-
Cell membrane is a barrier
- Separates inside of cell from outside fluid
- -Inside = cytosol = intracellular
- -Outside = extracellular = interstitial
- -Allows inside concentration of electrolytes
- and other solutes to be different from
- extracellular concentration of solutes
- -Higher inside:K+, proteins (negatively charged;A-)
- -Higher outside:Na+, Cl, Ca+2
-
Permeability
- The ease with which substances can cross the cell membrane
- -Nothing passes through an impermeable barrier(if 100%)
- -Anything can pass through a freely permeable barrier
- -Diff cells are permeable to diff substances (b/c of diff transport mechanisms)
-
What level of permeability are cell membranes?
Selectively permeable (because of different transport mechanisms)
-
Passive Transport
Cell doesn't expend energy (No ATP consumed)
-
Active Transport
Cell expends energy (ATP consumed from going against concentration gradient)
-
Diffusion (in a solution or across a membrane)
- Passive; Random motion of ions and molecules down their concentration gradient
- -High to low concentration
-
Carrier Mediated Transport (across membrane)
Passive or active; requires transport protein in membrane
-
Why can't anything hydrophilic or large pass thru a membrane alone?
They MUST have a transport protein
-
Diffusion (definition)
Movement of a substance from an area of high concentration to low concentration
-
How do molecules with no electrical charge diffuse?
Diffuse down or along the chemical concentration gradient of the molecule
-
How do charged ions and molecules diffuse?
- -Diffuse based on electro-chemical gradient
- -Chemical concentration gradient is one driving force
- �Electrical concentration gradient is another driving force
- -----positives go from positives to negatives on gradient
-
Diffusion in body fluids (examples)
- -O2 moves from lungs into blood, into interstitial spaces, into cells
- -CO2 moves from cells into interstitial spaces, into blood, out through lungs
- -Water moves across epithelium of digestive tract into body tissues
- -Anesthetics diffuse into cells
-
Do membranes need to be permeable to the substance for diffusion to occur?
YES
-
Diffusion: Lipid Bilayer of cell membranes
- -permeable to O2, CO2 and most hydrophobic molecules (steroids)
- -NOT permeable to most large molecules and most hydrophilic molecules (glucose, glycerol)
-
What do membrane proteins provide for diffusion?
They provide channels for passive diffusion
-
Osmosis
- -Diffusion of water across a semi-permeable
- membrane in response to solute differences
- -Concentration of water is related to total concentration of all solutes (dissolved materials) including ions, proteins,
- monomers, polymers, etc.
- -Water moves by diffusion down its concentration gradient
-
Water diffuse from _____________ to ______________
low solute concentration to high solute concentration
-
Osmotic Pressure
The force of water movement into a solution (pulling)
-
Solute
Something that is dissolved in a liquid
-
Tonicity
The effects of extracellular solutions on cells
-
Isotonic solution
No net osmosis, no net gain or loss of water (equail in and out - RBC's)
-
Hypotonic solution
- Net gain of water into cell
- -Can result in cytolysis (add too much H2O to inside, overfilling cell - may burst)
-
Hypertonic solution
- Net flow out of the cell (way more solutes outside of cell)
- -Can result in crenation (shrivels) - extreme dehydration
-
Hypotonic extracellular solution (low tone)
- Less solutes, more water than intracellular solution
- -Water will flow INTO the cell
-
Hypertonic extracellular solution (high tone)
- More solutes, less water than intracellular solution
- -Water will flow OUT of cell
-
Factors Influencing Diffusion
- *Distance � concentration gradients effective only over short distances � few cells are more than 125 �m from a blood vessel
- *Diffusion is faster if
- -Molecule is smaller
- -Temperature is higher
- -Concentration gradient is higher
