Skeletal Muscle Tissue 2 - BIOL 310

Learning Objectives

By the end of this lesson, students should be able to:

  • Identify the Features of the Sarcomere: Recognize the individual components and structures within the sarcomere.

  • Describe the Sliding Filament Theory: Understand the mechanics behind muscle contraction.

Review of the Muscle Contraction Cycle

Overview of Processes

  1. Neural Control:

    • Initiation starts with neural inputs.

  2. Excitation-Contraction Coupling:

    • Summarizes the chain of events from neural stimulation to muscle contraction.

  3. Calcium Ion Release:

    • Triggered at the axon terminal and linked to an action potential traveling through T-tubules to the sarcoplasmic reticulum.

The Sliding Filament Theory

Mechanism of Contraction

  • As the thin filaments slide past the thick filaments toward the M line, each myofibril shortens or creates tension.

  • Muscle fibers can shorten by about 30% during a contraction.

Structural Components

Thick Filament

  • Arrangement of Filaments:

    • Contains thick myosin filaments.

    • Includes critical landmarks: M line, A band, I band, Z line, and titin.

  • Myosin Protein Structure:

    • Composed of myosin molecules with a tail and a hinge-like connection that allows pivoting and a free head.

Thin Filament

  • Composition:

    • Made of actin (specifically G actin) with tropomyosin and troponin proteins included.

    • Troponin has binding sites for tropomyosin, actin, and calcium.

The Cross-Bridge Cycle

Overview of Steps (Detailed)

  1. Cocking of Myosin Heads:

    • If ATP is available, it binds to myosin heads, which allows their cocking (extended position).

    • Energy from ATP breakdown produces ADP + P, facilitating myosin heads' ATPase function.

  2. Calcium Ion Interaction:

    • Calcium ions released from the sarcoplasmic reticulum bind to troponin, leading to a shape change that pulls tropomyosin off the active sites on actin.

    • This exposes active sites for myosin head binding.

  3. Cross-Bridge Formation:

    • The cocked myosin heads attach to the newly exposed active sites on actin, creating cross bridges.

  4. Power Stroke:

    • The myosin heads pivot, pushing thin filaments toward the M line, which forms the contraction phase.

    • During this stage, ADP and P are released from the myosin head.

  5. Detachment of Cross-Bridge:

    • Myosin heads can detach from actin when a new ATP molecule binds to the myosin head.

  6. Myosin Reactivation:

    • The ATP is broken down, which recocks the myosin head, making it ready for another cycle.

Cycle Continuation and Muscle Contraction

  • The cross-bridge cycle will repeat, allowing contractions to persist until action potentials cease within the T tubules.

Calcium Ion Management

Role of Calcium Ions

  • When action potentials stop, calcium ions are actively pumped out of the sarcoplasm back into the SR via Ca2+ pumps.

  • Outcome: No calcium ions result in no cross-bridge formation, halting contraction.

ATP Utilization in Muscle Contraction

Energy Source Breakdown

  1. Cocking Myosin Heads:

    • ATP binds to myosin heads but is not immediately broken down until the cocking phase.

  2. Calcium Ion Pumping:

    • ATP is necessary to pump Ca2+ ions back into the SR against their concentration gradient.

  3. Source of ATP:

    • The energy needed for these processes is derived from numerous mitochondria present within muscle fibers.

Review of Key Concepts

Essential Terms to Understand

  • Acetylcholine (ACh)

  • Acetylcholinesterase (AChE)

  • Actin, Myosin, Troponin, Tropomyosin

  • ATP, ADP + P

  • Calcium Ions (Ca2+)

  • Synaptic Cleft, Neuromuscular Junction

  • Excitation-Contraction Coupling

  • Z line, M line, H band

  • Motor Neuron

Integration Task

  • Collaborate with a neighbor to outline the process a muscle contraction follows from initiation at the neuromuscular junction to conclusion (including what stops the contraction).

Rigor Mortis Explanation

Process of Rigor Mortis

  • No ATP Production:

    • Subsequent to death, ATP production halts, preventing pumps from moving calcium ions back to the sarcoplasmic reticulum.

  • Calcium Leakage:

    • Breakdown of the SR allows Ca2+ to leak out.

  • Active Site Exposure:

    • As a result, active sites on actin remain uncovered by tropomyosin.

  • Continuous Cross-Bridge Formation:

    • Myosin heads stay bound to actin, maintaining tension until the myofibrils decompose.