Ch9: Muscles and muscle tissue

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  1. What are the muscle Types using two classifications

    1. What is their special characteristics

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  1. What are the muscle Types using two classifications

    1. What is their special characteristics

  1. Voluntary

    1. Skeletal :

      1. Striated

      2. Elongated cylindrical

      3. multinucleated

  2. Involuntary:

    1. Cardiac :

      1. Striated

      2. Branches at intercalating discs

      3. Mononucleated

    2. smooth :

      1. Non-striated

      2. Sheet like

      3. Elongated

      4. Spindle shaped cells

      5. mono nucleated

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  1. What is the special name of muscles cells in which type of muscles and why in those types ?

  2. What prefixes belong to muscles

  1. Muscle cell is called muscle fiber in smooth and skeletal muscle but not in cardiac because they are elongated

  2. Myo and mys and sarco

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  1. What are the characteristics of a muscle tissue (4)

    1. What does each mean

  1. Excitability /responsiveness,

    1. Ability to receive and respond to a stimulus by changing membrane potential

  2. Extensibility : Ability to extend / stretch

  3. Elasticity : ability of muscle to recoil to resting length after stretch

  4. contractility : ability to shorten forcibly when stimulated

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  1. What are the functions of muscles (4)

  1. Produce movement

  2. Maintain posture and body position

  3. Stabilizes joints

  4. generate heat

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  1. What serves the muscle with it’s needs

  2. where do they pass through

  3. how do they reach to all the cells

  4. How do skeletal muscles differ from other types

  1. The muscle is served with :

    1. One nerve

    2. One artery

    3. One / more veins

  2. They pass through the central part of the muscle

  3. They branch through connective tissue sheaths

  4. Each muscle fiber of skeletal muscle is served with a nerve ending to control it’s voluntary action unlike cardiac and smooth which can sometimes not have one

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What is the function of connective tissue sheaths (5)

  1. Supporting each cell

  2. holding together the muscle

  3. prevent the muscles from bursting during strong contractions

  4. Transmit pulling force to bone to be moved

  5. Provide routes for entery and exit of Blood vessles and nerve fibers

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What are muscle sheaths continuous with

  1. they are continuous with each other

  2. They are continuous with aponeurosis and tendons connecting to the muscle

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  1. What are the connective tissue sheath types

    1. What do they surround

    2. what are they made of

  2. What is a fascicle

  1. Epimysium :

    1. Surrounding the whole muscle

    2. Dense irregular CT

    3. Sometimes blends with other neighboring facia

  2. Perimysium :

    1. Surrounding each fascicle

    2. Dense irregular CT

  3. Endomysium :

    1. Surrounding each muscle fiber

    2. Areolar CT

A fascicle group of muscle fibers surrounded by perimysium

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  1. At how many points do muscles attach to bones

  2. What are the names of those points

    1. what is the difference

    2. where is the location

  3. Towards where does motion of muscle occur

  1. At least at two points

  2. Two types :

    1. Insertion :

      1. The attachment to a bone that can move

      2. Distal

    2. Origin :

      1. The attachment to a bone that can’t move or moves less

      2. proximal

  3. The muscle’s insertion moves towards the muscle’s origin

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  1. What are the types of muscles attachments

    1. Characteristics of the attachment

    2. Types if applicable

  2. Between what does attachment occur generally

  3. Which type is common and why

  1. Muscle attachment:

    1. Direct/ fleshy attachment :

      1. Epimysium of muscle is fused to the periosteum of the bone or the perichondrium of the cartilage

    2. Indirect attachments :

      1. Epimysium of muscle fuses to Dense Regular which connects to periosteum (all of which are CT)

      2. Through two types :

        1. Tendons : rope like

        2. Aponeurosis: Sheet like

  2. Occurs generally between connective tissues one that belongs to the muscle (epimysium) and other that belongs to bone (periosteum) and mostly something in between (tendon / aponeurosis ) which are also connective tissues

  3. Indirect attachment is better because

    1. It doesn’t require much space

    2. can withstand abrasion from bones unlike muscles

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  1. What are the most important organelles of the muscle fiber and what are their normal cell equivalents

  2. How were the muscle fibers formed

  1. Organelles :

    1. Sarcolemma : Plasma Membrane of a muscle fiber

    2. Sarcoplasm : Cytoplasm of a muscle fiber

    3. Sarcoplasmic reticulum : endoplasmic reticulum

    4. Glycosomes : Granules that store glycogen which produces glucose when muscle needs

    5. Myoglobin : Red pigment that Stores Oxygen

  2. hundreds of embryonic cells fuse to form one muscle fiber

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What are the specialized structures of muscle fiber

