Muscular Contractions

 

The Neuromuscular Junction

Another specialization of the skeletal muscle is the site where a motor neuron’s terminal meets the muscle fiber—called the neuromuscular junction (NMJ).

• This is where the muscle fiber first responds to signaling by the motor neuron.
• Every skeletal muscle fiber in every skeletal muscle is innervated by a motor neuron at the NMJ.
  • Excitation signals from the neuron are the only way to functionally activate the fiber to contract.

 

Every skeletal muscle fiber is supplied by a motor neuron at the NMJ. Watch this video to learn more about what happens at the NMJ.

Part 1 of Muscle  Contraction

 

Excitation-Contraction Coupling

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 signaling 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.

 

Although the term excitation-contraction coupling confuses or scares some students, it comes down to this: for a skeletal muscle fiber to contract, its membrane must first be “excited”—in other words, it must be stimulated to fire an action potential.

• The muscle fiber 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 center, shortening the muscle fiber.

 

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 signaling from the nervous system.

 

• At the NMJ, the axon terminal releases ACh.
  • The motor end-plate is the location of the ACh-receptors in the muscle fiber sarcolemma.
• When ACh molecules are released, they diffuse across a minute space called the synaptic cleft and bind to the receptors.

 

The motor neurons that tell the skeletal muscle fibers to contract originate in the spinal cord, with a smaller number located in the brainstem for activation of skeletal muscles of the face, head, and neck.

• These neurons have long processes, called axons, which are specialized to transmit action potentials long distances— in this case, all the way from the spinal cord to the muscle itself (which may be up to three feet away).
• The axons of multiple neurons bundle together to form nerves, like wires bundled together in a cable.

 

Signaling begins when a neuronal action potential travels along the axon of a motor neuron, and then along the individual branches to terminate at the NMJ.

• At the NMJ, the axon terminal releases a chemical messenger, or neurotransmitter, called acetylcholine (ACh).
• The ACh molecules diffuse across a minute space called the synaptic cleft and bind to ACh receptors located within the motor end-plate of the sarcolemma on the other side of the synapse.
• Once ACh binds, a channel in the ACh receptor opens and positively charged ions can pass through into the muscle fiber, causing it to depolarize, meaning that the membrane potential of the muscle fiber becomes less negative (closer to zero.)
• As the membrane depolarizes, another set of ion channels called voltage-gated sodium channels are triggered to open.
• Sodium ions enter the muscle fiber, and an action potential rapidly spreads (or “fires”) along the entire membrane to initiate excitation-contraction coupling.

 

Things happen very quickly in the world of excitable membranes (just think about how quickly you can snap your fingers as soon as you decide to do it).

• Immediately following depolarization of the membrane, it repolarizes, re-establishing the negative membrane potential.
• Meanwhile, the ACh in the synaptic cleft is degraded by the enzyme acetylcholinesterase (AChE) so that the ACh cannot rebind to a receptor and reopen its channel, which would cause unwanted extended muscle excitation and contraction.

 

Propagation of an action potential along the sarcolemma is the excitation portion of excitation-contraction coupling.

• Recall that this excitation actually triggers the release of calcium ions (Ca++) from its storage in the cell’s SR.
• For the action potential to reach the membrane of the SR, there are periodic invaginations in the sarcolemma, called T-tubules (“T” stands for “transverse”).
  • You will recall that the diameter of a muscle fiber can be up to 100 μm, so these T-tubules ensure that the membrane can get close to the SR in the sarcoplasm.
  • The arrangement of a T-tubule with the membranes of SR on either side is called a triad.
  • The triad surrounds the cylindrical structure called a myofibril, which contains actin and myosin.

 

• Narrow T-tubules permit the conduction of electrical impulses.
• The SR functions to regulate intracellular levels of calcium.
  • Two terminal cisternae (where enlarged SR connects to the T-tubule) and one T-tubule comprise a triad—a “threesome” of membranes, with those of SR on two sides and the T-tubule sandwiched between them.
• The T-tubules carry the action potential into the interior of the cell, which triggers the opening of calcium channels in the membrane of the adjacent SR, causing Ca++ to diffuse out of the SR and into the sarcoplasm.
• It is the arrival of Ca++ in the sarcoplasm that initiates contraction of the muscle fiber by its contractile units, or sarcomeres.

 

It is extremely complicated.  This is only the first half of the sequence.  I just want you to appreciate the complicated system used to contract your muscles.  

Steps to part 1:

1. The nervous system sends a signal through a nerve to the muscle.
2. Ach neurotransmitter is released into the synaptic cleft from the nerve.
3. Ach binds to the receptor and triggers it to open allowing Na+ to enter cell
4. Depolarization occurs and the action potential (excitation) is started in the muscle.
5. Exciting of the membrane triggers Ca+ to be released from the SR (sarcoplasmic reticulum) into the sarcoplasm (by using T-tubules)

 

That wasn't that hard was it?  Now let's work on the second half.  

