Exam 3 Flashcards
1- muscle
2-muscle fiber
3-myofibril
4-myofilament
1-muscle attached to bones and the contraction is responsible for the support and movement of skeleton.
2-single skeletal muscle cell. large, elongated and cylinder shaped. run up the entire length of muscle
3-contractile elements of muscle fibers. numerous myofibrils make up one muscle fiber—each myofibril consists of repeating units called sarcomeres
4-ultramicroscopic filamentous structures where the contractile proteins are arranged into. Thick= myosin and thin= actin
Sarcomere
- functional unit
- has cytoskeletal elements made up of thick and thin
- bounded by Z lines—(anchors thin filaments)
- causes triations in skeletal and cardiac
Thick filament
- made up of myosin
- each myosin has 2 golf club shaped subunits w/ tails intertwined and has globular heads that have an actin binding site and an ATPase site.
- thick filament = myosin molecules lying parallel to one another
- half oriented in 1 direction while other half in other
- globular head= protrude= cross bridges
Thick Filaments
1-titin
2-myomesin
3-creatine kinase
4-c-protein
5-MLCK (myosin light chain kinase)
1-stretches entire length of half sarcomeres from M line to Z line and controls both length of sarcomere and its elasticity
2-found in M line and helps titin and myosin to maintain their 3D structure
3-found in M line and is enzyme that transfers phosphate group from creatine phosphate to ADP= energy fo muscle contraction
4-maintains width of thick filaments by restricting them to 200-400 molecules each
5-binds to thick filament and phosphorylates the light chain of myosin. sensitizes myosin to Ca activation
Thin Filament
1-Actin
2-Tropomyosin
3-Troponin (Tn)
1-specherical shaped protein w/ bidning site for myosin. molecules bind together to make 2 stranded actin helix string
2-threadlike regulatory protein in the groove between the 2 actin strands. when relaxed= blocks myosin binding sites on actin
3-regulatory protein thats bound to tropomyosin. has 2 subunits: TnI, TnT, TnC. binding of Ca to TnC= conformational change that displaces TnI, exposing myosin biding sites on actin molecules
Hexagonal Arrangement
w/in A bands (thick and thin)
- each thick furrounded by hexagon of 6 thin filaments
- each thin filament surrounded by triangle of 3 thick filaments
- w/in I band = thin filaments
- w/in H zone= thick filaments
Muscle Receptors
- joint movements, muscle tension, and muscle length is monitored by sensory receptors (propioreceptors) in muscle sent to CNS by neurons
- efferent info (CNS to periphery) is conducted by somatic alpha motor neurons for either contraction or relaxation of main contractile cells of skeletal muscle i.e. extrafusal muscle fibers
Proprioreceptor in Skeletal Muscle
—Muscle Spindles
- stretch receptors w/in muscle that monitor both absolute muscle length and the change in length
- muscle spindle arranged in parallel to extrafusal fibers
- ex= knee jerk reflex= external force passively stretches quads, pulls on intrafusal fibers of spindle = inc in firing rate. sends more AP to spinal cord via sensory neuron. sensory neuron synapses directly onto alpha motor neuron that excites the quad contraction= lower leg swinging.
- —while that is happening, the hamstring relaxes bc it is inhibited of alpha motor neuron. inhibition is bc of interneuron activation in spinal bc of same sensory neuron
Propioreceptors in skeletal muscle
-Golgi Tendon Organs
- w.in tendons near junction w/ muscle
- connection in series w/ extrafusal fibers, when the muscle contracts there is tension upon the tendon
- golgi tendon organ discharges in response to tension generated by contracting muscle
- activation of golgi tendon organs= widespread inhibition of contracting muscle and stimulation of antagonistic muscles
- protects muscle when large tension is generated
Sliding Filament Theory
- contraction of muscle occurs by sliding of thin filaments over thick. actual length=unchanged
- relaxed = low crossbridge cycling because the myosin bidning site on actin is covered by troponin-tropomyosin complex.
- excited= Ca binds w/ troponin pullin troponin-tropomyosin complex aside to expose crossbridge binding.
