Muscles II: Muscle Contraction Flashcards
Types of skeletal muscle
Muscle
Fascicle
Fibre
Myofibril
Muscle
These tissues include the skeletal muscle fibres, blood vessels, nerve fibres, and connective tissue
Fascicle
Functional muscular unit. Receives individual input from nervous system.
Fibre
Individual contractile unit
Myofibril
Source of contraction.
membrane potential
All living cells have membrane potentials, or electrical gradients across their membranes. The inside of the membrane is usually around -60 to -90 mV, relative to the outside. This is referred to as a cell’s membrane potential. Neurons and muscle cells can use their membrane potentials to generate electrical signals. They do this by controlling the movement of charged particles, called ions, across their membranes to create electrical currents. This is achieved by opening and closing specialized proteins in the membrane called ion channels. Although the currents generated by ions moving through these channel proteins are very small, they form the basis of both neural signalling and muscle contraction.
Both neurons and skeletal muscle cells are electrically excitable, meaning that
they are able to generate action potentials. An action potential is a special type of electrical signal that can travel along a cell membrane as a wave. This allows a signal to be transmitted quickly and faithfully over long distances.
excitation-contraction coupling
for a skeletal muscle fibre to contract, its membrane must first be “excited”—in other words, it must be stimulated to fire an action potential. The muscle fibre action potential, which sweeps along the sarcolemma as a wave, is “coupled” to the actual contraction through the release of calcium ions (Ca++) from the SR. Once released, the Ca++interacts with the shielding proteins, forcing them to move aside so that the actin-binding sites are available for attachment by myosin heads. The myosin then pulls the actin filaments toward the centre, shortening the muscle fibre.
In skeletal muscle, this sequence begins with signals from the somatic motor division of the nervous system. In other words, the “excitation” step in skeletal muscles is always triggered by signalling from the nervous system.
neuromuscular junction
achemical synapsebetween amotor neuronand amuscle fibre. It allows the motor neuron to transmit a signal to the muscle fibre, causingmuscle contraction.
Describe a neutron transmitting a signal
Muscles require innervation to function—and even just to maintainmuscle tone, avoidingatrophy. In theneuromuscular systemnerves from thecentral nervous systemand theperipheral nervous systemare linked and work together with muscles.
Synaptic transmission at the neuromuscular junction begins when anaction potentialreaches the presynaptic terminal of a motor neuron, which activatesvoltage-gated calcium channelsto allow calcium ions to enter the neuron.
Calcium ions bind to sensor proteins (synaptotagmin) on synaptic vesicles, triggering vesicle fusion with the cell membrane and subsequentneurotransmitterrelease from the motor neuron into thesynaptic cleft.
Invertebrates, motor neurons releaseacetylcholine(ACh), a small molecule neurotransmitter, which diffuses across the synaptic cleft and binds tonicotinic acetylcholine receptors(nAChRs) on the cell membrane of the muscle fibre, also known as thesarcolemma.
nAChRs areionotropicreceptors, meaning they serve asligand-gatedion channels.
The binding of ACh to the receptor can depolarize the muscle fibre, causing a cascade that eventually results in muscle contraction.
sarcoplasmic reticulum
is a network of tubules that extend throughoutmuscle cells, wrapping around (but not in direct contact with) themyofibrils(contractile units of the cell). Cardiac and skeletal muscle cells contain structures calledtransverse tubules (T-tubules), which are extensions of thecell membranethat travel into the centre of the cell. T-tubules are closely associated with a specific region of the SR, known as theterminal cisternaein skeletal muscle, with a distance of roughly 12nanometers, separating them. This is the primary site of calcium release.The longitudinal SR are thinner projects, that run between the terminal cisternae/junctional SR, and are the location where ion channels necessary for calcium ion absorption are most abundant.These processes are explained in more detail below and are fundamental for the process of excitation-contraction coupling inskeletal,cardiacandsmooth muscle.
