muscle tissue A&P Flashcards
muscle tissue percentage body weight
40-50%
depending on body fat, gender, muscle mass etc.
4 functions of muscle tissue
motion
stabilize/posture
store/move substance
(blood, food, urine,)
–> peristalsis
heat via shivering (thermogenesis)
5th function? store glycogen
circular muscles that act as gate-keepers…
sphincter muscles
regulating movement from one part of body to another
smooth muscles move
food (GI tract)
blood
_____ is an involuntary response using voluntary muscles
shivering
3 types of muscle tissue
cardiac
skeletal
smooth
smooth muscle function in BV
e.g. regulates diameter of arteries
skeletal muscle fibres
elongated,
cylindrical
multinucleated
striated (VIA ARRANGEMENT OF contractile proteins)
skeletal muscle fibres – note these functions
protect internal organs
protects entrance/exit to digestive, respiratory, urinary tracts (I.e. sphincter muscles)
cardiocytes
short, branched, USUALLY SINGLE NUCLEUS
interconnected via intercalated discs
striated, involuntary
MOVES BLOOD, MAINTAINS BP
intercalated discs
transverse thick portion of membrane
VIA DESMOSOMES & GAP JUNCTIONS
desmosomes stronger (INTERMEDIATE FILAMENTS VIA KERATIN)
gap junctions for electrical signal (ion movement)
desmosomes also via glycoprotein ____
cadherin
smooth muscle cells
short, spindle-shaped, nonstriated,
SINGLE nucleus, INVOLUNTARY
smooth muscle cells functions
Move food (PERISTALSIS), urine, reproductive secretions
diameter of respiratory pathway (bronchi**)
DIAMETER OF BLOOD VESSELS
sphincter pupillae and dilator pupillae
dilate and constrict pupils
muscle cell types by speed of contraction
skeletal = FAST
cardiac = INTERMEDIATE
smooth = SLOW
muscle cell types by Nervous system type
skeletal = SOMATIC
cardiac = AUTONOMIC
smooth = AUTONOMIC
muscle cell types by shape
skeletal = CYLINDER
cardiac = BRANCHED/CYL
smooth = FUSIFORM
muscle cell types by # of nuclei
skeletal = MANY (PERIPHERAL)
cardiac = (GENERALLY ONE – CENTRE)
smooth = (ONE – CENTRE)
muscle cell types via connection
Cardiac = INTERCALATED DISCS (GAP + DESM)
smooth muscle cells = GAP JUNCTIONS
4 properties of muscle tissue
1) CONTRACTILITY
2) EXCITABILITY
3) EXTENSIBILITY
4) ELASTICITY
2) excitability
ability to receive and respond to stimulus from NERVOUS SYSTEM, or ENDOCRINE SYSTEM
3) Extensibility
Same as plasticity (?)
ability to stretch/lengthen
4) Elasticity
ability to return to original length
epimysium
covers outer later of skeletal muscle
CONTINUOUS with tendon
CONTINUOUS with PERIOSTEUM
epimysium composition
DENSE IRREGULAR CT
epimysium function
separates skeletal muscle from other muscles, or organs
epimysium vs tendons
continuous with tendons
HOWEVER, tendons DENSE REGULAR CT (?)
epimysium DENSE IRREGULAR CT
Epimysium VS deep fascia
epimysium connected to DEEP FASCIA
PERIMYSEUM
covers muscle fascicles
ALSO DENSE IRREGULAR CT
collaged + elastic fibres
muscle fascicles
GROUP OF MUSCLE FIBRES
ENDOMYSIUM
surrounds individual muscle fibres
FASCIA
DENSE IRREGULAR CT
“Deep” fascia covers EPIMYSIUM
fascia other functions
lines body walls, limbs
SUPPORTS/surrounds muscles
two types of fascia
1) SUPERFICIAL fascia
2) DEEP fascia
Superficial fascia
below dermis (?)
AKA SUBCUTANEOUS layer
AKA HYPODERMIS
blends w/ deepest part of skin
SEPARATE muscle from skin (DERMIS)
Deep fascia
BELOW superficial fascia (?)
OVER muscle (over epimysium)
Superficial fascia densely packed with
nerves, blood vessels, adipose tissue (and other CT), & LYMPH vessels
Deep fascia …
DENSE (IRREGULAR?) CT
fills space between individual skeletal muscles –
FACILITATES MOVEMENTS BETWEEN SKELETAL MUSCLES (reduce friction)
Deep fascia can surround individual muscles or GROUPS of muscles
.
When around groups of muscles, deep fascia forms _____
fascial compartments with groups of muscles (perhaps with similar function/actions?)
E.G. (lower leg)
ANTERIOR compartment
DEEP POSTERIOR compartment
SUPERFICIAL POSTERIOR compartment
LATERAL compartment
Tendon
DENSE REGULAR CT
extend via muscle fibres to bone
TENDON CAN BE continuous w/
a) Epimysium
b) Perimysium
c) Endomysium
I.e. INVOLVES STRUCTURES OF EACH
Aponeurosis
similar structure to TENDON
Broad and flat instead of cylindrical
MUSCLE TO BONE or MUSCLE TO MUSCLE
E.g.
Epicranial APONEUROSIS (GALEA Aponeurotica
THORACOLUMBAR fascia
SYNOVIAL TENDON SHEATHS
skin for tendons
CERTAIN PARTS – tendons experience more wear/stress
E.G.