- bidning of actin + myosin crossbridges triggers power stroke, pulling thin inward during contraction
Cross Bridge Cycle
- during each cycle the myosin head binds w/ actin molecule, bending to pull the thin filament inward during the power stroke…it will then detach and return to resting conformation= repeat of cycle
- during muscle contraction, each sarcomere shortens as thin filaments slide closer together between thick filaments so that the Z lines are pulled closer together
- A bands width dont change, but the I and H zones become shorter
Cross Bridge Cycling
1-myosin head is activated—ATP is hydrolyzed so myosin has ADP bound to it. Myosin ADP is activated form of myosin. but it cant yet to bind to actin because myosin is blocked by troponin-tropomyosin complex.
2-Cross bridge formation—Cat2 binds to troponin and troponin-tropomyosin complex moves, exposin myosin binding sites on actin. myosin binds actin
3-power stroke—release of ADP and P from myosin head. Head undergoes conformational change. thin filament sliding along thick filament. thin pulled 10 nm
4-cross bridge detachment—ATP binds to myosin, so myosin dissociates from actin and the cross-bridge breaks. hydrolysis of ATP to ADP and P returns myosin to original activated confromation
5-if there isnt enough ATP then myosin wont dissociate from actin…so cross bridge remains intact.
Rigor Mortis
- ATP insufficiency in skeletal muscle
- stiffness in skeletal muscle after death
ATP in skeletal muscle contraction
-ATP gives energy for 2 actions
1-binding of ATP to myosin dissociates the cross bridge between actin and myosin. the hydrolysis of ATP into ADP and P by myosin ATPase activates myosin heads
2-Ca-ATPase in SR transports Ca ions into SR which lowers cytosolic free Ca. terminates contraction and allows muscle fiber to relax
Velocity of Muscle Contraction
- rate of ATP hydrolysis is determinant of rate of cross bridge cycling= determines maximal muscle contraction velocity
- fast twitch fibers have isoform of myosin ATPase that splits ATP into ADP and Pi quickly
- slow twitch fibers have isoform of myosin ATPase that split ATP into ADP slowly
- cardiac and smooth muscles have diff isoforms of myosin ATPase
Neuron Muscle Synapse—Neuromuscular Junction
- muscle fiber plasma membrane beneath nerve terminal = motor end plate
- axon terminal + motor endplate= neuromuscular junction
Neuromuscular Junctions
1-neurotransmitter
2-Ach Receptors
3-Neurotrans Degradation/Removal
4- Acetylcholinesterase
1-Ach is a transmitter used at NM junctions. synthesized from acetyl coA and choline and is w/in vesicles in the axon terminal
2-on motor end plate w/in Ach receptros (nicotinic) receptors are ligand gated, cation selective channels that open when bound to Ach. amount of Ach released during AP will open 400000 channels in motor end plate
3-activation of Ach receptors terminates Ach degradation
4-post synaptic membrane degrades Ach. choline is taken back into presynaptic motor nerve for resynthesis of Ach. some diffuse away from cleft
Transmission at Neuromuscular Junction
- AP generated in motor neuron
- depolarization of motor neuron axon terminal by AP opens VG Ca channels and Ca moves into axon terminal
- exocytosis of ACh containing vesicles-# of vesicles released is dependent upon con of Ca in terminal
- Ach diffuses across synapse and binds to nicotinic Ach receptors on motor end plate of muscle membrane
- sarcolemma is folded to synaptic cleft, and Ach receptors are present in junctional folds
- after binding of Ach the nicotinic Ach receptor opens allowing an influx of Na and effluc of K= depolarizing end-plate potential (EPP)
- EPP= AP down muscle membrane
- Achesterase breaks down ACH in junction to stop contraction
End Plate Potentials
