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Denervated muscles are characterized by extensive muscle atrophy, intramuscular fat infiltration, and fibrous tissue formation. They exhibit abnormal spontaneous activity, with an increased number of acetylcholine receptors on the muscle membrane, resulting in hypersensitivity and spontaneous depolarization. To elicit muscular contractions, the cellular membrane of each target muscle fiber must be depolarized. This can be achieved through electrical stimulation, such as functional electrical stimulation (FES) using direct current (DC) or alternating current (AC). DC stimulation involves a constant flow of electrons in one direction, while AC can be delivered at high frequencies to reduce skin impedance and deliver more current to the target area. The intensity and duration of the electrical stimulus play a crucial role in depolarizing denervated muscles effectively.
| Characteristics | Values |
|---|---|
| Denervated muscle contraction | Requires depolarization of the T-tubules |
| Denervated muscle contraction and relaxation | More sluggish than innervated muscle |
| Denervated muscle stimulation | Requires long duration pulses |
| Denervated muscle sensitivity | Insensitive to short duration stimuli |
| Denervated muscle pulse duration | Below 100 ms requires higher stimulus intensity |
| Denervated muscle pulse frequency | Cannot exceed 10 Hz for 100 ms pulse duration |
| Denervated muscle depolarization | Requires higher stimulus intensity if pulse duration is decreased |
| Denervated muscle | Has a higher number of acetylcholine receptors |
| Denervated muscle | Is more liable to depolarize spontaneously |
| Denervated muscle | Has a higher rate of rise in the earlier denervation stages |
| Denervated muscle | Has a reduced transmembrane K+ gradient |
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What You'll Learn
Denervated muscle is relatively insensitive to short-duration stimuli
Denervation is the loss of nerve supply to a muscle, which can occur due to nerve damage or various disorders. This can lead to muscle atrophy, degeneration, and a reduction in muscle fibre size and quantity. The denervated muscle undergoes an inexorable course of atrophy, eventually leading to a state where functioning muscle tissue is replaced by fibrous connective tissue and fat.
One of the earliest indications of denervation is the presence of spontaneous fibrillation activity, which is associated with the spread of acetylcholine receptors along the muscle fibre membrane. This hypersensitivity results in a spontaneous muscle fibre action potential, leading to fibrillation potentials that are of short duration and low amplitude.
The denervated muscle fibres must be stimulated directly rather than via nerve supply. The sensitivity of denervated muscle decreases for stimulus frequencies above 10 Hz, and this behaviour is evident from the strength-duration curve of denervated muscle. For pulse durations below 100 ms, the stimulus intensity required for contraction increases, and this intensity should be sufficient to elicit strong contractions.
The average pulse duration used for individuals with LMN denervation is 100-200 ms, and the pulse duration should be greater than or equal to the chronaxie of denervated muscles. Biphasic rectangular direct current (DC) impulses with durations between 30-150 ms and a frequency of 2-22 Hz may be applied to denervated muscles to restore muscle size.
In summary, denervated muscles are relatively insensitive to short-duration stimuli due to the increased stimulus intensity required for contraction for pulse durations below 100 ms. The sensitivity decreases further for stimulus frequencies above 10 Hz. To effectively stimulate denervated muscles, longer pulse durations and higher intensities are necessary.
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DC depolarization can cause chemical changes
DC depolarization is a technique that has been obtained using a dynamic mercury electrode. The process of depolarization involves reducing polarization in a galvanic cell by introducing a chemical compound, which changes the nature of the electrode reaction, allowing for a more efficient current flow. This is achieved by adding a chemical compound, such as calomel, which is used as a laboratory reagent, a fungicide, and a depolarizer in dry batteries.
In the context of denervated muscles, DC depolarization is used to elicit muscular contractions. The cellular membrane of each target muscle fiber is depolarized using a specific pulse duration and current intensity to induce strong contractions. This application of DC impulses can lead to chemical changes within the muscle fibers, potentially involving calcium and sodium ion channels.
Furthermore, DC depolarization can induce chemical changes in muscle cells, specifically smooth muscle cells (SMCs). It has been observed that DC depolarization causes the direct activation of G protein-coupled receptors, leading to local Ca2+ release in SMCs. This release of Ca2+ drives mechanical force and cellular responses, including muscle contraction. The underlying molecular processes can vary between skeletal and cardiac muscle cells, with distinct mechanisms of Ca2+ release.
Overall, DC depolarization has the ability to initiate chemical changes by modifying electrode reactions and influencing ion channels, ultimately impacting cellular functions and muscle contractions.
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Denervated muscle contraction is sluggish
To elicit muscular contractions in denervated muscles, the cellular membrane of each target muscle fibre must be depolarized. This can be achieved through electrical stimulation, such as functional electrical stimulation (FES) or direct current (DC) impulses. The intensity of the current needs to be sufficient to induce strong contractions, and the pulse duration should be equal to or greater than the chronaxie of denervated muscles.
