochondria, and capillaries. Their capacity to produce ATP through oxidative metabolism is high. FOG fibers split ATP rapidly producing high contraction velocities. These fibers show less resistance to fatigue than SO fibers. These fibers comprise a large percentage of a sprinter's leg muscles.
Fast glycolytic (FG) fibers are also called fast twitch B fibers. These white fibers are poor in myoglobin, mitochondria, and capillaries, but contain considerable stores of glycogen. FG fibers produce ATP using anaerobic metabolism that cannot continuously supply needed ATP. As a result, these fibers fatigue easily. FG fibers split ATP rapidly producing high contraction velocities. Arm muscles contain a high proportion of these fibers.
Exercise can change the properties, but not the number, of muscle fibers. Endurance exercises like running can slowly transform FG fibers into FOG fibers, increasing diameter, mitochondria, capillaries, and strength. In contrast, exercises like weight lifting that require explosive force for brief periods increase FG fiber size and strength.
Muscle biopsies of chronic pain patients raise the possibility that their postural muscles contain a disproportionate number of FG fibers that fatigue more rapidly than SO fibers. Increased vulnerability to fatigue could result in buildup of muscle contraction byproducts (like lactate and hydrogen ions) that can stimulate pain receptors (Tortora & Derrickson, 2006).
The SEMG records muscle action potentials from skeletal motor units. Inserted electrodes can detect signals from 2 to 10,000 Hz. The upper limit for surface recording is 1,000 Hz since tissue (skin, subcutaneous fat, muscle, and connective tissue) absorbs higher frequencies.
Below is a BioGraph ® Infiniti SEMG FFT display of a frontales placement. Note that the bulk of the signal energy is below 100 Hz with the peak frequency (highest amplitude frequency) under 40 Hz. Note that lower frequency amplitude increases with stronger muscle contraction.
The amplitude or strength of an electromyogram reflects the number of active motor units, their firing rate, and distance from the electrodes.
The greatest concentration of SEMG power (energy) lies between 10 and 150 Hz. Strong muscle contraction shifts the distribution of SEMG power upwards (more μV) and to the right toward higher frequencies (Stern, Ray, & Quigley, 2001).
Skeletal muscle fiber depolarization (which produces the SEMG signal) lasts 1 to 2 ms and ends before a muscle fiber starts to contract. The SEMG reflects muscle depolarization, not muscle contraction. The period of mechanical contraction is considerably longer and lasts from 10-100 ms due to the removal of calcium ions and muscle elasticity (Tortora & Derrickson, 2006).
A muscle action potential depolarizes the interior of the muscle fiber and releases stored calcium ions from the sarcoplasmic reticulum. The presence of calcium ions allows actin (thin) and myosin (thin) myofilaments to bind to each other forming cross bridges. Simple contact will not shorten a muscle. Myosin must bind to actin, push it inward, break contact, and bind again. These power strokes use stored energy released by splitting ATP.
Robert Sabbadini, Ph.D. and Jeff Sale produced this animation based on the Color atlas of physiology by Agamemnon Despopoulos and Stefan Silbernagl (1991), New York: Thieme Medical Publishers, Inc.
Remember that actin is attached to the Z discs that define each sarcomere (muscle compartment). When myosin ratchets actin inward toward a sarcomere's center, the entire sarcomere shortens to up to 50 percent of its resting length. Sarcomere shortening produces the force of muscle contraction that can move or stabilize limbs. A sarcomere's average length is 2.5 µm, it can shorten to about 1.5 µm, and can stretch to about 3 µm.
A skeletal muscle fiber consists of I bands, A bands, H bands, Z discs, and M lines. I bands are comprised of actin filaments. A bands contain overlapping actin and myosin filaments. H bands only contain myosin filaments. Z discs are regions where the actin myofilaments of two adjacent sarcomeres appose each other via the protein alpha-actinin. Finally, M lines are made up of vertical connections between myosin myofilaments mediated by proteins like myomesin (Slomianka, 2004; Tortora & Derrickson, 2006).
Muscle contraction can be isometric or isotonic. Muscles produce tension with minimal fiber shortening during isometric contraction. For example, when you press your hands against themselves, muscles do not appreciably shorten due to the resistance of the opposing hand. Posture results from continuous isometric contraction. SO fibers are specialized for this contraction due to their resistance to fatigue.
