Body Movement Year 2 Unit 1

Body Movement - Year 2, Unit 1

• Course: Body Movement
• Year: 2
• Unit: 1
• Academic Year: 2024-2025
• Instructor: Dr. Tariq Alshaibani

Learning Objectives

• Describe the neuromuscular junction (NMJ) and how action potentials in the motor neuron lead to skeletal muscle excitation and contraction.
• Detail the molecular and electrical makeup of muscle cell excitation-contraction coupling.
• Define the elements of the sarcomere that underlie striated muscle contraction.

Skeletal Muscle Contraction & Body Movement

• Skeletal muscles contract and relax to move the body (e.g., walking, running, manipulating objects).
• Skeletal muscle works with bones to create body movements.
• Muscle fibers contract, generating tension transmitted through tendons to bones, enabling movement.

Neuromuscular Control

• Stimulation of skeletal muscle fibers (motor neurons in the spinal cord/brainstem) is the only way to make them contract.

The Neuromuscular Junction (NMJ)

• The NMJ is where the axon terminal of a motor neuron meets a muscle fiber.
• The synaptic cleft is a 20-30nm gap containing acetylcholinesterase (AChE).
• The motor end plate is the postsynaptic part of the NMJ; it features junctional folds increasing the surface area of the postsynaptic membrane.
• The motor end plate contains ACh receptors and voltage-gated sodium channels.

Acetylcholine Release

• Calcium channels are localized around dense bars on the presynaptic membrane where vesicles containing ACh fuse.
• Acetylcholine (ACh) receptors are located at the top of the subneural cleft, and voltage-gated sodium channels are found in the bottom half of the subneural cleft.
• Voltage-gated sodium channels facilitate action potential generation.

Main Schema for Neuromuscular Transmission

• Action potentials travel down motor neuron axons, triggering calcium release.
• Calcium release triggers the release of acetylcholine (ACh).
• ACh binds to receptors on the muscle fiber, initiating an action potential.
• This action potential triggers calcium release from the sarcoplasmic reticulum, leading to muscle contraction.

Disorders

• Eaton-Lambert syndrome: Autoimmune disorder affecting calcium channels in the presynaptic axon terminal.
• Botulism: Toxin produced by Clostridium botulinum bacteria, inhibiting the release of acetylcholine (ACh).
• Myasthenia gravis: Autoimmune disorder affecting cholinergic receptors in the postsynaptic membrane.

Excitation-Contraction Coupling

• Describes how the action potential entering the muscle cell causes a contraction within the muscle.

Ca+2 for Excitation-Contraction Coupling

• Action potentials travel through T-tubules.
• Calcium released from the sarcoplasmic reticulum (SR).
• Calcium binds to troponin, causing tropomyosin to shift, exposing binding sites on actin.
• Myosin heads bind to actin, producing a power stroke, pulling actin filaments.

Release of Ca+2 from Sarcoplasmic Reticulum

• Dihydropyridine (DHP) receptors sense the muscle action potential in the membrane.
• DHP receptors are linked to calcium release channels (ryanodine receptors).
• Triggering calcium release from the sarcoplasmic reticulum by activating DHP receptors in the T-tubules.

Organization of Skeletal Muscle

• Describes how skeletal muscle fibers, fascicles, and bundles are organized.

Skeletal Muscle Structure- Gross to Cellular

• Muscle, tendon, and bone relationships are described, from whole muscle to individual muscle fibers.
• Myofibril structure is described.

The Myofilaments

• Arrangement of thin (actin) and thick (myosin) filaments creates the sarcomere structure that is responsible for skeletal muscle contraction.

The Sarcomere

• The sarcomere is the fundamental unit of skeletal muscle contraction.
• A band contains thick filaments; an I-band contains thin filaments.
• The structure of Z-lines, A-bands, I-bands, and M-lines is detailed for understanding skeletal muscle contraction.

The Sliding Filament Theory of Contraction

• Myosin filaments pull actin filaments closer together, shortening sarcomeres within a muscle fiber.
• Sliding of actin past myosin generates muscle tension.

Ultrastructure of Skeletal Muscle – Molecular Basis of Contraction

• Description of the structural components related to skeletal muscle contraction.

Contractile Proteins of Skeletal Muscle

• Myosin and actin filament structure are described to explain how they enable skeletal muscle contraction.

The Molecular Basis of Skeletal Muscle Contraction

• How Ca+2 levels and ATP hydrolysis lead to skeletal muscle contraction and enable myosin to detach from actin are explained.

The Contraction Cycle - Role of Ca+2 and ATP

• The process, starting with ATP hydrolysis, of how myosin heads bind to actin followed by the power stroke (myosin heads pull actin) and detachment, and repeating to enable skeletal muscle contraction is explained.

Rigor Mortis

• After death, the process of rigor mortis, where muscles stiffen, occurs because there is no more ATP to detach myosin from actin.

In order for a skeletal muscle contraction to occur: (Summary)

• There must be a neural stimulus.
• There must be Ca+2 in the cytosol of the muscle cells.
• ATP must be available for energy.
• Relaxation occurs when Ca+2 levels decrease and ATP is available.