HAND, WRIST, FOOT, ANKLE
synovial tendon sheaths parts
Synovial lining / synovial cover of tendon
SYNOVIAL SHEATH
mesotendon, and SYNOVIAL CAVITY
Tenosynovitis
inflammation of tendons + Synovial sheaths
(E.G. In hands/feet)
E.g.
DeQuervain’s Tenosynovitis (Gamer’s thumb)
muscle fibres via ____blasts
myoblasts
note myocyte, cardiocyte, and cardiomyocyte
note muscle fibre, myocyte, myofibre
note myofibre
number of skeletal muscle fibres
predetermined at birth
(GENERALLY?) does NOT CHANGE via MITOSIS
can grow/heal but not increase in #
HYPERTROPHY but NOT HYPERPLASIA
mechanism of Hypertrophy
stress causing microtears –> Stimulates repairs, causing cell size increase
anabolic steroids and muscle fibre hyperplasia
.
embryonic development and muscle fibre hyperplasia
during embryonic development
When do muscle cells exit cell cycle?
@ G0 Phase
G0 PHASE?
“If cells don’t pass the G1 checkpoint, they may ‘loop out’ of the cell cycle and into a resting state called G0, from which they may subsequently re-enter G1 under the appropriate conditions. At the G1 checkpoint, cells decide whether or not to proceed with division based on factors such as: Cell size. Nutrients.”
ATROPHY
loss of MYOFIBRILS (and therefore, size)
Via lack of USE
E.g.
FRACTURE
Via innervation LOSS (Neurodegenerative Disease)
Satellite Cells (AKA myosatellite cells)
embryonic cells
remain in skeletal muscles throughout adulthood
Can REPLACE damaged muscle fibres (“to some degree”)
MUSCLE TISSUE REGENERATION AFTER INJURY
myofibre diameter and length
100microMETERS in DIAMETER
can span entire muscle length (“up to 30cm”)
(?) Longest fibres in sartorius, up to 600mm (60cm)
Muscle fibres
myofibre
cell membrane of muscle fibre
SARCOLEMMA
(underneath endomysium)
SURROUNDS myoFIBRILS and SARCOPLASM
Sarcolemma
selective permeability
DETERMINED RMP (resting membrane potential)
NOTE REVERSAL OF CHARGE (faciliates muscle contraction)
change in charge of muscle fibre via…
Via Neuron signal
SPREADS ACROSS ENTIRE SARCOLEMMA
MYOFIBRILS
contractile organelles
VIA MYOFILAMENTS (contractile proteins)
Myofilaments give muscles STRIATIONS
Myofibril diameter
1 MICROMETER
How many myofibrils per myocyte?
approximately 2000 myofibrils per MYOCYTE
I.e. MUSCLES OF UNTRAINED INDIVIDUAL
Hypertrophied muscles could have 4000 (?) or more (?) MYOFIBRILS
Myofilaments
within myofibrils
2 types of myofilaments
1) THICK FILAMENTS (myosin filaments)
2) THIN FILAMENTS (actin filaments)
thick filaments 15nm diameter
thin filaments 7nm diameter
Thick via MYOSIN protein
Thin via ACTIN protein
Myoglobin (within sarcoplasm)
binds O2 for ATP production
Sarcoplasmic reticulum
membranous sacs – SURROUND myofibrils
SPECIALIZED smooth ER
Sarcoplasmic reticulum stores Ca2+ – necessary ion for muscle contraction
T tubules (Transverse tubules)
invagination/holes of SARCOLEMMA
facilitate SARCOPLASMIC reticulum via nerve impulses
T-TUBULES surrounded by terminal cisternae of SR
Terminal cisternae of SR
dilated terminal regions of SR
FORMED on both sides of Transverse Tubules
Triads of myofibrils
trio consisting of TRANSVERSE tubule
+
two terminal cisternae
Triad
= 1 T-tubule from outside (via sarcolemma)
+ 2 terminal cisternae from within muscle fibre
3 categories of muscle proteins
1) contractile proteins
2) regulatory proteins
3) structural proteins
1) contractile proteins
found inside myofibrils
types:
i) MYOSIN
= THICK FILAMENTS
= GOLF CLUBS TWISTED TOGETHER
= has ACTIN binding sites
ii) ACTIN
= THIN FILAMENTS
= shaped like golf balls
= has MYOSIN binding sites
Sarcomere
functional unit of striated muscle
Z-disc
on ends of 1 sarcomere unit
M-line
mid-line of 1 sarcomere unit
Myosin molecule
2 golf clubs twisted together
MYOSIN TAIL
MYOSIN HEADS
thick filament
composed of molecules of Myosin aligned
SIDE TO SIDE
and
END TO END
– with heads facing away
2) REGULATORY PROTEINS
1) Troponin
2) Tropomyosin
Thin Filaments
composed not JUST of ACTIN
TROPOMYOSIN is part of thin filament COMPLEX
troponin is also part of complex
TROPONIN IS BINDING SITE FOR CALCIUM
function of tropomyosin
BLOCKS myosin binding site during muscle RELAXATION
Z-disc structure
THIN (Actin) filaments extend from Z-discs
THICK (Myosin) filaments aligned on M-line, in BETWEEN the thin filaments
4 structural proteins
1) Titin
2) Myomesin
3) Nebulin
4) Dystrophin
2) Myomesin
forms M-line
stabilizes THICK filaments
1) Titin
indirectly attached Thick filaments to Z-discs on either side
LIKE A COIL
helps to return filaments to original position after stretch or contraction
3) Nebulin
connects thin filaments to Z-discs
4) Dystrophin
links thin filaments to SARCOLEMMA (stability)
muscular dystrophy
protein dystrophin is lacking in this pathology
sarcomere
(from z disc to z disc)
THE UNIT THAT CONTRACTS
myofibril is repeating sarcomeres
WHEN SARCOMERES CONTRACT, MYOFIBRILS CONTRACT, MUSCLE FIBRE CONTRACTS, MUSCLE CONTRACTS
WHY STRIATED?