- *For charged ions, concentration gradient is one driving force, electrical gradient is another driving force
- ---very fast during exercise
-
Diffusion (in a solution or across a membrane)
- -Passive (going down gradient)
- -Random motion of substances down their chemical or electrical concentration gradient
- -Channel proteins allow diffusion of some hydrophilic substances across membranes
-
Carrier mediated transport (across membrane)
- -Passive (down gradient) or active (across or up gradient)
- -REquires transport protein in membrane
-
Carrier mediate transport
- -Membrane proteins biund and transport specific molecules or ions
- -Many carrier proteins transport one substance, one way only; some fo two at same time
-
Specificity
Carrier proteins are generally specific for a particular substance
-
Saturation limits
Rate of transport subject to number of transport proteins available
-
Regulation
Various control factors exist that affect activity of carrier proteins
-
Cotransport
- Both go same directions across membrane
- -uses less ATP
-
Counter-Transport
- Go opposite directions across membrane
- -Restores balance
-
Facilitated Diffusion (across membrane)
- -Substance moves DOWN conc. gradient (E supplied, no ATP)
- -Requires transport proteins (diff transport proteins for diff substances)
- -Differs from simple diffusion b/c of transport proteins (maximum rate is dependent on availability of transport proteins-can reach saturation)
-
Facilitated Diffusion (w/ co-transport against conc. gradient)
- -One substance moves down its conc. gradient (E supplied, no ATP)
- -Another substance moves against its conc, gradient (E supplied)
- -Requires transport protein
-
Active transport (across membrane)
- -Consumes ATP
- -Independent of Conc. gradient
- Examples: Ion pumps, secondary active transport
-
Trans-membrane potential
- -Difference in electrical potential between inside and outside a cell
- --Outside more (+), inside more (-) -->resting membrane potential
-
Electro-chemical gradient
- -Sum of forces of all chemical and electrical gradients acting across the cell membrane
- --->work together to make ONE gradient
-
Bio-electricity in nerve and muscle cells
- -Ion flow is a form of electrical current
- -Ions move across the membrane through protein channels
- --Driving force is diffusion along electrochemical gradient (trans-membrane potential is equivalent of a battery)
-
Gated channels
Open in response to various stimuli
-
Chemically regulated (gated) channels
Open or close when they BIND specific chemicals
-
Voltage regulated (gated) channels
- Open of close in response to level of trans-membrane potential
- --only open if change in chemical charge
-
Acetylcholine (ACh) gated sodium ion channel
- -Neuromuscular junction � synapse between nerve cell and muscle cell
- -Nerve cell process releases acetylcholine by exocytosis
- -ACh binds to receptor on gated sodium channels in muscle membrane, causing sodium channel to open
-
Ex. of Voltage regulated gated channel
- -Found in excitable membranes, those capable of having action potentials, closed at resting potential
- -Nerve cells and muscle cells are excitable
-
Voltage regulated ion channels
-Change in level of trans-membrane potentialopens or closes voltage regulated ion channels
-
Depolarization
Trans-membrane potential becomes LESS NEGATIVE (inside of cell becomes more positive)
-
Hyperpolarization
Trans-membrane potential becomes MORE NEGATIVE
-
Repolarization
Trans0membrane potential returns toward resting potential after being depolarized
-
Skeletal Muscle
- Attached to bone
- -Striated, voluntary
-
Cardiac Muscle
- Found in the heart
- -Striated Involuntary
-
Smooth Muscle
- Lines hollow organs, blood vessels, iris of eye, GI tract, uteris and ureter
- -Nonstriated, invlountary
-
Skeletal Muscle functions
- -Produce skeletal movement
- -Maintain posture and body position
- -Support soft tissues
