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135 Cards in this Set

  • Front
  • Back
Muscle Functions (5)
* movement (body & organ)
* posture & movement prevention
* comm (write, express, speech)
* control of openings & passageways
* body heat production
3 connective tissues of muscle
Epimysium - covers entire belly
Perimysium - covers fascicle
Endomysium - covers each fiber
2 types of fascia
Deep Fascia - between adjacent muscles

Superficial Fascia (hypodermis) - btw muscle & skin, adipose
another name for hypodermis
superficial fascia
Types of muscle attachments & examples of each (3)
* DIRECT (aka = fleshy) = intercostals
* INDIRECT - biceps, adbominal
* TO DERMIS - facial
Direct vs Indirect Muscle Attachment
DIRECT = epimysium > periosteum

INDIRECT = epimysium > tendon or aponeurosis > merges into periosteum as perforacting fibers
Aponeurosis
connective tissue between two muscles
3 parts of a skeletal muscle
ORIGIN - stationary end
BELLY - thicker middle region
INSERTION - attachment to mobile muscle end
Muscle shapes (5 - FCPCP)
Fusiform
Convergent
Parallel
Circular
Pennate
Fusiform muscles (details & example)
Thick in the middle & tapered at ends

Ex: biceps brachii
Convergent muscles (details & example)
Broad at origin, tapers to narrow insertion

Ex: pectoralis major
Parallel muscles (details & example)
Parallel fascicles

Ex: rectus abdominis
Circular muscles (details & example)
sphincters, rings around openings

Ex: orbicularis oris
Pennate muscles (details & example)
Fascicles insert obliquely on tendon. THREE TYPES - unipennate, bipennate, multipennate

Ex: palmer interosseus, rectus femoris & deltoid

* think of a feather pen
What are the muscles called that produce the most force?
Prime mover or Agonist
What are the muscles called that modify the direction of movement and stabilize nearby joints?
Synergist
What are the muscles called that prevent excessive movement or injury?
Antagonist (opposes prime mover)
What are the muscles called that prevent movement of the bone that prime mover is attached to?
Fixator
Elbow Flexion: Agonist, Synergist, Anatagonist & Fixator?
Agonist=biceps S=brachialis OR
Agonist=brachialis S=biceps
Anta=triceps
F = rhomboideus
What/where are intrinsic muscles?
Contained within the region they act on - ex: hand
What/where are extrinsic muscles?
Contained outside of the region the operate - muscles that move the fingers
2 types of nerves that innervate muscles?
Cranial - #1-12
Spinal - exist spinal cord thru intervertebral foramina
Nomina Anatomica
Latin system for naming muscles (1895). Updated since then.
Digiti
of a finger
Levator
elevates a body part
Profundus
deepest
(Quadri/Bi/Tri)ceps
having multi heads
Muscle Tissue
* 3 types - skeletal, cardiac, smooth
* Cells capable of shortening & converting chem energy into mechanical energy
Universal Characteristics of Muscle
(RCCEE)
* Responsiveness (excitability) - respond to chem & other signals, respond via electrical charge across PM
* Conductivity - electrical charge triggers wave of excitation along fiber
* Contractility- shortens
* Extensibility - stretches
* Elasticity - returns to resting length
Skeletal Muscle (NS system, visual characteristics)
* Voluntary
* Striated (overlapping of internal contractile proteins)
* Myofibers - muscle fibers
* up to 30cm long
What are series-elastic components?
* Connective tissue elements between fiber, bone & other attachments
* NOT excitable or contractile
* VERY extensible & elastic
* Ex: calcaneal tendon
How do series-elastic components work/behave?
* Internal tension stretch components when muscle contracts
* When taut, external tension moves load as muscle shortens
Transverse Tubules (T Tubules)
Infoldings of sacolemma that carry electrical current into cell interior
Sacroplasm
* "Cytoplasm" of muscle fibers
* Filled with myofibrils (larger units filled with myofilaments) / store glycogen for E & myoglobin for O2
Sarcolemma
* 'plasma membrane' of muscle fibers
* Carries electrical current
Order of linings (superficial to deep)
* DEEP FASCIA - exterior of entire muscle
* EPIMYSIUM - under deep fascia
* PERIMYSIUM - conn. tissue that lines fascicles
* ENDOMYSIUM - conn. tissue that lines fibers
* SARCOLEMMA - "plasma membrane" of muscle fiber
Sacroplasmic Reticulum are located__________ and form________
superficially around each myofibril

