Lesson Explainer: Muscle Contraction Biology

In this explainer, we will learn how to describe the structure of a neuromuscular junction and outline the sliding filament theory of muscle contraction.

Did you know that muscle contraction accounts for almost 85% of the total heat produced in your body? This is because the muscle cells carry out lots of cellular respiration to release the necessary energy for contraction and this releases heat. This explains why we get so warm when we exercise, as so many of our muscles are continuously contracting and respiring! The release of heat can also be used as an advantage for the body through involuntary muscle contractions. When we are cold, we shiver. Shivering is our muscles contracting, aiming to warm us up by respiring more and releasing more heat!

Muscle movements can be voluntary or involuntary. Voluntary movements are usually carried out by skeletal muscles, named as such because they are attached to the bones of our skeleton. These are the muscles that will be moving your legs and arms to help you exercise.

Most involuntary muscle contractions are conducted by smooth muscle and cardiac muscle. Smooth muscle, among its many other uses, contracts to help food move through our digestive system and to help blood move through our arteries. Cardiac muscle contracts to regulate our heartbeat. Both of these types of muscle contract and relax rhythmically without us needing to think about it, and so, they are involuntary.

To bring about movement in our skeletal muscles, the nervous, skeletal, and muscular systems work together. Let’s have a look at this coordination in more detail.

The skeletal system is involved in most voluntary responses by skeletal muscles, as these muscles are usually connected to bones. Bones provide a site that muscles can connect to, and the joints found between many bones allow flexibility of movement resulting from muscle contraction.

The nervous system is also involved in muscle contraction. Neurons conduct electrical impulses called action potentials. Action potentials involved in muscle contraction function to stimulate the muscle fiber. They do this by depolarizing the muscle fibers by changing the electrical, or potential difference, across their membranes. This instructs the muscle to contract.

Key Term: Action Potential

An action potential is the sudden and propagating change in the potential difference across the membrane of a neuron or a muscle fiber when stimulated.

Muscles are sometimes called effectors, as they cause an effect to occur. This effect is called a response. This response in muscles is usually movement. The neurons that connect to effectors such as muscles are called motor neurons. The point where the motor neuron and muscle fiber meet is called the neuromuscular junction. You can see some neuromuscular junctions in Figure 1.

Key Term: Neuromuscular Junction

A neuromuscular junction is a synaptic connection between the axon of a motor neuron and a muscle fiber.

Example 1: Identifying the Location of Neuromuscular Junction Formation

Where does a neuromuscular junction form?

  1. Between the dendrite of a sensory neuron and a muscle fiber
  2. Between the axon of a motor neuron and the dendrite of a sensory neuron
  3. Between the axon of a motor neuron and a muscle fiber
  4. Between the axon of a motor neuron and the dendrite of another neuron

Answer

The muscular system is responsible for movement. It does this through the contraction and relaxation of organs called muscles.

The nervous system is also involved in muscle contraction. Neurons conduct electrical impulses called action potentials. Action potentials involved in muscle contraction function to stimulate the muscle fibers. They do this by depolarizing the muscle fibers by changing the potential difference across their membranes. This instructs the muscle to contract.

Muscles are sometimes called effectors, as they cause an effect to occur. This effect is called a response. This response in muscles is usually movement. The neurons that connect to effectors, such as muscles, are called motor neurons. The point where the axon of a motor neuron and a muscle fiber meet is called a neuromuscular junction. You can see some neuromuscular junctions in the figure below.

Therefore, neuromuscular junctions form between the axon of a motor neuron and a muscle fiber.

All muscle fibers are stimulated by motor neurons. A single motor neuron and all the muscle fibers that it stimulates are called the motor unit. The motor unit is the functional unit of skeletal muscle, and it branches into several axon terminals.

Key Term: Motor Unit

A motor unit is the functional unit of skeletal muscle, consisting of a motor neuron and all the muscle fibers that it stimulates.

In humans, one motor unit can connect from 5 to over 1‎ ‎000 muscle fibers at neuromuscular junctions! This means that all the muscle fibers receive stimulation simultaneously and, therefore, contract at the same time too. The stimulation of all the motor units in the muscle adds together, or summate, to provide a powerful contraction.

