Exam 5 Part 2 Flashcards
(91 cards)
1
Q
•Nearly half of body’s mass can
A
transform chemical energy (ATP) into directed mechanical energy, which is capable of exerting force
2
Q
Terminologies:
A
•Myo, mys, and sarco are prefixes for muscle
–Example: sarcoplasm: muscle cell cytoplasm
3
Q
•Three types of muscle tissue
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–Skeletal
–Cardiac
–Smooth
•Only skeletal and smooth muscle cells are elongated and referred to as muscle fibers
4
Q
•Skeletal muscle
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–Skeletal muscle tissue is packaged into skeletal muscles - organs that are attached to bones and skin
–Skeletal muscle fibers are longest of all muscle and have striations (stripes)
–Voluntary muscle - consciously controlled
–Contract rapidly; tire easily; powerful
–Requires innervation to contract
5
Q
•Cardiac muscle
A
–Cardiac muscle tissue is found only in heart
•Makes up bulk of heart walls
–Striated
–Involuntary: cannot be controlled consciously
•Can contract on its own, but nervous system can increase rate
6
Q
•Smooth muscle
A
–Smooth muscle tissue: found in walls of hollow organs
•Examples: stomach, urinary bladder, and airways
–Not striated
–Involuntary: cannot be controlled consciously
•Can contract on its own without nervous system stimulation
7
Q
•All muscles share four main characteristics:
A
–Excitability (responsiveness): ability to receive and respond to stimuli
–Contractility: ability to shorten forcibly when stimulated
–Extensibility: ability to be stretched
–Elasticity: ability to recoil to resting length
8
Q
•Four important muscle functions
A
1.Produce movement: responsible for all locomotion and manipulation
•Example: walking, digesting, pumping blood
- Maintain posture and body position
- Stabilize joints
- Generate heat as they contract
•Additional functions
–Protect organs, form valves, control pupil size, cause “goosebumps”
9
Q
Skeletal muscle is an organ made up of
A
different tissues with three features: nerve and blood supply, connective tissue sheaths, and attachments
10
Q
Nerve and Blood Supply
A
•Each muscle receives a nerve, artery, and veins
–Consciously controlled skeletal muscle has nerves supplying every fiber to control activity
•Contracting muscle fibers require huge amounts of oxygen and nutrientsAlso need waste products removed quickly
11
Q
Connective Tissue Sheaths
A
- Each skeletal muscle, as well as each muscle fiber, is covered in connective tissue
- Support cells and reinforce whole muscle
- Sheaths from external to internal:
–Epimysium: surrounding entire muscle
–Perimysium: surrounding fascicles (groups of muscle fibers)
–Endomysium: surrounding each muscle fiber
12
Q
Attachments
A
- Muscles span joints and attach to bones
- Muscles attach to bone in at least two places
–Insertion: attachment to movable bone
–Origin: attachment to immovable or less movable bone
13
Q
•Attachments can be direct or indirect
A
–Direct (fleshy): epimysium fused to periosteum of bone or perichondrium of cartilage
–Indirect: connective tissue wrappings extend beyond muscle as ropelike tendon or sheetlike aponeurosis
14
Q
A
15
Q
Skeletal muscle fibers
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- are long, cylindrical cells that contain multiple nuclei
- Sarcolemma: muscle fiber plasma membrane
- Sarcoplasm: muscle fiber cytoplasm
- Contains many glycosomes for glycogen storage, as well as myoglobin for O2 storage
- Modified organelles:
Myofibrils
Sarcoplasmic reticulum
T tubules
16
Q
Myofibrils
A
•densely packed, rodlike elements
–Single muscle fiber can contain 1000s
–Accounts for ~80% of muscle cell volume
•Myofibril features
–Striations
–Sarcomeres
–Myofilaments
–Molecular composition of myofilaments
17
Q
Striations:
A
•stripes formed from repeating series of dark and light bands along length of each myofibril
–A bands: dark regions
•H zone: lighter region in middle of dark A band
–M line: line of protein (myomesin) that bisects H zone vertically
–I bands: lighter regions
•Z disc (line): coin-shaped sheet of proteins on midline of light I band
18
Q
•Sarcomere
A
–Smallest contractile unit (functional unit) of muscle fiber
–Contains A band with half of an I band at each end
•Consists of area between Z discs
–Individual sarcomeres align end to end along myofibril, like boxcars of train
19
Q
•Myofilaments
A
–Orderly arrangement of actin and myosin myofilaments within sarcomere
–Actin myofilaments: thin filaments
- Extend across I band and partway in A band
- Anchored to Z discs
–Myosin myofilaments: thick filaments
•Extend length of A band Connected at M line
20
Q
•Molecular composition of myofilaments
A
–Thick filaments: composed of protein myosin made up of two heavy chains that form the tail, and four light chains that form the two globular heads
