Chapter 10 Flashcards
Functions of Muscle Tissue (4)
1) excitable/irratable →
2) **contractile **→ can shorten in length
3) **extensible **→ extend/stretch
4) **elastic **→ can return to original shape
Other Functions of Muscle Tissue (5)
1) create motion
2) stabilize body positions & maintain posture
3) store substances within body using sphincters
4) move substances by contractions
5) generate **heat **through **thermogenesis **
(3) types of muscular tissue
1) Skeletal
2) Cardiac
3) Visceral
1) Skeletal muscle
- location
- function
- appearance
- control
- skeleton
- movement, heat posture
- striated, multi-nucleated (eccentric)
- fibers parallel
- voluntary
2) Cardiac muscle
- location
- function
- appearance
- control
- heart
- pump blood continuously
- striated, 1 central nucleus
- involuntary
3) **Visceral **muscle
- location
- function
- appearance
- control
- GI tract, uterus, eye, blood vessels
- peristalsis, BP, pupil size, erects hairs
- no striations, 1 central nucleus
- involuntary
Organization of Muscle Tissue
epimysium, perimysium & endomysium
→ all continuous with CT that forms tendons & **ligaments **
**→ **extend from **fascia **
Fascia
- function
dense sheet/broad band of irreg CT that lines body wall/limbs & supports/surrounds muscles/other organs
- holds muscles of similar functions together
- (connects muscles to other muscles to form groups)
Epimysium
outermost layer of **dense irregular CT **
- encircles entire muscle
Perimysium
layer of dense irregular CT surrounding groups of 10-100 muscle fibers seperating them in bundles (fascicles)
Endomysium
mostly reticular fibers
- seperates individual muscle fibers
What seperates muscle from skin?
Subcutaneous layer
Tendon
ropelike structure that extends beyond muscle fibers to attach muscle to periosteum of bone
Sarcolemma
plasma membrane of muscle cell beneath endomysium
- encloses sarcoplasm & myofibrils (striated)
Sarcoplasm
**cytoplasm **of muscle fiber within sarcolemma
Myofibrils
striated contractile organelles of skeletal muscle
(in the sarcoplasm)
Transverse (T) Tubules
tiny invaginations of sarcolemma filled with interstitial fluid *(open to outside of fiber) *
- tunnel in from surface toward center of each muscle fiber
Triad
T tubule + 2 terminal cisternae
Sarcoplasmic Reticulum (SR)
fluid-filled system of membranous sacs
- encircles each myofibril
- has **terminal cisternae **
- stores Ca2+ in relaxes muscle fiber
Terminal Cisternae
dilated end sacs of SR that butt against T tubule from both sides
What triggers muscle contraction?
Release of Ca2+ from **terminal cisternae **of **SR **
Sarcomere
basic functional units of myofibrils
- arrangement of thick & thin filaments sandwiched between 2 Z discs
Myofibrils
- composed of?
filaments
- thick filaments (myosin)
- thin filaments (actin)
Z disc
*narrow, plate-shaped region of dense protein material *
- seperates one sarcomere from the next
Sarcomere extends from?
one Z disc to the next Z disc
Extent of overlap of thick & thin filaments depends on?
whether muscle is contracted, relaxed or stretched
A band
dark middle region
- extends length of thick filaments
(includes part of overlap with thin filaments)
I band
lighter, less dense area
- contains rest of thin filaments
but NO thick filaments
- Z disc passes through center
Zone of overlap
Toward each **end of A band **
- where thin & thick filaments lie side by side
H Zone
center of A band containing ONLY thick filaments
M line
center of **H zone **
marks middle of sarcomere
formed by supporting proteins that hold thick filaments **together **
Z line is really __ __ when considered in 3D
Z disc
Muscle Proteins
**Myofibrils **built from (3) groups of proteins
- functions?