arrangement/contrast of thin/thick filaments (NOTE A BAND – region signifying entire length of thick filament in sarcomere unit) – darker band of striations)
“darker regions have more overlap” (???)
lines and bands
Z lines
I band
A band
M line
H band
Z lines (Z discs)
protein structures on edges of sarcomere unit
stabilize filaments
A band
entire length of thick filaments (including where overlapping with thin filaments)
CREATES DARKER striation
A in “dArk”
I band
signifies region of thin filaments with NO OVERLAP
I in “lIght”
M line
middle of sarcomere
PASSES THROUGH MIDDLE OF THICK FILAMENTS
H band (H zone)
signifies region of thick filaments with NO OVERLAP with thin filaments
Zones/lines/bands during contraction
Z-lines come closer together
H BAND becomes smaller and disappears
I BAND becomes SMALLER
and A BAND REMAINS SAME
SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION
MYOSIN HEADS of thick filaments attach to myosin binding sites of ACTIN proteins
— They then PULL actin (thus Z-discs) towards each other
— SHORTENS SARCOMERES, leading to muscle contraction
4 steps of the CONTRACTION CYCLE (sliding filament theory)
1) ATP hydrolysis (@ MYOSIN heads)
— 2) formation of “Cross bridges” – Myosin heads attaching to binding site on ACTIN
— 3) Power stroke = fast motion of myosin heads pulling thin filaments
— 4) breaking of cross bridge (ADP molecule detaches and New ATP molecule attaches)
1) ATP hydrolysis
ATPase in myosin heads breaks down ATP to ADP
— Causes myosin head to become energized
— positions myosin heads appropriately
2) formation of “Cross bridges”
Ca2+ from Sarcoplasmic reticulum is released
— Ca2+ attaches to TROPONIN
— Causes Tropomyosin to shift and REVEAL the MYOSIN BINDING SITES of the ACTIN proteins
— MYOSIN heads bind to MBS of ACTIN proteins, thus forming CROSS BRIDGES
3) Power stroke
ADP falls off myosin heads
— Myosin heads perform power stroke in direction of centre of sarcomere (towards M-line
— Sarcomere shortens
4) Breaking of cross bridges
another molecule of ATP binds to cross bridge
— Causes myosin head to release from ACTIN proteins
under what conditions do steps in SLIDING FILAMENT theory continue
as long as there is ATP and Ca2+
Ca2+ depends on
Nerve impulses stimulating Ca2+ release from sarcoplasmic reticulum
— If there is a nerve impulse, Ca2+ is present, and contraction takes placec
ATP availability and myosin heads
ATP is needed for Myosin head to release from Actin
— If no ATP, muscle stays contracted
— RIGOR MORTIS
Length-tension relationship
amount of overlap between thick and thin filaments determines the amount of force generated (% maximal)
— IDEAL OVERLAP = maximal possible force
— too little overlap = less possible
— too much overlap = less possible
— SARCOMERE TOO SHORT OR TOO LONG = LESS POTENTIAL FOR MAXIMAL FORCE
Excitation-contraction coupling
generation of AP in SARCOLEMMA –> Start of muscle contraction
— Signal from motor neuron reaches muscle fibre (sarcolemma)
— Ca2+ is released from sarcoplasmic reticulum via signal
— Ca2+ binds to troponin, which causes tropomyosin to shift and expose the MBS of ACTIN proteins
— Excitation-contraction coupling is the process of Ca2+ release & fibre contraction via NEURON signal
Steps of excitation-contraction coupling
1) neural control
2) Excitation
3) Ca2+ release
4) Contraction cycle begins
5) Sarcomeres shorten
6) muscle tension is produced
Steps of excitation-contraction coupling (outlined)
1) neural control
— AP @ NMJ begins process —
2) Excitation
— AP causes ACETYLCHOLINE (ACh) release via motor neurons
— leads to EXCITATION (AP) @ SARCOLEMMA —
3) Ca2+ release
— muscle fibre AP travels via T-tubules (transverse tubules)
— Via Terminal Cisternae (Sarcoplasmic reticulum)
— leads to release of Ca2+ in Sarcoplasmic reticulum) —
4) Contraction cycle begins
— Ca2+ binds to troponin
— Tropomyosin shifts off of MBS of Actin
— Cross bridges form
5) Sarcomeres shorten
6) muscle tension is produced
importance of neuron signalling
As long as motor neuron signals are present, Ca2+ will be present via Sarcoplasmic reticulum (Via T-tubules and T-Cisternae)
— Muscle will thus continue to contract (ATP must be present as well)
when neuron stimulus ends
SR calcium channel closes
— Ca2+ pumps return remaining Ca2+ into Terminal Cisternae
— CALSEQUESTRIN (protein) binds to Ca2+ in Sarcoplasmic reticulum
— Stores Ca2+ in SR for next contraction
— Tropomyosin resumes original position after Ca2+ leaves Troponin, thus preventing cross bridge formation
— MUSCLE RELAXES
misc fact about Ca2+ in SR vs cytosol @ rest
10,000x higher Ca2+ levels in SR than cytosol of muscle fibre, when muscle at rest
Muscle injuries, exercise, and other random facts
DOMS
— via microscopic tears after strenuous exercise
— pain, tenderness, stiffness, edema
— repair is done via SATELLITE CELLS
— SATELLITE CELLS use amino acids to build new proteins
— pre-workout & post-workout protein intake facilitates this process
muscle strains
muscle and tendon injuries
— excessive force on muscle fibres
— pain, dysfunction, fibrosis (scar tissue)
— note that muscles strain while ligaments sprain
muscle cramps
muscle spasms/pain
— extended usage
— lack of blood flow
— dehydration
— buildup of lactic acid & other wastes
skeletal muscle fibre types
1) Fast glycolitic (fast fibres)
2) fast oxidative (intermediate fibres)
3) slow oxidative (slow fibres)
how do skeletal muscle fibres differ. What variables?