- -Guard entrances and exits
- -Maintain body temperature
- -Nutrient Reserves
-
Origin and Insertion
- (attached to bone by tendon)
- O-attached to bone that remains relatively stationary during movement
- I-attached to bone that moves
-
Synergistic muscles
Muscles that work together for movement
-
Antagonistic muscles
- Muscles that work opposite (have opposite effect)
- -Flexors AND extensors
-
Endomysium
Covers individual muscle fibers (plasma membrane)
-
Perimysium
- Sheathes bundles of muscle fibers (muscle fasicles)
- -contain blood vessels and nerves
-
Epimysium
- Surrounds a muscle
- -contains blood vessels and nerves
-
Deep fascia
- Wrap groups of cooperating muscles together
- -Fascicles separated by Connective TIssue
-
Muscle cell = ___________
muscle fiber
-
Each muscle cell is as long as _____________
- the muscle
- -Multinucleate, very long cell
-
Skeletal muscle cells are formed during _______
-embryogenesis (by end-to-end fusion of uni-nucleate myoblasts)
-
Myoblasts
Fuse together to make one long muscle with mulit-nuclei
-
Adult muscle repair is _________
- limited
- -New skeletal muscle cells come from stemm cells called SATELLITE CELLS
-
Satellite cells
- Stem cells for muscle repair
- -Will divide and try to repair muscle injuries BUT doesn't repair quickly and scar tissue may form faster
-
Myofilaments
Protein filaments. Large quantities of myofilaments compose the muscle fiber
-
Myofibrils
- Bundles of myofilaments (proteins)
- -Can actively shorten; anchored to inner surface of sarcolemma at either end of cell
-
Actin has _______ myofilaments
thin, skinny strands
-
Myosin has _________ myofilaments
think
-
Sarcoplasm is the ______________ and is _______ to the muscle
muscle cell membrane, specific
-
Sarcolemma is the ______________
cell membrane (it's very excitable)
-
Sarcoplasmic REticulum (SR) holds __________
Calcium reserves (it's a modified ER)
-
Sarcolemma's T-tubules
- -Make muscle contract quickly together
- -NArrow tubes of sarcolemma that extend into cell at right angles to cell surface
- -Conduct action potential deep into cell
- -COmes in close contact with SR
-
SR=Lots of _____________; forms a ____________________ around each myofibril
- -Calcium (stores high conc. of ions needed for contraction);
- -tubular network (completely surrounds actin and myosin. Terminal cisternae form triads with T-tubules)
-
Sarcomeres
- Repeating units of myofilaments in myofibril
- -Arrangements of actin and myosin in fiber/cell
-
Striated sarcomeres
-Differences in distribution of thick and thin myofilaments gives banded appearance
-
I-bands
- lIght bands
- -contain only thin filaments
-
A-bands
- dArk bands
- -contain thick filaments, and some overlap with thin filaments
- -H band contains only thick filaments
-
Z disk (line)
border between sarcomeres
-
Muscles shorten during contraction because:
The mysoin and actin filaments slide between each other to shorten each sarcomere
-
How do you make muscles bigger?
Adding/producing more myofibrils
-
What are responsible for muscle contraction?
Interactions between thin and thick sarcomere filaments (actin and myosin)
-
Thin filaments slide over thick filaments shortening the _____________
sarcomere
-
Myofibrils consist of thousands of ____________ end to end
-sarcomeres
-
Shortening occurs in every ___________ in the myofibril, thus shortens the __________
sarcomere, myofibril
-
When is the sarcomere at maximum shortening?
- When it is the width of the A band, no I band or H band is visible
- --Actin has maximally overlapped myosin
-
Thin actin filaments are attached to __________
Z disk
-
What occurs as actin filaments move toward center of sarcomere
- -Thin filaments slide over thick filaments (myosin)
- -Z lines are pulled closer together
- -I bands and H bands are narrow
- -A band stays the same width
- ----The area with no myosin gets really small
-
What causes thin and thick myofilaments to slide across each other?