1) **Contractile **→ generate force during contraction
2) Regulatory→ help switch contraction process on/off
3) Structural→ keeps thick & thin filaments in proper alignment & links myofibrils to sarcolemma & ECM
1) Contractile Proteins
Actin
Mysoon
2) Regulatory Proteins
troponin
tropomyosin
3) Structural Proteins
Titan
Dystrophin
Myomesin
Myosin
- parts
main component of **thick **filaments
-functions as motor protein in all 3 types of muscle tissue
**myosin tail → **twisted gold club handles
- point toward M line in center of sarcomere
- form **shaft **
**myosin head **→ 2 projections of each myosin molecule
Actin
main component of **thin filaments **(anchored to Z discs)
- bead of pearls twisted into helix
myosin-binding site → where myosin head attaches
Tropomyosin
strands of **tropomyosin **cover **myosin-binding site **on actin
- held together by **troponin **molecules
Troponin
hold **tropomyosin strands **in place
When Ca2+ binds to troponin?
**troponin **undergoes change in shape
→ moves **tropomyosin **away from **myosin-binding sites **on actin
- muscle contraction begnis as myosin binds to actin
Structural Proteins → functions? (4)
contribute to **alignment, stability, elasticity & extensibility **of myofibrils
Titin
3rd most plentiful protein in muscle (after actin & myosin)
- extends from Z disc to M line & accounts for much of the elasticity of myofibrils
Dystrophin
links filaments to integral membrane proteins
reinforces **sarcolemma & **transmits tension from **sarcomeres **to tendons
Myomesin
binds to titin & links adjacent thick filaments
- forms **M line **
Troponin-Tropomyosin Complex
can slide back & forth depending on presence of Ca2+
- slides down into “gutters” of actin molecules ot unblock **myosin-binding sites **on actin
Levels of **Organization **within Skeletal Muscle
skeletal muscle
fascicle
muscle fibers (cells)
myofibrils
filaments
Sliding-Filament Mechanism
muscle contraction occurs b/c myosin heads attach to & walk along thin filaments at both ends of sarcomere
- progressively pulling thin filaments towards M line
- thin filaments meet at center of sarcomere
What happens to each band/zone as muscle contracts?
H Zone → disappears (thin filaments overlap more & more)
**I Band → **shortens & disappears (Z discs come closer together)
A Band → does not shorten (extends length of thick filaments which does not shorten)
Contraction Cycle
repeating sequence of events that cause filaments to slide
Contraction Cycle
at onset of contraction…
**SR **releases Ca2+ into sarcoplasm
→ bind to troponin → moves tropomyosin away from myosin-binding sites on actin
→ once binding sites are free - **contraction cycle **begins
Contraction Cycle
**- (4) steps **
1) ATP hydrolysis
2) **Attachment of myosin **to **actin **to form cross-bridges
3) Power stroke
4) Detachment of myosin from actin
1) ATP hydrolysis
myosin head include ATP-binding site & ATPase
hydrolysis rxn reorients & energizes myosin head
- ADP & P group still attached to myosin head
2) Attachment of myosin to actin to form cross-bridges
energized myosin head attached to myosin-binding site on actin (cross-bridge)
- releases P group
3) Power stroke
after cross-bridges form, power stroke occurs
during power stroke:
- site on cross-bridge where ADP is bound opens
- cross-bridge rotates & releases ADP
- cross-bridge generates force as it rotates towards center of sarcomere, sliding thin filament past thick filament toward M line
4) Detachment of myosin from actin
at end of power stroke, **cross-bridges **remain firmly attached to actin **until it binds another ATP molecule **
