Chapter 10 Muscular Tissue Flashcards
Muscular tissue and homeostasis
Contributes by
- Producing movement
- Moving substances through body
- Producing heat to maintain body temperature
Study of muscles
Myology
Three types of muscle tissue
Skeletal
Cardiac
Smooth
Skeletal muscle tissue..
Move bones
Striated (alternating light and dark)
Mainly voluntary
Subconsciously (diaphragm to breathe)
Cardiac muscle tissue..
Only in heart Most of heart wall Striated Involuntary Has natural pacemaker
Autorhythmicity
Built in rhythm in pacemaker
Smooth muscle tissue..
Located in walls of hollow internal structures (like blood vessels)
Nonstriated
Usually involuntary
Muscular tissue four main functions
- Produce body movements
- Stabilizing body positions
- Storing and moving substances within the body
- Generating heat
Producing body movements
Movements of the whole body and localized movements..
Requires muscular contractions,
Which rely on integrated functioning of skeletal muscles, bones, and joints
Stabilizing body positions
Skeletal muscle contractions stabilize joints and help maintain body positions
Postural muscles contract continuously when awake, like holding the head upright
Storing and moving substances within the body
-Storage held by sphincters
-Cardiac muscle contractions pump blood
-smooth: sperm, oocytes, bile and enzymes (GI), urine
Skeletal: lymph flow, return of blood to heart
Generating heat
As muscular tissue contracts, it produces heat (thermogenesis)
Maintain normal body temperature
Involuntary (shivering)
Properties of muscular tissue
Electrical excitability
Contractility
Extensibility
Elasticity
Electrical excitability
Ability to respond to certain stimuli by producing electrical signals called ‘action potentials (impulses)’
In muscles: muscle action potentials
In nerve: nerve “ “
Autorhythmic electrical signals arising in muscular tissue
Chemical stimuli, such as neurotransmitter a released by neurons, hormones distributed by blood, or even local changes in pH.
Contractility
Ability of muscular tissue to contract forcefully when stimulated by an action potential
When a skeletal muscle contracts, it generates tension while pulling on its attachment points
In some muscle contractions, the muscle develops tension but does not shorten
Extensibility
Ability of muscular tissue to stretch, within limits, without being damaged
The connective tissue within muscle limits the range of extensibility and keeps within contractile range of muscle cells
Smooth muscle is normally subject to the greatest amount of stretching
Elasticity
Ability of muscular tissue to return to its original length and shape after contraction or extension
Skeletal muscle tissue
Each skeletal muscle - separate organ
composed of hundreds to thousands of cells, called muscle fibers
Muscle cell = muscle fiber
Skeletal muscle contain connective tissue surrounding muscle fibers and whole muscles and blood vessels and nerves
Subcutaneous layer (hypodermis) Aid in muscle function..
- Separates muscle from skin
- areolar and adipose tissue
- Pathway for nerves, bv’s, lymphatic vessels to enter in/out of muscles
- adipose stores most of triglycerides in body
- insulating layer/protects muscles from trauma
Fascia
Dense sheet or broad band of irregular connective tissue that lines the body wall and limbs and supports and surrounds muscles and other organs
Holds muscles with similar movements together
Allows free movement of muscles
Carries nerves, blood vessels, and lymphatic vessels
Fills spaces between muscles
Three layers of connective tissue extend from fascia to protect and strengthen skeletal muscle
Epimysium
Perimysium
Endomysium
Epimysium
Outer layer encircling entire muscle.
Dense irregular connective tissue
Perimysium
Surrounds groups of 10 to 100 or more muscle fibers, separating them into bundles called fascicles
Endomysium
Penetrates the interior of each fascicle and separates individual muscle fibers from one another.
Mostly reticular fibers.
Aponeurosis
Connective tissue elements extend as a broad, flat sheet
Fibromyalgia
Chronic, painful, nonarticular rheumatic disorder that affects the fibrous connective tissue components of muscles, tendons, and ligaments.
