Unit 4 💪🏻 Flashcards
Excitable (functional properties)
Can generate an action potential, stimulated by nerves, hormones,local signals
Elastic (functional properties)
Can recall when stretched
Extensible (functional properties)
. Can stretch/expand
Contractile (functional properties)
Shorten w/ force/pull on attachments
Skeletal muscle
Voluntary,long, striated, multinucleated, attached to bone (mostly)
Smooth muscle
Involuntary, tapered,non-striated, single nucleus, hollow organs, vessels
Cardiac muscle
Involuntary, branched,striated, 1-2 nuclei, intercalated discs,🫀 only
Skeletal muscle functions
Movement (all locomotion), maintain posture,
Stabilize joints, protection, generate heat
Epimysium (💀 packaging)
Outermost dense irregular C.t. Layer (separates muscle from organs), allows independent moves
Perimysium (💀 packaging)
C.t. Surrounding fascicles ( bundles of muscle fibers), ‘grain’ of muscles, allow precise movements
Endomysium (💀 packaging)
C.t. Around each fiber
Aponeurosis (💀 packaging)
Sheet of collagen fibers, connect muscles to other muscles or to bone or skin
What do skeletal muscles contain?
Contains lots of blood vessels ( smallest capillaries, highly interconnected) each fiber connects to motor neuron
Myofibril💀
Contractile organelle (100s - 1000s per fiber) repeating sarcomere
Sacrolemma💀
Plasma membrane, conduct electrical impulses that trigger contraction
Sacroplasmic reticulum💀
Smooth Er (regulates ca +), striations due to myofilaments
Actin💀
Part of thin filament
Myosin💀
Make up thick filament
What does myofibril contain?
I band, A band, H zone, m line, sacromere, Z disc
Sacromere💀
Functional unit of skeletal muscle,. Thick/thin filaments, repeating unit in my fibril
What does sacromere contain?
Actin, troponin +tropomyosin, thick filaments, myosin
I band
Thin filaments only (light bond)
A band
Thick + thin filaments (dark band)
H zone
Thick filaments only W/ in A band
M line
Anchor thick filaments, elastic fibers
Z disc
Tie everything together, microscopic banding pattern, thin filaments are anchored
Actin
Myofilament w/ binding sites for myosin heads, thin filament
Myosin
Myofilament ( 300 / filament) w/ heads that bind actin
Troponin+ tropomyosin=
Regulatory problems
Sliding filament theory?
Actin filaments are pulled closer by myosin, z-discs move closer, h-bands shrink, A bands stay put (contraction, actin and myosin overlap completely)
Crossbridge
With Ca + present, ‘cocked’myosin heads bind to actin
Power stroke🌉
Myosin pulls actin toward m-line
Cross bridge cycling steps
Crossbridge, power stroke, an 300 myosin heads on thick filament, sacromere, myofibril, myosin head detached by ATP, ATP splits and recooks head, form crossbridge, continues until no ATP or Ca
① ATP and muscle contraction
Active site on actin exposed as Ca binds to troponin
② ATP and muscle Contraction
High energy (adp+p)myosin head binds actin =crossbridge
③ ATP and muscle contraction
During power stroke, p released and head pivots forward, ADP released =↓ energy state
(Notice crossbridge still intact)
④ ATP and muscle contraction
ATP attaches to myosin head, crossbridge detaches
⑤ ATP and muscle contraction
Myosin head hydrolizes ATP →adp+p= recocked/high energy
Source of ATP - creatine phosphate
- Stored ATP used up in seconds
- regenerates ATP for 15 seconds
Sources of ATP - anaerobic respiration
- High demand = rapid ATP delivery
- glycolysis (breaking glucose) =2 ATP lactic acid (from pyrurate)
- very rapid, very expensive (only 2 atp/gluccse)
- about 60 sec., O2 not required
Sources of ATP - aerobic respiration
- Lower demand = O2 can be used
- 2 ATP from glycolysis +pyruvate sent to mitochondria = 36 ATP per glucose.’