differ in SIZE, in INTERNAL STRUCTURE, in METABOLISM (type), in RESISTANCE TO FATIGUE
Slow oxidative fibres (slow fibres) – how much longer do they take to contract?
3x longer to contract compared to fast fibres (Fast glycolitic fibres)
slow oxidative fibres (slow fibres) – how much is diameter compared to fast fibres
1/2 diameter of fast fibres (Fast glycolitic fibres)
slow oxidative fibres (slow fibres) – resistance to fatigue compared to fast fibres
longer sustained contractions = fatigue resistance
how is ATP produced i slow oxidative fibres?
via aerobic ATP production
how does structure of slow oxidative fibres facilitate aerobic ATP production?
MANY MITOCHONDRIA
—Extensive capillary network (for oxygen exchange)
MYOGLOBIN –> (protein pigment) –> binds/stores O2 in muscle fibres (similar in function to Hemoglobin)
how do slow oxidative fibres appear in colour?
they appear red due to Myoglobin pigment protein, and DUE TO EXTENSIVE CAPILLARY NETWORK
fast Glycolitic fibres PEAK tension time
in <0.01 second
fast glycolitic fibres diameter and why large diameter? – storage of glycogen (where?)
large diameter
DENSELY PACKED WITH MYOFIBRILS = POWERFUL CONTRACTIONS
large glycogen reserve (in SARCOPLASM)
fast glycolitic fibres fatigue rate?
fatigue rapidly
fast glycolitic fibres ATP production (?)
ATP produced anaerobically
how do fast glycolitic fibres appear in colour?
appear white due to LACK OF MYOGLOBIN
Fast oxidative muscle fibres (intermediate muscle fibres) – how do they produce energy? contraction speed?
combination of aerobic and anaerobic metabolism
muscle contractions faster than SLOW OXIDATIVE but slower than FAST GLYCOLITIC
fast oxidative muscle fibres appearance in colour and structure
many mitochondria and Blood Capillaries
—- LOW MYOGLOBIN
—- light red colour
—- GLYCOGEN ALSO PRESENT = anaerobic glycolysis
the terms RED and WHITE muscle
Red muscle = lot’s of blood flow, MYOGLOBIN, Mitochondria
—- = high fatigue resistance
—- = slow
—- = small diameter muscle fibres
—- E.g. Postural muscles
White muscle
= Little blood flow, less MYOGLOBIN, less Mitochondria
—- low fatigue resistance
—- fast
—- large diameter muscle fibres
—- E.g. Eye muscles
Muscles have MIXTURE of fibre types
Mix reflects function
—- E.g. Back/calf = Slow
—- E.g. Eye/hand = fast
what determines ratio of fast to slow muscle fibres in different muscles?
there are some typical patterns of fast/slow ratio (such as push muscles usually having more fast twitch muscle fibres in untrained adults)
—- RATIO can be genetically determined
—- RATIO can be modified with training (Via Specific adaptation to imposed demands)
ORIGIN of a muscle tends to be more…
more stable, less mobile
Insertion tends to be less stable, more mobile
blood and nerve supply to muscles
all muscles are innervated by at least 1 nerve (often more)
—- All muscles will have multiple sources of blood supply (ARTERIAL/VENOUS) —- Usually 1 main artery/vein is present
AGONIST (AKA PRIME MOVER)
muscle which contributes the most in a specific movement
E.g.
BRACHIALIS IS THE PRIME MOVER IN ELBOW FLEXION
ANTAGONIST
primary opposition to prime mover (AGONIST)
E.g.
