Lecture 9: Muscle Anatomy and Physiology Part 1 Flashcards
(23 cards)
Motor units
A motor unit consists of a single motor neuron and the muscle fibers it controls
A motor unit controls only a few muscle fibers in an entire muscle
Large muscles have more motor units than do smaller muscles
Each muscle fiber obeys the all or none principle. A muscle fiber contracts completely or not at all
When a motor unit is stimulated all of muscle fibers under its control will contract
Properties of muscle tissue
Four unique characteristics of muscle tissue:
- Excitability: outside stimuli can initiate electrical changes in the muscle fiber (cell) leading to contraction of that muscle fiber (cell)
- Contractility: stimulation of muscle fiber can lead to contraction or shortening of the muscle fiber
- Elasticity: a muscle fiber’s ability to return to its original length when the tension of contraction is released
- Extensibility: the ability of a muscle fiber to be stretched beyond its relaxed state
Properties of whole muscles
Not all muscle cells in a muscle contract at the same time (only the ones activated by the same neuron)
The number of motor units that are activated determines the strength of the contraction small number of units = weak contraction; large number of units at greater frequency = stronger contraction
Muscle tone is the continued steady low level of contraction that stabilizes joints and maintains general muscle health
Dystonia
Disorder characterized by involuntary sustained muscle contractions resulting in twisting and repetitive movements or abnormal postures
Components of the NMJ
Synaptic knob: expanded end of the neuron
Synaptic vesicles: membrane bound sacs filled acetylcholine
Motor end plate: region of sarcolemma across from the synaptic knob that has folds and indentations to increase the surface area in that region
Synaptic cleft: narrow space separating the synaptic knob from the motor end plate
ACh receptors: in the motor end plate that bind to ACh
Acetylcholinesterase (AChE): an enzyme in the synaptic cleft that rapidly breaks down ACh
Steps of propagation
- Motor neuron action potential
- Ca2+ enters voltage gated channels
- Acetylcholine release
- ACh binding opens ion channels
- Na+ entry
- Local current between depolarized end plate and adjacent muscle plasma membrane
- Muscle fiber action potential initiation
- Propagated action potential in muscle plasma membrane
- Acetylcholine degradation
Muscle fiber terminology
Cytoplasm = sarcoplasam
Plasma membrane = sarcolemma
Smooth ER = sarcoplasamic reticulum
Excitation contraction coupling
- Somatic motor neuron releases ACh at NMJ
- Net entry of Na+ through ACh receptor channel initiates a muscle potential
- Action potential in t-tubules alters confirmation of DHP receptor
- DHP receptor opens ryanodine receptor Ca2+ release channels in sacrcoplasmic reticulum and Ca2+ enters cytoplasm
- Ca2+ binds to troponin allowing actin-myosin binding
- Myosin heads execute power stroke
- Actin filament slide toward center of sarcomere
Multiminicore disease
Disorder that primarily affects muscles used for movement (skeletal muscle) this condition causes muscle weakness and related health problems that range form milf to life threatening
Mutation in the RYR1 and SEPN1 genes cause multiminicore disease
RYR1 mutations are also associated with an increased risk of malignant hyperthermia
NMJ disorders
Myasthenia Gravis
Myasthenic syndrome (eaton lambert disease)
Muscular dystrophy (such be muscular dystrophy)
Mystonias
MS
Guilloan-Barre (acute idiopathic polyneuritis)
Amyotrophic lateral sclerosis (als)
Myasthenia Gravis
Post junctional alteration Auto immune response to ACh receptors Onset pharyngeal and ocular weakness Worsens with exercise Treatment: anticholinestrase
Myasthenic syndrome/ eaton lambert syndrome
Pre-junctional alteration Decreased ACh release Peripheral and pelvic muscles affected Improves with exercise Do not improve with anticholinestrases
Smooth muscle contraction
- Intracellular Ca2+ concentrations increases when Ca2+ enters cell and is released from sarcoplasamic recticulum
- Ca2+ binds to calmodulin (CaM)
- Ca2+ calmodulin activates myosin light chain kinase (MLCK)
- MLCK phosphorylates light chains in myosin heads and increases myosin ATPase activity
- Active myosin crossbridges slide along actin and create tension
Relaxation in Smooth Muscle
- Free Ca2+ in cytosol decrease when Ca2+ is pumped out of the cell or back into the sarcoplasamic reticulum
- Ca2+ unbinds from calmodulin
- Myosin phosphatase removes phosphate from myosin which decreases myosin ATPase activity
- Less myosin ATPase results in decreased muscle tension
Myofibrils
The sarcoplasam of a a muscle fiber contains 100-1000 of cylindrical structures that extend the entire length of the cell- myofibrils
Myofibrils have the ability to shorten resulting in contraction of the muscle and the production of motion
Myofilaments
Myofibrils are composed of short bundles of myofilaments
Myofilaments do not run the entire length of the muscle fiber but are organized into repetitive groupings
Myofilaments are of two types:
- Thin filaments: actin and associated proteins
- Thick filaments: myosin
Thin filaments
5-6nm
Comprised of two strands ( f-actin or filamentous actin) of bead-shaped (G-actin or globular actin) molecules twisted around each other
Two regulatory proteins part of thin filaments:
1. Tropomyosin
2. Troponin
Thick filaments
11nm in diameter (twice as thick as thin filaments)
Composed of bundled molecules of myosin
Myosin molecule has a head and elongated tail
The heads form crossbridges with thin filaments during contraction
Organization of a sarcomere
The sarcomere is the functional contractile unit in a skeletal muscle fiber
Defined by the are between 2 adjacent Z discs
Myofibrils contain multiple and repeating sarcomeres
Each sarcomere shortens as the muscle fiber contracts
Overview Muscle contraction
Muscle fibers shorten by the interaction between thin and thick filaments within each sarcomere
The mechanism for contraction is explained by the sliding filament theory
Sliding filament theory
Thin filaments slide across thick filaments towards the center of the sarcomere resulting in shortening of the H zone and I zone. A band does not change. The z lines move closer together
Molecular basis of contraction
1. Ca2+ levels rise in cytosol Actin binding 2. Power stroke 3. aDP release 4. ATP binding and cross bridge detachment 5. ATP hydrolysis
Muscle contraction
Muscle tension: force created by muscle Load: weight that opposes contraction Contraction: creation of tension in muscle Relaxation: release of tension Steps leading to muscle contraction: Events at the NMJ Excitation- contraction coupling Contraction-relaxation cycle