- Myosin heads contain binding sites for ATP and actin
- During contraction, heads link thick and thin filaments together, forming cross bridges
21
Q
•Molecular composition of myofilaments
A
–Thin filaments: composed of fibrous protein actin
•Actin is polypeptide made up of G actin (globular) subunits
–G actin subunits bears active sites for myosin head attachment during contraction
- G actin subunits link together to form long, fibrous F actin (filamentous)
- Two F actin strands twist together to form a thin filament
22
Q
Tropomyosin and troponin
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regulatory proteins bound to actin
23
Q
Sarcoplasmic reticulum
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•network of smooth endoplasmic reticulum tubules surrounding each myofibril
–Most run longitudinally
–Terminal cisterns form perpendicular cross channels
–SR functions in regulation of intracellular Ca2+ levels
Stores and releases Ca2+
24
Q
•T tubules
A
–Tube formed by protrusion of sarcolemma deep into cell interior
- Increase muscle fiber’s surface area greatly
- Lumen continuous with extracellular space
- Allow electrical nerve transmissions to reach deep into interior of each muscle fiber
–Tubules penetrate cell’s interior at each A–I band junction between terminal cisterns
•Triad: area formed from terminal cistern of one sarcomere, T tubule, and terminal cistern of neighboring sarcomere
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•Triad relationships
–T tubule and SR cistern contains integral membrane proteins that protrude into intermembrane space (space between tubule and muscle fiber sarcolemma)
* Tubule proteins act as voltage sensors that change shape in response to an electrical current
* SR integral proteins control opening of calcium channels in SR cisterns
–When an electrical impulse passes by, T tubule proteins change shape, causing SR proteins to change shape, causing release of calcium into cytoplasm
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Contraction
* the activation of cross bridges to generate force
* Does not necessarily shorten muscles
* Shortening occurs when tension generated by cross bridges on thin filaments exceeds forces opposing shortening
* Contraction ends when cross bridges become inactive
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Muscle Fiber Contraction
•Four steps must occur for skeletal muscle to contract:
1. Nerve stimulation
2. Action potential, an electrical current, must be generated in sarcolemma
3. Action potential must be propagated along sarcolemma
4. Intracellular Ca2+ levels must rise briefly
* Steps 1 and 2 occur at neuromuscular junction
* Steps 3 and 4 link electrical signals to contraction, so referred to as excitation-contraction coupling
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Skeletal muscles are stimulated by
* somatic motor neurons
* Axons (long, threadlike extensions of motor neurons) travel from central nervous system to skeletal muscle
* Each axon divides into many branches as it enters muscle
* Axon branches end on muscle fiber, forming neuromuscular junction (NMJ) or motor end plate
–Each muscle fiber has one neuromuscular junction with one motor neuron
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Axon terminal
* (end of axon) and muscle fiber are separated by gel-filled space called synaptic cleft
* Stored within axon terminals are membrane-bound synaptic vesicles
–Synaptic vesicles contain neurotransmitter acetylcholine (ACh)
* Infoldings of sarcolemma, called junctional folds, contain millions of ACh receptors
* NMJ consists of axon terminals, synaptic cleft, and junctional folds
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•Events at the neuromuscular junction
–Nerve impulse arrives at axon terminal, causing ACh to be released into synaptic cleft
–ACh diffuses across cleft and binds with receptors on sarcolemma
–ACh binding leads to electrical events that ultimately generate an action potential through muscle fiber
–ACh is quickly broken down by enzyme acetylcholinesterase, which stops contractions
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Resting sarcolemma
•polarized, meaning a voltage difference exists across the membrane
–Inside of cell is negative compared to outside
–Na+ and Ca2+ are high outside the cell and K+ is high inside the cell
* An action potential is caused by changes in electrical charges
* Action potentials occur in three steps
1. End plate potential
2. Depolarization
3. Repolarization
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1. End plate potential
–ACh released from motor neuron binds to ACh receptors on sarcolemma
