Chapter 8 Flashcards
Voluntary Muscles
-controlled by the somatic nervous system
-skeletal muscle
Involuntary Muscles
-innervated by autonomic nervous system
-cardiac muscle
-smooth muscle
Striated Muscle
-alternating light and dark bands are seen under microscope
-overlapping proteins
-skeletal muscle
-cardiac muscle
Unstriated Muscle
-smooth appearance; no bands
-smooth muscle
Skeletal Muscle
-most abundant
-32-40% of body weight
-make up the muscular system
Muscle Fibre
-single skeletal muscle cell
-muscle consists of several muscle fibres bundled together via connective tissue
Myoblasts
-smaller cells that make muscle fibres during embryonic development
-have multiple nuclei in a single muscle cell
-high amounts of mitochondria to meet energy demands
Myofibrils
-predominant structural feature of a muscle fibre
-80% of muscle fibre volume
Sarcolemma
-the plasma membrane
T-Tubules
-aka transverse tubules
-dips or hollow regions at the junction of an A band and an I band
-run perpendicular to the surface of the muscle cell membrane
-action potentials spread here to interior of muscle fibre
Presence of Nuclei
-muscle fibres have their own nucleus
-hence they can regenerate
Presence of Mitochondira
-in high amounts to meet energy demands
Skeletal Muscle Organization
Whole muscle (organ)➡️muscle fibre (cell)➡️myofibril (specialized intercellular structure)➡️thick and thin filaments (cytoskeletal elements)➡️myosin and actin (protein molecules)
Connective Tissue Covering
-covers each muscle
-primarily collagen and to the lesser extent, elastin
-provides structure to the muscle
-allows transfer of force to the bone
-tension for movement/stabilization
Epimysium
-covers whole muscle
Peromysium
-divides muscle fibres into bundles
Endomysium
-covers each muscle fibre
Tendons
-connect muscle to bone
Glycogen Reserves
-glycogen breaks down to produce glucose
-glucose is the substrate for ATP production
Sarcoplasmic Reticulum (SR)
-modified smooth endoplasmic reticulum
-stores calcium in terminal cisternae (aka lateral sacs)
Role of Calcium
Proteins
-make up contractile and regulatory regions
Contractile Proteins
-form filaments
-actin and myosin
Thick Filaments (myosin)
-assemblies of myosin protein
-look like golf clubs
-250 to 300
-head has ATP and actin binding sites
-hinge region allows for binding to occur and cross bridges to from
-considered a motor protein
Thin Filaments (actin)
-assemblies of actin protein
-pearl chain
-actin is the primary structural component of thin filaments
-bulbs have myosin binding sites
-thin filament also consists of troponin and tropomyosin
Cross Bridge
-where actin and myosin join together
-myosin heads
-results in contraction of the muscle fibre
Regulatory Proteins
-troponin and tropomyosin
Tropomyosin
-cover/hide the actin binding site on thin filaments
-blocks action that leads to muscle contraction
Troponin
-binds to calcium ions
-has three polypeptide units with three different binding sites, one for each: tropomyosin, calcium, actin
-exposes the actin binding site so the cross bridge can form
Binding of Troponin Units
-when troponin not bound to calcium: the protein stabilizes tropomyosin, blocking binding sites
-when calcium binds to troponin, protein shape is changes so tropomyosin slips away from blocking position
-this unblocking forms the cross bridge, then the contraction
Accessory Proteins
-nebulin and titin
Nebulin
-runs through thin filaments to stabilize them
Titin
-runs through thick filament to stabilize it
-largest protein in the body
-30 000 amino acid chain
-acts like a spring to augment muscle elasticity
Dystrophin Protein
-stabilizes entire structure
-attaches to sarcolemma
Sarcomere
-single unit of contraction
-functional unit of skeletal muscle (smallest component that can perform all the functions)
Z Lines
-zig zag line of proteins
-in the middle of each I band
-where thin filaments attach/anchor
-sarcomeres reside between the two Z lines
I Band
-remaining portion of the thin filament that does not project into the A band
-actin/thin filament
M Line
-middle line
-supporting proteins that hold the thick filaments together vertically
A Band
-overlapping region
-made of a stacked set of thick filaments
-thick filaments extend entire width of A band
H Zone
-lighter area in the middle of the A band where the thin filaments don’t reach
-central portions of thick filaments found in this region
Light Regions
-not over lapping
Dark Regions
-where thin and thick filaments overlap
Neuromuscular Junction (CH 5)
-gets excited with acetylcholine
-starts an action potential which originated as a graded potential
Sarcoplasmic Reticulum and T-Tubule Receptor Coupling
-are both in close proximity to each other
-both have receptors
that snap together like buttons
-troponin binds to the releases calcium ions (released from lateral sacs)
-tropomyosin is removed from the actin binding site
-several cross bridges are formed:)
Sarcoplasmic Reticulum and Contraction
-contains 4 receptor proteins that join with the T Tubule receptors
-“ryanodine proteins” aka foot proteins (calcium release channels)
-get excited by action potential
T-Tubules and Contraction
-contain 4 receptors that join with SR receptors
