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.