Muscles and Muscle Tissue Part 2: Recap

Learning Objectives

• Describe an end plate potential

• Explain excitation-contraction coupling

• Explain how the sliding filament mechanism (cross-bridge cycle) is controlled

• Define motor unit

• Describe the contractile response to an end plate potential (muscle twitch and muscle contraction)

Generation and Propagation of an Action Potential in a Skeletal Muscle Fiber

End Plate Potential

The end plate potential (EPP) is a local depolarization of the muscle fiber membrane at the neuromuscular junction, triggered by the binding of acetylcholine (ACh) to its receptors.

• Acetylcholine release: Motor neuron releases ACh into the synaptic cleft.

• ACh binding: ACh binds to receptors on the sarcolemma, opening ligand-gated ion channels.

• Ion movement: Na+ enters the muscle fiber, causing depolarization (EPP).

Action potential propagation: If the EPP is strong enough, it triggers an action potential that propagates along the sarcolemma and into the T tubules.

• Depolarization: Voltage-gated Na+ channels open, further depolarizing the membrane.

• Repolarization: K+ channels open, restoring the resting membrane potential.

Example: The rapid influx of Na+ ions initiates the muscle action potential, leading to contraction.

Excitation-Contraction Coupling

Mechanism and Sequence

Excitation-contraction (E-C) coupling is the process by which an action potential in the sarcolemma leads to muscle contraction via the sliding of myofilaments.

• Action potential travels along sarcolemma and down T tubules.

• Triggers release of Ca2+ from the sarcoplasmic reticulum (SR).

• Ca2+ binds to troponin, initiating contraction.

Example: The arrival of an action potential at the T tubule causes Ca2+ release, which is essential for contraction.

Muscle Fiber Contraction: Cross Bridge Cycling

Role of Calcium and Regulatory Proteins

Muscle contraction is regulated by the availability of Ca2+ and the interaction of regulatory proteins.

• Low Ca2+: Tropomyosin blocks actin's active sites; myosin cannot bind; muscle is relaxed.

• High Ca2+: Ca2+ binds to troponin, causing a conformational change that moves tropomyosin away from actin's binding sites.

• Myosin binds to actin: Cross bridge forms, initiating contraction.

• Contraction ends: Ca2+ is pumped back into SR when stimulation ceases.

Example: During muscle activation, Ca2+ influx allows myosin to interact with actin, resulting in sarcomere shortening.

Cross Bridge Cycle Steps

The cross bridge cycle is the sequence of events that enables muscle contraction at the molecular level.

1. Cross bridge formation: Myosin head (in high-energy state) attaches to actin.

2. Power stroke: Myosin head pivots, pulling actin toward the M line.

3. Cross bridge detachment: ATP binds to myosin, causing it to detach from actin.

4. Cocking of myosin head: ATP hydrolysis re-energizes the myosin head for the next cycle.

Equation:

Additional info: The energy from ATP hydrolysis is used for the power stroke in each cycle.

Motor Unit

Definition and Function

A motor unit consists of a single motor neuron and all the muscle fibers it innervates.

• Each muscle is served by at least one motor nerve.

• Motor nerve contains axons of multiple motor neurons.

• Axons branch to form neuromuscular junctions with muscle fibers.

• Smaller motor units: Allow for fine control of muscle contraction.

Example: Muscles controlling eye movements have small motor units for precise control.