-“dihydropyridine” aka DHP receptors
-leads to the release of calcium
Power Stroke
-caused by cross bridge bending
-uses ATP constantly
-SR releases calcium into sarcoplasm
-hydrolysis of ATP transfers energy to myosin head
-myosin heads bind to actin
-sarcomere pulled inward
-fresh ATP binds to myosin head and detaches it from actin
Cross Bridge Cycling
-pulls thin filaments inward relative to stationary thick filaments
-one myosin head attaches to actin at a time
-bridge changes shape and bends inward and pulls thin filament inward
-this cycle repeats and completes shortening
-at the end of one cycle the actin and myosin cross bridge breaks, then it binds to the next molecule
-ie. pulling a rope in hand over hand
What prevents the thin filaments from slipping away?
-cross bridges don’t stroke in unison
-it is a staggered system between the six surrounding thin filaments
-some hold on while others let go
Sliding Filament Theory
-increase in calcium starts filament sliding
-thin filaments on each side of the sarcomere slide inward over stationary thick filaments toward the centre of A band
-sarcomere shortens simultaneously
Z Lines during Sliding Filament Mechanism
-come closer together
I Bands during Sliding Filament Mechanism
-become shorter and almost disappear
M Line during Sliding Filament Mechanism
-remains the same
A band during Sliding Filament Mechanism
-width remains the same
H Zone during Sliding Filament Mechanism
-shrinks from over lap
Do the thick or thin filaments change length ever?
No, they just slide closer together.
Where does the energy come from?
-the splitting of ATP
Role of ATP during Power Stoke
-break down of ATP occurs on the myosin cross bridge before it links with actin
Role of ATP: Step 1
-ADP and P1 remain tightly bound to myosin, the generated energy is stored within the cross bridge
binds with actin molecule
Role of ATP: Step 2a
-when the muscle fibre is excited, calcium pulls troponin-tropomyosin complex out of its blocking position
-myosin cross bridge
Role of ATP: Step 3
-contact between myosin and actin “pulls the trigger” causing the cross bridge bending
-inorganic phosphate is released from cross bridge during power stroke
-ADP is released after the power stroke is completed
Role of ATP: Step 2b
-when muscle is not excited, calcium is not released, blocking position remains, no power stroking takes place
Role of ATP: Step 4a
-after P1 and ADP are released from myosin following power stroke: myosin ATPase site is free for attachment of another ATP molecule
-cross bridge remains linked until a fresh ATP attached to myosin to detach the cross bridge
-cross bridge is ready for another cycle
Role of ATP: Step 4b
-if no fresh ATP is available, actin and myosin remain together in RIGOR COMPLEX
Rigor Mortis
-muscle stiffness upon death
-locking of muscle in place
-no fresh ATP = no movement/separation of cross bridge
-calcium re-uptake doesn’t occur
-enzymatic degradation eats flesh
Relaxation
-the opposite of contraction
-acetylcholinesterase breaks down ACh at the neuromuscular junction
-action potential stops
-SR and T-tubules release from each other
-no action potential = calcium moves back into SR via the calcium ATPase pump
-tropomyosin back into blocking position
-cross bridge stops
Muscle Twitch
-a brief, weak contraction
-produced from a single action potential
-too short and weak to be useful
-doesn’t normally take place
Twitch Summation
-results from sustained elevation of cytosolic calcium
-sustained stimulation of the fibre before it has time to relax
-possible because duration of action potential is shorter than the twitch – action potential needs to finish before next one
2 factors to adjust gradation of a muscle
- number of fibres contracting
- firing frequency of each fibre
Most Tension
-larger muscles have more muscle fibres and hence generate more tension than smaller muscles
Motor Neurons
-have branches at their ends that supply each group of muscle fibres = motor unit
Tetanus (not the infection)
-occurs if muscle fibre is stimulated so rapidly that it doesn’t have a chance to relax between stimuli
-sustained contractile activity
-smooth contraction of maximal strength
Optimal Muscle Length
-form best cross bridges
-lots of power stroking
-myosin heads are in line with actin body
-relationship between length and tension before onset of contraction
-optimal = maximal forced achieved at subsequent tetanic contraction
-more tension achieved when beginning at optimal length
Lengths Greater than Optimal Length
-thin filaments pulled out from the thick
-decreases number of actin sites available for binding = less tension
-when muscle stretched 70% longer; no sites available = no contraction
Less than Optimal Length
-less tension because:
1. thin filaments from opposite side are overlapped = less available binding sites
2. ends of thick filaments forced against z lines = further shortening impeded
3. muscle lengths at less than 80%; not as much calcium is released = fewer sites are uncovered
Muscle Origin
-end of muscle attached to stationary part of the skeleton
Muscle Insertion
-end of the muscle attached to the skeletal part that moves
How is tension created?