-Cross bridges are formed and pull the actin over the mysoin
-
Cross bridges
- -When myosin heads bind to the active site of actin
- -Once formed, they change the sahpe pulling actin past the myosin
- -Use ATP to change shape and pull the actin - convert chemical energy to mechanical energy
-
Molecular anatomy of Myosin
- -Have elongated tail, globular head - golf club shape
- -arrayed with half facing each end, center is just tails
- -Heads form cross bridges during CONTRACTION
- -Interactions between myosin and actin prevented by tropomysin during rest
-
Tropomyosin
- Protein that sits on top of active sites of actin, prevents cross bridges
- -Attached by troponin (protein)
-
Molecular anatomy of Actin
- -Twisted strand composed of two rows of individual globular actin molecules
- -Each actin molecule in twisted strand has active site to which myosin head can attach (only attracted to head)
- -Strands of tropomyosin cover the actin active site during rest
-
Calcium is the _______that binds to ____________to unlock ___________, revealing the active site of actin
key, troponin, tropomyosin
-
Sliding filament theory
- -Cyclic process beginning with CALCIUM release from SR
- --Calcium binds to troponin
- --Troponin moves, moving tropomyosin and exposing actins active site
- --Mysoin head forms cross bridge to actin, bends toward center of sarcomere, pulling the actin closer to the M-line
- --ATP allows release of cross bridge
-
What's the role of ATP in muscle contraction?
- -ATP supplies the E for the movement of the mysoin head (converts chem E to mechanical E of movement)
- -ATP bins to un-energized myosin head (ATP is split to ADP&P, mysoin head moves into energized position)
- -Mysoin head in energized position binds to actin active site (releases ADP&P, pivots, pulling on and actin)
- -ATP binds to un-energized myosin head (detaches mysoin from actin, Actin is split and head is energized)
-
Role of Calcium ions in muscle contraction?
- -Concentration of Ca2+ around sarcomere controls contraction
- -Ca is low around sarcomere at rest
- -Action potential in sarcolemma and T-tubules result in contraction (opens Ca channels in SR, releases Ca in sarcoplasm)
- -Ca binds to troponin
- -Mysoin heads bind to active site until Ca levels fall
- -When Ca levels fall: tropomyosin covers actin ending contraction
-
Motor neuron
- Nerve cell that controls muscle contraction
- --once depolarized it realeases acetyl choline
- --action potential initiated in motor neuron in response to CNS commands
-
Neuromuscular junction
- Synapse between motor neuron and muscle cell
- --every muscle fiber has it's own neural junction
-
Action potentials travel through ______ ________ and arrives at the ______ ______.
motor neuron, synaptic terminal
-
Acetyl Choline (ACh) is released from ____________ and diffuses across _____________, then binds to receptors on ________ gated socium channels in muscle membrane
motor neuron terminal, synaptic gap, chemically
-
Sodium ions flow into muscle cells causing it to __________
Depolarize (an action potential starts in the muscle cell)
-
Chemically regulated gates stay open as long as ______ is present
ACh (acetyl choline)
-
Acetylcholine Esterase (AChE) location and function
- -lovated in synaptic gap
- -rapidly breaks down AcH (stops contraction by 'gobbling' up ACh and closing gates)
-
Action Potential in muscle cell membranes are conducted intot he interior of the muscle via __________ and cause Ca2+ to be released from _____.
T-Tubules, SR
-
Action potential along ______ causes release of calcium from ______ of SR
T-tubule, cisternae
-
Excitation/contraction of muscle cycle repeats until ________ ion concentrations fall to rsting level.
- Calcium
- -high frequenct creates a stronger contraction
-
How does Ca ion concentration return to resting level?
- -AP depolarization ends, voltage gated Ca channels in SR close (Ca flow in sarcoplasm stops)
- -Ca is actively transported out of sarcoplasm
- ---some acros sarcolemma to outside of cell (requires ATP)
- ---across SR to reticulum membrane into SR (requires ATP)
- ---Requires ATP for active transport protein to function
-
Duration of contraction depends on:
- 1. Duration of stimulation at nerve-muscle synapse (neuromuscular junction)
- 2. Fresence of calcium ions in sarcoplasm (contraction cycle continues until Ca ion conc. returns to resting levels)
- 3. Availability of ATP (No ATP = contraction cycle stops no matter what)
-
Conraction ends and relaxation occurs when:
- 1. AP stops in motor neuron
- 2. AChE breaks down ACh in the neuromuscular synaptic gap
- 3. ACh gated channels close (Na is no longer diffusing into cell)
- 4. Action potentials stop occuring in sarcolemma and T-tubules
- 5. Ca levels in sarcoplasm return to resting levels (no new cross bridges can form)
- 6. Relaxation requires ATP (to pump Ca into SR, to discunnect myosin heads from actin, no ATP=rigor mortis)
-
How does botulism affect ACh?