terminal cisternae (series of dilated, calcium storage sacs)
Thick Filaments
* entwined "golf clubs"
* 200-500 myocin protein molecules
* Heads on each end with central bare zone w/ no heads
* Titin protein strands thru center
Thin Filaments
* 2 strands of fibrous actin entwined
* subunits of actin chain are globular active w/ active sites
* Tropomyosin molecule strand sits in groove & blocks active sites
* Troponin stuck to tropomyosin
Fibrous Actin (F Actin)
strands of actin
Globular Actin (G Actin)
subunits of F Actin - have active sites
Tropomyosin
strands along F actin that block active sites of G actin
Troponin
calcium-binding molecules stuck to tropomyosin
Elastic Filaments
* Titin = springy proteins that run thru core of each thick filament
* Connect thick filaments to Z discs
FUNCTION:
- keep thick & thin fila's aligned
- resist overstretching
- helps cell recoil
Titin
springy muscle proteins
2 contractile proteins
Myosin & Actin - work to shorten muscle
2 regulartory proteins
Tropomyosin & Troponin - switches that start & stop shortening
What causes the striations?
* Dark A band regions alternating with lighter I band regions
* A = dArk= thick filament region
* I = lIght = thin filament region - bisected by Z disc proteins
Z disc proteins
* bisect I band filaments
* anchor thick & thin filaments
* 1 Z to the next = a sarcomere
Sarcomere
one z disc to the next
What is the action that makes a muscle shorten?
Shortening sarcomeres - Z discs get pulled closer together (horizontally on diagram)
Do filaments shorten during sacromere contractions?
NO - they just getting pulled over each other so that there is more overlapping
What stimulates a muscle to contract?
Stimulation signal from nerve
What is included in a motor unit?
a motor neuron + all fibers it innervates
Where are the cell bodies of somatic motor neurons?
in brainstem & spinal cord
Somatic motor fibers
Axons of somatic motor neurons - branch to individual fibers - 200 terminal branches, 1 branch per fiber
What happens when a motor units contract together? What is the point?
* causes a weak contraction over wide area
* provides ability to sustain long-term contraction as motor units take turns resting
* Ex = posture
Fine control motor units
as few as 20 muscle fibers per nerve

Ex = eye muscles
Example of a strength control motor unit
gastrocnemius has 1000 fivers per nerve fiber
Neuromuscular Junction (NMJ)
Synapse region where nerve fiber makes functional contact with muscular target cell
Neurotransmitters - what/example
released from nerve fiber to stimulate muscle cell

Ex = acteylcholine
Synaptic Knob
swollen end of nerve fiber with ACh filled vesicles
Motor End Plate
region of muscle cell surface, has ACh receptors
Schwann Cells
envelope & isolate NMJ
Acetylcholinesterase
Enzyme that breaks down ACh & causes muscle to relax
Effects of cholinesterase inhibitors in pesticides
* bind to acetylcholinesterase & prevent ACh breakdown
* spastic paralysis & possible suffocation
What is Tetanus/Lockjaw & what causes it?
* Cause = Clostridium bacteria
* Blocks glycine release in spinal cord, causes overstimulation of muscles
What does the presence of Curare cause?
* Flaccid paralysis with limp muscles unable to contract
* Curare competes with ACh for receptor sites but doesn't stimulate muscle
Botulism occurs when a bacteria releases neurotoxin that prevent motor neurons from releasing ACh. Which of the following is not an effect - flaccid paralysis, tetany, cardiac arrest, suffication, muscle weakness?
Without ACh muscle won't contract, so Tetany.
What is the cause of the resting membrane potential?
* Na+ outside cell / K+ and other anions inside cell.
* More Na than K, causing an imbalance & the inside to be less positive than the outside
What causes the voltage change in the plasma membrane?
* Ion gates open - Na rushes in, K rushes out - CREATES ACTION POTENTIAL