by the tightening of the series elastic component that are the non-contractile tissues of the muscle (tendons)
Isotonic Contraction
-equal stretch
-tension is constant
-force production is unchanged
-consists of concentric and eccentric contraction
Concentric Contraction
-bring weight toward the body
-create tension
-flexion
-usually muscle shortening
-actin pulled together
Eccentric Contraction
-weight goes away from centre of the body
-extension
-muscle lengthening
-usually results in injury when done poorly
-actin pulled apart
Isometric Contraction
-length is unchanged
-muscle fibre is prevented from shortening
-tension at constant length
-static
-ie. holding a heavy box in a constant position or plank
Dynamic Contraction
-changing force contraction
-length changes
-both concentric and eccentric
Static Contraction
-not in motion contraction
-increased tension but no change in body position
Creatine Phosphate
-source of energy
-involves the transfer of a high-energy phosphate from creatine phosphate to ADP
-aka creatine kinase enzyme breaks down creatine phosphate to get creatine + ATP
Glycolysis
-a source of energy
-splitting of glucose into 2 pyruvate molecules
=2 ATP molecules
Oxidative Phosphorylation
-citric acid/krebs cycle and ETC
-metabolize acetyl CoA to two CO2 molecules, resulting in NADH and FADH2
=34 ATP molecules
Creatine as a Supplement
-can cause severe GI disturbances
-dehydration
-muscle stores = weight gain
3 processes that require ATP
- provides energy for power stroke
- allows bridge to detach so cycle can be repeated
- active transport of calcium back to the SR during relaxation
Muscle Fibres
-classified based on differences in ATP hydrolysis and synthesis
Fast Twitch (type II)
-2-3x faster
-faster ATP use (splitting)
-faster calcium release
-used occasionally
-ie. pianist
-innervated by a1 motor neurons (are larger)
Slow Twitch (type I)
-slower in general
-slower ATP use
-slower calcium release
-frequently used
-ie. maintaining posture or walking
-innervated by a2 motor neurons
Oxidative Muscle Fibres
-need oxygen
-glycolysis, krebs cycle, etc = ATP
-more mitochondria
-high conc. of blood vessels
-increased oxygen
-myoglobin binds to oxygen giving a rich red color
-fatigue less often
Glycolytic Muscle Fibres
-oxygen doesn’t matter
-stops at glycolysis (anaerobic) = 2 ATP
-less mitochondria
-fewer blood vessels
-lower myoglobin = pale white color
-fatigue more often
Types of Muscle fibres
-these categories combine to create:
a. slow-oxidative (type 1) fibres
b. fast-oxidative (type 2a) fibres
c. fast-glycolytic (type 2x) fibres
Muscle Fatigue
-occurs when exercising muscle can no longer respond to stimulation with the same degree of contractile activity
-underlying causes unclear
-2 types: a. central fatigue & b. peripheral fatigue
Central Fatigue
-CNS no longer adequately activates motor neurons (somatic motor neuron/ANS issue)
-psychological (muscles still physically able to perform)
-monotony - same thing over and over again ie. assembly line
Peripheral Fatigue
-NMJ is vulnerable (Ch 5)
-SR and T-tubules
-can be a lack of ATP
-build up of lactic acid
-depleted glycogen levels
Circumventing Fatigue - EPOC
Excess
Post-exercise
Oxygen
Consumption
aka recharging
Control of Motor Movement
-three levels of input can control motor-neuron output:
1. input from afferent neurons
2. input from primary motor cortex
3. input from brain stem
Afferent Neurons
-input from afferent neurons usually through intervening interneurons at the level of the spinal cord: spinal reflexed
-ie. reflexes
Primary Motor Cortex
-fibres originating from neuronal cell bodies, pyramidal cells, descend directly to terminate on motor neurons without synaptic interruption
-basal nuclei: ie. parkinsons