Blockage of release of ACh
-
Polio (Muscular system disorders)
Loss of motor neuron
-
Myasthenia gravis (Muscular system disorders)
- Interference with binding of ACh to receptors
- -muscles don't resoind
-
Prolonged contraction (Muscular system disorders)
Interference with ACh Esterase activity
-
Peripheral nerve damage (Muscular system disorders)
loss of motor neuron axon
-
MS (Muscular system disorders)
Reduction of AP efficiency, damage to myelin
-
Tetanus (Muscular system disorders)
- Excessive stimulation of motor neuron
- -send to much ACh
-
Tension
- Sliding and pulling of actin and myosin filaments causes sarcomere shortening
- -in a muscle cell, all sarcomeres shorten causing the muscle cell to shroten
- -Pulls on CT and bone that it's attached to
-
Tension in a muscle cell depends on:
- -Tension that develops in individual muscle cells during contraction
- -Number of muscle cells that contract (neighbor cells may not contract)
- --muslce cells are grouped in motor units
-
Amount of tension depends on number of ______ _______ formed
- cross bridges
- --depends on degree of everlap of actin and myosin
-
Skeletal muscle contracts _____ forcefully over narrow ranges of resting ________
most, lengths (overlap)
-
Twitch (quick contraction)
- -Cycle of contraction, relaxation produced by a SINGLE action potential in a muscle cell
- -Not typical in normal muscle cell activity
- --can only be seen on a dissected muscle and forcing it to twitch
-
Latent phase (twitch)
- Action potential occurs
- -No contraction until Ca is released from SR
-
Contraction Phase (twitch)
- Tension rises to peak
- -Ca moves tropomyosin off of actin sites
- -Myosin cross bridges form, actin is pulled
-
Relaxation Phase (twitch)
- Tension fails to resting levels
- -Ca is pumped back into SR
- -Actin sites covered by tropomyosin
- -No cross bridges remain
-
Summation of tension produces ____________________
- greater tension
- -sum is greater than its individual parts
-
Summation
- Repeated stimulation produced before relaxation phase has been completed
- -summation of tension caused by build up of Ca ions in sarcoplasm
-
Complete tetanus
Maximum tension production in a muscle cell-maximum cross bridge formation
-
Atrophy
- muscle become smaller (lack of use)
- -decrease in diameter of a muscle
-
Hypertrophy
- Muscle become larger
- -increase in diameter of muscle (adds more myofibrils)
-
Motor units (muscle tension)
- -All muscle fibers innervated by one motor neuron
- -Amount of tension produced in a muscle determined by number of motor units activated (Max tension-all motor units active)
- -Asynchronous motor unit summation for sustained contractions (allows one to relax while others are still active)
-
Differences in number and size of motor units in different muscles determines what?
Precision of control of movements
-
Small motor unit=?
- Precise control
- -One motor neuron innervates a small number of muscle fibers - Fine motor skills
-
Large motor unit=?
- Gross movement control
- -One motor neuron innervates a large number of muscle fibers
-
Muscle Tone
- Resting tension in a skeletal muscle
- -In any muscle some motor units are always active, tense and firm
- -Stabilizes bones and joints
- -Greater resting muscle tone causes higher resting rate of metabolism
-
Why is it difficult to contract a muscle that has been overstretched?
