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Which types of muscle tissue are elongated and muscle fibers
Skeletal and smooth
Skeletal Muscle
longest of all muscle
has striations
voluntary
Multi nucleated
Cardiac muscle
Cardiac,
striated
Involuntary
Smooth Muscle
Visceral
Non-striated
Involuntary
Hollow organs ( large arteries, bladder, stomach
Skeletal Muscle anatomy
Nerve and blood supply
connective tissue sheaths
attachments
Epimysium
Dense irregular connective tissue surrounding entire muscle
Perimysium
fibrous connective tissue surrounding fascicles ( group of muscle fibers)
Endomysium
Fine areolar connective tissue surrounding each muscle fiber
Attachments
Direct: epimysium fused to periosteum of bone or perichondrium of cartilage
Indirect: connective tissue wrappings extend beyond muscle as rope-like tendon
Myofibril
long, cylindrical, contractile organelles within muscle cells
Sarcolemma
muscle fiber plasma membrane
Sarcoplasm
Muscle fiber cytoplasm ( contains many glycosomes ( glycogen storage, myoglobin O2 storage)
Sarcoplasmic Reticulum
Stores and releases Ca 2+
SR functions in regulation of intracellular Ca 2+ levels
surrounds skeletal muscle fiber
Sarcomere
smallest contractile unit of muscle fiber
consists of area between z discs
Actin myofilaments
thin filaments
anchored to Z discs
Extend across I band and pathway in A band
Myosin myofilaments
thick filaments
connected at M line
extend length of A band
Muscle Fiber Contraction
Muscle cells are excitable cells capable of action potentials
AP crosses from neuron to muscle via the neurotransmitter acetylcholine ( ACh)
Ion channels in muscle contractions
Chemically gated ion channels - opened by chemical messengers such as neurotransmitters Ex) ACh receptors on muscle cells
Voltage- gated ion channels- open or close in response to voltage changes in membrane potential
Skeletal muscles are stimulated by…
somatic motor neurons
Neuromuscular Junction ( skeletal muscle)
The region where the somatic motor neuron contacts the skeletal muscle, consists of axon terminals and the underlying junctional folds of the sarcolemma
Synaptic cleft
muscle fiber are separated by gel-filled space
Events at the Neuromuscular Junction
AP arrives at axon terminal
Voltage-gated calcium channels open, calcium enters motor neuron
Calcium entry causes release ACh neurotransmitter into synpatic cleft
ACh diffuses across to ACh receptors (Na+ chemical gates) on sarcolemma
ACh binding to receptors, open gates, allowing Na+ to enter resulting in end plate potential
Acetylcholinesterase degrades ACh
Generation of an Action Potential across the Sarcolemma ( Muscle fiber excitation)
1.Generation of end plate potential
2.Depolarization
3.Repolarization
End plate potential
ACh released from motor neuron binds to ACh receptors on sarcolemma
Causes chemically gated ion channels on sarcolemma to open
Na+ diffuses into muscle fiber ( K+ diffuses outward)
Because Na+ diffuses in, interior of sarcolemma becomes less negative
results in local depolarization
Depolarization in skelteal muscle ( sarcomere)
Generation and propagation of an Action potential
end plate potential causes enough change in membrane voltage to reach critical level called threshold, Lyigand gated ion Na+ channels in membrane will open
the influx of Na+ through channels into cell triggers AP that is unstoppable and will lead to muscle fiber contraction, this causes a series of voltage gated sodium channels opening all along the t-tubules
AP spreads across sarcolemma from one voltage-gated Na+ channel to next one in areas, causing that area to depolarize
Repolarization
restoration of resting conditions
Na+ voltage-gated channels close, and voltage-gated K+ channels open
K+ effux out of cell rapidly brings cell back to initial resting membrane voltage
Refractory period
Muscle fiber cannot be stimulated for a specific amount of time until repolarization is complete
ionic conditions of resting state are restored by Na+- K+ pump ( Na+ out, K+ in)
Excitation Contracting coupling
AP is propagated along sarcolemma and down into T tubules, where voltage- sensitive proteins in tubules stimulate Ca 2+ release from SR leading to sliding of myofilaments
Cross Bridge Cycling
at higher intracellular Ca2+ concentrations ca2+ binds to troponin, troponin changes shape and Move tropomyosin away from myosin-binding sites ( it blocks active sites on actin), Myosin head bind to actin forming cross bridge. Once Nervous stimulation ceases ca2+ is pumped back into SR, ending contraction
Cross bridge cycle steps
1) Cross bridge formation: Energized myosin head attaches to an actin myofilament, forming a cross bridge ADP and Pi are attached at this time
2) The power ( working) stroke: ADP and Pi are released and the myosin head pivots and bends changing to its bent low-energy state, pulling actin towards the M line ( In the absence of ATP myosin heads will not detach causing rigor mortis)
3)Cross bridge detachment: after adding ATP to myosin, the link between myosin and actin weakness and the myosin head detaches