- EPP are special excitatory Post synaptic potential at motor end plate
- EPP is analogous to EPSP at neuron neuron synapse
- binding of Ach to post syn receptor= electrical response of muscle cell membrane—depends only on Ach not voltage
- large magnitude (50mv) of EPP= exceed membrane threshold of adjacent muscle plasma membrane to trigger AP. EPP= only 20 mv above membrane threshold= safety to ensure AP in motor neuron= AP in muscle
Muscle Membrane Action Potentials
- EPP produces inward current flow at motor end plate
- initiates AP in muscle membrane that is propagated over surface of fiber
- Na current through VG Na channels generates the upstroke of AP in muscle membrane while K generates repolarization of muscle membrane
1-Alters release of Ach
2-blocks Ach receptors sites
3-prevents inactivation of Ach
1
- black widow spider venom
- clostridium botulinum toxin
- lamber-eaton syndrome
2
- curare
- myasthenia gravis
3
-organophosphates
1-black widow spider venom
2-clostridium botulinum toxin
3-lambert-eaton syndrome
4-curare
5-myasthenia gravis
6-organophosphates
1-explosive release of Ach
2-blocks release of Ach
3-self Ab to Ca diminishes Ca influx into presynaptic term during AP= reduced Ach release
4-reversibly binds w/ Ach receptors
5-self AB inactivate ACh receptor
6-irreversibly inhibits Ach
Excitation Contraction Coupling
- events linking electrical phenomena in plasma membrane to the cell shortening that results in muscle contraction
- delay (altent) between electrical signal (AP) and mechanical response (contraction) reprsents the excitation-contraction coupling
Steps of Excitation Contraction Coupling
1-Ach released by axon of motor neuron crosses cleft and binds to nicotinic receptors on motor end plate that form cation selective channels. if depolarization= threshold then AP is generated
2-AP is propagated across surface membrane and down T-tubulues of muscle cells. t-tubules are invaginations of surface membrane= deep into interior of muscle. they conduct AP into cells center to activate entire cell in sync
3-T-tubules AP activates VG Ca channels that associate w/ Ca release channels in SR. AP triggers Ca release from SR. Free Ca of sarcoplasm inc from resting to antive
4-Ca ions released from SR bind to troponin (tn-c) on actin filaments. tropomyosin is physically moved aside to uncover cross bridge binding sites on actin. myosin able to make crossbridge w/ actin
5-myosin heads bend, pulling actin towards center of sarcomere= shortening sarcomere. energy is provided by hydrolysis of ATP into ADP & P. cross bridge binding, power stroke, and detachment will continue if ATP and Ca are present. Single contraction= cross bridge attaches, pulls, & detaches many times as it progresses along actin towards Z
6-AP termination (repolarization) VG Ca channels in T-tubules close, terminating SR Ca release. Ca ions in cytosol are pumped back into SR by Ca-ATPase, Ca is reduced. Low Ca favors dissociation of Ca from TnC.
Role of Ca in Skeletal Muscle Contraction
- w/in skeletal muscles, the SR is main source of Ca. Ca is needed for cross bridging attachment of myosin to actin bc it removes blocking of the myosin binding by troponin
- Ca & ATP = cross bridge cycling
- but when SR removes Ca from cytoplasm there will be relaxation
Slow Oxidative FIbers
- Type 1 w/in muscles for low-intensity contractions for longperiods of time w/o fatigue
- muscles of back and legs that support bodys weight against gravity
- high oxidative capacity bc of many mitochondria
- high capillary density and low fatigability
- oxidative phosphorylation for ATP
- high myoglobin
- low glycogen
- slow contraction velocity
- small fiber diameter, small motor unit size and small motor neuron innervating fiber
Fast Oxidative Glycolytic Fibers
- Type IIa- share characteristics of both fibers.