Let’s see how a motor neuron stimulates contraction.

The way that neurons pass messages to the muscle fiber to stimulate it to contract is quite similar to how neurons pass messages to each other, as they both occur via synapses. Synapses are the junctions between two neurons, or between a neuron and an effector.

Key Term: Synapse

A synapse is the junction between two neurons, or a neuron and an effector.

A stimulus from the brain or spinal cord generates an action potential in the dendrites of a motor neuron, as we see in Figure 1. The action potential travels along the axon of the motor neuron until it reaches the axon terminals, which form a synaptic knob at each neuromuscular junction.

When an action potential arrives at the axon terminal of the motor neuron, it depolarizes it. This means that the space inside the motor neuron membrane becomes more positively charged than the space outside, which is the opposite of its resting state. This stimulates voltage-gated calcium ion channels in the membrane to open, and calcium ions (Ca)2+ diffuse into the motor neuron as we can see in Figure 2.

Key Term: Calcium Ions

An ion is a charged atom or molecule. Calcium ions (Ca)2+ are involved in the release of a neurotransmitter at a synapse.

There is a small gap at each neuromuscular junction between the motor neuron and muscle fiber called the synaptic cleft, which you can see in Figure 3.

Vesicles within the synaptic knob contain acetylcholine. Acetylcholine is the neurotransmitter at neuromuscular junctions in skeletal muscle. A neurotransmitter is a chemical that transmits information across a synapse from a neuron to another neuron or an effector.

Key Term: Neurotransmitter

A neurotransmitter is a chemical involved in communication across a synapse between adjacent neurons or a neuron and an effector.

Ca2+ diffusing into the motor neuron stimulates vesicles containing acetylcholine to move toward the motor neuron’s plasma membrane. These vesicles fuse with the plasma membrane and release the neurotransmitter into the synaptic cleft as you can see in Figure 3. This is called exocytosis. Exo means out of, and cyto means cell. This describes how a substance, like acetylcholine, moves out of a cell in large quantities.

Once it has been released from the motor neuron, acetylcholine diffuses across the synaptic cleft toward the muscle fiber, as you can see in Figure 4. Diffusion is the movement of particles from an area of high concentration to an area of lower concentration. Acetylcholine is in a higher concentration by the motor neuron membrane than by the muscle fiber, so it can diffuse passively without requiring any energy.

Key Term: Diffusion

Diffusion is the movement of molecules from a region of high concentration to a region of low concentration.

The membrane of a muscle fiber is called the sarcolemma. At this point, the space outside the sarcolemma is more positively charged than the space inside the muscle fiber. This is due to the difference in the concentration of charged ions inside and outside the sarcolemma. The sarcolemma is referred to as polarized at this point.

As you can see in Figure 5, there are sodium ion channels embedded in the sarcolemma of the muscle fiber.

These sodium ion channels are receptors that contain active sites complementary to acetylcholine. Once it has diffused across the synaptic cleft, acetylcholine binds to these active sites, causing the sodium ion channels to open. As shown in Figure 5, this allows sodium ions (Na)+ to diffuse from the synaptic cleft where they are high in concentration, into the muscle fiber where they are lower in concentration.

As these sodium ion channels are only located on the sarcolemma and not in the synaptic knob of the motor neuron, they ensure that the impulse only travels in one direction and the neuron itself is not stimulated again.

Key Term: Sodium Ions

An ion is a charged atom or molecule. Sodium ions (Na)+ are involved in the depolarization step in the transmission of an action potential.

When Na+ diffuses into the muscle fiber, it increases the positive charge inside the muscle fiber’s sarcoplasm, depolarizing it. This generates a new action potential in the muscle fiber.

Example 2: Describing the Series of Events at a Neuromuscular Junction

The flowchart provided describes the events that occur at a neuromuscular junction, with each step assigned a number. State the number sequence that would give the correct order of events.

Answer

A neuromuscular junction is a synaptic connection between the axon of a motor neuron and a muscle fiber.

