In this video, we will learn how to describe the structure of a neuromuscular junction, which is where the nervous and muscular systems meet. We will outline the processes that occur at neuromuscular junctions and explain the sliding filament theory that proposes a mechanism of how various protein filaments interact to cause muscular contractions.
Have you ever wondered why we shiver when we are cold? Shivering is actually our muscles contracting more to release more heat in order to warm us up. In fact, muscle contraction accounts for almost 85 percent of the total heat produced in your body. This is because our muscle cells carry out a lot of cellular respiration in order to release the energy necessary for contraction, and this process releases heat. This helps to explain why we get so warm when we exercise as so many of our muscles are continuously contracting and respiring.
While moving our arms to lift a weight is a voluntary action that we consciously choose to do, shivering is usually described as an involuntary action as we cannot decide to do it and we cannot simply decide to stop doing it. The muscle movements that carry out these actions are also described as either voluntary or involuntary. Voluntary movements are usually carried out by skeletal muscles, which are so named as they are attached to the bones of our skeleton, such as in the arm. Smooth muscle is exclusively involuntary muscle, and it can be found in the walls of some organs in the digestive system. For example, smooth muscle in the walls of the intestine can contract and relax to move food along.
Cardiac muscle is another type of involuntary muscle, which is only found in the heart and contracts and relaxes to regulate our heartbeat. As both smooth and cardiac muscles contract and relax without us needing to think about it, they’re described as involuntary muscles. In this video, we’re going to be focusing on skeletal muscles. So let’s take a closer look at how movement can be brought about in this type of muscle. This involves coordination of the nervous skeletal and muscular systems. The skeletal system is involved in most voluntary responses as skeletal muscles are attached 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.
By magnifying a part of this muscle, we can see a muscle fiber bundle made up of several individual muscle fibers. The nervous system is also highly important for any kind of muscular contraction. Neurons, like this motor neuron shown here in pink, conduct electrical impulses called action potentials which stimulate the muscle fiber. An action potential is a sudden and propagating change in the electrical or potential difference across the membrane of a neuron or muscle fiber when it’s stimulated. Action potentials depolarize the muscle fibers, which affects the electrical charges inside and outside of the motor neuron, stimulating the muscle fibers to contract. We’ll cover the process of depolarization in more detail later on in the video.
Muscles are sometimes called effectors as they cause an effect, sometimes called a response, to occur. The response in muscles is usually movement. All muscle fibers are stimulated by motor neurons. Let’s take a quick look at the structure of this motor neuron. Action potentials are first generated in the dendrites of a motor neuron stimulated by a signal from the brain or the spinal cord. Once these signals are gathered, they travel along a long threadlike structure called the axon. The axon ends in axon terminals that link the neuron to the muscle fiber. The points where the axon terminals and muscle fiber meet are called neuromuscular junctions. Neuromuscular junctions allow an action potential to depolarize the muscle fiber, stimulating it to contract.
A motor unit is the functional unit of skeletal muscle consisting of a motor neuron and all of the muscle fibers that it stimulates. In humans, one motor unit can connect to between five and over 1000 muscle fibers at neuromuscular junctions. This means that all of the muscle fibers receive stimulation simultaneously and therefore contract at the same time too. The stimulation of all the motor neurons in the muscle add together or summate to provide a powerful contraction.
Let’s take a closer look at a neuromuscular junction. The way that neurons pass messages to muscle fibers is similar to how neurons pass messages to each other as they both occur at synapses. Synapses are junctions between two neurons or between a neuron and an effector like this muscle fiber, which we can see a part of in this magnified view of a neuromuscular junction. As we now know, a stimulus from the brain or spinal cord first generates an action potential which propagates to the axon terminals at the end of a motor neuron. But what happens next?
Just like in a connection between two nerves, the region at the end of the axon terminal is called a synaptic knob. When an action potential arrives at the synaptic knob of a motor neuron axon terminal, it depolarizes it. In its resting state, the inside of the motor neuron is more negatively charged than the outside of the motor neuron. Depolarization flips this distribution of charge and means the inside of the motor neuron becomes more positively charged than the space outside. This causes voltage-gated calcium ion channels embedded in the presynaptic membrane to open. And calcium ions can now diffuse into the motor neuron. Remember that diffusion is the movement of particles like these calcium ions from an area of their high concentration to an area of their low concentration.