Triceps Vs flexion of forearm @ elbow
SYNERGIST
muscle that aids the PRIME MOVER (agonist)
E.g.
biceps brachii and brachioradialis are synergists of Brachialis during flexion of the forearm @ the elbow joint
Fixator/stabilizer
muscle that stabilizes a joint so AGONIST can perform its action
isotonic movements/contractions
skeletal muscle length changes
—- Concentric and eccentric
Isometric contractions/movements
muscle length does not change, but there is tension in the muscle
more about concentric contraction
muscle tension exceeds load
— muscle shortens and tension is constant (ISO-tonic)
— SPEED of contraction inversely related to weight of load
eccentric
muscle tension is less than the load
— muscle lengthens against load (elongates)
— rate of elongation depends on how much the load exceeds the muscle tension
what happens if muscle contraction ends, but load is not removed?
muscle stretches until
2) Tendon breaks
—
3) “ELASTIC RECOIL OPPOSES LOAD”
isometric
muscle length does not change
tension does not exceed load, load does not exceed tension
E.g.
Postural muscles
do muscles bulge during isometric contractions?
yes, but not as much as during ISOTONIC contractions
Lever and fulcrum
Lever = rigid beam + FULCRUM
—– EFFORT & LOAD are applied to each end of the beam
what is the fulcrum?
fulcrum is point on which beam pivots
3 types of levers
1st class lever, 2nd class lever, 3rd class lever
1st class lever (EFL)
Effort –> fulcrum –> load
E.g.
Posterior neck muscles holding head up
2nd class lever (FLE)
Fulcrum –> load –> Effort
— Load is between Effort and Fulcrum
— I.e. WHEELBARROW LEVER
— BIOMECHANICALLY THE STRONGEST IN BODY
E.g.
CALVES when doing calf raises on stairs
3rd class lever (FEL)
Fulcrum –> effort –> load
— effort is between load/fulcrum
— TWEEZER LEVER
E.g.
Hip Flexors raising leg
— NOTE: THIS is MOST COMMON LEVER IN BODY
proprioception and proprioceptors
proprioception = perceiving sense of position/movement in space (INDEPENDENT OF VISUAL SENSORY FEEDBACK) & perception of equilibrium and balance
proprioceptors
proprioceptors are responsible for proprioception
— proprioceptors read the muscle LENGTH, MOTION/POSITION, TENSION, etc
Examples of proprioceptors
1) Muscle spindles, AND 2) Golgi Tendon Organs
1) muscle spindles
proprioceptors in muscle belly
— Adjust via changes in muscle length (stretch)
— muscle spindle reflex contracts muscle to prevent tearing of muscle tissue during overstretch
1) muscle spindles structure
composed of INTRAFUSAL MUSCLE FIBRES
— = 3-10 specialized muscle fibres, embedded within muscle belly
— ITRAFUSAL MUSCLES FIBRES are specialized skeletal muscle fibres that served as sensory receptors (PROPRIOCEPTORS)
— Normal contractile muscle tissue is called EXTRAFUSAL MUSCLE FIBRES
note difference between INTRAFUSAL and EXTRAFUSAL muscle fibres
.
innervation of Muscle spindles
1) sensory nerve endings – deliver sensory information from INTRAFUSAL FIBRES of muscle spindle to the nervous system
2) motor nerve endings
MOTOR NERVE ENDINGS of INTRAFUSAL MUSCLE FIBRES of Muscle Spindles
GAMMA MOTOR NEURONS innervate intrafusal muscle fibres
— GAMMA MOTOR NEURONS regulate sensitivity of muscle spindle to stretch stimulation
(Perhaps depending on external factors that determine muscle receptiveness to a given stretch)
— NOTE that extrafusal muscle fibres are innervated via ALPHA MOTOR NEURONS (Skeletal muscle contractions)
Gamma motor neurons and what impact their firing rate has with how sensitive a muscle spindle (w/ intrafusal fibres) becomes to stretch
increased firing rate of Gamma motor neurons results in increased sensitivity to stretch in the Muscle Spindle
—- more firing = more sensitive muscle spindle
Muscle spindle and the stretch reflex
contractile reflex in response to rapid stretching of muscle
— protects muscle from tearing, and in the event of injury results in less severe damage, such as strain
GOLGI TENDON ORGAN
at musculo-tendinous junction
— monitors tension/force at tendon
GTO reflex
inhibits muscle to protect the muscle & TENDON from damage/strain
A few muscle pathologies
1) muscular dystrophy
2) Myasthenia Gravis
3) Fibromyalgia
1) muscular dystrophy
inherited
— destroys muscle tissue leading to degeneration of skeletal muscle fibres
— COMMON type is DUCHENNE MUSCULAR DYSTROPHY (DMD) – effects almost exclusively males
common type of muscular dystrophy and mechanism
DUCHENNE muscular dystrophy
— DYSTROPHIN protein is not produced, or barely produced
— leads to tears in SARCOLEMMA during muscle contraction
signs and symptoms of Muscular dystrophy including prognosis
signs/symptoms clear by age 2-5 = lack of coordination, falling, stumbling, etc.