Isotonic contraction produces movement by exerting tension on an attached structure (bone). These contractions may either be concentric or eccentric. A pull-up involves concentric contraction where fibers shorten as your body moves upward. In contrast, a squat involves eccentric contraction where fibers lengthen as you lower yourself (Tortora & Derrickson, 2006).
Muscles groups work together to perform actions. For example, you contract at least nine muscle groups in a specific sequence to open your mouth. You activate a different sequence to close your mouth. SEMG biofeedback records the electrical activity of surface muscles. The SEMG usually monitors the activity of muscle groups instead of individual muscles.
Muscle spindles are stretch receptors that lie in parallel with skeletal muscle fibers. When their annulospiral receptors stretch as a muscle lengthens, they activate alpha motor neurons to strengthen muscle contraction to increase muscle tone. Physicians assess the unisynaptic stretch reflex when they stretch the patellar tendon with a rubber mallet to elicit a knee jerk (Wilson, 2003).
Golgi tendon organs are force detectors that lie in series with skeletal muscle fibers. When excessive contraction threatens to damage muscle and tendon, they inhibit the responsible alpha motor neurons to prevent injury. This protective mechanism is called the tendon reflex (Wilson, 2003).
Skeletal muscles attach to the articulating bones of a joint and transmit force through the tendons to bones and tissues like the skin. Muscle contraction moves the two bones that comprise a joint unequally and pulls one of the articulating bones at a joint toward the more stationary bone. A muscle's attachment to the more stationary bone is called its origin and to the more movable bone is called its insertion. Movement produced by a muscle's contraction is its action. The same muscle can perform several different actions.
Muscles that operate a joint are arranged in opposing agonist-antagonist pairs. An agonist produces a specific movement and is opposed by an antagonist. When the biceps brachii (agonist) contracts to flex the forearm at the elbow joint, the triceps brachii (antagonist) must relax or else flexion will be prevented. When agonist and antagonist muscles contract concurrently in stroke patients, this can produce spasm and rigidity.
Synergists stabilize a joint to reduce the origin's interference with movement. The deltoid and pectoralis major anchor both the arm and shoulder when the biceps brachii (agonist) contracts to flex the forearm. The same muscle can be an agonist, antagonist, or synergist depending on its movement.
The quadriceps and tibialis anterior muscles of your leg contract together to dorsiflex (bend the foot upwards) during the forward swing phase of walking. The same muscle can be an agonist, antagonist, or synergist depending on its movement (Tortora & Derrickson, 2006).
Instructions: click on the magnifying glass icon to see movie clips
that illustrate muscle actions. Click on each movie clip to
start or replay it.
Flexors decrease the angle between two bones. Biceps brachii flexes and supinates (turns up) the forearm. Weight lifters flex forearms, not muscles.
Extensors increase the angle between two bones. Triceps brachii extends the forearm. The motor control system coordinates synergist, flexor, and extensor contraction to produce the needed limb position.
Abductors move a limb away from the center of the trunk or a body part. The abductor pollicis moves the thumb outward.
Adductors move a limb toward the center of the trunk or a body part. Adductor pollicis moves the thumb inward.
Levators produce upward movement. Levator scapulae elevates the shoulder blades.
Depressors produce downward movement. Pectoralis minor lowers the shoulder blades.
Supinators turn the palm upward (anteriorly). Supinator exposes the anterior side of the forearm.
Pronators turn the palm downward (posteriorly). Pronator teres exposes the posterior side of the forearm.
Dorsiflexors point the toes toward the shin (superiorly) through flexion at the ankle joint. Tibialis anterior dorsiflexes and inverts the foot during the swing phase of walking. This is disrupted during a neuromuscular disorder called foot drop in which the toes drag on the ground.
Plantar flexors point the toes downward (inferiorly) through extension at the ankle joint. Tibialis posterior plantar flexes and inverts the foot.
Invertors, turn the sole of a foot inward. Flexor digitorum longus plantar flexes, flexes toes, and inverts the foot.
Evertors turn the sole of a foot outward. Extensor digitorum longus dorsiflexes, extends toes, and everts the foot.
Tensors make a body part more rigid. Tensor fasciae latae flexes and abducts the thigh.
