Tissue types and excitable tissue physiology
Tissue type determines how the body responds to stimulation: a nerve sends an impulse, a muscle contracts and a gland releases a secretion. This article unpacks an old lecture-notes topic in plainer language, while keeping the core concepts that help explain how the neuromuscular system works.
When the bar suddenly feels heavy during a workout, it isn’t only a matter of willpower. Excitation, inhibition, synapses, calcium ions and motor units are all at play. These are the phenomena that link the nervous system to muscle work.
Why does tissue type matter for understanding excitation?
Irritability is the ability of living tissue to respond to influences from the external environment and to changes in the internal environment. Such influences are called stimuli. The body’s response to a stimulus can vary widely. In nervous tissue, a wave of excitation, also known as a nerve impulse, is generated and propagated. In muscle tissue, the response shows up as contraction, meaning the muscle fibers develop tension or shorten. In glandular tissue, the response is the release of a secretion.
The basic point is that the same stimulus does not affect every tissue in the same way. That is why tissue type is such an important concept in physiology. The form and duration of irritability also depend on the functional state of the tissue. A tired muscle responds differently from a rested one. The same applies to nervous tissue.
By their energetic nature, stimuli are divided into physical, chemical and physicochemical. Physical stimuli include temperature, sound, light, electricity, impact, pressure, stretch and movement through space. Chemical stimuli include hormones, metabolic products such as lactic acid and pyruvate, as well as drugs and toxins. Physicochemical stimuli include changes in osmotic pressure, acid-base balance (pH) and electrolyte composition.
By their physiological nature, we speak of adequate and inadequate stimuli. An adequate stimulus is one to which an organ or tissue type has adapted over the course of evolution. For the eye, that is light; for the ear, sound; for the skin’s tactile receptors, pressure; and for skeletal muscles, nerve impulses. An inadequate stimulus does not easily provoke the same response under normal conditions, but if it is strong enough, lasts long enough and is frequent enough, it too can cause a similar reaction. For example, electricity can stimulate skeletal muscle.
Stimulation is the effect of a stimulus on living tissue. By strength of effect, we distinguish subthreshold, threshold and suprathreshold stimulation. Subthreshold stimulation produces a weak local response but does not yet bring about the full functional effect characteristic of the tissue. Threshold stimulation is the minimum stimulation that evokes a response. Suprathreshold stimulation is stronger than that and usually leads to a clearly visible reaction.
Excitability is the property of nervous, muscle and glandular tissue to respond to stimulation by generating excitation. Excitable tissues are precisely those tissues that give such a response. Excitation itself is a response that involves energy consumption. In the process, both the physicochemical state and the metabolism of the tissue change.
Tissue type, depolarization and inhibition
The common hallmark of excitation in all excitable tissues is an ionic shift across the cell membrane. This is called depolarization. At rest, the inner surface of the cell membrane carries a negative charge. During depolarization, that negative charge decreases.
When the stimulus is weak and subthreshold, local excitation occurs. This is a small, localized depolarization. When depolarization reaches a critical point, propagated excitation occurs: a large-amplitude action potential arises in the stimulated part of the cell membrane, spreads to neighboring areas and causes depolarization there too.
In nervous tissue, the characteristic sign of excitation is the generation of nerve impulses. In muscle tissue, it is contraction. In glandular tissue, it is the release of secretion. The action potential arises before any visible functional effect. For example, before a muscle can develop strength, the muscle fiber must receive an electrical signal.
Conductivity of excitation means the ability to pass excitation on. This is a property of all excitable tissues. Excitation that arises in the body of a nerve cell is transmitted onward to the axon and, through it, via synapses to other nerve cells, to a muscle or to a gland.
Inhibition is a decrease or cessation of the functional activity of excitable tissues under the influence of stimuli. In the central nervous system, inhibition is just as important as excitation. Thanks to inhibition, excitation does not spread uncontrollably across the whole system. This is how coordinated reflexes and complete movements come about.