  1. Sarcoplasmic reticulum

  2. T-tubules

  3. Myofibrils

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  1. Myofibrils :

    1. What are they made of

      1. What is that made of

        1. What are they ?

  2. How many myofibrils does each muscle fiber have and how are they arranged

  1. myofibrils are made of a chain of sarcomeres that are linked end to end

    1. They are made of myofilaments :

      1. Thick filaments

      2. Thin filaments

  2. Many accounting up to 80 % of muscle fiber that are densely packed

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  1. What are striations

    1. What are their types

    2. draw the striations of a sarcomere

    3. which to which striation structure makes up a sarcomere

  1. Repeating series of dark and light bands evident along the length of each muscle fiber :

    1. A Bands :

      1. Extends along the thick filaments

    2. I Bands :

      1. The region with only the thin filaments

    3. H-zone :

      1. The central less dark region of thick filaments

    4. M-line :

      1. The line at the center of a thick filament formed by myomesin protein

    5. Z discs : Zig zag lines at the center of I bands

  2. A sarcomere is between Z-line to the adjacent Z-line

<ol><li><p>Repeating series of dark and light bands evident along the length of each muscle fiber : </p><ol><li><p>A Bands : </p><ol><li><p>Extends along the thick filaments </p></li></ol></li><li><p>I Bands : </p><ol><li><p>The region with only the thin filaments </p></li></ol></li><li><p>H-zone : </p><ol><li><p>The central less dark region of thick filaments </p></li></ol></li><li><p>M-line : </p><ol><li><p>The line at the center of a thick filament formed by myomesin protein</p></li></ol></li><li><p>Z discs : Zig zag lines at the center of I bands </p></li></ol></li><li><p>A sarcomere is between Z-line to the adjacent Z-line </p></li></ol>
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  1. What is the smallest contractile unit of a muscle fiber

  2. What striations does it have at which locations

  1. a sarcomere

  2. Between two successive Z-discs they have :

    1. Half I band at each side next to Z discs

    2. A band in center along thick filaments

    3. H zone and M line at the center of A bands

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  1. Thick filaments :

    1. What are they made of

      1. What is that made of

    2. As which enzyme does myosin act and which part of it exactly

    3. what striation is possible because of it

    4. What causes the H zone

    5. What is the role of Myomesin and what striation does it form

  1. 300 Myosin molecules bundled together the tails facing inward and the heads facing outwards

    1. Made of Six polypeptide chains :

      1. 2 heavy : twist to form the tail

      2. 4 light : form the 2 globular heads

      3. attached to each other by a flexible hinge

    2. The globular head acts as ATPase

    3. This structure causes A band (thick filament with myosin heads) and the H zone (thick filament without myosin heads/thin filaments)

    4. The H zone is caused by lack of myosin heads at the center of the thick filaments

    5. Myomesin connects thick filaments of one myofibril to thick filaments of another and they form the M line which helps in alignment of myofibrils

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  1. Thin filaments:

    1. What proteins is it made of

      1. What are the subunits of this protein if any

      2. Structure

      3. what is the function of the subunits

      4. what do they form only for 1

  1. Made of protein actin and regulatory proteins:

    1. Actin:

      1. The subunits are G-actin (globular) :

        1. Kidney shaped

        2. Has a myosin binding site where myosin heads attach to during a contraction

        3. They polymerize to form F-actin (filamentous)

        4. One thin filament has two F-actin interwinding each other to form a helix

    2. Regulatory proteins :

      1. Troponin :

        1. Is a globular protein

        2. Has three subunits :

          1. 1 Binds to Actin filament : to bind

          2. 1 binds to Ca

          3. 1 Binds to tropomyosin : to help position tropomyosin on actin

      2. Tropomyosin:

        1. Long rod

        2. Covers the actin filaments to block it’s binding sites and prevent contraction when not needed

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How is the hexagonal arrangement viewed

  1. Six thin filaments surround each thick filament

  2. Three thick filaments surround each thin filament

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  1. What is the other type of filaments

    1. What is it made of

    2. how is it placed

    3. what is it’s function and which part

  1. Elastic filaments :

    1. Made of Titin protein

    2. Extends from Z discs through the center of the thick filament to connect to the M-line

    3. The part of the titin that spans the I bands is extensible,

      unfolding when the muscle stretches and recoiling when the tension is released

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  1. What are the other important proteins