–Causes chemically gated ion channels (ligands) on sarcolemma to open
–Na+ diffuses into muscle fiber down its electrochemical gradient
•Some K+ diffuses outward, but not much
–Because Na+ diffuses in, interior of sarcolemma becomes less negative (more positive)
–This results in local depolarization called end plate potential
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2. Depolarization:
generation and propagation of an action potential (AP)
–If end plate potential causes enough increase in membrane voltage to reach critical level called threshold, voltage-gated Na+ channels in membrane will open
–Large influx of Na+ through channels into cell triggers AP that is unstoppable and will lead to muscle fiber contraction
–AP spreads across sarcolemma from one voltage-gated Na+ channel to next one in adjacent areas, causing that area to depolarize
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Repolarization:
restoration of resting conditions
–Na+ voltage-gated channels close, and voltage-gated K+ channels open
–K+ efflux out of cell rapidly brings cell back to initial resting membrane voltage
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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
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Excitation-contraction (E-C) coupling:
•events that transmit AP along sarcolemma (excitation) are coupled to sliding of myofilaments (contraction)
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•At low intracellular Ca2+ concentration
–Tropomyosin blocks active sites on actin
–Myosin heads cannot attach to actin
–Muscle fiber remains relaxed
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At higher intracellular Ca2+ concentrations
* Ca2+ binds to troponin
* Troponin changes shape and moves tropomyosin away from myosin-binding sites
* Myosin head is then allowed to bind to actin, forming cross bridge
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•Four steps of the cross bridge cycle
1. Cross bridge formation: high-energy myosin head attaches to actin thin filament active site
2. Power (working) stroke: myosin head pivots and pulls thin filament toward M line
3. Cross bridge detachment: ATP attaches to myosin head, causing cross bridge to detach
4. Cocking of myosin head: energy from hydrolysis of ATP “cocks” myosin head into high-energy state
•This energy will be used for power stroke in next cross bridge cycle
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•Rigor mortis
–3–4 hours after death, muscles begin to stiffen
•Peak rigidity occurs about 12 hours postmortem
–Intracellular calcium levels increase because ATP is no longer being synthesized, so calcium cannot be pumped back into SR
•Results in cross bridge formation
–ATP is also needed for cross bridge detachment
•Results in myosin head staying bound to actin, causing constant state of contraction
–Muscles stay contracted until muscle proteins break down, causing myosin to release
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Isometric contraction:
no shortening; muscle tension increases but does not exceed load
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Isotonic contraction:
muscle changes length because muscle tension changes relative to load
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•Each muscle is served by at least one motor nerve
–Motor nerve contains axons of up to hundreds of motor neurons
–Axons branch into terminals, each of which forms NMJ with single muscle fiber
•Motor unit is the nerve-muscle functional unit
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Motor unit
•consists of the motor neuron and all muscle fibers (four to several hundred) it supplies
–Smaller the fiber number, the greater the fine control
•Muscle fibers from a motor unit are spread throughout the whole muscle, so stimulation of a single motor unit causes only weak contraction of entire muscle
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Muscle twitch:
•simplest contraction resulting from a muscle fiber’s response to a single action potential from motor neuron
–Muscle fiber contracts quickly, then relaxes
•Twitch can be observed and recorded as a myogram
–Tracing: line recording contraction activity
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•Three phases of muscle twitch
–Latent period: excitation-contraction coupling is occurring but no muscle tension seen yet
–Period of contraction: cross bridge formation
•Tension increases
–Period of relaxation: initiated by Ca2+ reentry into SR
* Tension declines to zero
* Muscle contracts faster than it relaxes
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Differences in strength and duration of twitches are due to
•variations in metabolic properties and enzymes between muscles