- hour sustained activity+ resting ATP
Oxygen debt (post exercise excess oxygen consumption)
- Oxygen intake Î after exercise
- resting ATP, cp, and other fuels restored
- lactic acid metabolism, cell repair adaption
- until resting conditions restored (3-40hrs)
Muscle strength
Of fibers / muscle does not change, genetically determined
Stress (muscle)
Production of more sarcomeres and myofibrils = stronger, losing it=atrophy
Use IT OR lose IT
Muscular dystrophy = inherited disorder
- Muscle fibers degenerate (atrophy) abnormally
- duchenne muscular dystrophy (dmd ) fatal by early 20’s
- sarcolemma
Isotonic
Muscle moves load (maintain same tone)
Concentric (isotonic)
Muscle shortens
Eccentric ( isotonic)
Muscle lengthens
Isometric
Muscle contracts, but load remains still, often load exceeds strength of muscle
Motor unit
-1 motor neuron + all associated muscle fibers
- small (4 fibers) to large (1000’S fiber)
-Small control fine movements (like eyes)- easily excited
-Large units - gross movements
Recruitment
Larger motor units ‘recruited’ until goal reached
- small more excitable units recruited 1st
- larger, less excitable units recruited later
- muscles exhibit ‘graded’ response, ex. Matches load
What does fiber length affect?
Tension
What do thick and thin filaments have to do to develop tension?
Must overlap
80% -120% resting muscle length =
Greatest possible tension
Muscle twitch=
Single contraction (1 AP)
Latent period (muscle twitch)
AP along sarcolemma down tubules
Contraction period (muscle twitch)
Ca binding troponin, cross bridges forming
Relaxation period (muscle twitch)
Ca pumped back to SR, tropomyosin covering binding site
- last 100 m sec, depending on fiber type
Single AP =
Twitch
Wave summation
- If 2nd AP arrives before end of relaxation period,
- more ca in sarcaplasm = more active sites exposed = more cross bridges
-↑ frequency than motor = greater tension per muscle fiber
Stimulation frequency, tetanus
When max tension achieved
Incomplete tetanus
Fiber quivers due to relaxation phases
Complete tetanus
Stimulation frequency ↑ enough
Treppe - ‘staircase’ effect
- max stimulation of dormant muscle generates 50% of max tension
- repeated max stimulus = gradual ↑ to max tension
- due to heat and extra ca
Muscle tone
Some fibers are contracting even at ‘rest’
What does muscle tone provide?
Fiber contraction alternates to provide tone,
-Involuntary, keeps muscles ready for action
Hypotonia ( muscle tone)
Damage to direct nerves= lack of tone (atrophy)
Hypertonia. (Muscle tone)
Excessive tone, inhibitory nerve damage = spastic when stretched
Types of muscle fibers
Speed of ATPases (ATP splitters), ATP forming pathways (oxidative/glycatic), slow oxidant fibers, fast oxidative fibers, fast glycolytic fibers
Speed of ATPases (ATP splitters)
2 general fiber types = slow and fast (2x faster)
ATP forming pathways
- Oxidative fibers - use aerobic respiration
- glycolic fibers - use anaerobic respiration
Slow oxidative fibers (so)- slow ATPases
- Aerobic ATP production - lots o’ mitochondria
- myoglobin - 02 carrying molecule = dark meat,
- thin, less tension, fatigue resistant (posture, joint stability)
Fast oxidative fibers (fo)- fast ATPase (intermediate fibers)
- aerobic ATP, lots o’ mitochondria
- little myoglobin, intermediate tension (walking)
Fast glycolytic fibers (fg) - fast ATPase
- Anaerobic few mitochondria/myoglobin
- lots o’ glycogen
Endurance exercise = mainly slow fibers
- More mitochondria = more aerobic ATP
- more myoglobin = extra 02
- more capillaries = angiogenesis
- not so much hypertrophy= ↓ blood flow
- all= greater endurance
Resistance exercise = mainly Fg fibers
Short term, powerful movements required (anaerobic)
-↑ in my fibril #=↑ in muscle fiber size
-↑ in c.t.