When an action potential arrives at a neuromuscular junction, it first depolarizes the synaptic knob at the end of the motor neuron. This means that the space inside the motor neuron membrane becomes more positively charged than the space outside, which is the opposite of its resting state.

This stimulates calcium ion channels in the membrane to open, and calcium ions (Ca)2+ diffuse into the motor neuron.

Ca2+ diffusing into the motor neuron stimulates vesicles containing acetylcholine to move toward and fuse with the plasma membrane of the motor neuron. Acetylcholine is released into the synaptic cleft by exocytosis.

Acetylcholine diffuses across the synaptic cleft toward the muscle fiber. The membrane of a muscle fiber is called the sarcolemma. There are sodium ion channels embedded in the sarcolemma of the muscle fiber. These sodium ion channels are receptors that contain active sites complementary to acetylcholine. Once it has diffused across the synaptic cleft, acetylcholine binds to these active sites.

This causes the sodium ion channels to open. This allows sodium ions (Na)+ to diffuse from the synaptic cleft, where they are high in concentration, into the muscle fiber, where they are lower in concentration.

When Na+ diffuses into the muscle fiber, it increases the positive charge inside the muscle fiber’s sarcoplasm, depolarizing it. This generates a new action potential in the muscle fiber.

The correct order of stages is therefore 6, 2, 1, 4, 3, 5.

Once an action potential has been generated in the muscle fiber, acetylcholine is broken down by an enzyme called acetylcholinesterase into choline and ethanoic acid. These products will then be reabsorbed into the synaptic knob of the motor neuron to be recycled into acetylcholine using energy released by the motor neuron’s many mitochondria. Acetylcholine is broken down in the synaptic cleft so that it does not continue to bind to the receptors on the sarcolemma and overstimulate the muscle.

Figure 6 shows us how the motor neuron connects to the structures within the muscle fiber.

As you can see in Figure 6, T tubules, short for transverse tubules, are deep indentations of the sarcolemma into the muscle fibers. T tubules, with the help of voltage-gated ion channels embedded into their membranes, allow action potentials to be transported from the surface of the muscle fiber to the sarcoplasmic reticulum that surrounds the myofibrils. Let’s see how the sarcoplasmic reticulum plays a role in muscle contraction.

The sarcoplasmic reticulum contains stored Ca2+. When an action potential travels along the T tubules to the sarcoplasmic reticulum, it causes calcium ion channels to open in the sarcoplasmic reticulum membrane. Ca2+ diffuses from an area of high concentration in the sarcoplasmic reticulum into the sarcoplasm of the muscle fiber where there is a lower concentration of Ca2+.

Muscle fibers possess organelles called myofibrils. Myofibrils contain thin protein filaments called actin and thicker ones called myosin. They also contain thin filaments called tropomyosin that regulate the interaction of actin and myosin to control muscle contraction. The release of Ca2+ from the sarcoplasmic reticulum stimulates this muscle contraction, but how does this happen?

Key Term: Myosin

Myosin is a thick filament within a myofibril of a muscle fiber, consisting of long rod-shaped fibers with globular heads that project outwards.

Key Term: Actin

Actin is a thin filament within a myofibril of a muscle fiber, consisting of two strands twisted around each other.

Key Term: Tropomyosin

Tropomyosin is a thin filament that controls muscle contraction by regulating the interactions of actin and myosin.

The most widely accepted idea of how muscle contraction occurs was theorized by a scientist named Huxley. He observed muscle fibers with an electron microscope in a state of both relaxation and contraction. He saw that actin and myosin filaments slide over each other when a muscle fiber is stimulated, using Ca2+ to form links between the two filaments. He called this the sliding filament theory.

Key Term: Sliding Filament Theory

The sliding filament theory describes the movement of actin and myosin filaments in relation to each other to cause muscle contraction.

Let’s see how this sliding filament theory works in more detail.

Myofibrils are made up of many repeating units called sarcomeres, two of which are shown in Figure 7 below. A sarcomere is the functional unit of a myofibril and two Z lines mark the sarcomere’s boundary. A sarcomere is therefore the distance between each two successive Z lines, as you can see in a relaxed and contracted muscle sarcomere in Figure 7 below.