–Example: eye muscles contraction are rapid and brief, whereas larger, fleshy muscles (calf muscles) contract more slowly and hold it longer
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Graded muscle responses
•vary strength of contraction for different demands
–Required for proper control of skeletal movement
•Responses are graded by:
Changing frequency of stimulation
Changing strength of stimulation
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•Muscle response to changes in stimulus frequency
–Single stimulus results in single contractile response (i.e., muscle twitch)
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Wave (temporal) summation
–results if two stimuli are received by a muscle in rapid succession
•Muscle fibers do not have time to completely relax between stimuli, so twitches increase in force (tension) with each stimulus
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•Muscle response to changes in stimulus strength
–Recruitment (or multiple motor unit summation): stimulus is sent to more muscle fibers, leading to more precise control of contraction force
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–Types of stimulus involved in recruitment:
* Subthreshold stimulus: stimulus not strong enough, so no contractions seen
* Threshold stimulus: stimulus is strong enough to cause first observable contraction
* Maximal stimulus: strongest stimulus that increases to maximum contractile force
–All motor units have been recruited
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–Recruitment works on size principle
* Motor units with smallest muscle fibers are recruited first
* Motor units with larger and larger fibers are recruited as stimulus intensity increases
* Largest motor units are activated only for most powerful contractions
* Motor units in muscle usually contract asynchronously
–Some fibers contract while others rest
–Helps prevent fatigue
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Muscle Tone
* Constant, slightly contracted state of all muscles
* Due to spinal reflexes
–Groups of motor units are alternately activated in response to input from stretch receptors in muscles
•Keeps muscles firm, healthy, and ready to respond
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Isotonic contractions:
•muscle changes in length and moves load
–Isotonic contractions can be either concentric or eccentric:
•Concentric contractions: muscle shortens and does work
–Example: biceps contract to pick up a book
•Eccentric contractions: muscle lengthens and generates force
–Example: laying a book down causes biceps to lengthen while generating a force
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•Isometric contractions
–Load is greater than (or equal to) the maximum tension the muscle can generate, so the muscle neither shortens nor lengthens
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•Electrochemical and mechanical events are same in isotonic or isometric contractions, but results are different
–In isotonic contractions, actin filaments slide and cause movement
–In isometric contractions, cross bridges generate force, but actin filaments do not slide
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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
* Available stores of ATP depleted in 4–6 seconds
* ATP is the only source of energy for contractile activities; therefore it must be regenerated quickly
**•ATP is regenerated quickly by three mechanisms:**
**–Direct phosphorylation of ADP by creatine phosphate (CP)**
**–Anaerobic pathway: glycolysis and lactic acid formation**
**–Aerobic respiration (mitochondria)**
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•Direct phosphorylation of ADP by creatine phosphate (CP)
–Creatine phosphate is a unique molecule located in muscle fibers that donates a phosphate to ADP to instantly form ATP
* Creatine kinase is enzyme that carries out transfer of phosphate
* Muscle fibers have enough ATP and CP reserves to power cell for about 15 seconds
Creatine phosphate + ADP ® creatine + ATP
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Anaerobic pathway:
•glycolysis and lactic acid formation
–ATP can also be generated by breaking down and using energy stored in glucose
•Glycolysis: first step in glucose breakdown
–Does not require oxygen
–Glucose is broken into 2 pyruvic acid molecules
–2 ATPs are generated for each glucose broken down
•Low oxygen levels prevent pyruvic acid from entering aerobic respiration phase
–In the absence of oxygen, referred to as anaerobic glycolysis, pyruvic acid is converted to lactic acid
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•Anaerobic pathway: glycolysis and lactic acid formation (cont.)