Whereas excitation is accompanied by depolarization, inhibition is linked to the opposite process: hyperpolarization of the cell membrane. This means an increase in the negative charge on the inner surface of the membrane. Transmarginal inhibition can arise as a result of excitation that is too frequent or too prolonged. In that case, the lability of the nerve cells drops and recovery after each excitation cycle takes longer.
Direct inhibition is linked to the activity of inhibitory neurons and synapses. In presynaptic inhibition, inhibitory neurons form synapses on the axon terminals of excitatory neurons. The neurotransmitter released prevents impulses from spreading along the presynaptic membrane. Postsynaptic inhibition arises, for example, through the action of gamma-aminobutyric acid on the postsynaptic membrane. This hyperpolarizes the next neuron and makes it harder for excitation to occur.
Renshaw inhibition, or recurrent inhibition, is a special type of postsynaptic inhibition. Renshaw cells receive impulses from the collaterals of spinal alpha motor neurons and form inhibitory synapses on the same alpha motor neuron or on other motor neurons. The stronger the excitation of the alpha motor neuron, the stronger the inhibitory effect of the Renshaw cells. This is a form of autoregulation whose job is to limit excessive excitation.
Measuring the excitability of nerve and muscle tissue
In physiology and medicine, electrical stimulation is used to assess the functional state of the neuromuscular apparatus. Its advantage is easy dosing: the strength, voltage, duration and frequency of the direct current can all be adjusted precisely. Electric current is an inadequate stimulus for nerve and muscle tissue, but it is closer to them than many chemical or mechanical influences, because the activity of these tissues is itself accompanied by natural electrical phenomena.
In direct electrical stimulation, the electrical stimulus is delivered through an electrode straight to the muscle. In indirect electrical stimulation, the nerve that innervates the muscle is stimulated. According to the polar law, excitation arises in the area of the cathode, the negative electrode, when the current is switched on, and in the area of the anode, the positive electrode, when the current is switched off.
Electrotonus means a change in tissue excitability under the influence of electric current. When the current is switched on, excitability rises around the cathode and falls around the anode. When the current is switched off, the hyperpolarization in the anode area disappears, which can also raise excitability. At the cathode, meanwhile, excitability drops as a result of repolarization.
The generation of excitation depends on current strength, the duration of the stimulus and the current gradient. The lower the threshold stimulus, the higher the tissue’s excitability. Local subthreshold changes must reach the threshold level, and that takes time. The minimum time required to elicit excitation in living tissue is called the utilization time.
If the voltage of the current is raised slowly, the membrane of a nerve or muscle cell can accommodate, that is, adapt. In that case excitation may not arise even with a relatively strong current. If the voltage is increased abruptly, a contraction is much more likely. Electrode area matters too. With a point electrode, the current density is higher and the threshold stimulus, or rheobase, appears at a lower current strength than with a large plate electrode.
Rheobase is the minimum voltage V or current strength mA of direct current required to elicit excitation in living tissue when the stimulus duration is unlimited. The smaller the rheobase, the higher the tissue’s excitability. Chronaxie is the minimum time in ms required to elicit the smallest response under direct current at twice the rheobase strength. The shorter the chronaxie, the faster the excitation wave arises.
The lability of excitable tissues means their functional mobility. It is used to describe the speed at which the excitation process spreads. The concept was introduced by Nikolai Vvedensky in 1892. Lability is not a fixed property. It is usually assessed by the maximum frequency of rhythmic electrical stimuli to which the tissue can respond without transforming the rhythm.
The optimum stimulus frequency is the frequency that elicits the maximum effect, for example the maximum contraction of a skeletal muscle. Pessimum occurs when, as the stimulus frequency is increased further, the contraction weakens and the muscle eventually relaxes. Parabiosis, or the “near-life” state, is a form of inhibition associated with a decline in lability. When lability falls, the organ’s excitability and function disappear as well.
Tissue type and bioelectrical phenomena
Membrane theory is used to explain bioelectrical phenomena. According to it, biopotentials arise from the uneven distribution of ions across cell membranes and from the movement of ions through the membrane. At rest, the cell membrane is electrically polarized: the outer surface is positive and the inner surface negative. This potential difference is called the membrane resting potential.