The response of denervated muscles to electrical stimulation differs from that of innervated muscles in terms of contraction type, pulse shape, and duration. Denervated muscles are relatively insensitive to short-duration stimuli and require longer pulses for effective stimulation. This is because the accommodation effect is much smaller in denervated muscles compared to nerves, allowing for the use of various pulse shapes, such as sawtooth, trapezoidal, or triangular, with adjustable duration and intensity to adequately stimulate the denervated muscle while minimising stimulation of nearby sensory and pain nerve fibres.
The duration of the pulse plays a crucial role in denervated muscle stimulation. For pulse durations below 100 ms, the stimulus intensity required for contraction increases. At 100 ms, the pulse frequency cannot exceed 10 Hz, providing no 'rest' time between stimuli. By increasing the frequency above 10 Hz, the pulse duration must decrease to allow separation between pulses. Therefore, a longer duration pulse with relatively low intensity or a shorter duration pulse with higher intensity can be used to charge the muscle fibre membrane sufficiently for depolarization.
In summary, denervated muscle contraction is sluggish due to the loss of motor nerve supply, increased acetylcholine receptor sensitivity, and the need for specific electrical stimulation parameters to induce contraction. The response to electrical stimulation differs from innervated muscles, requiring longer pulses and specific intensities to effectively stimulate denervated muscles and evoke contraction.
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Calcium release is induced by depolarization
Calcium release induced by depolarization is a process that occurs in skeletal and cardiac muscle cells. This process, known as voltage-induced calcium release (VICR), is initiated by the activation of voltage-dependent Ca2+ channels (VDCCs) in the plasma membrane.
During depolarization, the cellular membrane of a muscle fiber undergoes a change in electrical potential, which can be induced by a current. This change in potential activates VDCCs, which are transmembrane proteins that allow the passage of Ca2+ ions. The opening of VDCCs facilitates the release of Ca2+ ions from intracellular stores, particularly the sarcoplasmic reticulum (SR).
The SR is a specialized endoplasmic reticulum found in muscle cells that plays a crucial role in regulating intracellular calcium levels. During depolarization, the SR releases Ca2+ ions through ryanodine receptors (RyRs). This release of Ca2+ ions from the SR is essential for muscle contraction and other cellular responses.
The mechanism of calcium release induced by depolarization varies slightly between skeletal and cardiac muscle cells. In skeletal muscle cells, depolarization of the T system, a network of tubular invaginations of the sarcolemma, may induce a potential change across the SR membrane, leading to calcium release. This process is not yet fully understood. In cardiac muscle cells, depolarization activates VDCCs, resulting in a small influx of extracellular Ca2+ ions. This initial influx then triggers the opening of RyR2 channels and a subsequent large release of Ca2+ ions from the SR, known as calcium-induced calcium release (CICR).
Additionally, in smooth muscle cells, depolarization has been found to directly activate G protein-coupled receptors, leading to local Ca2+ release. This activation triggers a signaling cascade involving G proteins, phospholipase C, and inositol 1,4,5-triphosphate (IP3), ultimately resulting in Ca2+ release through IP3 receptors and RyRs.
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Denervated muscle has a higher number of acetylcholine receptors
Denervated muscle fibres induce muscle atrophy, and active acetylcholine receptors can prevent this. Acetylcholine is a neurochemical that acts as a chemical messenger, allowing neurons to communicate with one another and with other specialised cells. It is released by motor neurons and binds to receptors at the neuromuscular junction.
Acetylcholine has a wide variety of functions in the brain and body, including regulating cardiac contractions and blood pressure, intestinal peristalsis, glandular secretion, and muscle movement. It is also involved in memory, learning, and REM sleep. In the body, it is made at the end of nerve cells and is stored there until it is triggered to be released. Once released, it moves into the synaptic cleft, where it can bind to nicotinic or muscarinic receptors.
The denervation of muscle fibres causes atrophy via mechanisms that are not yet fully understood. However, it has been shown that the binding of acetylcholine to its receptor at the neuromuscular junction prevents the expression of connexins 43 and 45, which promote atrophy. This binding also prevents the increase of sarcolemmal permeability, the fall of RMP, and the increase of Ca2+ and Na+ signals in cultured skeletal myofibers.
In addition, the in vivo increase in the half-life of acetylcholine decreased atrophy in denervated mice. This protective effect is carried out by nicotinic acetylcholine receptors (nAChRs) through a post-transcriptional mechanism that controls Cxs mRNA translation. Therefore, it can be concluded that denervated muscle has a higher number of acetylcholine receptors to prevent atrophy and favour reinnervation.
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Frequently asked questions
Muscle denervation refers to the loss of motor nerve supply to a muscle. This can result in abnormal activity while the muscle is at rest, such as fibrillation potentials and positive sharp waves.
Denervated muscles can be stimulated by applying electrical impulses. Depolarization of the muscle fiber membrane triggers the release of calcium ions, resulting in contraction.
Long duration pulses with relatively low intensity or shorter duration pulses of higher intensity can be used. The average pulse duration used for individuals with LMN denervation is 100-200 ms.
Depolarization of denervated muscles can help restore muscle size and function after spinal cord injuries. It can also be used to study the behavior of denervated muscles and their response to electrical stimulation.
