Recording-2025-01-28T18_53_53.679Z

Axon Terminal and Acetylcholine

• Axon Terminal

  • The end of the axon where it terminates; typically wider than other parts.

  • Contains synaptic vesicles which are membrane-bound sacs.

• Acetylcholine

  • The neurotransmitter released from synaptic vesicles into the synapse.

  • Essential for stimulating skeletal muscle; no other neurotransmitter can communicate with skeletal muscle fibers.

  • Contains an acetyl group, indicating it is a more complex molecule than simple neurotransmitters.

Membrane Potential and Action Potential

• An electrical signal travels down the axon due to a voltage change along the excitable membrane.

• Resting Membrane Potential (RMP): Charge difference across the membrane in a resting state.

• Voltage-gated Channels: Channels that open in response to changes in voltage.

  • Calcium Voltage-gated Channels: Open when an electrical signal reaches the axon terminal, allowing calcium to enter the axon terminal.

Neurotransmitter Release Process

• Influx of calcium allows for the release of acetylcholine into the synaptic cleft via exocytosis.

• Acetylcholine binds to chemically gated channels (acetylcholine receptors) on the muscle fiber.

• This binding opens channels, allowing sodium (Na+) to enter and potassium (K+) to exit the cell, leading to a change in membrane voltage and muscle contraction.

Role of Acetylcholinesterase

• Acetylcholinesterase: An enzyme that breaks down acetylcholine in the synaptic cleft to stop the muscle contraction signal.

• Ensures acetylcholine doesn’t linger too long, which is crucial for muscle relaxation:

  • Without it, acetylcholine would keep muscles contracted.

  • Following breakdown, components are recycled to form new acetylcholine.

Excitation-Contraction Coupling

• Excitation: An action potential is generated, leading to acetylcholine release.

• Excitation-Contraction Coupling: Refers to events that connect the electrical signal to muscle contraction.

• Action potential travels along the muscle fiber's sarcolemma and into the T-tubules, signaling the release of calcium from the sarcoplasmic reticulum.

• Calcium binds to troponin, resulting in the movement of tropomyosin to expose binding sites on actin for myosin heads to attach.

Contraction Mechanisms

• Myosin heads bind to actin and undergo a power stroke, pulling actin filaments closer, resulting in muscle contraction.

• ATP is essential for muscle contraction:

  • Binds to myosin head to prepare for the next cycle.

  • Breakdown of ATP provides energy for the subsequent contraction.

Muscle Relaxation Phase

• When the signal from the nerve stops, calcium is pumped back into the sarcoplasmic reticulum.

• Troponin reverts to its original shape, and tropomyosin covers the binding sites on actin, terminating muscle contraction.

Mechanisms of Muscle Contraction

• Muscle Twitch: A single contraction-relaxation cycle occurs in response to a stimulus.

  • Characterized by phases: latent period (no contraction immediately), contraction phase, and relaxation phase.

• Recruitment: Recruitment of muscle fibers occurs based on the stimulus intensity; smaller motor units are activated first before larger ones as more tension is required.

Types of Muscle Contractions

• Isometric Contraction: Muscle generates tension without changing length (e.g., holding an object steady).

• Isotonic Contraction: Muscle changes length while generating tension; subcategories:

  • Concentric: Muscle shortens while staying under tension.

  • Eccentric: Muscle lengthens while maintaining tension (e.g., lowering a weight).

Energy Sources for Muscle Contraction

• ATP is crucial for muscle contractions and its availability depends on:

  • Oxygen levels

  • Availability of glucose or fatty acids.

• Anaerobic Fermentation and Aerobic Respiration provide ATP through different pathways depending on oxygen supply.

  • Anaerobic fermentation results in lactate and is limited in energy production (2 ATP).

  • Aerobic respiration maximizes ATP output with sufficient oxygen.

Fatigue Mechanisms

• High-Intensity Workouts: Potassium accumulation in the T-tubules impacts the muscle's electrical excitability, while excess ADP and phosphate hinder energy production.

• Low-Intensity Workouts: Prolonged activity leads to fuel depletion and a need for external energy replenishment (glucose/electrolytes).

Rigor Mortis Explanation

• After death, calcium leaks into the sarcoplasm, allowing cross-bridging between actin and myosin without ATP to release it, causing muscle stiffness.

• Eventually, connective tissue deteriorates, allowing for muscle flexibility as structures break down.

Key Terms

• Threshold: Minimum voltage required for voltage-gated channels to open.

• Tetanus (Incomplete/Complete): Repeated stimuli causing sustained muscle contractions; can lead to fatigue if prolonged.

• Motor Units: Group of muscle fibers innervated by a single motor neuron; size influences recruitment during muscle contraction.