- contract quicker than slow oxidativefibers and maintain contraction for longer than fast glycolytic
- medium oxidative w/ moderate fatigue
- oxidative phosphorylation
- many mitochondria, high myoglobin
- intermediate glyocgen, intermediate fatigue, intermediate contraction velocity
- intermediate contraction velocity
- intermediate fiber and motor unit size and innervating fiber
Fast Glycolytic FIbers
- type IIb- whire- w/in muscles for high intensity contraction for short periods of time
- arm muscles for heavy lifting
- low oxidative capacity
- few mitochondria
- low capillary density
- high fatigability
- glycolysis for ATP
- low myoglobin
- high glycogen
- low contraction velocity
- large fiber, motor size and inenrvating fiber
1-tension
2-load
3-types of contraction
1-force exerted on object by a contracting muscle
2-force on the muscle exerted by the weight of an object
3-isotonic, isometric, and eccentric (lengthening)
Isotonic Contraction
- muscle tension remains constant as the muscle changes length
- muscle shortens, causing a load to be moved
- concentric contraction
- muscle tension is greater than load
Isometric Contraction
- muscle is prevented from shortening so tension develops at constant muscle length
- contraction occurs when muscle supports a load in a constant position (doesnt move)
- muscle tension is equal to the opposing load
Lengthening Contraction
- load pulls the muscle to a longer length in spite of opposing forces being made by cross bridges
- eccentric contraction
- not an active process but is a consequence of external forces being applied to the muscle
- muscle tension is less than the opposingl oad
- ex: knees extensor muscles in your thighs are used to lower you to a seat from a standing position—-the muscle lengthens
Latent Period
- delay between muscle stimulation and onset of contraction
- AP in skeletal muscle fiber lasts less than 5 ms
- onset of resultant contractile response lags behind the action potential because the entrie excitation-contraction coupling process must be before cross bridge activity
Frequency Tension Relationship
-summation of contractions
- inc in muscle tension from successive AP occurring during the phase of mechanical activity
- caused bc Ca removal from cytoplasm takes time
- tension (force) being summated not voltage
- AP of muscles DONT summate, but the contractions do
Frequency Tension Relationship
-Tetanus
- sustained contraction where the individual twitches are no longer distinguishable from each other
- rapid, repetitive stimulus
- inc the frequency of stimulation doesnt allow muscle fiber to fully relax between successive APs
- = an inc in produced muscle tension as individual twitches summate
- fused tetanus= maximal tension is reached
Role of Ca in muscle fiber force production
- cutosolic Ca levels remain elevated after the AP terminates
- if 2nd AP excites the muscle during this period, the new Ca release from SR will inc the cytosolic Ca= larger muscle tension
Single Muscle Twitch
- w/in individual muscle a single AP = maximal release of Ca from SR= single muscle twitch
- each single muscle twitch= produced by same amount of Ca releases from SR (Ca release is NOT regulated)
High Cytosolic Ca
- duration is important in development of graded forces w/ summation.
- w/ single AP the duration of the high Ca is short even tho Ca released from the SR is maximal=single AP doesnt make maximal tension in muscle
- –however at high frequency, Ca rises= inc in cytosolic Ca during summation.—if elevated for a long time= maximal tension in muscle
- muscle tensions depends on amt of cytoplasmic Ca
Length Tension Relationship
- max tension is achieved when muscle fiber length at the beginning of twitch, allows max overlapping between actin and myosin
- resting length is the optimum length
- if muscle is overstretched then there is no overlap of A & M so there are no crossbridges
- if overshortenedand A & M physically overlap= interference w/ crossbridges
Whole Muscle Contraction
-Motor Unit
- when reaching a muscle the axon of a motor neuron divides into branches and each branch makes a single junction w/ a muscle fiber
- single motor neuron innervates many muscle fibers but each fiber is controlled by one motor neuron
- motor neuron + muscle fibers innervates motor unit
- AP generated in motor neuron all fibers in unit contract
Motor Unit Recruitment