    1. Function of 1 and 5 only

    2. What are their general functions

  1. Dystrophin: Links thin filaments to integral proteins of sarcolemma which are anchored to the ecm

  2. Nebulin:

  3. myomesin

  4. C-protiens

  5. Intermediate (desmin) filaments extend from Z disc and connect each myofibril to the next one through the muscle fiber

Their general functions is to bind to filaments or sarcomeres and maintain their alignment

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  1. What is a disease related to the proteins above

  2. To what family of diseases does it belong to

  3. when do they appear

  4. inheritance and gender

  5. What causes it

  6. cure

  1. DMD : Duchenne muscle dystrophy

  2. belongs to Muscular dystrophy family

  3. appear during childhood (2-7)

  4. sex linked recessive mostly to males

  5. Caused by a defective gene for dystrophin which causes the sarcolemma to tear and allow Ca2+ to enter which causes muscle cells to go through apoptosis

  6. Death

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  1. What are the type of sets of intracellular tubules that the muscle fiber has

  2. What do they form

  3. why is it called that way

  1. 2 types of sets :

    1. Sarcoplasmic Reticulum

    2. T-tubules

  2. They form a triad

  3. because it houses two terminal cisterns with a T-tubules in the center

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  1. What is the function of Sarcoplasmic reticulum

  2. How do they run along what

  3. Where do they communicate with each other and what does that form

  1. Functions include :

    1. Stores and regulates intracellular levels of Ionic Ca2+

    2. Releases Ca2+on demand when muscle fiber is stimulated

  2. They run longitudinally (same direction as myofilaments) along a Myofibril to surround it

  3. they communicate with each other at two points :

    1. H zones (forms a network of interconnecting tubules)

    2. A–I band junction (forms the Terminal cisterns of Triad)

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  1. What are the T-tubules

  2. What is the function of the T-tubules

  1. they are invaginations of the Sarcolemma going down along the circumference of each microfibril which is continuous with extracellular space

  2. They increase surface area which allows changes in membrane potential to occur fast so they act as voltage sensors

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  1. What is considered a contraction

  2. when does shortening occur

  3. when does contraction end and what is that stage called

  4. What model explains whats stated up

    1. What does it say

  5. what happens to the striations during shortening

  1. Formation of cross bridges (myosin heads binding to actin filaments)

  2. only occurs if the force generated is greater than the opposite tension force

  3. cross bridges become inactive (relaxed)

  4. sliding filament model of contraction

    1. It says that the myosin heads cause the thin filaments to overlap to a greater degree which causes shortening

  5. Striations :

    1. A band : length Doesn’t change but move closer to each other

    2. I band : shortens

    3. H zone : shortens / disappears

    4. Z discs: distance between them decrease

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  1. What does excitable cell mean

  2. examples

  3. what are the types of signals

    1. What is the type that we work with

      1. 1 benefit 1 drawback

  1. cells that respond to external stimuli by changing their resting membrane potential.

  2. two :

    1. Muscle fibers

    2. Neurons

  3. Two types :

    1. Electrical signal :

      1. AP (action potential / nerve impulse) :

        1. Travels long distance

        2. cannot pass from cell to cell

    2. Chemical signal:

      1. Neurotransmitters (Acetyl-choline)

        1. Can pass from cell to cell

        2. Travels short distance

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  1. What are the types of Ion channels important for excitation and contraction of skeletal muscles

    1. What are they opened with

    2. What do they cause

    3. The example that we are working with

  1. Chemically-gated :

    1. Opened by chemical messengers (AcH)

    2. cause a small local depolarization which triggers voltage gated channels

    3. ACh receptor

  2. Voltage gated:

    1. open or close in response to membrane potential changes (Action potential)

    2. They cause the next voltage gated to open as they carry the message

    3. Voltage gated K+ and voltage gates Na+

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  1. What gives the order for the skeletal muscle to contract

  2. Where do they reside

  3. how do they communicate

  4. where

  5. how many

  1. Somatic motor neurons

  2. They are present in the spinal cord except for brain and neck which is in the brain

  3. The neurons have axons which branch alot as they enter the muscle then they branch to form a neuromuscular junction / motor end plate

  4. near the center if the muscle fiber

  5. each muscle fiber has 1 neuromuscular junction no more no less

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  1. Draw the neuromuscular junction and label its parts