Tender points
Somatic motor neuron
Stimulate skeletal muscle contractions
Has threadlike axon that extends from the brain or spinal cord to a group of skeletal muscle fibers
Branching to different skeletal muscle fibers
Blood capillaries in muscular tissue
Plentiful
Bring in oxygen and nutrients and remove heat and waste products of muscle metabolism
Sarcolemma
Plasma membrane of muscle cell
Transverse tubules
Thousand of tiny invaginations of sarcolemma, tunneling from surface toward center of each muscle fiber
Filled with interstitial fluid
Muscle action potentials travel along sarcolemma and through T tubules
-ensures action potential excites all parts of the muscle fiber
Sarcoplasm
Cytoplasm of the muscle fiber
Includes substantial amount of glycogen
-for synthesis of ATP
Contains red colored protein (myoglobin)
-only in muscles/binds oxygen molecules that diffuse into muscle fibers from interstitial fluid
Myoglobin releases oxygen needed by mitochondria for ATP production
Mitochondria lie in rows throughout muscle fiber, strategically close to contractile muscle that use ATP during contraction so that ATP can be produced quickly
Myofibrils
“Little threads in sarcoplasm”
The contractile organelles of skeletal muscle
Sarcoplasmic reticulum
Fluid filled system of membranous sacs, encircling each myofibril
Terminal cisterns
Dilated end sacs of the Sarcoplasmic reticulum
Triad
Formation of a transverse tubule and the two terminal cisterns on either side of it
Denervation atrophy
If nerve supply is disrupted or cut
Over a period of 6 months to 2 years, the muscle shrinks to about 1/4 the original size and it’s fibers are irreversibly replaced by fibrous connective tissue
Microscopic organization of skeletal muscle
During embryonic development
- myoblasts form muscle fiber
- loses ability to cell divide, except satellite cells
- sarcolemma encloses sarcoplasm and myofibrils
- Sarcoplasmic reticulum wraps around each myofibril
- thousands of T tubules invaginate from sarcolemma to center of muscle
Filaments
Within myofibrils
Involved in contractile process
Around compartments (sacromeres)
-z discs separate sacromeres
A band
Darker middle part of sacromere
I band
Lighter less dense area than A band containing the rest of thin filaments but no thick filaments
H zone
Narrow, in center of A band, contains thick but no thin filaments
M Line
Center of H zone
Proteins of myofibrils
Contractile proteins - generate force during contraction
Regulatory proteins - help switch the contraction process on and off
Structural proteins - keep thick and thin filaments in proper alignment, give elasticity and extensibility, and link the myofibrils to sarcolemma and extra cellular matrix
Two contractile proteins
Myosin - main component of thick filaments and functions as a motor protein in all three types of muscle tissue
Heads point to M line
Actin - main component of thin filaments, has myosin-binding site where myosin heads bind during contraction
Regulatory proteins
Tropomyosin - tropomyosin blocks myosin from binding to actin by covering myosin binding site
Tropomyosin strands are held in place by troponin molecules
Structural proteins
Titin a-Actinin Myomesin Nebulin Dystrophin
Titin
Connects Z disc to M line
Stabilize thick filament position
Stretch and spring back
a-Actinin
In Z disc
Connects actin molecules to Titin
Myomesin
Form M line
Bind Titin and adjacent thick filaments
Nebulin
Wraps around thin filament
Anchor thin filament to Z discs
Regulates length of thin filament
Dystrophin
Links thin filaments to integral membrane proteins in sarcolemma
- which are attached to CT matrix surrounding muscle fibers
Thought to help reinforce sarcolemma and help transmit tension generated by sacromeres to tendons
Sliding filament mechanism
Myosin heads attach and walk along the thin filaments and both ends of a sacromere
I band and H zone disappear
Contraction cycle
At onset of contraction
The Sarcoplasmic reticulum release Calcium ions into sarcoplasm
They bind to troponin
-cause tropomyosin to move away from myosin binding sites on actin
Contraction cycle steps
ATP hydrolysis
Attachment of myosin to actin to form cross-bridges
Power stroke
Detachment of myosin from actin
ATP hydrolysis
Myosin head includes ATP binding site and an ATPase, an enzyme that hydrolyzes ATP into ADP and a phosphate group
Reorients and energizes myosin head
Attachment of myosin to actin to form cross-bridges
Energized myosin head attaches to myosin binding site on actin and releases the previously hydrolyzed phosphate group
When myosin heads attach to actin during contraction, they are referred to as cross-bridges
Power stroke
The site on the cross-bridge where ADP is still bound opens.
As a result, the cross bridge opens and releases the ADP.
The cross-bridge generates force as it rotates towards the center of the sacromere, sliding the thin filament past the thick filament toward the M line.
Detachment of myosin from actin
At the end of the power stroke, the cross bridge remains firmly attached to actin until it binds another molecule of ATP, causing myosin head to detach from actin
Excitation-contraction coupling
As muscle action potential propagates along the sarcolemma and into T tubules,
It causes Calcium release channels in SR membrane to open.
-Ca2+ flows out SR to sarcoplasm
Ca2+ rises 10fold
Ca ions combine w/ troponin causing a change in its shape
-moves tropomyosin to move away from myosin-binding sites on actin
Ca2+ active transport pumps
Use ATP to move Ca2+ constantly from sarcoplasm into SR
Calsequestrin
Molecules of calcium-binding protein inside the SR.