— most pass away by 20 years old, due to cardiac/respiratory failure
— currently, there is no cure, and stem cell & genetic research is on-going
2) Myasthenia Gravis
autoimmune disorder
— antibodies that bind to ACh receptors, at the NMJ —-> Block them from binding ACh (Acetylcholine)
myasthenia gravis signs, symptoms, prognosis
chronic, progressive weakening and fatigue of muscles
— could lead to eventual death due to paralysis of RESPIRATORY/CARDIAC muscles
— first affects muscles of face/neck/jaw – arms/legs affected later
— Drug therapy done, but no cure
—> immunosuppressants
—> cholinesterase inhibitors (CHOLINESTERASE breaks done ACh (Acetylcholine))
why does MG worsen with activity and improve with rest?
because immune system activity increases with activity
3) Fibromyalgia
IDIOPATHIC
— Pain/tenderness around the body, including muscles and related connective tissues such as ligaments, tendons, Sheaths/fascia
— diagnosed in past 20 years
— affects women more than men
— pain during rest and activity, as well as when pressure is applied
other symptoms of FM
headaches, insomnia, fatigue, depression
treatments for FM
antidepressants, NSAID, massage, physiotherapy, chiropractic heat, exercise
“abnormal pain perception processing” and FM
more sensitive to pain than people without FM
NMJ
TERMINAL END of Somatic Motor Neuron
MEETS WITH…
Skeletal muscle (@ Motor end plate)
SYNAPTIC CLEFT in b/w
“Synapse”
they “synapse” (connect) together
I.E. axon terminal synapses w/ Motor end plate
SITE for transmission of AP from nerve to muscle
“Somatic”
pertaining to body
somatic neurons
nerves/neurons that extend from brain/Spinal cord (CNS)
RESPONSIBLE for somatic movements
SOMATIC MOTOR NEURONS terminate @ SARCOLEMMA OF MUSCLE FIBRE
NMJ 2
junction b/w neuron and muscle fibre
Synaptic cleft
space b/w axon terminal and motor end plate
DIFFERENT nerves communicate via SYNAPSE
Neurotransmitters
chemicals that propagate AP signal across SYNAPTIC CLEFT
how many types of Neurotransmitters
hundreds of NTs
some excitatory, some inhibitory
Acetylcholine (ACh)
NT released @ NMJ
Presynaptic terminal
Axon terminal before synapse
ACh stored in…
pre-synaptic terminal in VESICLES
motor end plate
post-synaptic membrane @ NMJ (on muscle fibre)
motor end plate consists of…
muscle fibre Sarcolemma containing ACh receptors (ligand-gated receptors / ION CHANNELS)
the (receptors) LIGAND-GATED ION CHANNELS of motor end plate
ligand-gated
which ligand?
ACh is the ligand
SODIUM ION CHANNELS
PRESYNAPTIC TERMINAL (2)
AKA presynaptic Membrane
MOTOR NEURON, axon terminal
POSTSYNAPTIC MEMBRANE / TERMINAL
Motor end plate of muscle fibre
the process @ NMJ of AP –> Ca2+ release from Sarcoplasmic reticulum
nerve impulse arrives at AXON TERMINAL
cause VOLTAGE GATED Ca2+ Channels to open
Ca2+ causes ACh VESICLES to undergo EXOCYTOSIS
ACh goes across synaptic cleft to ligand gated Na+ Ion channels
Na+ FLOWS INTO MUSCLE FIBRE (SARCOPLASM)
INCREASE OF POSITIVE CHARGE IN CELL (DEPOLARIZATION*****)
influx of Na+ increases charge of muscle fibre
Na+ ion channels @ synaptic cleft vs. adjacent to synaptic cleft
@ synaptic cleft = LIGAND gated
Elsewhere = VOLTAGE GATED
I.e.
CHANGE in voltage in cell (DEPOLARIZATION) LEADS TO Voltage gated Na+ ION CHANNELS opening
after Na+ ligand gated and voltage gated ION CHANNELS open
AP propagated along sarcolemma into T-TUBULES (Transverse tubules)
—–> TO TRIADS –> @ Terminal Cisternae of Sarcoplasmic reticulum —> Ca2+ released from SR
Depolarization & Repolarization
depolarization = away from RMP –> less negative / more positive
repolarization = towards RMP –> less positive / more negative
Terminating AP (3 methods)
1) ACh moves out of synaptic cleft via DIFFUSION
2) ACh broken down by enzyme Acetylcholinesterase (AChE)
3) (NOT APPLICABLE TO ACh) –> Other small NTs removed from Syn Cleft via REUPTAKE
REUPTAKE
“the absorption by a presynaptic nerve ending of a neurotransmitter that it has secreted.”
Note Sodium Potassium pump
brings cell environment back to RMP
Acetylcholinesterase @ ACh – End products are…
“the end products are recycled back into the axon terminal to make new ACh molecules for the next time they’re needed”
after Ca2+ is released from SR (review)
“Ca+2 binds to troponin in the sarcoplasm causing tropomyosin to change position (revealing the myosin-binding sites on actin)
“ATP attached to myosin heads is hydrolyzed to ADP plus phosphate (energizing myosin heads and allowing crossbridges to occur)
“Muscle contraction occurs”
Botox
clinical use of botulinum toxin
“poison derived from clostridium botulism (anaerobic bacterium)”
blocks the ACh release from presynaptic motor neurons
no muscle contraction – muscle paralyzed
Botulinum toxin
one of themost lethal substances known
1 nanogram (10-9) per kilogram can kill a human
intravenous dose of just 10-7g would be fatal to a 70kg person
I.e.
0.000001g (one millionth of a gram)
heart is
hardest working muscle in body
how many beats per day
over 100,000 times
how many beats per minute
average 75
cardiac muscle tissue is ____ and ____
striated
involuntary
heart uses which ion
Ca2+ from SR and Interstitial fluid
why heart prolonged contraction
high levels of Ca2+
how much longer contraction?