There’s a small gap at each neuromuscular junction between the motor neuron and the muscle fiber called the synaptic cleft. As the concentration of calcium ions was higher in the synaptic cleft than it was in the motor neuron axon terminal, they can diffuse in passively. There are vesicles within the synaptic knob containing a substance called acetylcholine. Acetylcholine is the neurotransmitter in neuromuscular junctions in skeletal muscle. A neurotransmitter is a chemical that transmits information across the synapse from a neuron to another neuron or from a neuron to an effector. In this case, the effector is our muscle fiber.
The diffusion of calcium ions into the motor neuron stimulates these vesicles that contain acetylcholine to move towards the motor neuron’s plasma membrane. This is otherwise known as the presynaptic membrane because it comes before the synaptic cleft. The vesicles then fuse with the presynaptic membrane and release acetylcholine into the synaptic cleft. This occurs by a process called exocytosis. The prefix exo- means out of, and -cyto- means cell, describing how a substance like acetylcholine can move out of a cell in large quantities. Once it has been released from the motor neuron, acetylcholine diffuses across the synaptic cleft towards the muscle fiber. The plasma membrane of a muscle fiber is called the sarcolemma.
At rest, the space outside the sarcolemma is more positively charged than the space inside the muscle fiber. At this point, it’s referred to as polarized. There are sodium ion channels, which are shown here in pink, embedded in the sarcolemma of the muscle fiber. These sodium ion channels contain acetylcholine binding sites. Once it’s diffused across the synaptic cleft, acetylcholine which is shown here in red attaches to these binding sites causing the sodium ion channels to open. This allows sodium ions which are shown here as pink dots to diffuse from the synaptic cleft where they’re in a high concentration into the muscle fiber, where they’re in a comparatively lower concentration.
As the acetylcholine binding sites are only located on the sarcolemma and not in the motor neuron itself, this ensures that the signal only travels in one direction. When sodium ions diffuse into the muscle fiber, it increases the positive charge inside the muscle fiber sarcoplasm. When enough sodium ions diffuse in, the sarcolemma becomes depolarized. This generates a new action potential in the muscle fiber. Once a new action potential has been generated, acetylcholine is broken down using an enzyme called acetylcholinesterase in the synaptic cleft into choline and ethanoic acid, which are shown here as small orange dots. These products will then be reabsorbed into the synaptic knob of the motor neuron. There, it can be recycled back into acetylcholine using energy released by the motor neuron’s many mitochondria.
Acetylcholine is broken down in the synaptic cleft so it does not continue to bind to receptors on the sarcolemma and overstimulate the muscle. Let’s take a look at how this new action potential can stimulate changes within the muscle fiber next. T-tubles are indentations of the sarcolemma that allow action potentials to be transported to the sarcoplasmic reticulum, which surrounds organelles called myofibrils and contains stored calcium ions. When it stimulates by an action potential, calcium ion channels open in the sarcoplasmic reticulum’s membrane, and calcium ions diffuse into the sarcoplasm. The calcium ions can then interact with protein filaments within the myofibrils to stimulate muscle contraction.
But how exactly does this happen? To understand this, let’s take a quick look at the basic structure of the repeating units of myofibrils which are called sarcomeres. The sarcomere is the functional unit of a myofibril, and it’s marked as the distance between two Z lines as you can see in this diagram. Each sarcomere contains thin filaments called actin, which is shown in this diagram in blue and consists of two strands twisted around each other. The sarcomere also contains thicker filaments called myosin, consisting of long rod-shaped fibers with globular heads that project outwards. The myofibrils also contain thin filaments called tropomyosin, which have been shown in this diagram in pink.
Tropomyosin regulates the interaction of actin and myosin to control muscle contraction. Muscles can move between states of relaxation and contraction. A scientist named Huxley used an electron microscope to observe muscle fibers in a state of relaxation and contraction, which we can see the sarcomere of in a simplified view on the right of the screen. He saw that actin and myosin filaments slide over each other when a muscle fiber is stimulated using calcium ions to form links between the two filaments. He called this the sliding filament theory, and it’s the most widely accepted idea of how muscle contraction occurs. You can see in the contracted muscle that the length of the sarcomere has shortened as the distance between the two Z lines has decreased compared to in the relaxed muscle.