* Spreads as a nerve signal or impulse
Four phases of muscle contraction
* EXCITATION - action potential in nerve lead to formation of action potential in muscle fiber
* EXCITATION-CONTRACTION COUPLING: refers to APs on sarcolemma activating myofilaments
* CONTRACTION: shortening of muscle fiber or formation of tension
* RELAXATION: return of fiber to its resting length
Sequence of EXCITATION during muscle contraction
1st: Nerve signal stimulates voltage-gated Ca channels > results in exocytosis of ACh synaptic vesicles

2nd: ACh binds to ligand-gated Na/K channels > Na in, K out > results in an end-plate potential (EPP) bc voltage jumps from -90mV to +75mV

3rd: Voltage change in EPP opens nearby voltage-gated channels in sarcolemma (Na & K channels separate) > Na in & K out > produces AP

* MUST BE ABLE TO IDENTIFY PICTURES
Sequence of EXCITATION-CONTRACTION during muscle contraction
1st: AP spreads over sarcolemma, reaches T tubules > v-gated channels open in T tubes that are linked to Ca gates that open out of SR into cytosol

2nd: Ca releases & binds to Troponin > causes myosin to bind to active sites on G actin
Sequence of CONTRACTION during muscle contraction
1st: Myosin head w/ ATP of thick filament froms cross-bridge between thin filament & thick

2nd: Myosin head releases ADP & PO4, flexes as it pulls thin filament along > more ATP then binds & releases head from thin filament
Sequence of RELAXATION of a muscle contraction
1st: Stimulation ceases - AChE removes ACh from receptors so stimulation stops

2nd: Active transport pumps Ca back into SR - Ca binds to calsequestrin

3rd: loss of Ca from SR results in hiding of G actin active sites again & cessation of tension
Is ATP needed during muscle contraction or relaxation?
BOTH
C: needed to bind myocin to g-actin & cock the head
R: replaces ADP (used ATP) on myocin head, which releases it from the g-actin AND for the active transport pumps that move Ca back into the SR cisternae
Causes for a muscle not to contract
Nerve doesn't send signal
Ca doesn't enter knob
Cell can't release ACh
ACh can't bind to receptor
Electrolite imbalances
Ca can't be released from SR
Ca doesn't bind to Troponin
Not enough ATP for binding
Causes for a muscle to not relax
Lack of ATP
AChE not breaking down ACh
If Ca is not put back into SR
The amount of tension generated depends on....
length of muscle before stimulation.

length-tension relationship
Result of overly contracted muscle
weak contraction - thick fila's too close to Z discs & can't shorten enough
Result of a muscle that is too stretched
weak contraction - little overlap of thin/thick fila's doesn't allow for enough cross-bridges to form
What maintains optimum resting length, which produces the greatest contraction force?
muscle tone or partial contraction maintains optimum length
Rigor Mortis (what, stages, sequence of events)
* Stiffening of body 3-4 hrs after death, peaks in 12 hours, diminishes over next 48hrs
* Deteriorating sarcoplasmic reticulum releases Ca
* Ca activates myosin-actin cross bridging & muscle contraction
* No ATP present to relax muscles (none is being produced & amount present at death is used for contraction)
* Fibers remain contracted until myofilaments decay
What is a muscle twitch?
A single brief voltage stimulus produces quick cycle of contraction & relaxation
Sequence of a muscle twitch (4)
* LATENT PERIOD - 2msec - delay between stimulus & twitch onset
* CONTRACTION - tension develops & muscle shortens
* RELAXATION - loss of tension & return to resting length
* REFRACTORY PERIOD - muscle will not respond to new stimulus
Why do muscle twitches vary in strength even when the stimulus is a constant voltage?
* Stimulation frequency
* Concentration of Ca
* Length-tone relationship
* Temperature> Warm-up = stronger contraction
* pH
* Hydration of muscle fiber
Isometric muscle contraction
tension develops without length change
Isotonic muscle contraction
tension develops while shortening (Concentric) or lengthening (Eccentric) the muscle
Concentric vs Eccentric Isotonic muscle contractions
Concentric = shortening
Eccentric = lengthening