Sarcoplasmic Reticulum (Calcium Storage)
The SR containsion channel pumps, within its membrane that are responsible for pumping Ca2+into the SR. As the calcium ion concentration within the SR is higher than in the rest of the cell, the calcium ions won’t freely flow into the SR, and therefore pumps are required, that use energy, which they gain from a molecule calledadenosine triphosphate (ATP). These calcium pumps are calledSarco(endo)plasmic reticulum ATPases (SERCA). There are a variety of different forms of SERCA, with SERCA 2a being found primarily in cardiac and skeletal muscle.
Sarcoplasmic Reticulum (Calcium Release)
Calcium ion release from the SR, occurs in the junctional SR/terminal cisternaethrough aryanodine receptor (RyR)and is known as acalcium spark.[10]There are three types of ryanodine receptor,RyR1(inskeletal muscle),RyR2(incardiac muscle) andRyR3(in thebrain).[11]Calcium release through ryanodine receptors in the SR is triggered differently in different muscles. In cardiac and smooth muscle an electrical impulse (action potential) triggers calcium ions to enter the cell through anL-type calcium channellocated in the cell membrane (smooth muscle) or T-tubule membrane (cardiac muscle). These calcium ions bind to and activate the RyR, producing a larger increase in intracellular calcium. In skeletal muscle, however, the L-type calcium channel is bound to the RyR. Therefore, activation of the L-type calcium channel, via an action potential, activates the RyR directly, causing calcium release (seecalcium sparksfor more details). Also,caffeine(found in coffee) can bind to and stimulate RyR. Caffeine makes the RyR more sensitive to either the action potential (skeletal muscle) or calcium (cardiac or smooth muscle), thereby producingcalcium sparksmore often (this is partially responsible for caffeine’s effect on heart rate).
For a muscle cell to contract…
, the sarcomere must shorten. However, thick and thin filaments—the components of sarcomeres—do not shorten. Instead, they slide by one another, causing the sarcomere to shorten while the filaments remain the same length. The sliding filament theory of muscle contraction was developed to fit the differences observed in the named bands on the sarcomere at different degrees of muscle contraction and relaxation. The mechanism of contraction is the binding of myosin to actin, forming cross-bridges that generate filament movement.
E-C Coupling: Sliding Filament Model of Contraction
When a sarcomere shortens, some regions shorten whereas others stay the same length. A sarcomere is defined as the distance between two consecutive Z discs or Z lines; when a muscle contracts, the distance between the Z discs is reduced. The H zone—the central region of the A zone—contains only thick filaments and is shortened during contraction. The I band contains only thin filaments and also shortens. The A band does not shorten—it remains the same length—but A bands of different sarcomeres move closer together during contraction, eventually disappearing. Thin filaments are pulled by the thick filaments toward the center of the sarcomere until the Z discs approach the thick filaments. The zone of overlap, in which thin filaments and thick filaments occupy the same area, increases as the thin filaments move inward.
Crossbridge cycling
is a sequence of molecular events that underlies the sliding filament theory.
The motion of muscle shortening occurs as myosin heads bind to actin and pull the actin inwards. This action requires energy, which is provided by ATP. Myosin binds to actin at a binding site on the globular actin protein.
Myosin has another binding site for ATP at which enzymatic activity hydrolyses ATP to ADP, releasing an inorganic phosphate molecule and energy.
ATP binding causes myosin to release actin, allowing actin and myosin to detach from each other. After this happens, the newly bound ATP is converted to ADP and inorganic phosphate, Pi. The enzyme at the binding site on myosin is called ATPase. The energy released during ATP hydrolysis changes the angle of the myosin head into a “cocked” position. The myosin head is then in a position for further movement, possessing potential energy, but ADP and Piare still attached. If actin binding sites are covered and unavailable, the myosin will remain in the high energy configuration with ATP hydrolysed, but still attached.
If the actin binding sites are uncovered, a cross-bridge will form; that is, the myosin head spans the distance between the actin and myosin molecules. Piis then released, allowing myosin to expend the stored energy as a conformational change. The myosin head moves toward the M line, pulling the actin along with it. As the actin is pulled, the filaments move approximately 10 nm toward the M line. This movement is called the power stroke, as it is the step at which force is produced. As the actin is pulled toward the M line, the sarcomere shortens and the muscle contracts.