–Lactic acid
* Diffuses into bloodstream
* Used as fuel by liver, kidneys, and heart
* Converted back into pyruvic acid or glucose by liver
–Anaerobic respiration yields only 5% as much ATP as aerobic respiration, but produces ATP 2½ times faster
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•Aerobic respiration
–Produces 95% of ATP during rest and light-to-moderate exercise
•Slower than anaerobic pathway
–Consists of series of chemical reactions that occur in mitochondria and require oxygen
•Breaks glucose into CO2, H2O, and large amount ATP (32 can be produced)
–Fuels used include glucose from glycogen stored in muscle fiber, then bloodborne glucose, pyruvic acid from glycolysis and free fatty acids
•Fatty acids are main fuel after 30 minutes of exercise
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•Energy systems used during sports
–Aerobic endurance
•Length of time muscle contracts using aerobic pathways
–Light-to-moderate activity, which can continue for hours
–Anaerobic threshold
•Point at which muscle metabolism converts to anaerobic pathway
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Muscle Fatigue
* Physiological inability to contract despite continued stimulation
* Usually occurs when there are ionic imbalances
–Levels of K+, Ca2+, Pi can interfere with E‑C coupling
–Prolonged exercise may also damage SR and interferes with Ca2+ regulation and release
•Lack of ATP is rarely a reason for fatigue, except in severely stressed muscles
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•For a muscle to return to its pre-exercise state:
–Oxygen reserves are replenished
–Lactic acid is reconverted to pyruvic acid
–Glycogen stores are replaced
–ATP and creatine phosphate reserves are resynthesized
•All replenishing steps require extra oxygen, so this is referred to as excess postexercise oxygen consumption (EPOC)
–Formerly referred to as “oxygen debt”
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Force of Muscle Contractions
•Force of contraction depends on number of cross bridges attached, which is affected by four factors:
1. Number of muscle fibers stimulated (recruitment): the more motor units recruited, the greater the force.
2. Relative size of fibers: the bulkier the muscle, the more tension it can develop
•Muscle cells can increase in size (hypertrophy) with regular exercise
3. Frequency of stimulation: the higher the frequency, the greater the force
•Stimuli are added together
4. Degree of muscle stretch: muscle fibers with sarcomeres that are 80–120% their normal resting length generate more force
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•How fast a muscle contracts and how long it can stay contracted is influenced by:
–Muscle fiber type
–Load
–Recruitment
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•Muscle fiber type
–Classified according to two characteristics
1.Speed of contraction – slow or fast fibers according to:
–Speed at which myosin ATPases split ATP
–Pattern of electrical activity of motor neurons
2.Metabolic pathways used for ATP synthesis
–Oxidative fibers: use aerobic pathways
–Glycolytic fibers: use anaerobic glycolysis
–Based on these two criteria, skeletal muscle fibers can be classified into three types:
•Slow oxidative fibers, fast oxidative fibers, or fast glycolytic fibers
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–Different muscle types are better suited for different jobs
•Slow oxidative fibers: low-intensity, endurance activities
–Example: maintaining posture
•Fast oxidative fibers: medium-intensity activities
–Example: sprinting or walking
•Fast glycolytic fibers: short-term intense or powerful movements
–Example: hitting a baseball
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•Load and recruitment
–Load: muscles contract fastest when no load is added
* The greater the load, the shorter the duration of contraction
* The greater the load, the slower the contraction
–Recruitment: the more motor units contracting, the faster and more prolonged the contraction
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Aerobic (Endurance) Exercise
* such as jogging, swimming, biking leads to increased:
* Muscle capillaries
* Number of mitochondria
* Myoglobin synthesis
–Results in greater endurance, strength, and resistance to fatigue
–May convert fast glycolytic fibers into fast oxidative fibers
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Resistance exercise
•(typically anaerobic), such as weight lifting or isometric exercises, leads to
–Muscle hypertrophy
•Due primarily to increase in fiber size
–Increased mitochondria, myofilaments, glycogen stores, and connective tissue
Increased muscle strength and size
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Disuse atrophy
•(degeneration and loss of mass)
–Due to immobilization or loss of neural stimulation
–Can begin almost immediately
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Smooth Muscle
* Found in walls of most hollow organs, except heart
* Microscopic structure:
–Spindle-shaped fibers: thin and short compared with skeletal muscle fibers
•Only one nucleus, no striations
–Lacks connective tissue sheaths
* Contains endomysium only
* All but smallest blood vessels contain smooth muscle organized into two
layers of opposing sheets of fibers
–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
* Allows peristalsis: alternating contractions and relaxations of layers mix and squeeze substances through lumen of hollow organs