The resting potential is maintained by several factors: the uneven distribution of the main cations and Na+ and of the anions A-, Cl- and HCO-, the selective permeability of the cell membrane to different ions, and the active transport of Na+ and K+ ions by the Na+/K+ pump. This pump runs on metabolic energy.
Depolarization is a decrease in the resting potential. Hyperpolarization is an increase in the resting potential. Repolarization means the restoration of the resting potential to its baseline level. Understanding these three terms makes much of nerve and muscle physiology far easier to follow.
An electrotonic potential arises with a weak subthreshold stimulus, when the stimulus stays below 0.5 of the critical limit of depolarization. A local response arises when the stimulus grows into the range of 0.5–0.9 of the critical limit of depolarization. Both phenomena depend on the strength of the stimulus, stay at the site of stimulation and do not spread to neighboring areas of the cell.
An action potential is a brief change in the membrane resting potential that occurs when a cell is excited. It is also called the activity potential. In the spike potential, three phases are distinguished: 1) rapid depolarization, 2) reversal of polarity and 3) rapid repolarization. The after-potential is lower in voltage and longer in duration. It includes the negative after-potential and the positive after-potential.
An action potential arises when the drop in the membrane’s resting potential reaches the critical threshold of depolarization. At that point, the influx of Na+ ions into the cell becomes unstoppable. Within a very short time, the inner surface of the cell membrane becomes electropositive and the outer surface electronegative. This is polarity reversal, or inversion.
Once the action potential reaches its maximum amplitude, the membrane’s permeability to Na+ ions falls and its permeability to K+ ions rises. K+ ions leave the cell, which triggers repolarization. This restores the membrane polarization and ion distribution typical of the resting state.
The action potential follows two important rules. First, threshold and suprathreshold stimulation always produce a response of the same maximum amplitude. This is known as the all-or-none law. Second, an action potential travels along a nerve or muscle fiber without decrement, that is, without any drop in amplitude.
An excitatory postsynaptic potential is a local depolarization of the postsynaptic membrane caused by a transmitter such as acetylcholine. When it reaches the critical threshold of depolarization, an action potential is generated and spreads along the cell membrane. An inhibitory postsynaptic potential is the opposite: it is a hyperpolarization of the nerve cell membrane caused by an inhibitory transmitter substance.
Laws of conduction of excitation in nerve and muscle
An action potential generated in one part of nerve or muscle tissue spreads onward along the fiber. This happens through local equalizing currents. At the site of stimulation, the membrane depolarizes. This creates currents in the neighboring areas that stimulate the next sections of membrane. In this way, the excitation shifts to a new location.
The first law is the law of anatomical and physiological integrity of tissue. A wave of excitation can only spread through nerve and muscle tissue if the tissue is intact. Mechanical damage to the cell membrane, toxins, substances with an anesthetic effect or severe dehydration can disrupt the conduction of excitation.
The second law is the law of isolated conduction. Excitation travelling along a nerve or muscle fiber does not normally pass to neighboring fibers. Thanks to this, the different fibers of a mixed nerve can carry impulses independently of one another, and each impulse reaches its own destination. The same principle applies to muscle fibers.
The third law is the law of bidirectional conduction of excitation. A wave of excitation generated at one point of a nerve or muscle fiber spreads in both directions. In the body as a whole, however, excitation in nerve fibers travels in a fixed direction: in afferent fibers from the periphery toward the center, and in efferent fibers from the center toward the periphery.
The fourth law is the all-or-none law. The amplitude of an action potential travelling along the membrane of a nerve or muscle fiber does not depend on the strength of the stimulus that triggered it. Once the threshold has been exceeded, the response is constant under physiological conditions.
As a wave of excitation spreads, the excitability of the tissue itself also changes. During the local response, excitability rises. In the depolarization phase of the action potential, excitability disappears completely for a short time. This is called the absolute refractory period. In a motor nerve fiber, it lasts 0.5 1 ms.
