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Skeletal
Striated, voluntary
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Cardiac
Striated, involuntary
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Smooth
- Non-striated, involuntary
- Blood vessels, airways, many organs
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Gap junction
- Allows for all cells to connect
- By allow flow of electronegativity and nutrients
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Functions of muscles
- 1. Producing body movements (walking and running)
- 2. Stabilizing body positions (posture)
- 3. Moving substances within the body (heart muscle pumping blood; moving substances in the digestive tract)
- 4. Generating heat (contracting muscles produces heat; shivering increases heat production)
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Properties of muscle
- 1. Enable muscle to function and contribute to homeostasis
- 2. Excitability – ability to respond to stimuli
- 3. Contractility- ability to contract forcefully when stimulated
- 4. Extensibility- ability to stretch without being damaged (resilient)
- 5. Elasticity- ability to return to an original length
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Connective Tissue components
- Fascia- white connective tissue
- Tendon- cord that attaches to bone
- Aponeurosis- broad, flattened tendon
- Epimysium- outer most layer of muscle
- Perimysium- surrounds the bundles
- Endomysium- separates muscle fibers
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Hypertrophy
Muscle growth by testostrome and growth hormone
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Sarcolemma
Plasma membrane
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Sarcoplasm
- Cytoplasm of muscle fiber
- Contains glycogen and myoglobin
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Glycogen
Used for synthesis of ATP
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Myoglobin
Binds to O2 and releases it when needed for ATP
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Myofibrils
Threadlike structures which have contractile functions
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Sarcoplasmic Reticulum
- Membranous sacs which encircles each myofibril
- Stores Ca2+
- Releases Ca- triggers muscle contraction
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Filaments
- Function in the contractile process
- 2 types- 2 thin for every 1 thick
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Somatic motor neuron
Neuron that stimulates skeletal muscle to contract
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Motor Unit
- Motor neuron
- Skeletal muscles it innervates
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Z-line
Separates one sarcomere from the next
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A band
Actin and myosin overlap
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Myosin
- Stabilizes myosin
- Accounts for elasticity and extensibility of myofibrils
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Dystrophin
Stabilizes actin
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During contraction… I band
Decreases
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During contraction… A band
Increases
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During contraction… H zone
Decreases
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Riger Moris
Body becomes stiff bc not ATP- so cant contract
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Myasthenia Gravis
- Progressive, Autoimmune disease
- Make antibodies to AcH receptors -> so AcH cant bind to receptor
- Person has extreme fatigue- muscle weakness
- Die from respiratory problems b/c diaphragm stops working
- Treatment-
- 1. More AcH to give greater chance of binding
- 2. Inhibit AcHesterase- make receptors open longer
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Contraction cycle
- ATP hydrolysis- reorients and energizes myosin heads
- Formation of cross bridges- myosin head attaches to myosin binding site on actin
- Power stroke- cross bridges rotate, sliding the filament
- Detachment of myosin from actin- ATP binds to myosin head releasing actin
- AcHesterase ends muscle contraction
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Under stretched – short
Actin overlap and actin active sites are not exposed
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Overstretched- long
Myosin cant attach to actin
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Optimal tension
Actin and myosin can touch
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Why is length- tension relationship and U shaped graph?