* No neuromuscular junction, as in skeletal muscle
* Instead, autonomic nerve fibers innervate smooth muscle
–Contain varicosities (bulbous swellings) of nerve fibers
–Varicosities store and release neurotransmitters into a wide synaptic cleft referred to as a diffuse junction
* Smooth muscle does not contain sarcomeres, myofibrils, or T tubules
* Sarcolemma contains pouchlike infoldings called caveolae
–Caveolae contain numerous Ca2+ channels that open to allow rapid influx of extracellular Ca2+
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•Smooth muscle also differs from skeletal muscle in following ways:
–Thick filaments are fewer and have myosin heads along entire length
–No troponin complex
•Protein calmodulin binds Ca2+
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Smooth Muscle Filaments
–Thick and thin filaments arranged diagonally
•Myofilaments are spirally arranged, causing smooth muscle to contract in corkscrew manner
–Intermediate filament–dense body network
* Contain lattice-like arrangement of noncontractile intermediate filaments that resist tension
* Dense bodies: proteins that anchor filaments to sarcolemma at regular intervals
Correspond to Z discs of skeletal muscle
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•Mechanism of contraction
–Slow, synchronized contractions
–Cells electrically coupled by gap junctions
•Action potentials transmitted from fiber to fiber
–Some cells are self-excitatory (depolarize without external stimuli)
* Act as pacemakers for sheets of muscle
* Rate and intensity of contraction may be modified by neural and chemical stimuli
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–Contraction in smooth muscle is similar to skeletal muscle contraction in following ways:
* Actin and myosin interact by sliding filament mechanism
* Final trigger is increased intracellular Ca2+ level
* ATP energizes sliding process
* Contraction stops when Ca2+ is no longer available
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–Contraction in smooth muscle is different from skeletal muscle in following ways:
* Some Ca2+ still obtained from SR, but mostly comes from extracellular space
* Ca2+ binds to calmodulin, not troponin
* Activated calmodulin then activates myosin kinase (myosin light chain kinase)
* Activated myosin kinase phosphorylates myosin head, activating it
–Leads to crossbridge formation with actin
–Stopping smooth muscle contraction requires more steps than skeletal muscle
•Relaxation requires:
–Ca2+ detachment from calmodulin
–Active transport of Ca2+ into SR and extracellularly
–Dephosphorylation of myosin to inactive myosin
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•Energy efficiency of smooth muscle contraction
–Slower to contract and relax but maintains contraction for prolonged periods with little energy cost
* Slower ATPases
* Myofilaments may latch together to save energy
–Makes ATP via aerobic respiration pathways
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•Regulation of contraction
–Controlled by nerves, hormones, or local chemical changes (hormones, CO2, pH)
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•Special features of smooth muscle contraction
–Response to stretch
•Stress-relaxation response: responds to stretch only briefly, then adapts to new length
–Retains ability to contract on demand
–Enables organs such as stomach and bladder to temporarily store contents
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Types of Smooth Muscle
•All smooth muscle is categorized as either:
–Unitary or multiunit
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•Unitary (visceral) smooth muscle
–Electrically coupled by gap junctions (so work together as a unit)
–In all hollow organs except heart
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•Multiunit smooth muscle
–Located in large airways, large arteries, arrector pili muscles, and iris of eye
–Few Gap junctions
–Independent muscle fibers; innervated by autonomic NS; graded contractions occur in response to neural stimuli
–Has motor units; responds to hormones
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•Difference in muscle mass between sexes:
–Female skeletal muscle makes up 36% of body mass
–Male skeletal muscle makes up 42% of body mass, primarily as a result of testosterone
•Males have greater ability to enlarge muscle fibers, also because of testosterone
–Body strength per unit muscle mass is the same in both sexes
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Muscular dystrophy:
•group of inherited muscle-destroying diseases
–Generally appear in childhood
•Muscles enlarge as a result of fat and connective tissue deposits, but then atrophy and degenerate
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Duchenne muscular dystrophy (DMD)
•most common and severe type
–Caused by defective gene for dystrophin
–Inherited, sex-linked trait, carried by females and expressed in males (1/3600)
–Dystrophin is a cytoplasmic protein that links the cytoskeleton to the extracellular matrix, stabilizing the sarcolemma
•Fragile sarcolemma tears during contractions, causing entry of excess Ca2+
–Leads to damaged contractile fibers
* Inflammatory cells accumulate
* Muscle mass declines
* Victims become clumsy and fall frequently
–Usually appears between ages 2 and 7
No cure is known
•Patients usually die of respiratory failure in their early 20s