When the myosin head is “cocked,” it contains energy and is in a high-energy configuration. This energy is expended as the myosin head moves through the power stroke; at the end of the power stroke, the myosin head is in a low-energy position. After the power stroke, ADP is released; however, the cross-bridge formed is still in place, and actin and myosin are bound together. ATP can then attach to myosin, which allows the cross-bridge cycle to start again and further muscle contraction can occur.
E-C Coupling: summary (long, list as much as you can)
Excitation–contraction coupling is the link (transduction) between the action potential generated in the sarcolemma and the start of a muscle contraction. The trigger for calcium release from the sarcoplasmic reticulum into the sarcoplasm is a neural signal. Each skeletal muscle fiber is controlled by a motor neuron, which conducts signals from the brain or spinal cord to the muscle. The area of the sarcolemma on the muscle fiber that interacts with the neuron is called themotor end plate. The end of the neuron’s axon is called the synaptic terminal, and it does not actually contact the motor end plate. A small space called the synaptic cleft separates the synaptic terminal from the motor end plate. Electrical signals travel along the neuron’s axon, which branches through the muscle and connects to individual muscle fibers at a neuromuscular junction.
The ability of cells to communicate electrically requires that the cells expend energy to create an electrical gradient across their cell membranes. This charge gradient is carried by ions, which are differentially distributed across the membrane. Each ion exerts an electrical influence and a concentration influence. Just as milk will eventually mix with coffee without the need to stir, ions also distribute themselves evenly, if they are permitted to do so. In this case, they are not permitted to return to an evenly mixed state.
The sodium–potassium ATPase uses cellular energy to move K+ions inside the cell and Na+ions outside. This alone accumulates a small electrical charge, but a big concentration gradient. There is lots of K+in the cell and lots of Na+outside the cell. Potassium is able to leave the cell through K+channels that are open 90% of the time, and it does. However, Na+channels are rarely open, so Na+remains outside the cell. When K+leaves the cell, obeying its concentration gradient, that effectively leaves a negative charge behind. So at rest, there is a large concentration gradient for Na+to enter the cell, and there is an accumulation of negative charges left behind in the cell. This is the resting membrane potential. Potential in this context means a separation of electrical charge that is capable of doing work. It is measured in volts, just like a battery. However, the transmembrane potential is considerably smaller (0.07 V); therefore, the small value is expressed as millivolts (mV) or 70 mV. Because the inside of a cell is negative compared with the outside, a minus sign signifies the excess of negative charges inside the cell, −70 mV.
If an event changes the permeability of the membrane to Na+ions, they will enter the cell. That will change the voltage. This is an electrical event, called an action potential, that can be used as a cellular signal. Communication occurs between nerves and muscles through neurotransmitters. Neuron action potentials cause the release of neurotransmitters from the synaptic terminal into the synaptic cleft, where they can then diffuse across the synaptic cleft and bind to a receptor molecule on the motor end plate. The motor end plate possesses junctional folds—folds in the sarcolemma that create a large surface area for the neurotransmitter to bind to receptors. The receptors are actually sodium channels that open to allow the passage of Na+into the cell when they receive a neurotransmitter signal.
Acetylcholine (ACh) is a neurotransmitter released by motor neurons that binds to receptors in the motor end plate. Neurotransmitter release occurs when an action potential travels down the motor neuron’s axon, resulting in altered permeability of the synaptic terminal membrane and an influx of calcium. The Ca2+ions allow synaptic vesicles to move to and bind with the presynaptic membrane (on the neuron), and release neurotransmitter from the vesicles into the synaptic cleft. Once released by the synaptic terminal, ACh diffuses across the synaptic cleft to the motor end plate, where it binds with ACh receptors. As a neurotransmitter binds, these ion channels open, and Na+ions cross the membrane into the muscle cell. This reduces the voltage difference between the inside and outside of the cell, which is called depolarization. As ACh binds at the motor end plate, this depolarization is called an end-plate potential. The depolarization then spreads along the sarcolemma, creating an action potential as sodium channels adjacent to the initial depolarization site sense the change in voltage and open. The action potential moves across the entire cell, creating a wave of depolarization.