Few if any mysoin-actin cross bridges can form when sarcomeres are overextended
-
Isotonic Contracion
Tension rises, length of muscle changes (gets shorter or longer)
-
Concentric
Muscle tension exceeds resistnace and muscle SHORTENS
-
Eccentric
Peak tension developed is less than the resistance, muscle ELONGATES
-
Isometric Contraction
- Tension rises, length of muscle remains constant
- -Tension produced never exceeds resistance
- -Muscle as a whole doesn't shorten until individual fibers shorten until internal CT and tendons are rigid
- -Cannot shorten further b/c tension doens't exceed resistance
-
No ______ mechanism for muscle fiber elongation
- Active
- -A muscle cell doens't cause itself to lengthen after contraction process ends - relaxes
-
Muscle returns to resting length after contraction because:
- -Recoil in elastic components in CT
- -Contraction of opposing muscle groups
- -Gravity
-
How often must cells regenerate ATP?
Muscle cell must generate ATP at apporximately the same rate as it is used for the remainder of contraction
-
What are Creatine Phosphate reserves for
- -ATP isn't used for long term storage of E
- -At rest, muscle cell makes more ATP than needed, extra ATP transfers P to creatine for storage
- -CP reserves release stored energy to convert ADP to ATP when ATp is needed at start of contraction
-
________ _________ provides most ATP needed for resting muscle and for moderate levels of muscle activity
Aerobic repsiration (PRESENCE OF O)
-
At peak activity, alson need _______ (glycolysis) to generate additional ATP
- Anaerobic
- ----In addition to aerobic!!!
-
Aerobic Metabolism
- -Cellular Respiration (Uses O2- Releases CO2)
- -Occurs in Mitochondria: Citric Acid Cycle (CO2 produced), ETC (ATP synthesis, O2 used)
-
Resting muscle fibers rely on ________ metabolism of _____ ______ to generate ATP
- Aerobic, fatty acids
- -FAtty acids absorbed from circualtion
- -Broken down to Acetyl CoA
- -Excess aTP used to store glucose into GLYCOGEN, creates Creatine Phosphate
-
Contracting muscle cell fibers rely on _____ AND ______ metabolism of glucose
Aerobic, anaerobic
-
Anaerobic Metabolism
- -Produces ATP rapidly (allows muscle cell to generate extra ATP when aerobic isn't enough)
- -Disadvantages: Inefficient use of glucose, lactic acid LOWERS intracellular pH (donates H electrons)
-
Recovery Period
- -Begins immediatley after activity ends
- -Oxygen debt (excess post-exercise O consumption - panting)
- -Rebuild ATP and CP levels
- -Recycle lactic acid to make pyruvate
- -Rebuild glycogen reserves
-
People in good condition make more __________, making them able to exercise more.
Mitochondria
-
Fatigued muscle
A muscle that can no longer perform a required level of activity
-
Causes of muscle fatigue
- -Exhaustion of E resources
- -Build up of lactic acid and lowering of pH (acidosis)
- -Psychological fatigue
-
Force
(Power, strength) Maximum amount of tension produced by a muscle or muscle group
-
Endurance
- Amount of time during which an individual can perform a particular activity
- -size doesn't matter, efficiency does(amount of mitochondria)
-
Factors that determine performance capabilities of skeletal muscle:
- 1. Types of muscle fibers present in the muscle
- 2. Physical conditioning or training
-
Types of muscle fibers (3):
- 1. Type 1-Slow fibers (Red)
- 2. Type 2-A-Intermediate fibers
- 3. Type 2-B-Fast fibers (white)
-
Red fibers
- Type 1; Slow twitch oxidative fibers
- -Have lots of mitochondria (efficient without O)
- -Rich blood supply (why it's red)
- -"legs of the chicken"
- -Low prolonged movements, marathons
-
White fibers
- Type 2-B; fast twitch glycolytic fibers
- -Most efficient: anaerobic (glycolysis only)
- -For quick movements, sprinting
- -"Breast meat of chicken"
- -Large in diameter
-
Slow fibers are _____ the diameter of fast fibers
half
-
Slow fibers have a high concentration of ________ and can contract for ______ periods of time
Myoglobin (binds O in muscles-makes more red and has iron), long
-
Slow fibers have abundant ________, and take ______ times as long to contract after stimulation
Mitochondria (aerobic, oxidative metabolism), three
-
Slow fibers are _______ resistant meaning they can contract for long periods of time
Fatigue
-
Fast fibers have large ______ reserves and contain densely packed _______
glycogen, myofibrils (tons of actin and myosin)
-
Fast fibers have few _______ making them prone to _________ metabolism
mitochondria, anaerobic (glycolytic metabolism)
-
Fast fibers produce ______, powerful contractions of ______ duration making them ________ rapidly
rapid, short, fatigue
-
Pink fibers
- Fast twitch oxidative fibers - Type 2-A
- -Fast fibers that gain greater resistance to fatigue
- --Have additional capillary supply
- --More mitochondria
- --Smaller in diameter
- --Not as dependant on anaerobic metabolism
- -Adapt to endurance
-
We are born with a unique amount of each of the three fibers, however, which fibers can be CONVERTED?