Rigor mortis
After death cell membranes leak
Ca2+ leak from SR to sarcoplasm
-allow myosin heads to bind to actin
ATP synthesis ceases shortly after breathing stops (cross bridge cannot detach from actin)
Muscles in a state of rigidity
Begins 3-4 hours after death
Lasts about 24 hours
Disappears as proteolytic enzymes from lysosomes digest the cross-bridge
Length-tension relationship
Indicates how the forcefulness of muscle contraction depends on the length of sarcomeres within a muscle before contraction begins
Neuromuscular junction
NMJ
Synapse between a somatic motor neuron and a skeletal muscle fiber
Where muscle action potentials rise
Synapse
Region where communication occurs between two neurons or between a neuron and a target cell
Synaptic cleft
Small gap separating two cells at most synapses
Because the cells do not touch, the action potential cannot ‘jump’ between the two
-instead, the first cell communicates with the other by releasing a chemical messenger called a neurotransmitter
Axon terminal
At NMJ, end of motor neuron
Divides into cluster of synaptic end bulbs
Synaptic vesicles - hundreds of membrane enclosed sacs in the cytosol
Inside each synaptic bulb are thousands of molecules of Acetylcholine (the neurotransmitter released at the NMJ)
Motor end plate
Region opposite the synaptic end bulbs
Muscle fiber part of NMJ
Within are 30-40 million acetylcholine receptors
Nerve impulse (nerve action potential) elicits a muscle action in the following way
Release of acetylcholine
Activation of ACh receptors
Production of muscle action potential
Termination of ACh
Release of acetylcholine
Nerve impulse at synaptic end bulb stimulates voltage-gated channels to open
Ca2+ flows inward through open channels (ions more concentrated in extra cellular fluid)
-stimulates synaptic vesicles to undergo exocytosis
–synaptic vesicles fuse with motor neurons plasma membrane, liberating ACh into synaptic cleft
—ACh diffuses across synaptic cleft between motor neuron and motor end plate
Activation of ACh receptors
Binding of two molecules of ACh to the receptor on the motor end plate opens an ion channel in the ACh receptor
Once the channel is open, small cations, most importantly Na+, can flow across the membrane
Production of muscle action potential
The inflow of Na+ makes the muscle fiber more positively charged
This change in the membrane potential triggers a muscle action potential
Each nerve impulse normally elicits one action potential
The muscle action potential then propagates along the sarcolemma into the system of T tubules
This causes sarcoplasmic reticulum to release it’s stored Ca2+ into the sarcoplasm and the muscle fiber subsequently contracts
Termination of ACh activity
The affect of ACh binding lasts only briefly because ACh is rapidly broken down by an enzyme called acetlycholinesterase
This enzyme is attached to collagen fibers in the extracellular matrix of the synaptic cleft
AChE breaks down ACh into acetyl and choline, products that cannot activate the ACh receptor
Electromyography
A test that measures the electrical activity in resting and contracting muscles
Resting produce less activity
Needle inserted into muscle
-played through loudspeaker
Determine if weakness is due malfunction of the muscle or the nerves supplying the muscle
Botulinum toxin
Curare
Botox* - blocks exocytosis of synaptic vesicles at the NMJ
Poison used South American Indians in blow darts - causes muscle paralysis by binding to and blocking ACh receptors
Ways for muscle fibers to produce ATP
From creating phosphate
By anaerobic glycolysis
By anaerobic respiration
Creating phosphate
High energy-rich molecule that is found in muscle fibers
Comes from excess ATP produced while muscle fibers are relaxed
Enzyme creating kinase catalyze a the transfer of one of the high energy phosphate groups from ATP to creatine, forming creatine phosphate
Creatine
Amino-acid like molecule that is synthesized in the liver, kidneys, and pancreas and then transported to muscle fibers
Anaerobic glycolysis
Process of the breakdown of glucose to give rise to lactic acid when oxygen is absent or at low concentration
1 glucose molecule -> 2 lactic acid + 2 ATP
- most lactic acid diffuses into blood
- liver cells convert back to glucose
- -reduces acidity of blood
Provides enough energy for two minutes of maximal muscle activity
Breaks down glucose into 2 pyruvic acid molecules
Aerobic respiration
A series of oxygen-requiring reactions that produce ATP, carbon dioxide, water, and heat
(When pyruvic acid enters mitochondria)
If enough oxygen is present
1 molecule glucose -> 30-32 of ATP
Myoglobin + hemoglobin
Oxygen sources
Myoglobin - only in muscle cells
Hemoglobin - only in red blood cells
Oxygen binding proteins that bind when it’s plentiful and release when it’s scarce
Muscle fatigue
Inability of a muscle to maintain force of contraction after prolonged activity
Central fatigue - tiredness before actual fatigue
Oxygen debt
Recovery Oxygen uptake
After heavy exercise, heavy breathing -> pay back oxygen
For..