ACh is broken down by the enzymeacetylcholinesterase(AChE) into acetyl and choline. AChE resides in the synaptic cleft, breaking down ACh so that it does not remain bound to ACh receptors, which would cause unwanted extended muscle contraction.
After depolarization, the membrane returns to its resting state. This is called repolarization, during which voltage-gated sodium channels close. Potassium channels continue at 90% conductance. Because the plasma membrane sodium–potassium ATPase always transports ions, the resting state (negatively charged inside relative to the outside) is restored. The period immediately following the transmission of an impulse in a nerve or muscle, in which a neuron or muscle cell regains its ability to transmit another impulse, is called the refractory period. During the refractory period, the membrane cannot generate another action potential. The refractory period allows the voltage-sensitive ion channels to return to their resting configurations. The sodium potassium ATPase continually moves Na+back out of the cell and K+back into the cell, and the K+leaks out leaving negative charge behind. Very quickly, the membrane repolarizes, so that it can again be depolarized.
energy demand of muscle contraction:
Cross-bridge formation occurs when the myosin head attaches to the actin while adenosine diphosphate (ADP) and inorganic phosphate (Pi) are still bound to myosin, Pi is then released, causing myosin to form a stronger attachment to the actin, after which the myosin head moves toward the M-line, pulling the actin along with it. As actin is pulled, the filaments move approximately 10 nm toward the M-line. This movement is called the power stroke, as movement of the thin filament occurs at this step. In the absence of ATP, the myosin head will not detach from actin.
Contraction Energetics
One part of the myosin head attaches to the binding site on the actin, but the head has another binding site for ATP. ATP binding causes the myosin head to detach from the actin. After this occurs, ATP is converted to ADP and Pi by the intrinsic ATPase activity of myosin. The energy released during ATP hydrolysis changes the angle of the myosin head into a cocked position. The myosin head is now in position for further movement.
When the myosin head is cocked, myosin is in a high-energy configuration. This energy is expended as the myosin head moves through the power stroke, and at the end of the power stroke, the myosin head is in a low-energy position. After the power stroke, ADP is released; however, the formed cross-bridge is still in place, and actin and myosin are bound together. As long as ATP is available, it readily attaches to myosin, the cross-bridge cycle can recur, and muscle contraction can continue.
Note that each thick filament of roughly 300 myosin molecules has multiple myosin heads, and many cross-bridges form and break continuously during muscle contraction. Multiply this by all of the sarcomeres in one myofibril, all the myofibrils in one muscle fibre, and all of the muscle fibres in one skeletal muscle, and you can understand why so much energy (ATP) is needed to keep skeletal muscles working. In fact, it is the loss of ATP that results in the rigor mortis observed soon after someone dies. With no further ATP production possible, there is no ATP available for myosin heads to detach from the actin-binding sites, so the cross-bridges stay in place, causing the rigidity in the skeletal muscles.
Role of atp in Contraction Energetics
ATP supplies the energy for muscle contraction to take place. In addition to its direct role in the cross-bridge cycle, ATP also provides the energy for the active-transport Ca++ pumps in the SR. Muscle contraction does not occur without enough ATP. The amount of ATP stored in muscle is very low, only sufficient to power a few seconds worth of contractions. As it is broken down, ATP must therefore be regenerated and replaced quickly to allow for sustained contraction. There are three mechanisms by which ATP can be regenerated: creatine phosphate metabolism, anaerobic glycolysis, and aerobic respiration.
Creatine phosphate
is a molecule that can store energy in its phosphate bonds. In a resting muscle, excess ATP transfers its energy to creatine, producing ADP and creatine phosphate. This acts as an energy reserve that can be used to quickly create more ATP. When the muscle starts to contract and needs energy, creatine phosphate transfers its phosphate back to ADP to form ATP and creatine. This reaction is catalysed by the enzyme creatine kinase and occurs very quickly; thus, creatine phosphate-derived ATP powers the first few seconds of muscle contraction. However, creatine phosphate can only provide approximately 15 seconds worth of energy, at which point another energy source must be used.