  2. provide brief explanation of the parts

  1. Axon terminal : end of the neuron

  2. synaptic cleft : Fluid filled area rich in glycoproteins and collagen fibers

  3. Synaptic vesicles : membrane bound granules that contain acetylcholine

  4. junctional folds of sarcolemma : increase surface area

  5. Note : Axon never touches the muscle

<ol><li><p>Axon terminal : end of the neuron </p></li><li><p>synaptic cleft : Fluid filled area rich in glycoproteins and collagen fibers </p></li><li><p>Synaptic vesicles : membrane bound granules that contain acetylcholine </p></li><li><p>junctional folds of sarcolemma : increase surface area </p></li><li><p>Note : Axon never touches the muscle </p></li></ol>
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How are the steps that lead to contraction divided

  1. Events at the neuromuscular junction

  2. Excitation of a muscle fiber

  3. Excitation contraction coupling

  4. Cross bridge cycling

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  1. Events at the neuro muscular junction

    1. What are the steps

  1. Action potential arrives at the axon terminal

  2. Ca2+ ion channels are opened which allows it to move into the axon terminal down it’s electrochemical gradient

  3. Ca2+ entry causes ACh to be released by exocytosis.

  4. ACh diffuses across the synaptic cleft and binds to ACh receptors on the sarcolemma.

  5. ACh binding opens chemically gated ion channels which allow K+ to move out and Na+ to move in at the same time which creates a local depolarization called (End plate potential)

  6. ACh effects are terminated by acetylcholinesterase which breaks down acetylcholine to acetic acid and choline

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  1. What are the steps of excitation of muscle fiber

  2. What is a refractory period

  3. What are the cellular conditions after the end of the stimulation

  1. opening of chemically gated channels causes Endplate potential which is a local depolarization

  2. Depolarization: opens voltage gated sodium channel which allows sodium to move in

  3. sodium moving in causes depolarization by which + charge is increasing in the cell which also triggers the same gated channel to close

  4. depolarization triggers potassium voltage gated channels to open

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  1. What is one disease related to ACh

  2. what are it’s signs

  3. what causes it

  1. Myasthenia gravis

  2. signs include drooping eyelids and muscle weakness

  3. it is caused when immune system destroys ACh receptors

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  1. draw the graph that shows depolarization and repolarization

  2. what is that one period and why is it important

  3. what does repolarization restore and what does it not

  4. What can cause problems with contraction

  5. What fixes it

  6. what is special about AP

  1. Refractory period is the period of repolarization

  2. it is important because no matter how strong the stimulation is the muscle cannot be stimulated until the refractory period has ended because the Na+ ion channels cannot be opened

  3. repolarization only restore electrical conditions not the ionic conditions which is restored by the ATP-Na-K-pump

  4. ionic imbalances ain’t a problem until thousand of contractions

  5. Ionic imbalances are fixed with Na K+ ATPase

  6. once started it cannot be stopped

<ol><li><p>Refractory period is the period of repolarization</p></li><li><p>it is important because no matter how strong the stimulation is the muscle cannot be stimulated until the refractory period has ended because the Na+ ion channels cannot be opened</p></li><li><p>repolarization only restore electrical conditions not the ionic conditions which is restored by the ATP-Na-K-pump</p></li><li><p>ionic imbalances ain’t a problem until thousand of contractions</p></li><li><p>Ionic imbalances are fixed with Na K+ ATPase</p></li><li><p>once started it cannot be stopped</p></li></ol>
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  1. What are the steps of excitation contraction coupling

  2. what happens after contraction is done (opposite)

  1. The AP is carried along the sarcolemma down the T-tubules

  2. AP reaches the area of T-tubules that has terminal cisterns which causes the the voltage sensitive tubule proteins on the T-tubules to change shape

  3. This shape change opens the Ca2+ release channels in the terminal cisterns, allowing Ca2+ to flow into the cytosol.

  4. Ca2+ binds to troponin

  5. troponin rolls tropomyosin to groove of actin helix exposing it’s binding sites which allows them to bind to thick filaments

  6. myosin binds and the next step starts

After math :

  1. The voltage sensitive tubules return to normal shape which closes the Ca2+ channels

  2. Ca2+ is actively pumped back to sarcoplasmic reticulum

  3. without Ca2+ troponin returns to normal and the tropomyosin blocks the binding sites of acting

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How many Ca2+ is required to expose the binding site of the actin filaments ?