- as ATP binds to ATP-binding site on myosin head, myosin head detaches from actin
Steps of Contraction Cycle (4)
- general concept
1) myosin heads hydrolyze ATP → become reoriented & energized **
2) myosin heads bind to actin forming cross-bridges
3) mysoin cross-bridges rotate toward center of sarcomere (power stroke**)
4) as myosin head binds ATP, cross-bridges detach from actin
Rigor Mortis
muscles remain in a state of rigidity because no ATP to bind to myosin head
- can’t detach from actin
Length-Tension Relationship
indicates how forcefulness of muscle contraction depends on length of sarcomeres within muscle before contraction begins
max tension occurs when zone of overlap b/w thick & thin extends from edge of H zone to 1 end of thick filament
understretched - compressed thick filaments
overstretched - limited contact b/w actin & myosin
Neuromuscular Junction (NMJ)
synapse between somatic motor neuron & **skeletal muscle fiber **
Somatic motor neurons
neurons that stimulate muscle fibers to contract
Somatic Motor Neuron - axon
extends from brain/spinal cord to group of skeletal muscle fibers
Synapse
region where communication occurs between 2 neurons or between neuron & target cell
Synaptic cleft
small gap at most synapses that seperates the 2 cells
Neurotransmitter
chemical released that transmit signals across **synapse **
Axon Terminal
End of **motor neuron **at NMJ
Synaptic end bulbs
neural part of NMJ
- axon terminal divides into cluster of synaptic end bulbs*
- expanded distal end of axon terminal that contains **synaptic vesicles **
Synaptic Vesicles
Hundreds of membrane-enclosed sacs in synaptic end bulbs that are suspended in the cytosol
- contain **Acetylcholine (ACh) **
Acetylcholine
neurotransmitter within synaptic vesicles that are released at NMJ
Motor End Plate
muscle fiber part of NMJ
region of sarcolemma opposite of synaptic end bulbs
- **contain millions of **ACh receptors **(integral transmembrane proteins) - **ligand-gated ion channels **
- gated Na+ channels that respond to ACh
Nerve impulse (nerve AP) elicits muscle action potential in **(4) steps **
1) Release of ACH
2) Activation of ACh receptors
3) Production of muscle action potential
4) Termination of ACh activity
1) Release of ACh
(7)
nerve impulse arrives at synaptic end bulbs
stimulates voltage‐gated channels to **open **
b/c [Ca2+] is higher in ECF, Ca2+ flows inward
Ca2+ stimulates synaptic vesicles to undergo exocytosis
synaptic vesicles fuse with motor neuron’s PM
release ACh into synaptic cleft
diffuses across synaptic cleft b/w motor neuron & motor end plate.
2) Activation of ACh receptors
2 ACh molecules bind to receptor on **motor end plate **→ ion channel **opens **
Na+ flows inward
3) Production of Muscle AP
inflow of Na2+ → inside of muscle fiber **more (+) **
→triggers muscle AP
→propogates along sarcolemma into T tubules
→ causes SR to release Ca2+ into sarcoplasm
muscle fiber contracts
4) Termination of ACh activity
ACh broken down by **acetylcholinesterase (AChE) **
- attached to collagen fibers in ECM of synaptic cleft
when APs in motor neuron stop…
ACh no longer released - broken down in synaptic cleft
**Ca2+ moves form sarcoplasm back into SR **
Ca2+ release channels in SR close
Where is NMJ?
usually near midpoint of skeletal muscle fiber
- muscle APs that arise at NMJ propogate towards ends of fiber
location of
- Presynaptic membrane
- postsynaptic membrane
1) on neuron
2) motor end plate on muscle cell
Conscious thought (to move muscle) causes?
