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Understanding Muscle Relaxation and Physiology
Sep 13, 2024
Muscle Relaxation and Related Physiology
Introduction
This lecture focuses on the relaxation phase of muscle contraction.
Review of muscle contraction and the transition to relaxation.
Action Potential and Ion Channel Dynamics
Voltage-Gated Channels
Sodium channels open, causing peak contraction at +30mV.
Potassium channels open at peak potential, allowing efflux of K+.
Repolarization Phase
Efflux of K+ leads to repolarization.
Inactivation gates of potassium channels slowly close, completing at resting membrane potential (-90mV).
Calcium Dynamics
Calcium binds to troponin during contraction, changing tropomyosin configuration.
Upon relaxation, calcium returns to the sarcoplasmic reticulum via calcium ATPase and sodium-calcium exchangers.
Sarcomere and Muscle Relaxation
Tropomyosin blocks actin-binding sites as calcium detaches, preventing myosin binding.
Sarcomere returns to resting state: H-zone reappears, I-band returns to normal.
Clinical Correlations
Autoimmune Disorders
Myasthenia Gravis
Autoimmune disorder where antibodies block nicotinic receptors, preventing acetylcholine binding.
Leads to muscle weakness, paralysis.
Lambert-Eaton Syndrome
Antibodies block calcium channels, preventing acetylcholine release.
Toxins and Drugs
Tetanus and Botulinum Toxins
Tetanus: Prevents GABA release, causing spastic paralysis.
Botulinum: Prevents acetylcholine release, used in Botox.
Snake Venoms
Dendrotoxin
: Blocks K+ channels, leading to convulsions.
Bungarotoxin
: Blocks nicotinic receptors, causing paralysis.
Succinylcholine
Mimics acetylcholine, causes temporary muscle relaxation.
Pharmacological Interventions
Acetylcholinesterase Inhibitors
Drugs like neostigmine increase acetylcholine levels by inhibiting breakdown.
Used to manage myasthenia gravis symptoms.
Conclusion
Understanding action potentials and muscle physiology is critical in both clinical and pharmacological contexts.
Important to recognize the impact of disorders and toxins on muscular function.
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