•Convert lactic acid back into glycogen stores in the liver
•Resynthesize creatine phosphate and ATP in muscle fiber
•Replace the oxygen removed from myoglobin
Motor unit
Consists of a somatic motor neuron and all of the skeletal muscle fibers it stimulates
Twitch contraction
Brief contraction of all muscle fibers in a motor unit responsible to a single action potential in its motor neuron
Myogram - record of muscle contraction
Last 20-200msec
Action potential only 1-2msec
Latent period
2msec delay in beginning of twitch contraction
Contraction period
Second phase of twitch contraction
Lasts 10-100msec
Relaxation period
Third phase of twitch contraction
10-100msec
Refractory period
Period of lost excitability
When a muscle receives enough stimulation to contract
Wave summation
When a second stimulus occurs after the refractory period of the first stimulus is over, but before the skeletal muscle fiber has relaxed, the second contraction will be stronger. This is what it’s called.
Occur when additional Ca2+ is released from the sarcoplasmic reticulum by subsequent stimuli while the levels of Ca2+ in the sarcoplasm are still elevated from the first stimulus.
Unfused tetanus
Muscle fiber is stimulated at a rate of 20-30 times per second, and can only partially relax
Fused tetanus
Skeletal muscle is stimulated at a higher rate of 80-100 times per second, does not relax at all
Individual twitches cannot be detected
Motor unit recruitment
Process in which the number of active motor units increases
Weakest motor units are recruited first
Progressively stronger added if task requires
Hypertonia
Increased muscle tone
Spasticity - stiffness, increase tendon reflexes
Rigidity - increase muscle tone not affecting reflexes (tetanus)
Isotonic contraction
Concentric - great enough to overcome the resistance of the object to be moved, muscle gets shorter
Eccentric - resists movement of the load, muscle gets longer
Isometric contraction
Not enough to exceed resistance of the object to be moved, muscle does not change in length
Red muscle fibers
High hemoglobin content of skeletal muscle fibers
(Dark meat in chicken legs and thighs)
More mitochondria and capillaries
White muscle fibers
Low hemoglobin content of skeletal muscle fibers
White meat in chicken breasts
Muscle fiber speed groups
Slow oxidative fibers
Fast oxidative-glycolytic fibers
Fast glycolytic fibers
Slow oxidative fibers
SO
Appear dark red - many capillaries and myoglobin
Generate ATP mainly by aerobic respiration
ATPase hydrolyzes ATP slowly
Resistant to fatigue
Capable of prolonged sustained contractions for many hours,
-posture, aerobic activities
Fast oxidative-glycolytic fibers
FOG
Many capillaries and myoglobin
Generate considerable ATP
Higher intercellular glycogen = generate ATP by anaerobic glycolysis
ATPase in myosin heads hydrolyzes ATP 3-5 times faster than in SO
*walking and sprinting
Fast glycolytic fibers
FG
Low myoglobin, few capillaries
Few mitochondria
Appear white in color
Ability to hydrolyze ATP rapidly = intense anaerobic movements of short duration
Intercalated discs
Irregular transverse thickenings of sarcolemma that connect ends of cardiac muscle fibers to one another
Contains desmosomes which hold the fibers together
Contains gap junctions which allow muscle action potentials to spread from one cardiac muscle fiber to another
Cardiac muscle tissue
Contain intercalated discs
Has endomysium and perimysium, but to epimysium
Contraction lasts longer than skeletal muscle because Ca2+ in interstitial fluid
Physiological enlarged heart
Cardiac muscle hypertrophy due to increased workload.
Smooth muscle tissue
Usually involuntary
Two types:
Visceral (single-unit) smooth muscle tissue
Multiunit smooth muscle tissue
Visceral (single-unit) smooth muscle tissue
In skin, arteries, veins, hollow organs
Autorhythmic
Fibers connect through gap junctions
-where action potentials spread
Multiunit smooth muscle tissue
Individual fibers with own motor neuron terminals, few gap junctions
Stimulation of one Multiunit fiber causes contraction of that fiber only
In walls of large arteries
- airways of lungs, arrector pili, muscles of iris, ciliary body
Dense bodies
Structures that thin filaments attach to, in smooth muscle fibers
Functionally similar to z discs in striated muscle fibers
Caveolae
Small pouch like invaginations of the plasma membrane in smooth muscle
Like ‘transverse tubules’
Physiology of smooth muscle
Contractions Start more slowly and lasts longer than skeletal and cardiac
Can shorten and stretch to greater extent
Increase in Ca2+ concentration in cytosol initiates contraction
No transverse tubules = takes longer for Ca2+ to reach filaments
-slow contraction onset
Calmodulin
Regulatory protein in smooth muscle
Binds to Ca2+ in cytosol, activates enzyme myosin light chain kinase -> then uses ATP to add a phosphate group to a portion of the myosin head
Smooth muscle tone
A state of continued partial contraction
from the prolonged presence of Ca2+ in the cytosol
Where most muscles are derived.
From the mesoderm