4) Cocking of myosin head, As ATP is hydrolyzed to ADP, and Pi the myosin head returns to its prestoke high energy position
Rigor mortis
Due to ATP needed for cross bridge detachment, resulting in myosin head staying bound to actin causing state of contraction,
Intracellular calcium levels increase because ATP is no longer being synthesized so calcium cannot be pumped back into SR
Isometric contraction
no shortening; muscle tension increase but does not exceed load ( muscle neither shortens nor lengthens) Muscle tension matches external load
isometric contractions, cross bridges generate force, but actin filaments do not shorten
Myosin heads “ spin their wheels” on same actin-binding site
Isotonic contraction
Muscle shortens because tension exceeds load ( Muscle changes in length and moves load
Actin filaments shorten and cause movement
Muscle twitch
simplmest contraction resulting from a muscle fiber repsonse to a single AP from motor neuron
The muscle twitch steps
1) Latent period: events of excitation-contraction coupling ( no muscle tension seen)
2) Period of contraction: cross bridge formation ( Tension declines to zero)
3) Period of relaxation: Ca2+ reentry into SR ( Tension declines to zero)
muscle tone
Constant, slightly contracted state of all muscles, due to spinal reflexes,
Concentric contractions
Muscle shortens and does work Ex) biceps contract to pick up a book
Eccentric contractions
Muscle lengthens and generates force Ex) laying a book down causes biceps to lengthen while generating a force
ATP providing Energy for Contraction
ATP supplies the energy needed for the muscle fiber to
Move and detach cross bridges
Pump calcium back into SR
Pump Na+ out of and K+ back into cell after excitation-contraction coupling
storage of ATP is depleted in 4-6 seconds
ATP regeneration quickly by three mechanisms
Direct phosphorylation of ADP by creatine phosphate
Anaerobic pathway: glycolysis and lactic acid formation
Aerobic pathway
Direct phosphorylation of ADp by creatine phosphate (CP)
Creatine Phosphate donates a phosphate to ADP to instantly form ATP
Creatine Kinase is an enzyme that carries out transfer of phosphate
the muscle fiber have enough ATP and CP reserves to power the cell for about 15 seconds
Anaerobic pathway
glycolysis and lactic acid formation
breaking down and using energy stored in glucose
Glycolysis: doesn’t require oxygen, glucose is broken into 2 pyruvic acid molecules, 2 ATP are generated for each glucose broken down
In the absence of oxygen , pyruvic acid is converted to lactic acid
lactic acid diffuses into bloodstream, used as fuel by liver, kidney and heart
converts back to pyruvic acid or glucose by liver
Anaerobic respiration vs Aerobic Repiration
Anaerobic respiration yields only 5% as much ATP as aerobic Respiration, but produces ATP 2.5 times faster
-Aerobic Respiration produces 95% of ATP during rest and ligth to moderate exercise ( requires oxygen) ( 32 ATP produced)
Anaerobic threshold
point at which muscle metabolism converts to anaerobic pathway
Aerobic endurance
Length of time muscle contracts using aerobic pathways
Muscle Fatigue
Inability to contract muscle despite continued stimulation
due to K+, Na+ and Ca+ disrupting membrane potential of muscle
Why would Muscle fatigue happen>
Decreased ATP and increased magnesium ( magnesium can interfere with Voltage sensitive T tubule proteins
Decreased glycogen
Ionic imbalances ( K+, Na + and Ca+ disrupting membrane potential of muscle cell
Increased inorganic phosphate from CP and ATP breakdown may interfere with calcium release from SR
For a muscle to return to its pre-exercise state EPOC has to happen, what happens during EPOC
Excess Post exercise Oxygen Consumption
Oxygen reserves are replenished
Lactic acid is reconverted to pyruvic acid
Glycogen stores are replaced
ATP and creatine phosphate reserves are resynthesizes
factors that increase the force of skeletal Muscle Contraction
High frequency of stimulation
Large number of muscle fibers recruited
Large muscle fibers
Muscle and sarcomere stretched to slightly over 100% of resting length
Increase force of skeletal muscle contraction leads to
More cross bridges attached
Optimal sarcomere operating length
80%-120% of resting length
Slow oxidative muscle fibers are good for
low- intensity, endurance actvities Ex) maintaing posture
Fast oxidative muscle fibers
Medium- intensity activities Ex) sprinting or walking
Fast glycolytic muscle fibers
Short-term intense or powerful movements Ex) hitting a baseball
Aerobic Endurance Excercise
Ex) joining, swimming, biking leads to increased muscle capillaries, number of mitochondria, myoglobin synthesis
Resistance Exercise
Ex) weight lifting, isometric exercises
leading to Muscle hypertrophy ( increase in fiber size)
Increased mitochondria, myofilaments, glycogen stores, and connective tissue
increased muscle strength and size
Smooth Muscle
Found in wall so hollow organs, Respiratory , digestive, urinary, reproductive, circulatory ( not in the heart though!)