- determines total tension that a muscle can develop is number of fibers contracting at any one time
- # of fibers contracting at one time depends on # of fibers in each motor unit and # of motor units
- motor units w/ lowest threshold activate first and then the recruitment adds additional units =’ing greater force
Motor Unit Order of Recruitment
- excitable first===slow oxidative type 1 (w/in postural muscles and fine motor movememnts)
- intermediate
- least excitable= fast glycolytic type 2b white—during high intensity when quick bursts of power are needed
Control of Whole Muscle Tension
- tension developed in muscle depends upon amt of tension developed by each fiber and # of fibers contracting at a time
- graded force production w/in muscle is determined by AP frequency w/ summation of contractions and the recruitment of motor units
-length tension relationship isnt imp. for force generation bc attachment to bone limits muscles ability to change length
1-frequency tension (summation)
2-length tension (fiber length)
3-fiber diameter (#of myofibrils)
4-fatigue
1-# of fibers per motor unit
2-#of active motor units (recruitment)
1-Soleus
2-extraocular muscles
1-fatigue resistant & maintain tension for a long time
2-contract rapidly but infrequently
1-slow twitch
2-fast twitch a
3-fast twitch b
1-type 1, fatigue resistant, red (myo), oxidative, high mito, low glyco
2-type 2a, fatigue resistant, red (myo), oxidative, higher mito, abundant glyco
3-type 2b, fatigable, white (low myo), anaerbox, few mito, high glyco
Sources of Energy
- cell processes provide biochemical energy to contractile mechanisms, dependent on ADP–>ATP
- metabolic pathway used to supple ATP depends on type of muscle and conditions
- Phosphocreatine= readily available energy. creatine phosphotransferase transfers hhigh energy phosophate to ADP making ATP
- glycogen= abundant energy source—into pyruvate then lactate via anerobic= 2 ATP
- pyruvate w/ O2= CAC=36 ATP
Muscle Fatigue
- end of muscle activity the creatine phosphate and glycogen stores will have decreases and need to be replenished—need energy so muscle uses O2 at inc rate (o2 debt) for time after activity stopped
- when muscle is repeatedly stimulated the max tension that muscle produces will decrease=muscle fatigue
- additional characteristics of fatigue= decreased shortening velocity and slower rate of relaxation
- onset + rate of fatigue depends on fiber type and intensity and duration of stimulation
1-Growth of Skeletal Muscle
2-Lengthening
3-Hypertrophy
4-hyperplasia
1-# is determined prenatally and is constant through life
2-growth by adding new sarcomeres at the ends of the myofibrils
3-formation of added myofibrils w/in cells
4-adding new cells
Hypertrophy
- total mass of muscle to increase
- adds more sacomeres in parallel = inc in size of individual muscle fibers and inc force that is developed by muscle fiber
- short duration, high intesity resistance exercise= hypertrophy in fast glycolytic fibers while low intensity but long duration = changes in slow oxidative and fast oxidative glycolytic fibers
- maybe bc cell damage bc of overloading= hypertrophy to prevent future muscle damage
- muscle fibers in men are thicker, larger, and stronger than womenthis is bc of androgenic steroid = inc in males
1-Atrophy
2-disuse atrophy
3-denervation atrophy
1-total muscle mass to decrease
2-if muscle not used for long periods of time (immobile) there is a dec in muscle size
3-motor neurons innervating muscle are destroyed the denervatied fibers become smaller—if not reinnervated then fibers degenerate and eliminate
Hyperplasia
- # of muscle fibers increase
- limited ability to form new fibers
- new fibers from differentiation of satellite cells w/in tissues
- major destruction= scar tissue replacement
- may happen as result of high volume moderate intesnity weightlifting protocol by body builder—but overall= minimal
Postnatal growth
-lengthening and hypertrophy
Smooth Muscle
- surrounds hollow organs and tubes (BV, bronchi, GI, reproductive, and urinary)
- eye for pupil diameter and hairs in skin
- propels contents through tubes
- maintains pressue against contents w/in organ and tube
- regulates internal flow of contents by changing tube diameter (resistance)
1- Muscle Contraction
2-Basal Tone
3-Phasic Contraction
4-Tonic Contraction
1-changes in Ca control muscle: high Ca= more cross bridge + stronger force…SM is slower than Skeletal