-White(fast fibers) to pink (intermediate) but NONE TO WHITE
-
Percentage of slow fibers and fast fibers are ________ determined and can vary among muscles
- genetically
- -Pale (white) muscles:mostly fast fibers
- -Dark (red) muscles:dominated by slow fibers
-
Training can change the percentage of _______ fibers that have intermediate properties to build endurance
Fast
-
Change in muscle size is due to an increase or decrease in ________ of muscle fibers within the muscle
- Diameter
- -Based on activity level
-
Muscle Fiber A is 2x the diameter of Muscle Fiber B. A can produce greater tension than B because:
A has more myosin to actin cross bridges forming during a contraction
-
Anaerobic Endurance
Time period in which muscular contractions are sustained by GLYCOLYSIS after depeting ATP/CP reserves
-
Aerobic Endurance
Time period in which muscle can continue to contract while supported by MITOCHONDRIAL activites after depleting ATP/CP reserves
-
How do you improve Anaerobic Endurance
- -Frequent, brief intensive workouts
- -Increase muscle mass
- -Increase ATP/CP reserves
- -Increase glycogen stores
- -Increase ability to tolerate lactic acid buildup
-
How do you improve Aerobic Endurance
- -Sustained low levels of activity
- -Increase blood supply to muscles
- -Imporve cardiovascular activity
-
Primary disorders
- Result from problems with the muscular system itself
- -Muscle trauma
- -Muscle infections
- -Inherited disorders
- -Tumors
-
Secondary disorders
- Result of problems originating in other systems (mostly nervous system)
- -NS disorders that affect the coordination or control of muscle contraction (MS)
- -Nutritional or metabolic problems that affect electrolyte concentrations of the available E supply (spasms and cramps)
- -Cardiovascular disorders that restrict or reduce blood flow to skeletal muscles
-
Most muscle disorders are __________ disorders
Secondary
-
Muscle spasm (cramp)
- Strong, sudden, usually painful, unwanted CONTRACTION
- -Mostly from electrolyte imbalance
-
Muscle spasticity
- Excessive muscle tone
- -Muscles contract at rest to make it look more tone
-
Muscle flaccidity
- Very low muscle tone
- -Muscle doesn't contract at rest
-
Muscle atrophy
Deterioration or wasting due to disease, immobility, or interference with normal motor neuron innervation (of acetyl choline)
-
Myositis
- Muscle inflammation (swollen)
- -Polymyositis & dermatomyositis - autoimmune
-
Muscle Strain
- Tears in muscle tissue
- -Usually can repair itself
-
Muscle sprain
Tears in ligament or tendon or joint capsule
-
Paralysis
- Loss of voluntary motor control
- -Flaccid or spastic (can be from excessive spasming)
-
Blockage of release of Acetyl choline results in ________ paralysis (ex. botulism)
Flaccid
-
Interference with binding of ACh to receptors results in _______ paralysis
Flaccid
-
Interference iwth ACh Esterase activity results in _______ paralysis
Spastic
-
Loss of motor neuron results in ______ paralysis (ex. polio)
Flaccid (increased branching of remaining motor neurons
-
Loss of motor neuron axon results in _______ paralysis (ex. peripheral nerve damage)
Flaccid
-
Excessive stimulation of motor neuron results in _______ paralysis (ex. tetanus)
Spastic
-
Muscular dystrophies
- -Duchenne's MD-gene on X chromosome
- -Early onset
- --Don't do transcription and translation properly
- --Dystrophy if formed improperly affects actin, myosin, all protein for muscles
-
Myotonic dystrophy
- -Chromosome 19 disorder
- -Typically onset is after puberty
- --Don't do transcription and translation properly
- --Dystrophy if formed improperly affects actin, myosin, all protein for muscles
-
Compartment syndrome
- Bleeding/inflammation in muscle
- -Swelling damages cells in same compartment
-
Minor trauma to muscles:
Damage to myofibrils, sarcolemma from excessive activity
-
Major trauma to muscles:
Lacerations, crushing, deep bruise, muscle tear (strain)
-
_______ problems can affect the energy supply available to the muscles from _________, like anorexia or bulimia
Nutritional, starvation
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__________ problems can affect electrolyte concnetration, like dehydration or kidney disease