 

10.3 | Muscle Fiber Contraction and Relaxation

By the end of this section, you will be able to:

• Describe the components involved in a muscle contraction
• Explain how muscles contract and relax
• Describe the sliding filament model of muscle contraction

 

Starting Part 2:

• The Ca++ then initiates contraction, which is sustained by ATP.
  • As long as Ca++ ions remain in the sarcoplasm to bind to troponin, which keeps the actin-binding sites “unshielded,” and as long as ATP is available to drive the cross-bridge cycling and the pulling of actin strands by myosin, the muscle fiber will continue to shorten to an anatomical limit.

 

 

Contraction of a muscle fiber: A cross-bridge forms between actin and the myosin heads triggering contraction. As long as Ca++ ions remain in the sarcoplasm to bind to troponin, and as long as ATP is available, the muscle fiber will continue to shorten.

 

Muscle contraction usually stops when signaling from the motor neuron ends, which repolarizes the sarcolemma and Ttubules, and closes the voltage-gated calcium channels in the SR.

• Ca++ ions are then pumped back into the SR, which causes the tropomyosin to reshield (or re-cover) the binding sites on the actin strands.
• A muscle also can stop contracting when it runs out of ATP and becomes fatigued.

  

Relaxation of a muscle fiber: Ca++ ions are pumped back into the SR, which causes the tropomyosin to reshield the binding sites on the actin strands.

• A muscle may also stop contracting when it runs out of ATP and becomes fatigued.

 

The release of calcium ions initiates muscle contractions.

• Watch this video to learn more about the role of calcium.

Part 2 of Muscle Contraction

 

The molecular events of muscle fiber shortening occur within the fiber’s sarcomeres.

• The contraction of a striated muscle fiber occurs as the sarcomeres, linearly arranged within myofibrils, shorten as myosin heads pull on the actin filaments.

 

The region where thick and thin filaments overlap has a dense appearance, as there is little space between the filaments.

• This zone where thin and thick filaments overlap is very important to muscle contraction, as it is the site where filament movement starts.
• Thin filaments, anchored at their ends by the Z-discs, do not extend completely into the central region that only contains thick filaments, anchored at their bases at a spot called the M-line.
• A myofibril is composed of many sarcomeres running along its length; thus, myofibrils and muscle cells contract as the sarcomeres contract.

 

The Sliding Filament Model of Contraction

When signaled by a motor neuron, a skeletal muscle fiber contracts as the thin filaments are pulled and then slide past the thick filaments within the fiber’s sarcomeres.

• This process is known as the sliding filament model of muscle contraction.
• The sliding can only occur when myosin-binding sites on the actin filaments are exposed by a series of steps that begins with Ca++ entry into the sarcoplasm.

 

 

The Sliding Filament Model of Muscle Contraction  - When a sarcomere contracts, the Z lines move closer together, and the I band becomes smaller.

• The A band stays the same width.
• At full contraction, the thin and thick filaments overlap.

 

Tropomyosin is a protein that winds around the chains of the actin filament and covers the myosin-binding sites to prevent actin from binding to myosin.

• Tropomyosin binds to troponin to form a troponin-tropomyosin complex. The troponin-tropomyosin complex prevents the myosin “heads” from binding to the active sites on the actin microfilaments.
• Troponin also has a binding site for Ca++ ions.

 

To initiate muscle contraction, tropomyosin has to expose the myosin-binding site on an actin filament to allow cross-bridge formation between the actin and myosin microfilaments.

• The first step in the process of contraction is for Ca++ to bind to troponin so that tropomyosin can slide away from the binding sites on the actin strands.
• This allows the myosin heads to bind to these exposed binding sites and form cross-bridges.
• The thin filaments are then pulled by the myosin heads to slide past the thick filaments toward the center of the sarcomere.
  • But each head can only pull a very short distance before it has reached its limit and must be “re-cocked” before it can pull again, a step that requires ATP.

 

HERE IS YOUR SUMMARY AND WHAT YOU WILL NEED TO KNOW FOR THE QUIZ

• • YOU WILL ALSO NEED TO KNOW THE NAMES OF YOUR MUSCLES.  

 

Part 1 and Part 2:

1. The nervous system sends a signal through a nerve to the muscle.
2. Ach neurotransmitter is released into the synaptic cleft from the nerve.
3. Ach binds to the receptor and triggers it to open allowing Na+ to enter cell
4. Depolarization occurs and the action potential (excitation) is started in the muscle.
5. Exciting of the membrane triggers Ca+ to be released from the SR (sarcoplasmic reticulum) into the sarcoplasm (by using T-tubules)
6. Ca+ binds with the shielding proteins troponin.
7. Tropomyosin slide away from the actin binding sites.
8. The actin binding sites are unshielded allowing myosin to attach to actin.
9. Myosin pulls the actin filaments toward center to shorten the muscle.
10. Muscle contraction stops when Ach is degraded from the synaptic cleft.
11. Na+ is pumped out of the cell and the membrane is repolarized with a negative charge on the inside.
12. Ca+ is taken back into the SR and troponin will rebind to actin.

 

One more video from start to finish.