The H zone, a region in the center of the sarcomere, which contains only the thick myosin filament, shortens when the muscle contracts. This is because the myosin filament is pulling the actin filament towards the M line in the middle of the sarcomere. But how did the actin and myosin molecules move to change between these two states? ATP, or adenosine triphosphate, is a molecule that stores chemical energy in living organisms. It’s made up of adenine attached to a ribose sugar and three phosphate groups. ATP is sometimes referred to as energy currency in cells of living things as it stores a lot of chemical energy in the bond between its two outer phosphate groups.
ADP, or adenosine diphosphate, is formed through the hydrolysis of ATP. Hydrolysis breaks the high energy bond between the two outer phosphate groups in an ATP molecule, which releases a phosphate group and energy that the cells can use. This energy is especially useful in muscle cells where it can be used to move these actin and myosin filaments for movement of the muscle. Through addition of energy that’s usually obtained through food and an inorganic phosphate group, ATP can be reformed from ADP. This cycle happens continuously in ourselves very, very quickly. But how is this conversion between ATP and ADP used in the sliding filament theory to contract muscle fibers? Let’s take a closer look.
When a muscle fiber is relaxed, a filament called tropomyosin which has been shown here in pink coils around each of the actin filaments. Tropomyosin acts to block the binding sites for myosin, which are found on the actin molecule. We can recognize the myosin molecule as it’s got globular heads that project outwards. When the muscle fibers relaxed, each myosin head has ADP and an inorganic phosphate bound to it. When calcium ions are released from the sarcoplasmic reticulum, they cause tropomyosin to pull away from and expose the myosin binding sites found on the actin molecule. This allows the myosin heads to bind to the actin filament by forming a cross bridge, sometimes called a transverse link. This cross bridge temporarily links the actin and myosin filaments together.
This binding releases an inorganic phosphate molecule from each of the myosin heads. The myosin head then changes angle, which pulls along the hole of the actin filament. This process, which is sometimes known as the power stroke, releases ADP from the myosin heads. ADP detaching from myosin allows ATP to bind to myosin instead. When ATP binds to the myosin head, this breaks the cross bridge between the actin of myosin filaments, which causes the myosin heads to detach. This is because the myosin head has lost its affinity for the actin filament, so the head returns to its original position. But now each myosin head is further along the actin filament than it was previously as the actin filament has been pulled to the side.
The ATP molecule bound to the myosin head is then hydrolyzed back into ADP and an inorganic phosphate. This process involves an enzyme called ATPase. ATPase activity is dependent on the presence of calcium ions as the enzymes only activated when the myosin heads combined to the actin filament, which itself is only permitted when calcium ions stimulate tropomyosin to pull away from these binding sites. The hydrolysis of ATP releases energy needed for the myosin head to be ready for another power stroke. The myosin heads will now be ready to bind to another binding site further along the actin molecule to repeat the process once more and pull the actin filament even further along.
Overall, this process shortens the H zone in the contracted sarcomere, reducing the distance between the two Z lines through this continual cycle of myosin heads binding and unbinding, pulling the actin filaments closer together. 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. When stimulation stops, the sarcomere will return to its relaxed state and the muscle becomes thinner and longer. There are two different forms of cellular respiration that produce the ATP that’s required for muscular 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 much less ATP, however, and it also releases a byproduct called lactic acid. At rest, the oxygen supply to the muscles is sufficient for aerobic respiration. The muscles also have a store of glycogen, which can be broken down into glucose molecules if it’s 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 occurs in the muscle cells, then lactic acid can build up in these cells, which might lead to muscle fatigue.
Too much anaerobic respiration also means that less ATP will be released overall. You might recall that myosin heads require ATP to detach from the actin filament. When deficient in ATP, the myosin does not detach, which means that the muscle remains contracted, leading to painful muscle spasms and even tearing in subsequent bleeding.
Let’s recap some of the key points that we’ve covered in this video. Muscle contraction can be voluntary or involuntary. Skeletal muscle contractions are coordinated by the muscular, skeletal, and nervous systems. Electrical impulses are transmitted from a nerve to a muscle fiber at a neuromuscular junction. And the sliding filament theory describes muscle contraction as a result of the interaction of actin and myosin filaments.