- Under stretched- cant bind
- Optimal tension- can touch and bind
- Overstretched- cant touch
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Neuromuscular junction
Muscle, neuron, and synapse
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Synapse
Where communication occurs between a somatic motor neuron and muscle fiber
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Synaptic cleft
Gap that separates the 2 cells
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Neurotransmitter
Chemical released by initial cell communicating with the second cell (AcH)
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Synaptic vesicles
Sacs within the synaptic end bulb containing AcH go through Voltage Gated Ca2+ channel
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Motor endplate
Opposite the synaptic end bulb- activates ligand gated channels
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Depolarization
When Na2+ added to cell
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Botox
- Blocks release of AcH from synaptic vesicles
- Affects diaphragm
- Temporarily helps these problems
- Strabismus (cross eyes)
- Blepharospasm (uncontrolled blinking)
- Spasms of the vocal cords
- Relax muscle that cause wrinkles
- Alleviate chronic back pain due to spasms
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Curare
- Plant poison
- Causes paralysis by blocking AcH receptors
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Anticholinesterase
- Slows actions of AcHe and removal of AcH
- Can strengthen weak muscle contractions
- Treatment for myasthenia gravis
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Production of ATP in Muscle fibers
- 1. from creatine phosphate
- 2. Glycogen
- 3. by anaerobic CR
- 4. by aerobic CR
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Myokinase
Make ATP from AMP
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Creatine Phosphate
Excess ATP is used to synthesize creatine phosphate (15 sec of energy)
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Anaerobic CR
Convert pyruvic acid to lactic acid (30 -40 s)
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Aerobic CR
Breakdown of glucose (more than 30 s)
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Muscle fatigue
Inability of muscle to maintain force of contraction after prolonged activity
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Factors that contribute to muscle fatigue
- Inadequate release of Ca2+ from SR
- Depletion of creatine phosphate
- Insufficient O2
- Depletion of glycogen and other nutrients
- Buildup of LA and ADP
- Failure of the motor neuron to release enough AcH
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O2 consumption after exercise
- 1. Breathe heavily to release CO2
- 2. LA converted to glycogen
- 3. Synthesizes creatine phosphate
- 4. Replaces the O2 removed from myoglobin
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Maximum tension (force) dependent on
- 1. Rate nerve pulses arrive
- 2. Amount of stretch before contraction
- 3. Nutrient and O2 availability
- 4. Size of motor unit
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Phases of muscle tension
- Latent
- Contraction
- Relaxation
- Refraction
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Latent period
Action potential sweeps over the sarcolemma and Ca2+ is released from SR
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Contraction period
- Ca2+ binds to troponin
- Actin active sites exposed
- Cross bridge form
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Relaxation period
- Ca2+ transferred into SR
- Myosin head release
- Actin active sites covered by tropomyosin
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Refractory period
Time after muscle contraction where the muscle cant respond to another action potential
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Muscle tone
- A small amount of tension in the muscle due to weak contractions of motor units
- Keeps skeletal muscle firm and head from slumping
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Types of contractions
- Isotonic contraction
- Isometric contraction
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Isotonic contraction
- Tension (weight) same, length change
- Concentric- contract
- Eccentric- extension
- Bicep curls
- Isometric contraction
- Tension change, length same
- Holding book with outstretched arm
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Muscle contraction
- Increase tension
- 1. Motor unit
- -----a. motor neuron
- -----b. fibers it innovates
- + mu= + tension
- 2. stimulus- frequency of motor neuron firing
- + frequency = + tension
- 3. AcH
- Longer time available = + tension
- AcHe-I- more ability to bond for longer time
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Types of skeletal muscle fibers
- Red muscle fibers
- White muscle fibers
- Slow oxidative fibers
- Fast oxidative- glycolytic fibers
- Fast glycolytic fibers
- Determined primarily by genes
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Red muscle fibers
- Have high myoglobin content (O2 binding protein in blood)
- Appear darker in color
- Contain more mitochondria (oxidative phosphloration)
- High blood supply
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White muscle fibers
- Low content of myoglobin
- Lighter in color
- High glycogen content – more oxidative
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Slow oxidative fibers
- Red
- Long distance runners
- Rich in O2
- Rich in myoglobin
- Rich in mitochondria
- Least powerful
- Generate ATP from ACR
- Slow speed of contraction
- High resistant to fatigue
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Fast oxidative- glycolytic fibers
- Light red
- Intermediate
- Contain O2
- Contain myoglobin
- Contain mitochondria
- Contain glycogen
- ATP from ACR
- Moderate resistance to fatigue
- Walking
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Fast glycolytic fibers
- White
- Sprinters; weight lifting
- Glycogen
- Powerful contractions
- ATP from glycolysis
- Fatigue quickly
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Distribution and Recruitment of different types of muscle fibers
- Most muscles mixture of all 3
- SO- neck, back, legs
- FG- shoulders, arms
- FOG- legs
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Intercalated discs
Connect the ends of cardiac muscle to fibers to another
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Cardiac muscle
- Many large mitochondria
- Depends on ACR for ATP
- Contraction longer than skeletal muscle
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Smooth muscle
- Connected by gap junctions
- Contain dense bodies opposed to z lines
- Able to sustain long term muscle tone
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Myosin light chain kinase (MLCK)
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Smooth muscle contracts and relaxes in response to:
- 1. Action potentials from the autonomic nervous system- pupil constriction due to light
- 2. Stretching- digestive tract stretches intestinal walls initiating peristalsis
- 3. hormones- epinephrine causes relaxation of smooth muscles
- 4. Changes in pH, O2, CO2
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