activation of motor neuron
→ release of neurotransmitter acetylcholine (ACh) at NMJ
→ Enzyme Acetylcholinesterase breaks down ACh after short period of time
ACh Receptors
on **ligand-gated Na+ channels **on motor end plate
Muscle AP
- phases (3)
Resting Potential → (-70 mV)
ACh stimulus at motor end plate → (-55 = Threshold)
Depolarizing phase → (+30) - Na+ gates open → inflow
Action Potential
Repolarizing phase → back to (-70) - K+ gates open → outflow
(Na+ gates close)
**After-hyperpolarizing **phase → K+ channels take too long to close
Generating AP on muscle membrane involves transfer of info from:
Electrical signal (down neuron) → chemical signal (at NMJ) → electrical signal (depolarization of sarcolemma)
Excitation-Contraction Coupling
(8) steps
1) AP at axon terminal of motor neuron → release of ACh
2) **ACh **across synaptic cleft → binds to receptors in motor end plate → triggers muscle AP
3) AChE destroys ACh so only more ACh for AP
4) muscle AP: T Tubules → opens Ca2+ release channels in SR → Ca2+ into sarcoplasm
5) Ca2+ binds to troponin
6) Contraction Cycle
7) Ca2+ release channels in SR **close **→ transport pumps restore low Ca2+ in sarcoplasm
8) T-T complex back into position
9) muscle **relaxes **
**Excitation-Contraction Coupling **
- general process (6)
- Thought process going on in brain
- AP arriving at NMJ
- Regeneration of AP on muscle membrane
- Release of Ca2+ from SR
- Sliding of thick on thin filaments in sarcomeres
- Generation of muscle tension (work)
Role Players in Excitation-Contraction Coupling
(16)
**brain →motor neuron **→ **ACh **→AChE
ACh receptors → **Na+/K+ channels ** → Na+ flow in → K+ flow out
Regenerate AP →T-Tubules → SR → Ca2+ release → T/T
ATP →myosin binding → filaments slide → muscles contract
Sources of Muscle Energy (4)
1) stored ATP → 3 secs
2) Energy from **Creatine Phosphate → 12 secs
3) Anaerobic Glucose Use (Glycolysis) → 30-40 s
4) Aerobic ATP production (aerobic cellular resp**) → mins-hours
Creatine Phosphate
relaxed muscle:
Creatine + ATP → Creatine Phosphate + ADP
contracting muscle:
Creatine Phosphate + ADP → Creatine + ATP
ATP → Energy for muscle contraction + ADP
Anaerobic Glucose Use
Anaerobic Cellular Respiration = Anaerobic Glycolysis
Muscle Glycogen or Blood Glucose
Glucose → 2 ATP + 2 Pyruvic Acid → 2 Lactic Acid (→ into blood)
Aerobic ATP production
**Aerobic Cellular Respiration **
FAs (from adipose cells)
Pyruvic acid (from glycolysis)
Amino acids (from protein breakdown)
Oxygen (from hemoglobin in blood/myoglobin in muscle fibers)
→ **36 ATP **+ CO2 + H2O + heat
Muscle Fatigue
inability of a muscle to maintain force of contraction after prolonged activity
Types of Fatigue (2)
1) Central
2) Peripheral
1) Central Fatigue
**before actual muscle fatigue begins **
- feeling tired & wanting to stop activity
- caused by changes in **CNS **
2) Peripheral Fatigue
inability to supply sufficient energy to contracting muscles to meet increased energy demands
Sources of Fatigue (6)
- Inadequate release of Ca2+ from ** SR**
- Reduced O2
- Reduced Cr Ph
- Reduced glycogen
- Buildup of H+
- Problems with Ach receptors or release
Oxygen Debt (**Excess Post-Exercise Oxygen Consumption - EPOC) **
amount of O2 repayment required after exercise in skeletal muscle to:
- replenish ATP, Creatine phosphate & myoglobin
- convert lactic acid back into purivate (so it can be used for CAC to replenish ATP)
Motor Unit
composed of **motor neuron + all muscle cells it innervates **
Motor Units
1) high precision
2) low precision
1) fewer muscle fibers per neuron
- laryngeal & extraocular muscles (2-20)
2) many muscle fibers per neuron
- thigh muscles (2,000-3000)
Force of muscle contraction depends on (4)
frequency of stimulation - rate at which APs arrive at NMJ (# of impulses/second)
size of motor units
# of motor units activated
type?