Rotators move a bone around a longitudinal axis. Obturator externus rotates the thigh laterally (Tortora & Derrickson, 2006).
Basmajian and Blumenstein (1980) and Neblett (2006) were the references for sensor placement. Tortora and Derrickson (2006) was the resource for muscle action.
Action: draws the scalp forward, raises eyebrows, and wrinkles the forehead
Sensor placement: locate the actives between the eyebrows and hairline
Clinical application: anxiety, stress profile, and tension-type headache
Action: elevates and retracts the mandible (jaw)
Sensor placement: locate actives above the zygomatic arch (horizontal bony ridge from temporomandibular joint to the cheek)
Clinical application: tension-type headache
Action: elevates and protracts the mandible
Sensor placement: locate actives using the angle of the jaw as a landmark
Clinical application: temporomandibular joint disease (TMD)
Action: draws the corner of the mouth upward and outward when you smile
Sensor placement: locate actives above and at approximately a 45o angle from corner of the mouth
Clinical application: Bell's palsy and stroke
Action: closes the eyelids and wrinkles the forehead
Sensor placement: locate actives immediately below the center of each eye
Clinical application: Bell's palsy, blepharospasm, and stroke
Action: flexes the vertebral column and rotates the head to the opposite side (contract left SCM and head twists to right)
Sensor placement: center the actives 50% of the distance from the mastoid (bulge behind the outer ear) to the medial end of the clavicle (collarbone), which places them below the jaw along a vertical line
Clinical application: torticollis
Action: rotates and elevates the scapula (shoulder blade), extends, flexes, and rotates the head and neck
Sensor placement: center the actives between C7 (seventh cervical vertebra) and the angle of the acromion (posterior to bony triangle at the top of the shoulder)
Clinical application: shoulder pain and tension-type headache
Action: abducts, flexes, extends, and rotates the arm
Sensor placement: locate the actives behind the angle of the acromion (posterior to the bony triangle at the top of the shoulder)
Lateral head of triceps brachii
Action: extends the elbow joint
Sensor placement: center the actives 50% of the distance between the angle of the acromion (posterior to bony triangle at the top of the shoulder) and the olecranon process (behind the elbow)
Action: flexes and supinates the forearm
Sensor placement: center the actives over the bulge in this muscle
Action: extends, adducts, rotates the arm, and moves the arm inferiorly and posteriorly
Sensor placement: center the actives under the inferior angle of the scapula (shoulder blade)
Extends carpi ulnaris
Action: extends and adducts the hand at the wrist joint
Sensor placement: center the actives 1/3 of the distance between the posterior medial epicondyle and the posterior styloid process of the forearm
Abductor pollicis brevis
Action: abducts the thumb and assists in opposition
Sensor placement: center the actives over the most prominent bulge at the proximal end of the thumb
Action: adducts the thumb
Sensor placement: center the actives within a triangle that starts at the skin web
Vastus lateralis (VL) and vastus medialis (VMO)
Action: each muscle extends the leg at the knee joint
Sensor placement: locate the actives vertically within the oval bulges above the patella (kneecap) for the vastus lateralis (VL) and vastus medialis obliquus (VMO) sites, respectively.
Action: dorsiflexes and inverts the foot
Sensor placement: center the actives vertically within an oval region the tuberosity of the tibia (shin bone)
Clinical application: foot drop
Action: plantar flexes the foot and flexes the knee joint
Sensor placement: center the actives vertically over the bulges of either head of this muscle
Erector spinae (sacrospinalis)
Action: maintains erect position of the spine and extends the vertebral column
Sensor placement: locate active pairs lateral to the spine, above the iliac crest (rounded upper margins of the ilium bone above the buttocks) about L4 and below the bottom of the ribs at about L2. Clinicians should palpate these landmarks to achieve consistent lumbar placements
Clinical application: low back pain
Now that you have completed this module, identify the muscles you monitor and train in your clinical practice using the muscle diagram shown above.
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Basmajian, J. V., & Blumenstein, R. (1980). Electrode placement in EMG biofeedback. Baltimore: Williams & Wilkins.
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Neblett, R. (2006). Personal communication.
Stern, R. M., Ray, W. J., & Quigley, K. S. (2001). Psychophysiological recording (2nd ed.). New York: Oxford University Press.
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