Isotonic = muscle length changes, but no tension change
ATP sources
Primary: Aerobic Respiration & Anaerobic Fermentation
Other: Phosphagen system (immediate E only)
Anaerobic Fermentation
* limited ATP production (2 molecules)
* Toxic lactic acid byproduct - lowers pH, which can inhibit contractions, and stimulates nerve receptors causing a 'burn'
* no O2 needed
Aerobic Respiration
* 36-38 ATP molecules produced
* requires continuous O2 supply
* H2O & CO2 byproducts
Sources for immediate energy
* Myoglobin (provides O2 for limited term aerobic respiration)
* Phosphagen System
Phosphagen System
* process of transferring P from one molecule to another to create ATP
* Myokinase or Creatine Kinase used
Myokinase
Transfers P group from 1 ADP to another, transforming the second to ATP
Creatine Kinase
Pulls P from groups of Creatine Phosphate & donates them to ADP, changing it to ATP
Short-Term Energy Sources
* Glycogen-lactic acid system produces ATP for 30-40 sec of maximum activity
* Kick in when Phosphagen system is exhausted
* Muscles obtain glucose from blood & stored glycogen, anerobic fermentation
Long-Term Energy Source (when is it used, what does it do, what limits ability)
* kicks in after 40 seconds of exercise - respiratory & cardio systems begin to deliver enough O2 fo aerobic respiration
- O2 rates increase for first 3 min, then levels off to a steady state
- ATP production keeps pace with demand
* Limits are set by depletion of glycogen & blood glucose, loss of fluid & electrolytes thru sweating, lactic acid buildup occurs
What is muscle fatigue?
progress weakness & loss of contractility due to prolonged use
What causes muscle fatigue?
* ATP synthesis declines while glycogen is consumed
* ATP shortage causes NaPO4 pumps to be unable to maintain membrane potential & excitability (active transport pumps)
* Lactic acid lowers pH of sarcoplasm inhibiting enzyme function
* accumulation of extracellular K lowers membrane potential & excitability
* motor nerve fibers use up ACh
Endurance
* determined by max O2 uptake
* VO2 (max O2 vol per breath) proportional to body size, peaks at 20, larger in athletes/males
* Supply of organic nutrients - fatty acids, amino acids, glucose, carbohydrates (glycogen)
Oxygen Debt
* About 11 liters extra O2 needed after strenuous exercise
* Replaces O2 reserves (myoglobin, hemoglobin, lungs, plasma)
* Replenishes phosphagen system
* Converts lactic acid to glucose
* Serves elevated metabolic rate that occurs as long as body temp remains elevated during exercise
Fatigue can be caused by all of the following except - low ACh supply, low pH in sarcoplasm, excess myoglobin, excess lactic acid, reduced ATP concentrations?
Excess myoglobin
Slow-Twitch Fibers (dark meat)
* more mitochondria, myoglobin & capillaries
* continuously used, don't fatigue easy
* adapted for aerobic resp

Ex: soleus & postural muscles of back
Fast-Twitch Fibers (light meat)
* rich in enzymes from phosphagen & glycogen-lactic acid system
* not used as often, they fatigue
* sarcoplasmic reticulum releases Ca quickly

Ex: gastrocnemius muscle
Factors that increase strength & contraction (6)
* muscle size
* fascicle arrangement
* motor unit size
* motor unit recruitment
* frequency of stimulations
* length of muscle at start of contraction & fatique
What does resistance training due?
stimulates cell enlargment due to synthesis of more myofilaments (some splitting may occur)
What is the purpose of endurance training?
increases mitochondria, glycogen & density of capillaries
Angiogenisis
formation of new blood vessels
Astronauts in zero-gravity conditions do not have which of the following problems - bone loss, cardiac muscle atrophy, joint luxation, skeletal muscle atrophy?
joint luxation
Cardiac Muscle
* shorter, thicker cells than skeletal muscle
* branched & linked by intercalacted discs
* SR is less developed bu T tubules are large to admit Ca
* Autorhythmic
* Exclusively aerobic respiration
Gap junctions of cardiac muscle (electrical & mechanical)
* electrical gap junctions allow cells to stimulate neighbors