Key Term: Sarcomere

A sarcomere is the functional unit of a myofibril, marked as the distance between two Z lines, which shortens when a muscle contracts.

Figure 7 displays the orientation of actin and myosin in a relaxed muscle on the left and a contracted muscle on the right. You can see that in the contracted muscle, the sarcomere has shortened as the distance between the two Z lines has decreased compared to the relaxed muscle. The H zone, a region in the center of the sarcomere that only contains myosin, shortens when the muscle contracts as the myosin pulls the actin filaments toward the M line.

But how do the actin and myosin molecules move to change between the two states?

ATP, or adenosine triphosphate, is the molecule that stores chemical energy in living organisms. ADP, or adenosine diphosphate, is a molecule formed by the hydrolysis of ATP. By breaking down ATP with water through hydrolysis, ADP, an inorganic phosphate ion (Pi), and energy are released. This energy can be used for movement.

Key Term: ATP (adenosine triphosphate)

ATP is the molecule that stores chemical energy in living organisms.

Key Term: ADP (adenosine diphosphate)

ADP is the molecule formed by the hydrolysis of ATP, releasing a phosphate ion and energy.

Let’s see how the conversion between ATP and ADP is used in the sliding filament theory to contract muscle fibers.

When a muscle fiber is relaxed, a filament called tropomyosin coils around each actin filament, blocking binding sites for myosin on its surface. The Ca2+ released from the sarcoplasmic reticulum causes tropomyosin to pull away from binding sites on the actin filament. You can see this process occurring in Figure 8. This makes space for the myosin heads to bind to the actin filament through a crossbridge, sometimes called a transverse link. A crossbridge is the interaction between the actin and myosin filaments, temporarily connecting them to each other.

The myosin head binds to actin, which releases Pi, and then changes angle as you can see in Figure 9. The change in angle pulls the actin filament along. This process, which is sometimes called the power stroke, releases ADP from the myosin head.

ADP detaching from myosin allows ATP to bind to myosin instead. ATP binding to myosin causes the myosin head to detach from the actin filament that breaks the crossbridges, as you can see in Figure 10. This is because the myosin head loses its affinity for the actin filament, so the head returns to its original position.

The ATP molecule bound to the myosin head will then be hydrolyzed back to ADP and Pi. This process involves an enzyme called ATPase. ATPase activity is dependent on the presence of Ca2+, as ATPase activation only occurs when myosin heads bind to the actin binding sites. This is only permitted when Ca2+ stimulates tropomyosin to pull away from these binding sites. The hydrolysis of ATP releases the energy needed for the myosin head to be ready for another power stroke in the cocked position that we saw in Figure 8. Myosin can now bind to another binding site further along the actin filament to repeat the process.

Example 3: Describing the Action of Myosin in the Sliding Filament Theory

In the sliding filament theory of muscle contraction, what initiates the detachment of the myosin head from the binding site on the actin filament?

  1. A molecule of ATP binding to the myosin head
  2. Calcium ions binding to tropomyosin
  3. A molecule of ADP being released from the myosin head
  4. The hydrolysis of an ADP molecule on the actin filament

Answer

The sliding filament theory describes the movement of actin and myosin filaments in relation to each other to cause muscle contraction.

When a muscle fiber is relaxed, a filament called tropomyosin coils around each actin filament, blocking binding sites for myosin on its surface. The Ca2+ released from the sarcoplasmic reticulum causes tropomyosin to pull away from binding sites on the actin filament. This makes space for the myosin heads to bind to the actin filament through crossbridges, sometimes called transverse links.

The myosin head binds to actin, which releases Pi, and then changes angle. The change in angle pulls the actin filaments closer together, as you can see in the figure below. This process, which is sometimes called the power stroke, releases ADP from the myosin head.

Therefore, a molecule of ATP binding to the myosin head is what causes the myosin head to detach from the actin filament binding site. The correct answer is option A.