- no significant î in mitochondria or capillaries (02 delivery not critical)
-Hypertrophy= ↑ muscle size
Atrophy
- Loss of muscle mass
- lack of use=atrophy
- atrophy due to aging= sarcopenia
What does cardiac muscle do?
- Pumps blood
- lots o’ mitochondria + myoglobin (aerobic atp)
- autorythmic
-î and ↓ by ANS (autonomic nervous system)
Cardiac muscle contraction
-Functional synoytium (contracts-like 1 big cell) due to gap junctions.
-Long AP’S due to influx of Ca from extracellalar fluid (long contraction time)
- ca triggers contraction, but most from outside cell
Autorhythmic (cardiac)
Contractions via self-excitable ‘ pacemaker’ cells
Contraction of smooth muscle
- ca enters sarcoplasm (from outside cell + sr)
- calmodulin activated → myosin kinase activated
- ATP on myosin heads.→ ADP + p
- maintain contractions for long periods, ↓power contract., not much ATP
- some ca in sarcoplasm = maintain tone
- latch bridges = some intact w/o ca
What stimulates smooth muscle contraction?
Ca, most stored outside cell, no sr
Smooth muscle stimulation
- Natural (ANS) stimulation of smooth MT= neurotransmitters released from varicosites
-Digestive tract smooth muscle contains pacesetter cells = rhythmic contraction - other triggers include hormones and local factors ‘’
Single unit (smooth muscle organization)
- Single-unit = smooth muscles linked by gap junctions (aka visceral muscle)
- most common, 1 cell stimulated causes entire layer to contract
- often exhibit stretch-relaxation response(for storage stomach/ bladder)
Multi-unit (smooth muscle organization)
-Few gap junctions, each cell requires stimulation
-Much finer control (eyes,respiratory)
Origin
-Anchoring point, music attachment site does not move
Insertion
Muscle attachment sites that moves when muscle contracts
- insertion always moves toward origin
Prime mover(muscle interactions)
(Aka against)- muscle that contributes most to a particular movement
- biceps brachii = prime mover during elbow flexion
Synergism (muscle interactions)
Muscle that aids/help coordinate desired movement
- brachialis+brachioradialis help prevent undesirable rotation and also assist an elbow flexion
Antagonist(muscle interactions)
- Muscle w/ opposite action to prime mover
- helps maintain position /control rapid movements
Fixator (muscle interactions)
Type of synergism that keeps joint stable
Parallel(non -fusiform) fascicle arrangements
- Flat, fascicles along long axis
Parallel-fusiform(fascicle arrangements)
Rounded and tapered to tendons(thick middle =belly)
- circular, convergent
Unipernate (fascicle arrangements)
Like a feather, fascicles angled along on side of tendon
Step 1: the neuromuscular junction(excitable contraction)
-Each fiber innovated by motor neuron
- connection = neuromuscular junction(NMJ)
- 3 parts= synaptic end bulb (knob),synaptic cleft, motor end plate
Synaptic end bulb(knob)
- end of motor neuron, stores acetylcholine (ACH)
Synaptic cleft
- gap b/n cells, ACH diffuses across
Motor end plate
- sarcoma section, contains ACH receptors
Step 2: excitation contraction coupling
- Action potential arrives at synaptic knob
-Voltage-gated Ca channels open, ca enters knob - 3 key paints of ACH and receptors
- voltage gated Na channels that trigger AP along sarcoma fiber officially excited
- ACH quickly degraded by acetylcholnesterace = precise control of contraction
Key points of excitation contraction coupling
- ACH released via exocytosis from synaptic vesicles
- ACH diffuses across synaptic cleft, bind w/ACH receptors on motor end plate
- receptors open and allow Na intosarcoplasm= depolarization
Resting membrane potential. (Don’t need for essay) step 3?
- Muscle fibers maintain a voltage across sarcolemma, i.e. Polarized
If enough Na, voltage gated Na channels open, propagate AP like dominos)
Step 4: ap travels ↓ t-tubules
- T-tubule - transverse’ tubule, extension of sarcolemma w/in sarcopiasm
- terminal cistern-sr surrounding t-tubules,store Ca
5th step: contraction phase
- AP ↓ t-tubules stimulate Ca channels on terminal cistern to open
- Ca floods sarcoplasm
- ca binds to troponin
- troponin moves tropomyosin to reveal actin binding sites, contraction!