It is followed by the relative refractory period, which lasts 3 5 ms in a motor nerve cell. During this time, excitation can only be triggered by a stronger suprathreshold stimulus. In the final part of the negative after-potential, excitability is heightened, which is known as the supernormal phase; in a motor nerve fiber it lasts ~15 ms. The positive after-potential coincides with the subnormal phase, which lasts ~50 ms in a motor nerve fiber. The shorter the refractory period, the more impulses a cell can conduct and the greater its lability.
The neuromuscular synapse and muscle work
Excitation is transmitted from a motor nerve to a muscle through the neuromuscular synapse. Synapses can be chemical or electrical. The neuromuscular synapse is a chemical synapse in which the transmitter substance acetylcholine takes part in the transmission of excitation.
When a nerve impulse arrives, acetylcholine is released into the synaptic cleft from the active zones of the presynaptic membrane in the axon terminal. There it moves to the end plate of the muscle fiber and binds to the cholinergic receptors of the postsynaptic membrane. As a result, Na+ channels open, Na+ ions flow into the cell and an end-plate potential is generated.
The end-plate potential triggers an action potential that spreads along the muscle fiber membrane. Acetylcholine that has entered the synaptic cleft is quickly broken down by the enzyme acetylcholinesterase into choline and acetate. This readies the postsynaptic membrane to receive a new impulse.
The neuromuscular synapse has several special features. Excitation spreads nearly 100 times more slowly than in a nerve fiber. It takes the wave of excitation 1 ms to cross the synaptic cleft, which is 0.1 mm wide. This is called synaptic delay. Unlike nerve and muscle fibers, which conduct excitation in both directions, the neuromuscular synapse passes excitation on in one direction only: from nerve to muscle.
Muscle contraction is preceded by a chain of electrical, chemical and mechanical events. This is called the excitation–contraction coupling mechanism. The work of a skeletal muscle begins with a nerve impulse from an alpha motor neuron. This triggers depolarization of the sarcolemma of the muscle fibers. The action potential travels through the T-tubules to the membranes of the sarcoplasmic reticulum and increases their permeability to Ca2+ ions.
Ca2+ ions leave the terminal cisternae and enter the sarcoplasm. There they bind to troponin and make it possible for actin and myosin to interact. Tropomyosin, which blocks the attachment of the cross-bridges at rest, moves out of the way. The myosin heads can then bind to the active sites on actin. ATP hydrolysis provides the energy for this.
According to the sliding filament theory, the length of the thick myosin filaments and the thin actin filaments does not change during contraction. What changes is the length of the sarcomere, because the filaments slide past each other. The cross-bridges attach to actin, generate pulling force, detach and start a new cycle. Each cross-bridge attachment-detachment cycle is linked to the hydrolysis of one ATP molecule. The direction of cross-bridge movement is described as an angle of roughly 45o.
A muscle relaxes when the Ca2+ concentration in the myofibrillar space falls below a critical level. The links between myosin and actin break, the cross-bridges become inactive, and the tropomyosin-troponin complex blocks the active sites on actin again. Ca2+ ions are pumped back into the sarcoplasmic reticulum using ATP energy.
In response to a single stimulus, a muscle produces a brief contraction known as a twitch. It has a latent phase, a contraction phase and a relaxation phase. A higher proportion of fast muscle fibers, especially FG-type fibers, makes the twitch shorter and its force greater.
The staircase phenomenon refers to a gradual increase in twitch amplitude under rhythmic low-frequency stimulation. Post-tetanic potentiation refers to a marked increase in twitch force and a shortening of the contraction phase immediately after a brief 2-5 s tetanic contraction. In voluntary efforts, it appears when the size of the effort exceeds 50% of voluntary maximal strength.
Tetanic contraction occurs when individual twitches summate. Unfused (incomplete) tetanus occurs when human muscles are stimulated at a frequency of 5–10 Hz. Fused (complete) tetanus occurs at a frequency of 15–20 Hz. Slow motor units already work in fused tetanus at a stimulation frequency of 20 Hz, whereas fast motor units often need 35–40 Hz. In voluntary movement, muscle contractions are usually tetanic.