Glycolysis
is an anaerobic (non-oxygen-dependent) process that breaks down glucose (sugar) to produce ATP; however, glycolysis cannot generate ATP as quickly as creatine phosphate. Thus, the switch to glycolysis results in a slower rate of ATP availability to the muscle. The sugar used in glycolysis can be provided by blood glucose or by metabolizing glycogen that is stored in the muscle. The breakdown of one glucose molecule produces two ATP and two molecules ofpyruvic acid, which can be used in aerobic respiration or when oxygen levels are low, converted to lactic acid.
If oxygen is available, pyruvic acid is used in aerobic respiration. However, if oxygen is not available, pyruvic acid is converted tolactic acid, which may contribute to muscle fatigue. This conversion allows the recycling of the enzyme NAD+from NADH, which is needed for glycolysis to continue. This occurs during strenuous exercise when high amounts of energy are needed but oxygen cannot be sufficiently delivered to muscle. Glycolysis itself cannot be sustained for very long (approximately 1 minute of muscle activity), but it is useful in facilitating short bursts of high-intensity output. This is because glycolysis does not utilize glucose very efficiently, producing a net gain of two ATPs per molecule of glucose, and the end product of lactic acid, which may contribute to muscle fatigue as it accumulates.
Aerobic respiration
is the breakdown of glucose or other nutrients in the presence of oxygen (O2) to produce carbon dioxide, water, and ATP. Approximately 95 percent of the ATP required for resting or moderately active muscles is provided by aerobic respiration, which takes place in mitochondria. The inputs for aerobic respiration include glucose circulating in the bloodstream, pyruvic acid, and fatty acids. Aerobic respiration is much more efficient than anaerobic glycolysis, producing approximately 36 ATPs per molecule of glucose versus four from glycolysis. However, aerobic respiration cannot be sustained without a steady supply of O2to the skeletal muscle and is much slower. To compensate, muscles store small amount of excess oxygen in proteins call myoglobin, allowing for more efficient muscle contractions and less fatigue. Aerobic training also increases the efficiency of the circulatory system so that O2can be supplied to the muscles for longer periods of time.
Muscle Contractions: Overview
To move an object, referred to as load, the sarcomeres in the muscle fibers of the skeletal muscle must shorten. The force generated by the contraction of the muscle (or shortening of the sarcomeres) is called muscle tension. However, muscle tension also is generated when the muscle is contracting against a load that does not move, resulting in two main types of skeletal muscle contractions: isotonic contractions and isometric contractions
isotonic contractions
where the tension in the muscle stays constant, a load is moved as the length of the muscle changes (shortens). There are two types of isotonic contractions: concentric and eccentric
concentric contraction
concentric contraction involves the muscle shortening to move a load. An example of this is the biceps brachii muscle contracting when a hand weight is brought upward with increasing muscle tension. As the biceps brachii contract, the angle of the elbow joint decreases as the forearm is brought toward the body. Here, the biceps brachii contracts as sarcomeres in its muscle fibres are shortening and cross-bridges form; the myosin heads pull the actin
eccentric contraction
occurs as the muscle tension diminishes and the muscle lengthens. In this case, the hand weight is lowered in a slow and controlled manner as the amount of cross-bridges being activated by nervous system stimulation decreases. In this case, as tension is released from the biceps brachii, the angle of the elbow joint increases. Eccentric contractions are also used for movement and balance of the body.
isometric contraction
occurs as the muscle produces tension without changing the angle of a skeletal joint. Isometric contractions involve sarcomere shortening and increasing muscle tension, but do not move a load, as the force produced cannot overcome the resistance provided by the load. For example, if one attempts to lift a hand weight that is too heavy, there will be sarcomere activation and shortening to a point, and ever-increasing muscle tension, but no change in the angle of the elbow joint. In everyday living, isometric contractions are active in maintaining posture and maintaining bone and joint stability. However, holding your head in an upright position occurs not because the muscles cannot move the head, but because the goal is to remain stationary and not produce movement. Most actions of the body are the result of a combination of isotonic and isometric contractions working together to produce a wide range of outcomes
motor unit.