10-15 times longer for cardiac muscle tissue
cardiac muscle tissue has auto-_____
autorhymicity / auto-excitability
NO NERVE SUPPLY NEEDED
self-generated APs
pace-maker cells
Self-excitable
RHYTHMIC waves of contraction to adjacent cells throughout heart
Where are pacemaker cells
@ 2 nodes:
1) SINOATRIAL NODE
2) ATRIOVENTRICULAR NODE
= Automatic rhythmic contractions of upper/lower portions of heart
SMOOTH MUSCLE IS ____ and ____
Non-striated & Involuntary
is smooth muscle autorhythmic
can be autorhythmic – but is also influenced by NERVOUS system
how does AP travel b/w smooth muscle cells
AP in one smooth muscle fibre transmitted to neighbouring fibres —-> CONTRACTION IN UNISON
how nervous system influence smooth muscle
digestive control centre in brain send nerve signal to stomach / small intestine
ONLY ONE/FEW ACTION POTENTIALS ARE NEEDED TO STIMULATE ENTIRE ORGAN TO CONTRACT
Structure of smooth muscle
THICK FILAMENTS ATTACHED TO DENSE BODIES (similar functionally to Z-disc)
INTERMEDIATE FILAMENTS interconnect Dense Bodies —> Receive tension from contraction
Caveolae of Smooth Muscle tissue (AND NOTE about Ca2+ & SR)
pouchlike invagination containing Ca2+
LESS SR in smooth muscle cells – NO TRANSVERSE TUBULES
I.e.
MORE RELIANCE ON EXTRACELLULAR Ca2+ than intracellular (from SR)
Calmodulin and Smooth muscle tissue
protein in smooth muscle that binds to Ca2+
REGULATORY protein –> similar to TROPONIN in skeletal muscle
CALMODULIN eventually activates MYOSIN heads –> contraction occurs
what happens mechanically when smooth muscle contracts?
MYOSIN/ACTIN complex pulls on DENSE BODIES, which pulls on INTERMEDIATE FILAMENTS —> cell contracts
3 energy systems
Creatine phosphate (CP) aka Phosphagen System
Anaerobic glycolysis
Aerobic respiration aka Oxidative System
“All 3 Systems active at any given time, but magnitude and contribution of each depends on INTENSITY and DURATION of activity”
Creatine phosphate (CP) system
high energy bond in creatine phosphate (CP) aka phosphocreatine (PCr) to create ATP
ATP + creatine –> creatine phosphate + ADP –> ATP + creatine
where is creatine produced
liver, kidneys & pancreas, then transferred to muscles.
creatinine
breakdown product of creatine is creatinine, a metabolite excreted in the urine
creatine phosphate system duration
Provides ATP for short-term (15 secs), high intensity exercises
CREATINE KINASE
ENZYME
transfers a phosphate (PO4) group from ATP to creatine making creatine phosphate (reversible reaction)
elevated Creatine kinase
Elevated CK-MM = skeletal muscle damage
Elevated CK-MB (myoglobin?) = cardiac muscle damage
ANAEROBIC GLYCOLYSIS
Takes place in the sarcoplasm
breakdown of glucose to yield 2 x pyruvate molecules
2 molecules of ATP & 2 molecules of pyruvic acid (pyruvate?)
pyruvate can…
can go to aerobic respiration to form more ATP if oxygen is present (aerobic)
can get converted into lactic acid if no oxygen is present (anaerobic)
pyruvate duration
ATP for moderate to high intensity, short term exercise
2 minutes (30-40 seconds of maximum contraction)
pyruvate –> lactic acid (anaerobic process) —> CORI CYCLE
ATP synthesis occurs faster – is limited in duration
inefficient:
6 ATP used, 2 ATP gained
Cori cycle
@ MUSCLE:
glucose –> 2 ATP + 2 Pyruvate (GLYCOLYSIS)
2 Pyruvate –> 2 Lactate
@ LIVER:
2 lactate –> 2 pyruvate + 6ATP –> GLUCOSE (Via Gluconeogenesis)
Back to muscle:
Glucose goes to muscle
Lactic acid buildup misunderstood
Not entirely responsible for muscle burn during exercise
(Protons created during breakdown of ATP created at a faster rate then can be cleared –> H+ ions)
Lactic acid 3 myths
Myth 1:
“Burn” from lactic acid
—> Not from lactic acid –> from H+ ions during ATP breakdown = increased acidity
Myth 2:
Lactic acid is waste
–> NOT waste –> 75% is recycled –> lactate to glucose
Myth 3:
lactic acid causes DOMS
–> lactic acid flushed in 30-60mins –> DOMS is via microtrauma
aerobic respiration
mitochondria
oxygen
aerobic respiration and pyruvate
Uses pyruvic acid
LARGE AMOUNT OF ATP via KREB’S CYCLE and ELECTRON TRANSPORT CHAIN
aerobic respiration can also use
FATTY ACIDS
AMINO ACIDS
Duration of aerobic respiration
several minutes to hours
ATP generated
30-32 ATP
+ Heat, CO2, & H2O
oxygen for aerobic respiration
HEMOGLOBIN (blood) & MYOGLOBIN
3 systems – durations
0-6s = Phosphagen = very intense
6-30s = phosphagen & Fast glycolysis = intense
30s-2m = fast glycolysis = heavy
2-3m = fast glycolysis & oxidative = moderate
3+ mins = oxidative = light
Muscle fatigue – possible reasons
1) O2 lack
2) CO2 buildup
3) ATP lack (no glycogen)
(Or depleted Phosphagen system)
4) metabolic waste buildup
phosphagen depletion / repletion
rapidly depleted (15 secs)
fatigue partially from phosphagen depletion
repletion = within 8 minutes (Via aerobic metabolism and glycolysis)
phosphagen pre-exercise concentrations increased via
1) supplementation
2) Aerobic and anaerobic training / conditioning
glycogen depletion / repletion (HOW MUCH GLYCOGEN?