Regulation of muscle tension and the effect of training
Specific muscle strength is the maximal isometric strength of a muscle divided by its physiological cross-section. It is usually expressed in kilograms-force per square centimeter, or kg/cm2. Maximal muscle strength is the force that appears when all muscle fibers contract maximally. It can be assessed with supramaximal electrical stimulation, using a pulse duration of 0.5–1 ms and a stimulation frequency of 50 100 Hz.
Voluntary maximal strength is the force a person can produce under maximal effort. It depends on neural and peripheral factors. The neural factors include intramuscular and intermuscular coordination. The peripheral factors include the conditions under which force is applied, muscle length, joint angle, muscle cross-section and muscle fiber composition.
Intramuscular coordination rests on three mechanisms: the number of active motor units, their firing frequency and the timing of their impulses relative to one another. The more motor units are working, the more tension the muscle develops. This is called recruitment.
Recruitment takes place at the level of the motoneuron pools. Small alpha motoneurons with a low excitation threshold are switched on first. As the intensity of excitatory input rises, large alpha motoneurons with a higher excitation threshold are added. This is known as the size principle. It is associated with the researcher E. Hennemann.
A motor unit’s firing frequency determines how much tension that unit develops. During a light effort, slow motor units with a low excitation threshold fire at a low frequency. As the effort increases, new motor units are recruited and the frequency of those already working goes up. In maximal voluntary efforts, the firing frequency of motor units is usually 50–60 Hz, and in exceptional cases, such as a fast ballistic movement, up to 100 Hz.
The timing of impulses also affects strength. If some motor units fire synchronously, muscle tension may rise. Most of the time, however, motor units fire asynchronously, because this gives movement its smoothness. In fatigue, synchrony may increase and fatigue tremor may appear.
Intermuscular coordination means choosing the right synergist muscles, inhibiting excessive activity in the antagonist muscles and getting the fixator muscles to work optimally. It is based on the reciprocal relationships between the alpha motoneurons of synergist and antagonist muscles. When the nerve center controlling the flexors is excited, the center for the extensors is generally inhibited, and vice versa.
Training changes this system. Systematic physical training can improve both intramuscular and intermuscular coordination. This is called neural adaptation. It means that the control of the neuromuscular apparatus becomes more precise. Together with muscular adaptation, especially muscle fiber hypertrophy, it is the physiological basis for the development of strength and speed-strength.
In practice, this means a beginner’s strength numbers can improve before the muscle visibly gets much bigger. The nervous system learns to activate the muscles better. Recruitment, firing frequency and muscle coordination all improve. That is why learning technique is not a side issue in strength training but part of the physiology.
Practical notes on excitation and strength
If you want to understand training more intelligently, keep an eye on three things. First, a muscle needs a strong enough signal. If the stimulus stays below the threshold, a full response doesn’t occur. Second, fatigue affects the excitability of nerve and muscle tissue. The more fatigue builds up, the harder it is to maintain the same strength and the same precise movement. Third, coordination is trainable.
So what actually happens when your reps slow down at the end of a set? Part of the reason lies in the muscle, part in the nervous system. Ca2+ ion movement, ATP use, motor unit recruitment and inhibitory mechanisms all work at the same time. From the outside, it simply looks like the weight no longer moves as well.
Honestly, the vocabulary of physiology can be dry at times. But the point is very practical: your body doesn’t lift weight with muscle size alone. It lifts with nerve impulses, synapses, muscle fibers, coordination and energy. Once you understand these links, it’s easier to see why rest breaks, technique, increases in training load and fatigue management matter in training.
FAQ: tissue type and the neuromuscular system
What is a tissue type in physiological terms?
A tissue type is a group of cells with a similar structure and function. When it comes to excitation, nervous tissue, muscle tissue and glandular tissue are the important ones, because they respond to a stimulus with a clearly distinct function.
Why doesn’t a muscle respond to every stimulus?
A stimulus has to exceed the threshold and last long enough. If its effect is too weak or too slow, only a local response or membrane adaptation may occur, rather than a full contraction.
How does training develop the neuromuscular system?
Training improves motor unit recruitment, firing rate and intermuscular coordination. Later, muscle adaptation follows, including hypertrophy of the muscle fibers.
Author: EKFL
Source: WHO – physical activity.
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