Overall, this process functions to pull the actin filaments closer together, shortening the length of the H zone in the sarcomere, as you can see in the contracted muscle on the bottom right of Figure 11. This pulls the Z lines closer together, shortening the whole length of the sarcomere. When this happens to thousands of sarcomeres at once, it causes the whole muscle to shorten and contract! This will happen as long as the muscle is stimulated. You can see this shortened contracted muscle on the top right of Figure 11.

When stimulation stops, the sarcomere will return to its relaxed state, as you can see on the bottom left of Figure 11, and the muscle will become thinner and longer, as you can see in the top-left image.

Example 4: Describing the Stages of the Sliding Filament Theory

The diagram provided shows the stages of the sliding filament theory. State the correct order.

Answer

The sliding filament theory describes the movement of actin and myosin filaments in relation to each other to cause muscle contraction.

When a muscle fiber is relaxed, a filament called tropomyosin coils around each actin filament, blocking binding sites for myosin on its surface. The Ca2+ released from the sarcoplasmic reticulum causes tropomyosin to pull away from binding sites on the actin filament.

This makes space for the myosin head to bind to the actin filament through a crossbridge, sometimes called a transverse link.

The myosin head binds to actin, which releases Pi, and then changes angle. The change in angle pulls the actin filaments closer together as you can see in the figure below. This process, which is sometimes called the power stroke, releases ADP from the myosin head.

ADP detaching from myosin allows ATP to bind to myosin instead. ATP binding to myosin causes the myosin head to detach from the actin filament, which breaks the crossbridges.

The ATP molecule bound to the myosin head will then be hydrolyzed back to ADP and Pi. This process involves an enzyme called ATPase. The hydrolysis of ATP releases the energy needed for the myosin head to move back to its original position.

Therefore, the correct order of stages is 3, 2, 5, 7, 8, 6, 4, 1.

There are two different forms of cellular respiration that can release the ATP needed for muscle contraction: aerobic respiration and anaerobic respiration.

Both reactions break down glucose to release ATP. While aerobic respiration also requires oxygen, anaerobic respiration does not. Anaerobic respiration releases far less ATP than aerobic respiration, however, and it also produces a toxic byproduct called lactic acid.

Reaction: Aerobic Respiration

Glucose+OxygenCarbonDioxide+Water(+ATP)

Reaction: Anaerobic Respiration

GlucoseLacticAcid(+ATP)

At rest, the oxygen supply to the muscles is sufficient for aerobic respiration. The muscles also have a store of glycogen that can be converted into glucose molecules if needed. When the supply of oxygen to muscle cells via the blood is insufficient to meet the demands of aerobic respiration, this glucose can only be used in anaerobic respiration. If too much anaerobic respiration is carried out, lactic acid builds up in muscle cells and can cause muscle fatigue.

Too much anaerobic respiration also means that less ATP will be released overall. You may recall that the myosin heads require ATP to detach from the actin filament. When deficient in ATP, myosin does not detach, which means that the muscle remains contracted leading to painful muscle spasms and even tearing and subsequent bleeding.

Smooth muscle contraction is also dependent on calcium ions released from the sarcoplasmic reticulum and on the interactions between actin and myosin filaments in spite of these muscles appearing unstriated. Interestingly, in smooth muscle, the activity of ATPase is low compared to skeletal muscle, which means that fewer crossbridges are formed between myosin heads and actin filaments over the same period of time. This means that smooth muscles tend to have longer periods of contraction but can overall generate a potentially larger force of contraction!

Let’s recap some of the key points we have covered in this explainer.

Key Points

  • Muscle contraction can be voluntary in striated skeletal muscle or involuntary in smooth muscle and cardiac muscle.
  • Striated muscle contraction is coordinated by the muscular, skeletal, and nervous systems.
  • Electrical impulses are transmitted from a nerve to a muscle fiber at a neuromuscular junction.
  • The sliding filament theory, which describes muscle contraction as the movement of actin and myosin filaments across each other, is the most widely accepted theory of muscle contraction.
  • Muscles can become fatigued if they are not supplied with enough oxygen by the blood.

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