Rhythmic contraction(smooth muscle stimulation
Digestive tract smooth muscle contains pacesetter cells = rhythmic contraction
Tendons
Tough, rope -like structures that connect muscle →bone
Sarcoplasm💀
Cytoplasm of muscle fibers, contains enzymes and organelles for muscle function
Terminal cisternal
Large chambers in sr of muscle cells that store ca and release to start contraction
Why does skeletal fiber appear striated?
Highly organized arrangement of contractile proteins- actin and myosin, w/in their myofibrils, creating bands of light and dark sarcomeres
Thick filaments
- Main protein: myosin,
- function: provide motor protein that generate force for contraction
Thin filaments
- Protein: actin
- function: act as the track along which the myosin heads moving during contraction
Neuromuscular junction (Nmj)
•Synaptic connection between the terminal end of a motor nerve and a muscle
• synaptic knob, synaptic deft-motor end plate
What stimulates ACH release?
- Neurotransmitter released by motor neurons at NMJ
What is action potential?
- Rapid electrical signal that travels along a nerve cell membrane, generated by opening of voltage gated Na, cause rapid depolarization of membrane, propagating signal
What is ache, why is it important?
- acetylcholinesterase in NMJ,
-Immediately breaks down and hydrolyses ACH
Triad
- Substructure of SKM that coordinates excitation contraction, made up of 2 terminal cistern of s/r
Function of triad
- Translate: action potential from plasma membrane to sr, initiates calcium flow to cytoplasm/ contraction
Role of ATP
Provide energy needed for myosin head to detach from actin, allowing muscle to relax and prepare for new contraction
Why does rigor morris occur?
When someone dies, ATP prod. ↓, leading actin and myosin becoming permanently bound tg, causing muscles to stiffen and remain contracted due to lack of energy to detach
What causes muscles to relax?
When motor protein myosin in sarcomere releases actin
Tetanus
Serious bacterial infection that affects nervous system and muscle
Intercalated disc
Correction point between. Individual cardiac cells, allowing ↑ electrical impulses and mechanical fro force through heart
Varicosity (smooth)
Enlargement of neuron that ↑ neurotransmitter,
Dense body (smooth)
Anchor thin filaments n sm,
Calmodulin
Protein that regulates calcium dependent signals
Fascicle
Bundle of skeletal muscle fibers running parallel to each other, enveloped by perimysium
What is role of acetylcholine ( ACH )
Stimulate muscle contraction
What is a myofibril?
Rod - like unit within muscle fibers
What structure is responsible for the striated look of a skeletal muscle
Sarcomere
What protein blocks the myosin-binding site?
Tropomyosin
What causes muscles to relax?
Break ↓ of acetylcholine
What are the sources of ATP in skeletal muscle
Creative phosphate, glycolysis, and oxidative phosphorylation
What is oxygen debt *
Amount of oxygen required to oxidize lactic acid and replenish ATP stores after exercise
What is a isotonic contraction
Contraction where muscle length changes while generating force
What is an isometric contraction?
Contraction where the muscle length remains constant while generating force
How does recruitment help determine overall contraction strength?
Increasing the # of of motor units activated
How does stimulation frequency affect contraction strength?
Higher frequency of stimulation leads to stronger contractions
What is wave summation *
↑ in muscle contraction strength due to rapid stimulation
What is tetanus?
Sustained muscle contraction due to rapid stimulation
What are the 3 different skeletal muscle fiber types?
Slow oxidative, fast oxidative, fa fast glycolytic
What determines each category of skeletal muscle finer type?
ATPases activity and respiratory pathway
What are slow oxidative fibers adapted for?
Endurance and continuous contraction
What are fast glycolytie fibers adapted for?
Short bursts of power and speed
How do muscles adapt to resistance exercise?
↑ in muscle fiber size and strength
What is a variscosity in smooth muscle?
Swelling along a nerve finer that releases neurotransmitters