As you have learned, every skeletal muscle fibre must be innervated by the axon terminal of a motor neuron in order to contract. Each muscle fibre is innervated by only one motor neuron. The actual group of muscle fibres in a muscle innervated by a single motor neuron is called a motor unit. The size of a motor unit is variable depending on the nature of the muscle.
small motor unit
is an arrangement where a single motor neuron supplies a small number of muscle fibres in a muscle. Small motor units permit very fine motor control of the muscle. The best example in humans is the small motor units of the extraocular eye muscles that move the eyeballs. There are thousands of muscle fibres in each muscle, but every six or so fibres are supplied by a single motor neuron, as the axons branch to form synaptic connections at their individual NMJs. This allows for exquisite control of eye movements so that both eyes can quickly focus on the same object. Small motor units are also involved in the many fine movements of the fingers and thumb of the hand for grasping, texting, etc.
large motor unit
is an arrangement where a single motor neuron supplies a large number of muscle fibres in a muscle. Large motor units are concerned with simple, or “gross,” movements, such as powerfully extending the knee joint. The best example is the large motor units of the thigh muscles or back muscles, where a single motor neuron will supply thousands of muscle fibres in a muscle, as its axon splits into thousands of branches.
recruitment
There is a wide range of motor units within many skeletal muscles, which gives the nervous system a wide range of control over the muscle. The small motor units in the muscle will have smaller, lower-threshold motor neurons that are more excitable, firing first to their skeletal muscle fibres, which also tend to be the smallest. Activation of these smaller motor units, results in a relatively small degree of contractile strength (tension) generated in the muscle. As more strength is needed, larger motor units, with bigger, higher-threshold motor neurons are enlisted to activate larger muscle fibres. This increasing activation of motor units produces an increase in muscle contraction known as recruitment. As more motor units are recruited, the muscle contraction grows progressively stronger. In some muscles, the largest motor units may generate a contractile force of 50 times more than the smallest motor units in the muscle. This allows a feather to be picked up using the biceps brachii arm muscle with minimal force, and a heavy weight to be lifted by the same muscle by recruiting the largest motor units.
When necessary, the maximal number of motor units in a muscle can be recruited simultaneously, producing the maximum force of contraction for that muscle, but this cannot last for very long because of the energy requirements to sustain the contraction. To prevent complete muscle fatigue, motor units are generally not all simultaneously active, but instead some motor units rest while others are active, which allows for longer muscle contractions. The nervous system uses recruitment as a mechanism to efficiently utilize a skeletal muscle.
Muscle Contractions: Length-Tension Relationship
When a skeletal muscle fibre contracts, myosin heads attach to actin to form cross-bridges followed by the thin filaments sliding over the thick filaments as the heads pull the actin, and this results in sarcomere shortening, creating the tension of the muscle contraction. The cross-bridges can only form where thin and thick filaments already overlap, so that the length of the sarcomere has a direct influence on the force generated when the sarcomere shortens. This is called the length-tension relationship.
The ideal length of a sarcomere to produce maximal tension occurs at 80 percent to 120 percent of its resting length, with 100 percent being the state where the medial edges of the thin filaments are just at the most-medial myosin heads of the thick filaments. This length maximizes the overlap of actin-binding sites and myosin heads. If a sarcomere is stretched past this ideal length (beyond 120 percent), thick and thin filaments do not overlap sufficiently, which results in less tension produced. If a sarcomere is shortened beyond 80 percent, the zone of overlap is reduced with the thin filaments jutting beyond the last of the myosin heads and shrinks the H zone, which is normally composed of myosin tails. Eventually, there is nowhere else for the thin filaments to go and the amount of tension is diminished. If the muscle is stretched to the point where thick and thin filaments do not overlap at all, no cross-bridges can be formed, and no tension is produced in that sarcomere. This amount of stretching does not usually occur, as accessory proteins and connective tissue oppose extreme stretching.
Muscle twitch
A single action potential from a motor neuron will produce a single contraction in the muscle fibres of its motor unit. This isolated contraction is called a twitch. A twitch can last for a few milliseconds or 100 milliseconds, depending on the muscle type. The tension produced by a single twitch can be measured by a myogram, an instrument that measures the amount of tension produced over time. Each twitch undergoes three phases.