2-low level of contraction in absence of extrinsic factors. intrinsic of SM (mygenic). Cytosolic Ca is sufficient for low level cross bridging
3-brief stimulurus w/ rapid force (contraction) and rapid relaxation as Ca goes back to basal. GI, urogenital
4-continous production of force in presence of falling Ca that remain above basal levels. cross bridge cycling continues at low levels. Lungs, BV and GI sphincters have tonic contractions
Contraction of SM
- lacks striations but has order just doesnt detect small ordered arrays of overlapping filaments
- SM doesnt have t tubules, sarcomeres, troponin, and has less SR
- has myosin thick filaments and actin w/ thin
- regulation of cross bridge cycling in SM occurs on the thick myosin filament
Contraction of SM
steps
1- increase cytosolic Ca
2-Ca binds to calmodulin (binding protein) in cytosol
3-Ca calmodulin complex binds & activates enzyme MLCK (myosin light chain kinase)
4-MLCK uses ATP to phosphorylate myosin cross bridges
5-phosphorylated myosin forms cross bridges w/ actin filaments
6-cross bridge cycle produces tension and shortening
7-power stroke—release of ADP Pi from myosin head
8-cross bridge detachment needs ATP
Inc of Intracellular Ca
- extracellular Ca plays major role in inc of cytosolic Ca
- influc of extracell Ca into SM causes release of more Ca from SR===Ca induced Ca release
- small amt of extracell Ca= large inc in cyotosolic Ca
Extracellular Ca entering
- voltage gated Ca channels
- ligand (2nd messengers) gated Ca channels
- receptor gated Ca channels
- stretch activated Ca channels
-autonomic, hormones and paracrine control SM tone, contraction and relaxation
1-RMP
2-AP
3-AP definition
1-Em= not constant but variable…from -65 mV to -45 mV, RMP is determined by Na and K fluxes
2-Ca dependent rather than Na dependent. single unit SM fires AP, most multiunit SM dont fire AP
3-depolarization of RMP to generate AP = activation of VG Ca channels in membrane of SM and an increase in intracellular Ca
spontaneous depolarization (of single unit)
1-pacemaker potential
2-slow wave potential
1-membrane potential graduall depolarizes until it reaches threshold for firing a single AP. spontaneous depolarization= from activation of small cationic current (mostly Na)
2-membrane potential slowly oscillates, alternating small depolarizations and slow hyperpolarizations. when threshold is reached the cell fires a burst of AP
RMP
1-depolarization
2-hyperpolarization
1-of RMP w/o generating AP = activation of VG Ca channels, intracellular Ca and force of contraction inc
2-of RMP = closing of VG Ca. intracellular Ca and force of contraction dec
Pharmaco Mechanical Coupling
-agonist (hormone, neurotransmitter) binds to receptor and inc/dec cytosolic Ca through 2nd messenger, w/o changing membrane potential
1-receptor operated channels
2-mechano mechanical coupling
1-receptors are coupled (direct/indirect) to Voltage independent channels which then open bc of voltage change (depol or hyperpol) the change in membrane potential will alter cytosolic Ca that same neurotrans may contract or relax
2-stretch acitvated channels (mixed cation) open when the SM cell membrane is distorted by stretch of the organ…depolarization inc the cytosolic Ca—contraction opposes the stretch
Relaxation of SM
1-dec in cytosolic Ca from:
- return of Ca into SR by SR Ca ATPase
- extrusion of Ca out of SM by: -sarcolemma Na/Ca exchanger—energy for extrusion of Ca against concentration gradient from inward driving force for Na (atpase retains gradient) -sarcolemman Ca ATPase
2-MLCK returns from inactive
3-enzyme myosin phosphatase removes phosphate from myosin
4-cross bridge reattachment is inhibited—dec in contractile force occurs when intracellular Ca decreases
1-Smooth Muscle Drugs
2-Ca Antagonisms
3-K Channel Openers
1-affect excitation-contraction coupling in vascular SM cells—drugs treat hypertension
2-drugs block VG dependent Ca. Reduce Ca influx and Ca induced Ca release——nifedipine, verapamil, diltiazem
3-drugs cause hyperpolarization of SM cells. hyperpolarization promotes relaxation of SM and vasodilation of peripheral vascular SM—pinacidil
Smooth Muscle Drugs
Nitric Oxide/Cyclic GMP Stimulator
- vasodilators produce NO or stimulate nitric oxide cyclic GMP pathway= elevated cGMP conc in cyotosol
- cyclic GMP relaxes SM= nitrovasodilators=nitroglycerin
- NO = imp physiological regulatior of vascular smooth muscle tone and BP
- NO= impor regulatory mechanis in cardio