* mechanical gap junctions prevent cells from pulling apart
What makes cardiac muscles autorhythmic
Pacemaker cells
2 ways cardiac muscle resist fatigue
aerobic respiration (almost exclussively)

Large mitochondria
Smooth Muscle (form, visual characteristics, filament & basic structure, NS system)
* Fusiform cells with 1 nucleus
* no visible striations, sacromeres or Z discs
* thin filaments attach to dense bodies scattered thru sarcoplasm & on sarcolemma
* SR is scanty & no T tubes (Ca comes from extracellular fluid)
* Autonomic
Types of smooth muscle
Multiunit & single-unit
M: motor units contract independently
S: motor units contract as a whole
Multi-unit smooth muscle
* in largest arteries, iris, pumonary air passages, erector pili muscles
* terminal nerve branches synapse individual myocytes in a motor unit
* independent contraction of each cell
Single-unit smooth muscle
* in most blood-vessels & viscera
* in circular & longitudinal muscle layers
* electrically coupled by gap junctions so ions can flow directly from one cell to another
* large number of cells contract as a unit
Stimulation of smooth muscle
* involuntary - hormones, CO2, low pH, stretch, O2 deficiency (hypoxia)
* Autonomic nerve fibers have varicosities containing synapse vesicles
Varicosities
beadlike swellings on autonomic nerve fibers of autonomic smooth muscle that contain synaptic vesicles
Responses to stretching smooth muscle (4)
* opens mechanically-gated Ca channels causing muscle response (ex = food entering esophagus brings on peristalisis)
*stress-relaxation response needed for hollow organs that fill gradually. When stretched, tissue briefly contracts then relaxes. (ex = bladder)
* Must contract forcefully when greatly stretched - no orderly filament arrangement, no Z discs
* plasticity - ability to adjust tension to degree of stretch (empty bladder is not flabby)
Peristalisis
contractions that start in one area and move along like a wave (ex = upper & lower GI tract)
Plasticity
ability to adjust tension to degree of stretch, prevents unstretched muscles from being flabby
Muscular Dystrophy
* Group of hereditary diseases
* Skeletal muscle degenerates & is replaced with adipose
* Normal allele makes dystrophin (protein that links actin to cell membrane) - without it cell membranes tear
* Duchenne MD (sex-linked) - most common, mainly male, fatal
* Fascioscapulohumeral MD - facial & shoulder only, not fatal
Fascioscapulohumeral MD
face & shoulder muscles only
Duchenne MD
* Sex-linked
* Appears as child beings to walk
* Rarely live over 20 yrs
* Mostly a male disease bc sex-linked
Myasthenia Gravis
* Autoimmune - antibodies attack NMJ & bind ACh receptors into clusters
* Muscle fibers remove receptors, muscles become less sensitive to ACh
* Women, ages 20-40, but any demographic can be affected
* Treatment - cholinesterase inhibitors, thymus removal, immunosuppressive agents
* Symptoms: drooping eyelids, double vision, difficulty swallowing, weakness of limbs, respiratory failure (worst case)
Symptoms/side-effects of Myasthenia Gravis
Symptoms: drooping eyelids, double vision, difficulty swallowing, weakness of limbs, respiratory failure (worst case)
Athletic Injuries
* Vulnerable to sudden & intense stress
* Conditioning & warmup needed
* Rest, ice, compression & elevation
* Common injuries - shinsplints (general term for shin pain), pulled hamstring, tennis elbow, golfers elbow
lateral epicondylitis
aka - tennis elbow
medial epicondylitis
aka - golfers elbow
calsequestrin
protein in SR chisternae that Ca binds to during storage
Why is ATP needed for muscle relaxation?
2 reasons:
*Ca is pumped from the cytosol back into the SR cisterna during relaxation via active transport pumps

* It binds to the myocin head, releasing it from the g-actin and 'reloading' it for the next cocking
correct order of muscle parts (the fibers)
muscle > fasicle > fiber > myofibrils > myofilaments