Activities requiring extreme precision (subtle/rapid movements of eye) involve muscles with?
small motor units (1-4 muscle fibers/neuron)
All-or-none principle of muscle contraction
(2)
When individual muscle fiber is stimulated to depolarization & AP propagates along its sarcolemma → must contract to it’s full force
Also, when single motor unit is recruited to contract, all muscle fibers in that motor unit must all contract at the same time
twitch contraction
the brief contraction of all muscle fibers in motor unit in response to single AP in its motor neuron
Latent period
brief delay as AP sweeps aover sarcolemma & Ca2+ released from SR (point of no return)
2 msec
- delay between application of stimulus & beginning of contraction
Contraction Period
10-100 msec
Ca2+ binds to troponin, myosin-binding site on actin exposed
cross-bridges form
peak tension develops in muscle fiber
Relaxation Period
10-100 msec
Ca2+ **actively transported **back in SR
myosin-binding sites covered again by tropomyosin
myosin heads detach from actin
tension in muscle **decreases **
Refractory Period
5 msec (skeletal) - 300 msec (cardiac)
**temporary loss of excitability **
muscle fibers in motor unit won’t respond to stimulus during this short time
Wave Summation
phenomenon in which stimuli arriving at dif times causes **larger contractions **
- after refractory period is over but **before skeletel muscle has relaxed **
(2nd contraction stronger than first)
Unfused (incomplete) Tetanus
skeletal muscle fiber is stimulated at rate of **20-30 times/sec **
- can only partially relax between stimuli
result is sustained but wavering contraction
Fused (Complete) Tetanus
when skeletal muscle fiber is stimulated at rate of **80-100 times/sec **
- does not relax at all
- result = sustained contraction in which individual twitches can’t be detected
Applying increased numbers of APs to muscle fiber (or **fascicle/muscle**/muscle group) results in?
fusion of contractions (tetanus) & performance of useful work
Motor Unit Recruitment
process in which **# of active motor unit **increases
- allows muscle to accomplish increasing gradations of contractile strength
Muscle FIber Types by **appearance (2) **
1) Red Muscle Fibers
2) White Muscle Fibers
1) Red Muscle Fibers
high myoglobin content
more mitochondria
more energy stores
greater blood suppluy
(dark meat)
2) **White **muscle fibers
less myoglobin
less mitochondria
less blood supply
(white meat)
Types of Muscle Fibers by function
1) Slow Oxidative
2) Fast Oxidative-Glycolytic
3) Fast Glycolytic
1) Slow Oxidative
smallest, dark red
least powerful
very fatigue resistant
endurance (walking)
2) Fast Oxidative-Glycolytic
intermediate, red-pink
moderately resistant to fatigue
jogging/most weightlifting activities
3) Fast Glycolytic
large, white
powerful
intense anaerobic activity of short duration
Within a particular motor unit, skeletal muscle fibers are…
all the same type
Different motor units in muscle are recruited depending on?
task being performed
Muscle Contractions
(2) types
1) Isotonic
2) Isometric
1) Isotonic Contraction
tension (force of contraction) developed in muscle remains constant while muscle changes length
- results in movement
2) Isometric Contraction
tension generated not enough to exceed resistance of object being moved
tension = resistance
muscle does NOT change length
(2) types of Isotonic Contraction
1) Concentric
2) Eccentric
1) **Concentric **Isotonic Contraction
tension generated > resistance of object
muscle shortens while generating force
2) **Eccentric **Isotonic Contraction
length of muscle **increases **
contraction in which muscle tension < resistance
Aging - Muscle
partly due to decreased levels of physical activity…
humans undergo slow, progressive loss of skeletal muscle mass that is replaced largely by fibrous CT & adipose tissue
Muscle Strength
age 85 **vs **age 25
muscle fiber types
Muscle strength at 85 is about 1/2 that at age 25
Compared to other 2 fiber types, relative # of slow oxidative fibers appears to increase
Sarcopenia
degenerative loss of skeletal muscle mass, quality, and strength associated with aging
(0.5–1% loss per year after age 25)