Single Unit SM
- function syncitium bc of gap junction
- phasic contractions—superimposed on basal tone
- spontaneos contraction due to pacemakers or enteric nervous system
- common stretch initiated contactions (SI)
- common stretch initiated relaxations (rectum, bladder)
- modulate ongoing phasic contractions, altering basal tone (extrinsic factors)
- ex= GI tract, ureter, bladder, uterus, small diameter BV
Multiunit SM
- each cell is independent of its neighbor
- tonic contraction dependent on external stimuli
- controlled by extrinsic—ANS, hormones, and local paracrines
- stretch initiated contraction/relaxation= not common
- extrinsic factors= strong influence on contraction
- large diameter BV, airways of lungs, eye muscle, piloerector in skin
Shoulder and Pectoral Girdle
- clavicle
- scapula
- sternum
Scapula
- glenoid cavity (fossa)
- supraglenoid and infraglenoid tubercles
- fossae—shallow depressions for joint articulations or muscle attachments
- spine and acromion process
- suprascapular notch (foramen when bridged by suprascapular ligament)
- coracoid process
Arm (brachium)
Humerus:
- head and bicipital (intertubercular) groove
- greater and lesser tubercle
- deltoid tuberosity
- radial (spiral) groove
- olecranon fossa
Forearm (antebrachium)
-Ulna
- olecranon process
- coronoid process
- ulnar tuberosity
-Radius
- head
- radial (bicipital) tuberosity
Glenohumeral (GH:Shoulder) joint
-between glenoid fossa of scapula and head of the humerus
Shoulder Muscles
- deltoid
- supraspinatus
- infraspinatus
- subscapularis
- teres minor
- rotator cuff
- teres major
Deltoid
- origin
- insertion
- action
- innervation
- blood supply
1-lateral 1/3 of clavicle, acromion and spine of scapula
2-deltoid tuberosity
3-abducts arm
anterior fibers assist w/ flexion & medial rotation posterior fibers extend & lateral rotate the arm
4-axillary n
5-posterior circumflex humeral a
Supraspinatus
1-origin
2-insertion
3-action
4-innervation
5-blood supply
1-supraspinous fossa
2-greater tubercle of humerus
3-abduction of arm
4-suprascapular n
5-suprascapular a
Infraspinatus
1-origin
2-insertion
3-action
4-innervation
5-blood supply
1-infraspinous fossa
2-greater tubercle (inferior to supraspinatus insertion)
3-lateral rotation of arm
4-suprascapular n
5-suprascapular a
Subscapularis
1-origin
2-insertion
3-action
4-innervation
5-blood supply
1-subscapularis fossa
2-lesser tubercle
3-medial rotation of arm
4-upper and lower subscapular n
5-subscapular a
Teres Minor
1-origin
2-insertion
3-action
4-innervation
5-blood supply
1-lateral portion of axillar border
2-greater tubercle (inferior to inraspinatus insertion tendon)
3-lateral rotation of arm
4-axillary n
5-circumflex scapular a and scapular anastomoses
Rotator Cuff
-musculotendinous ring around GH join formed by tendons of the:
- supraspinatus
- infraspinatus
- teres minor
- subscapularis
- tendons of rotator cuff fuse w/ and reinforce fibrous capsule of GH joint
- tonic contractions of cuff muscles help hold head of humerus against glenoid fossa
Teres Major
1-origin
2-insertion
3-action
4-innervation
5-blood supply
1-lateral portion of axillar border inferior to teres minor
2-medial lip of intertubercular groove
3-extends, adducts, and medially rotates the arm
4-lower subscapular n
5-circumflex scapular and thoracodorsal aa
Pectoral Region Muscles
- pectoralis major
- pectoralis minor
- subclavius
- serratus anterior
Pectoralis Major
1-origin
2-insertion
3-action
4-innervation
5-blood supply
1-sternum, ribs 2-6, clavicle
2-lateral lip of intertubercular groove
3-adducts and medially rotates arm, flexes arm and extends it when you flexed, depresses and protracts shoulder by pulling on humerus
4-medial & lateral pectoral nn
5-thoracoacromial, lateral thoracic, and perforating internal thoracic
Pectoralis Minor
1-origin
2-insertion
3-action
4-innervation
5-blood supply
1-Ribs 2-5
2-coracoid process of scapula
3-depresses and protracts pectoral girdle
4-medial pectoral n
5-thoracoacromial and lateral thoracic a
Subclavius
- from 1st costal cartilage to inferior portion of clavicle
- depresses and resists lateral dislocation of clavicle
- innervated by ‘nerve to subclavius’
Serratus Anterior
1-origin
2-insertion
3-action
4-innervation
5-blood supply
1-ribs 1-9
2-ventral surface of scapular medial border
3-protracts and superiorly rotates scapula
4-long thoracic n
5-lateral thoracic and subscapular a