The first phase is the latent period, during which the action potential is being propagated along the sarcolemma and Ca++ ions are released from the SR. This is the phase during which excitation and contraction are being coupled but contraction has yet to occur.
The contraction phase occurs next. The Ca++ ions in the sarcoplasm have bound to troponin, tropomyosin has shifted away from actin-binding sites, cross-bridges formed, and sarcomeres are actively shortening to the point of peak tension.
The last phase is the relaxation phase, when tension decreases as contraction stops. Ca++ ions are pumped out of the sarcoplasm into the SR, and cross-bridge cycling stops, returning the muscle fibres to their resting state.
wave summation
Although a person can experience a muscle “twitch,” a single twitch does not produce any significant muscle activity in a living body. A series of action potentials to the muscle fibres is necessary to produce a muscle contraction that can produce work. Normal muscle contraction is more sustained, and it can be modified by input from the nervous system to produce varying amounts of force; this is called a graded muscle response. The frequency of action potentials (nerve impulses) from a motor neuron and the number of motor neurons transmitting action potentials both affect the tension produced in skeletal muscle.
The rate at which a motor neuron fires action potentials affects the tension produced in the skeletal muscle. If the fibres are stimulated while a previous twitch is still occurring, the second twitch will be stronger. This response is called wave summation, because the excitation-contraction coupling effects of successive motor neuron signalling is summed or added together. At the molecular level, summation occurs because the second stimulus triggers the release of more Ca++ ions, which become available to activate additional sarcomeres while the muscle is still contracting from the first stimulus. Summation results in greater contraction of the motor unit.
incomplete tetanus.
If the frequency of motor neuron signalling increases, summation and subsequent muscle tension in the motor unit continues to rise until it reaches a peak point. The tension at this point is about three to four times greater than the tension of a single twitch, a state referred to as incomplete tetanus. During incomplete tetanus, the muscle goes through quick cycles of contraction with a short relaxation phase for each.
complete tetanus.
. If the stimulus frequency is so high that the relaxation phase disappears completely, contractions become continuous in a process called complete tetanus.
During tetanus, the concentration of Ca++ ions in the sarcoplasm allows virtually all of the sarcomeres to form cross-bridges and shorten, so that a contraction can continue uninterrupted (until the muscle fatigues and can no longer produce tension).
Treppe
When a skeletal muscle has been dormant for an extended period and then activated to contract, with all other things being equal, the initial contractions generate about one-half the force of later contractions. The muscle tension increases in a graded manner that to some looks like a set of stairs. This tension increase is called treppe, a condition where muscle contractions become more efficient. It’s also known as the “staircase effect. It is believed that treppe results from a higher concentration of Ca++ in the sarcoplasm resulting from the steady stream of signals from the motor neuron. It can only be maintained with adequate ATP.
Muscle Tone
Skeletal muscles are rarely completely relaxed, or flaccid. Even if a muscle is not producing movement, it is contracted a small amount to maintain its contractile proteins and produce muscle tone. The tension produced by muscle tone allows muscles to continually stabilize joints and maintain posture.
Muscle tone is accomplished by a complex interaction between the nervous system and skeletal muscles that results in the activation of a few motor units at a time, most likely in a cyclical manner. In this manner, muscles never fatigue completely, as some motor units can recover while others are active.
hypotonia
The absence of the low-level contractions that lead to muscle tone is referred to as hypotonia, and can result from damage to parts of the central nervous system (CNS), such as the cerebellum, or from loss of innervations to a skeletal muscle, as in poliomyelitis. Hypotonic muscles have a flaccid appearance and display functional impairments, such as weak reflexes
hypertonia
Conversely, excessive muscle tone is referred to as hypertonia, accompanied by hyperreflexia (excessive reflex responses), often the result of damage to upper motor neurons in the CNS. Hypertonia can present with muscle rigidity or spasticity, a phasic change in muscle tone, where a limb will “snap” back from passive stretching.