-thalamus: a “loop”
-cerebellum: skilled, procedural memories
Brainstem
-midbrain
-pons
-MO
-final link in multineuronal pathways
Muscular Dystrophy
-genetic disease; carried in x chromosome, males more prone
-missing dystrophin protein that attaches sarcomere to sarcolemma
-sarcomere deforms when it tries to shorten
-affects hip muscles
-wheelchair bound
-leads to death
-gene therapy: manipulate gene that makes dystrophin
Parkinsons Disease
-basal nuclei disorder
-tremors, reptilian stare, shuffled gait, confusion, cognitive failure, sleep issues
-treatment = leva dopa
Muscle Spindle Structure
-consist of collections of specialized muscle fibres known as intrafusal fibres
-each spindle has its own private efferent and afferent nerve supply
-pay a key role in stretch reflex: how much a muscle can stretch
Intrafusal Fibres
-lie within spindle shaped connective tissue capsules, parallel to extrafusal fibres
-has noncontractile central portion
-contractile portion is limited to the ends
Extrafusal Fibres
-contain contracile elements (myofibrils) throughout its entire length
Pathways of the muscle spindle
-CNS➡️ a) gamma motor neuron➡️intrafusal fibre (receptor) or b) alpha motor neuron➡️extrafusal fibre
Golgi Tendon Organ
-in the tendons of the muscle
-respond to changes in tension rather than length
-consist of ending of afferent fibres intertwined with connective tissue = tendon
-tension causes golgi tendon organ receptors stretch causing afferent fibres to fire at the frequency of the developed tension
-reaches conscious awareness
-aware of tension but not length
-protect from injury: muscle stops creating force it can’t handle
Smooth Muscle
-found in the hollow tubes of internal organs
-no striations
-no sarcomere structure
-have actin and myosin
-form cross bridges
-no troponin; instead calmodulin
-has tropomyosin to hide actin binding site
-poor SR (stores calcium) and no T-tubules
-spindle shaped cells with a single nucleus arranged in sheets
-no z lines; instead has button like proteins called Dense bodies that hold actin and myosin together called
Smooth Muscle: Mechanism of Contraction
-globular structure creates forward motion
-calmodulin binds with calcium from SR and ECF
-calmodulin binds to inactive myosin light chain kinase (MLC kinase) enzyme and activates it
-breaks down ATP to do a power stroke (ATP = ADP + P1)
-activates myosin head which binds to actin
=cross bridge
2 Types of Smooth Muscle
a. multi unit smooth muscle
b. single unit smooth muscle
Multi Unit Smooth Muscle
-neurogenic (contraction is nerve produced; same as skeletal muscle)
-consists of discrete units that must be separately stimulated to contract
-found in: iris of the eye, large blood vessels, muscles in eye that adjust the lens
Varicosity
-stores neurotransmitters
-open during action potentials
Single Unit Smooth Muscle
-self-excitable
-aka visceral smooth muscle
-fibres become excited and contract as a single unit
-cells are electrically linked by gap junctions
-also described as a functional syncytium (1 cell)
-contraction is slow and energy efficient
-found in all hollow organs (ie. GI tract)
Pacemaker Potentials
-membrane potential gradually depolarizes on its own because of shifts in passive ionic fluxes
-when depolarized to threshold, action potential is initiated
-after repolarizing, depolarizes again
-cyclically generates action potentials
-dont have to reach tetanus
-stay in cross bridge longer
Slow Wave Potential
-gradually alternating hyperpolarizing and depolarizing swings in potential
Cardiac Muscle
-found only in walls of the heart
-striated
-cells interconnected by gap junctions
-fibres joined in branching network
-innervated by ANS
-held together by inter calculated discs