Longitudinal layer
Fibers run parallel to long axis of organ
Contraction causes organ to shorten
Circular layer
fibers run around circumference of organ
Contraction causes lumen of organ to constrict
Differences between Smooth and Skeletal muscle Fibers
Smooth muscle fibers are spindle-shaped fibers ( thin and short
Skeletal muscle fibers are wider and much longer
Smooth muscle fibers are one nucleated and have no striations
Skeletal Muscle fibers are multinucleate and have striations
Skeletal Muscle fibers has multiple connective sheaths ( Epimysium, Perimysium, Endomysium)
Smooth Muscle fibers has only one connective tissue ( contains endomysium only)
Smooth muscle fibers contain varicosities ( bulbous swellings) of nerve fibers
Skeletal muscle fibers contain neuromuscular junctions
Skeletal muscle fibers are innervated by voluntary somatic nervous system
Smooth muscle fibers are innervated by involuntary autonomic nervous system
Skeletal muscle fibers have junctional folding vs Smooth muscle fibers have diffuse junctions
Smooth muscle has less elaborate SR, and no T tubules vs the opposite for skeletal muscle fibers
Sarcolemma contains pouch like infolding called caveolae ( contain numerous Ca2+ channels) skeletal muscle fibers rely on T-tubules for singnaling SR for source of Ca2+
Smooth muscle fibers are usually electrically connected via gap junctions whereas skeletal muscle fibers are electrically isolated
smooth muscle have myosin heads along entire length,
Smooth muscle has both thick and thin filaments
thick filaments are fewer in smooth muscle than skeletal muscle fibers
No troponin complex in smooth muscle but does contain tropomyosin smooth muscle ( calmodulin regulates calcium for smooth muscle, skeletal has troponin regulate calcium)
Thick and thin filaments arranged diagonally ( smooth muscle , contracts in a corkscrew manner)
Intermediate filament-dense body network
Dense bodies are the ones that anchor the filaments to sarcolemma on the smooth muscle while Skeletal muscle filaments are anchored by z discs
There is no presence of myofibrils
metabolism is mainly aerobic for smooth muscle and aerobic and anaerobic for skeletal
Contraction of Smooth Muscle
Calcium is obtained mostly from extracellular space
Calcium binds to calmodulin, not troponin
Activated calmodulin then activates myosin kinase
Activated myosin kinase phosphorylates myosin head activating ATPases
Activated myosin forms cross bridges with actin of the thin filaments ( shortening begins
regulation of contraction in smooth muscle is done by
Neural regulation - neurotransmitter bind causes either graded ( local) potential or action potential
Results in increases in Ca2+ concentration in sarcoplasm
Response depends on neurotransmitter released and type of receptor molecules
Stopping smooth muscle contraction
Relaxation requires
Ca2+ detachment from calmodulin
-Active transport of Ca2 into SR and extracellularly
Dephosphorylation of myosin to inactive myosin
Smooth muscle contract without nerve signals due to
Reaction of hormones, oxygen levels or CO2 levels, they use G protein linked receptos to detect chemical changes
Unitary smooth muscle
organized in large sheets, connected by gap junctions, uses pacemaker cells , less innerveration
highly sensitive to stretch and chemical changes ( O2, hormones, ph)
presence of pacemaker
Rhythmic contractions
Multi-unitary smooth muscle fibers
independent muscle fibers, not that many gap junctions
richly supplied with autonomic nerve endings
Responds to neural stimuli
Cardiac characterstics
only Endomysium connective sheath
Has myofibrils
has t-tubules
-presence of gap junctions in intercalated discs
no neuromuscular junctions
Has pacemakerExcitation or inhibition of nervous system stimulation
metabolism is Aerobic