Metabolic
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Which organ systems are smooth muslces present
- -Integument (blood vessels, arrector pili)
- -Cardiovascular (help regulate bp)
- -Respiratory
- -Digestive
- -Urinary
- -Reproductive (uterus)
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Muscle ____________ moves everything
contraction
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Synctium
- Fused mass of cells
- -Most tissues
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Skeletal muscle is formed by ________________ cells which are formed by the fusion of many myoblasts during embryogenesis
Multinucleate
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Cells are linked by _________ (endomycium) that fuse to form tendons
connective tissue
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Cardiac muscle cells are linked by ________ and desmosomes into funcitonal synctium
gap junctions
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Smooth muscle cells are linked by gap junctions and ____ ______ into functional synctium
dense bodies (unique to smooth muscle, proteins where actin attache-no sarcomeres)
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Which muscle type DOESN'T have sarcomeres?
Smooth muscle
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Smooth Muscle thick filaments are _________ throughout sarcoplasm
scattered
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Smooth Muscle thin filaments are attached to _____ _______
Dense bodies
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Dense Bodies
- -Some at intersections of cytoskeletal framework
- -Some firmly attached to plasma membrane
- -Dense bodies can link adjacent muscle cells (communicate cell-cell)
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Sliding of thick and thin filaments in smooth muscle causes cell to ______ and _______ (ex. stomach)
shorten, twist
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Plasticity
- Strectched muscle adapts to new length and retains ability to contract and produce tension
- --adapts to change
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Smooth Muscles can undergo sustained _______ contractions
- Tetonic
- -All action potentials sum up and hold a HARD contraction ex. labor, vomitting
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Skeletal muscles are controlled by _____ _______ of voluntary nervous system
motor neurons
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Cardiac muscles are controlled by _________ cells, autonomic nervous system
- Pacemaker
- --Can contract on own outside of body
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Smooth muscles are controlled by ______ cells, hormones, autonomic nervous system
Pacesetter
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Rate of pacemaker cells and amount of tension can be modified by __________ nervous system
- autonomic
- -Innervated by motor neurons of ANS (sympathetic, parasympathetic)
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Visceral smooth muscle cells
- -Connected by gap junctions into large synctia arranged in sheets or layers
- -Automaticity-Pacesetter cells can trigger rhythmic contractions (local reflex)
- -Stimuli from autonomic nervous system can control contraction frequency
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Multi-unit smooth muscle cells
- -Not connected by gap junctions
- -Each cell innervated by one or more motor neurons of the autonomic nervous system
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Skeletal muscle E source
- -Aerobic metabolism at moderate activity
- -Anaerobic enhances metabolism at peak activity
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Cardiac muscle E source
-Aerobic metabolism ONLY (myoglobin and mitochondria content is high)
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Smooth muscle E source
- -Aerobic metabolism at moderate activity (typical)
- -Anaerobic metabolism enhances during peak activity (rare)
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