300-400g in muscle tissue
70-100g in liver
how glycogen pre-exercise concentration increase?
1) aerobic / anaerobic conditioning
2) carb-loading
how long till glycogen levels depleted
90+ minutes exercise
instead of carb-loading
replace lost glycogen during mid-exercise carbs
drinks, gels, bars etc
oxygen replenishment, oxygen debt, EPOC
Oxygen debt
recovery oxygen
EPOC (excess post-exercise oxygen consumption)
what is excess oxygen during EPOC used for
Resynthesis of ATP and creatine phosphate
Resynthesis of glycogen from lactate
tissue oxygen resaturation
venous blood oxygen resaturation
skeletal muscle oxygen resaturation
myoglobin oxygen resaturation
motor unit
somatic motor neuron and all muscle fibres it innervates
motor unit size varies
1 muscle fibre per neuron
> 3000 muscle fibres per neuron
motor unit average size
1 neuron for 150 muscle fibres
motor unit size vs precision
more precise movements = smaller motor unit (less muscle fibres per neuron)
muscle twitch length vs AP length
1-2 msec = AP
20-200 msec = muscle twitch
muscle twitch define
brief contraction of muscle fibres in motor unit via AP of neuron
muscle twitch duration varies
E.g.
eye muscle = quick
gastrocnemius = less quick
soleus = even less quick
Also note –> more precise & more delicate muscle (like eye muscle = smaller motor unit)
fasciculation
involuntary contraction of motor unit –> visible under skin
can occur under normal conditions or under pathological conditions of nervous system
motor unit contraction stages
1) latent period
2) contraction period
3) relaxation period
4) refractory period
latent period =
AP via sarcolemma –> Ca2+ released via SR – BUT NO TENSION YET***
contraction period
Ca2+ to troponin, tropomyosin change shape, crossbridge form, contraction occur
relaxation period
cross bridge break
Ca2+ taken up and restored
relative and absolute refractory period
absolute = no
relative = requires higher than usual stimulus (stronger AP?) to contract
Frequency of stimulus (AP?) as a variable
determines PEAK TENSION
how is tension determined in skeletal muscle?
1) amount of tension produced by each muscle fibre (VIA FREQUENCY OF STIMULATION?)
2) number of muscle fibres stimulated
Frequency of stimulation and Myogram
1) wave summation
2) Unfused tetanus
3) fused/complete tetanus
wave summation
second stimulus before muscle fully relaxes
SECOND CONTRACTION IS STRONGER THAN FIRST
I.e.
Wave summation
wave summation = stronger contractions —> up to ___x greater than single twitch
up to 5x stronger contraction
unfused tetanus
sustained contraction, but muscle fibre partially relaxing between summation (I.e. Wavering)
stimuli arriving @ 20-30 times/sec
Unfused tetanus = jagged curve on myogram
fused/complete tetanus
completely sustained –> muscle fibre has no time to relax partially
stimuli/AP arriving @ 80-100 times/sec
why fused?
sustain long/powerful contraction
motor unit recruitment
INCREASE OF ACTIVE MOTOR UNITS
–> “recruited”
Neuromuscular system efficiency –> greater efficiency of nervous system –> higher rate of stumuli/AP –> higher peak tension of single muscle fibre & muscle fibres within motor unit
–> AND HIGHER NUMBER OF MUSCLE FIBRES / Motor units activated —> = higher amount of tension produced
motor unit recruitment & movement/fatigue
smooth movement
delays muscle fatigue
motor unit recruitment – which fibres first?
smaller fibres recruited first
–> larger fibres recruited when duration/amount of force increase
flaccid paralysis
loss of muscle tone
hyporeflexia
muscle atrophy
why flaccid paralysis
Lower Motor Neuron injury/damage
Trauma
Nervous system disorders (e.g. ALS)
Guillain-Barre Syndrome
Polio
Nerve compression
Myasthenia Gravis
spastic paralysis
increased muscle tone
hyperreflexia
Upper motor neuron injuries/damage:
stroke
Multiple sclerosis
traumatic brain injury
spinal cord injury
cerebral palsy
Rigidity (“RIGOR”)
increase in muscle tone
no effect on reflexes
muscle cannot relax
can occur w/ tetanus (disease caused by bacterium Clostridium tetani)
tetanus can also cause tetany
tetany
“a condition marked by intermittent muscular spasms, caused by malfunction of the parathyroid glands and a consequent deficiency of calcium.”
muscle tone
amount of tightness/tension of muscle at rest
via small amount of subconscious contraction of motor units
muscle tone, blood vessels, GI organs, postural muscles
for maintaining adequate BP
for facilitating digestion/peristalsis
for maintaining posture
