Skeletal Muscle Physiology I, Chapter 10

• Lecture 11 covers Skeletal Muscle Physiology I, Chapter 10.

Skeletal System Physiology

• Key characteristics of muscle tissue include excitability, contractility, extensibility, and elasticity.
• Excitability refers to the ability to respond to stimuli.
• Contractility refers to the ability to shorten and thicken.
• Extensibility refers to the ability to be stretched when pulled.
• Elasticity refers to the ability to return to its original shape after contraction or extension.

Skeletal Muscle Function

• Key functions of skeletal muscle:
• Movement, like walking, breathing, and talking.
• Heat production, where heat comes as a waste product of metabolism in muscle fibers.
• Posture and facial expression.
• Visceral protection via abdominal muscles.

The Neuromuscular Junction

• A single muscle fiber is innervated by a single neuron.
• The axon of a motor neuron branches to innervate multiple muscle fibers.
• A motor unit includes one motor neuron and all the muscle fibers it innervates.
• One neuron can stimulate up to 150 muscle fibers within the same muscle, such as the biceps.
• All muscle fibers within a motor unit contract together.
• Motor units are distributed throughout a large muscle.
• The pre-synaptic neuron at the neuromuscular junction contains vesicles filled with acetylcholine.
• The post-synaptic cell is a muscle fiber, its sarcolemma contains acetylcholine receptors and is called the motor end plate.
• The synaptic cleft separates the pre-synaptic lower motor neuron from the post-synaptic muscle fiber.

Signal Transmission

• The action potential reaches the axon terminal and synaptic end bulb and results in exocytosis of acetylcholine.
• Calcium enters through voltage gates, triggering acetylcholine release.
• Acetylcholine binds to receptors on the post-synaptic sarcolemma at the motor end plate.
• Chemically gated sodium channels open in response to acetylcholine binding, producing a depolarizing end plate potential (EPP).
• The EPP is a graded potential that causes voltage-gated sodium channels to open on the adjacent sarcolemma, initiating an action potential in the muscle fiber.
• The action potential in the muscle fiber has the same properties as an action potential in a neuron.
• An action potential in a lower motor neuron always causes an action potential in the muscle fiber due to the large amount of acetylcholine released and high concentration of acetylcholine receptors.
• Inhibition of the lower motor neuron is necessary to prevent skeletal muscle contraction.

Contraction of Skeletal Muscle

• Tropomyosin covers myosin binding sites on actin filaments when the muscle is relaxed.
• The myosin head must be activated before contraction occurs.
• Once activated, the myosin head is ready to bind to myosin binding sites as soon as a stimulus arrives.
• Activation of the myosin head involves ATP converting to ADP + Pi + energy.
• The energy released from ATP breakdown is stored in the myosin head and later used for contraction.
• The sarcolemma is depolarized by the influx of sodium, creating an EPP, which leads to an action potential (AP).
• The action potential spreads down the T-tubules, penetrating deep into the muscle fiber.
• Excitation-contraction coupling links the electrical event of the action potential to the contractile event in the muscle fiber.
• The action potential in the T tubules triggers the release of calcium from the terminal cisternae of the sarcoplasmic reticulum through mechanically gated calcium channels.
• Calcium ions released bind to troponin.
• The troponin-tropomyosin complex shifts position, exposing the myosin binding sites on the actin filaments.
• Activated myosin heads attach to the newly exposed myosin binding sites on actin, forming cross-bridges.
• Energy stored in the myosin head is released as the myosin head pivots, creating the power stroke.
• ADP and Pi are released from the myosin head following the power stroke.
• The power stroke causes the actin filament to slide over the myosin filament, moving toward the center of the sarcomere, which is known as the sliding filament mechanism.
• A new molecule of ATP then attaches to the myosin head.
• ATP binding causes the myosin head to detach from the myosin binding sites on actin.
• The myosin head reactivates by converting ATP into ADP and Pi.
• The energy released is once again stored in the myosin head, ready for the next contraction event.
• If calcium levels remain high in the sarcoplasm, calcium will continue to bind to troponin.
• Activated myosin heads will continue to bind to actin, causing filaments to slide.
• ATP will attach to myosin, causing the myosin to be released from the actin, and the myosin head will reactivate.
• This cycle continues, resulting in the shortening of the muscle.
• During the sliding filament mechanism, sarcomeres shorten.
• The H zone and the I band become shorter.
• The A band does not change length.
• The myofibrils shorten, leading to shortening of the whole fiber.
• The length of thin (actin) and thick (myosin) filaments remains the same during this process.