Introduction
A key bioelectric signal that has diagnostic significance for various neuromuscular diseases is the electromyogram (EMG), which can be recorded from the skin surface with electrodes identical to those used for electrocardiography, although in some cases, the electrodes have smaller areas than those used for ECG ( <1 mm2). To record from single motor units (SMUs) or even individual muscle fibers (several of which comprise an SMU), needle electrodes that pierce the skin into the body of a superficial muscle can be employed. EMG recording is used to diagnose some causes of muscle weakness or paralysis, muscle or motor problems such as tremor or twitching, motor nerve damage from injury or osteoarthritis and pathologies affecting motor end plates.
Origin of EMGs
We have many types of muscle in the body e.g. cardiac, striated and smooth. Striated muscle in mammals can be further subdivided into fast and slow muscles. Fast muscles are used for fast movements; they include the two gastrocnemii, laryngeal muscles, extraocular muscles, etc. Slow muscles are used for postural control against gravity and include the soleus, abdominal, back and neck muscles among others. EMG recording is generally carried out on both types of skeletal muscles. It can also be done on less superficial muscles such as the extraocular muscles that move the eye balls, the eyelid muscles, and the muscles that work the larynx.
A specific striated muscle is stimulated to action by a group of motor neurons that have origin at a certain level in the spinal cord. In the spinal cord, motor neurons receive excitatory and inhibitory inputs from local feedback neurons from muscle spindles, Golgi tendon organs (responding to muscle tension), and Renshaw feedback cells. Individual motor neuron axons controlling the contraction of a specific striated muscle stimulate small groups of muscle fibers in the muscle called a single motor unit (SMU). Many SMUs comprise the entire muscle. The synaptic connections between the terminal branches of a single motor neuron axon and its SMU fibers are called motor end plates (MEPs). MEPs are chemical synapses in which the neurotransmitter, acetylcholine (ACh) is released presynaptically and then diffuses across the synaptic cleft or gap to ACh receptors on the subsynaptic membrane.
When a motor neuron action potential arrives at an MEP, it triggers the exocytosis or emptying of about 300 presynaptic vesicles containing ACh. (Approximately 3 x 105 vesicles are in the terminals of a single MEP; each vesicle is about 40 nm in diameter). Some 107 to 5 x 108 molecules of ACh are needed to trigger a muscle action potential. The ACh diffuses across the 20 to 30 nm synaptic cleft in approximately 0.5 ms; here some ACh molecules combine with receptor sites on the protein subunits forming the subsynaptic, ion-gating channels. Five high molecular weight protein subunits form each ion channel. ACh binding to the protein subunits triggers a dilation of the channel to approximately 0.65 nm. The dilated channels allow Na+ ions to pass inward; however, Cl– is repelled by the fixed negative charges on the mouth of the channel.
Therefore, the subsynaptic membrane is depolarized by the inward Na+ (i.e., its transmembrane potential goes positive from the approximately -85 mV resting potential), triggering a muscle action potential. The local subsynaptic transmembrane potential can go to as much as +50 mV, forming an end plate potential (EPP) spike fused to the muscle action potential it triggers with duration of approximately 8 ms, much longer than a nerve action potential. The ACh in the cleft and bound to the receptors is rapidly broken down (hydrolized) by the enzyme cholinesterase resident in the cleft, and its molecular components are recycled. A small amount of ACh also escapes the cleft by diffusion and is hydrolysed as well.
Once the postsynaptic membrane under the MEP depolarizes in a super-threshold end plate potential spike, a muscle action potential is generated that propagates along the surface membrane of the muscle fiber, the sarcolemma. It is the muscle action potential that triggers muscle fiber contraction and force generation. Typical muscle action potentials, recorded intracellularly at the MEP and at a point 2 mm from the initiating MEP are illustrated in the figure below:
A skeletal muscle fiber action potential propagates at 3 to 5 m/sec; its duration is 2 to 15 ms, depending on the muscle and its swings from a resting value of approximately -85 mV to a peak of approximately +30 mV. At the skin surface, it appears as a triphasic spike of 20- μV to 2000 –μV peak amplitude.
To ensure that all of the deep contractile apparatus in the center of the muscle fiber is stimulated to contract at the same time and with equal strength, many transverse, radially directed tubules penetrate the center of the fiber along its length. These T-tubules are open to the extracellular fluid space, as is the surface of the fiber, and they are connected to the surface membrane at both ends. The T-tubules conduct the muscle action potential into the interior of the fiber in several locations along its length.
Running longitudinally around the outsiders of the contractile myofibrils that make up the fiber are networks of tubules called the sarcoplasmic reticulum (SR). When the muscle action potential penetrates along the T-tubes, the depolarization triggers the cisternae to release calcium ions into the space surrounding the myofibrils’ contractile proteins. The Ca++ binds to the protein troponin C, which triggers contraction by the actin and myosin proteins.
Asynchronous stimulation of all the motor neurons stimulating a muscle produces what is termed to as a muscle twitch, i.e. the tension initially falls a slight amount, rises abruptly, and then falls more slowly to zero again. Sustained muscle contraction is caused by a steady (average) rate of (asynchronous) moto neuron firing. When the firing stops, the muscle relaxes.
Related: Electromyogram (EMG)
Muscle relaxation is an active process. Calcium ion pumps located in the membranes of the sarcoplasmic reticulum (SR) longitudinal tubules actively transfers Ca++ from outside the tubules to inside the SR system. The lack of Ca++ in proximity to troponin C allows relaxation to occur. In resting muscle, the contraction, [Ca++] is about 10-7 M in the myofibril fluid. In a twitch, [Ca++] rises to approximately 2 x 10-5 M and in a tetanic stimulation [Ca++] is about 2 x 10-4 M. The Ca++ released by a single motor nerve impulse is taken up by the SR pumps to restore the resting [Ca++] level in about 50 msec.
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