2 Ca2+ molecules are required to bind to troponin

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Cross bridge cycle

  1. upright myosin binds to actin

    1. It has ADP and Pi

  2. ADP and Pi leave causing myosin and the actin to move

  3. ATP binds which cause the Myosin to detach from actin

  4. ATP is hydrolyzed to ADP and Pi and the myosin head becomes upright ready to bind to another actin

<ol><li><p>upright myosin binds to actin </p><ol><li><p>It has ADP and P<sub>i</sub> </p></li></ol></li><li><p> ADP and P<sub>i</sub> leave causing myosin and the actin to move </p></li><li><p>ATP binds which cause the Myosin to detach from actin </p></li><li><p>ATP is hydrolyzed to ADP and Pi and the myosin head becomes upright ready to bind to another actin </p></li></ol>
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  1. What is one disease related to that

  2. what causes it

  3. what are it’s sign

  4. when does it end and why

  1. rigor mortis

  2. No ATP is present which means that the myosin head will not separate from the actin filament

  3. dead people have fully contracted muscles even tho they are dead

  4. after 3 days because the muscle proteins are broken down after death

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What are the two main opposing forces called

  1. Muscle tension : the force exerted by the muscle on the opposing force

  2. Load: the weight of the object to be moved

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  1. What is a motor unit

  2. what are the differences between different motor units

  1. A motor unit consists of :

    1. One motor neuron

    2. all the muscle fibers it innervates

  2. Differences in number of muscle fibers innervated in one motor unit :

    1. Larger motor units focus on larger force production (calves)

    2. smaller motor units focus on more precise movement (fingers)

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  1. what measures muscle contraction

  2. what is the simplest type of contraction and what is it’s description

  3. What are its phases and what occurs in them

  4. what is unusual about the phases

  1. a myogram

  2. Muscle twitch: Muscle response to a single stimulation by which the muscle contracts quickly then relaxes

  3. Three phases :

    1. Stimulus

    2. Latent period: Cross bridges begin to cycle but muscle tension not yet measurable

    3. Period of contraction: number of active Cross bridges is increasing

    4. period of relaxation: number of active Cross bridges is Decreasing

    5. Note: different type of muscles have different period legnth

  4. period of contraction is generally faster / shorter than the period of relaxation

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  1. Why is a muscle twitch not humanly

  2. what contraction is of humans

    1. what are it’s types

  1. because it is sudden and produces robot movements

  2. graded muscle contractions

    1. Temporal summation: Rate of firing of action potentials

    2. Recruitment: Number of motor neurons that are activated

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Temporal/wave summation :

  1. What does it cause

  2. What is the reason behind that function

  3. What are the types draw their myograms

  4. what types are rare and why

  5. What is it’s primary function

  1. is Increase in frequency of stimulation = stronger contraction by same muscles

  2. because the second stimulus arrives before the Ca2+ is fully pumped back which means that the tension is still there which allows the second stimulus to ride on its back and produce stronger contraction

  3. types are : in the picture

  4. fused and unfused tetanus are rare because physiological mechanisms prevent it

  5. To produce smooth, continuous muscle contractions

<ol><li><p>is Increase in frequency of stimulation = stronger contraction by same muscles</p></li><li><p>because the second stimulus arrives before the Ca2+ is fully pumped back which means that the tension is still there which allows the second stimulus to ride on its back and produce stronger contraction</p></li><li><p>types are : in the picture</p></li><li><p>fused and unfused tetanus are rare because physiological mechanisms prevent it</p></li><li><p>To produce smooth, continuous muscle contractions </p></li></ol>
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  1. Recruitment

    1. What is it also called

    2. what is it’s function and how does it occur

    3. How is it achieved in laboratory

    4. what is threshold

    5. what are the types of stimulus

    6. why do different types exist

    7. What principle dictates the recruitment and what does it explain

  1. Multiple motor unit summation

  2. Controls the force of contraction by :

    1. Different motor units have different thresholds by which

      1. According to stimulus intensity different motor units are recruited

  3. Achieved by increasing voltage

  4. Threshold is the point at which amount of depolarization required for the voltage gated channels to start an AP in muscle cells and start a contraction

  5. Three types :

    1. Subthreshold are APs that don’t cause contraction as they don’t cause depolarization enough to reach to threshold

    2. threshold stimulus is the one that causes the first observable contraction

    3. maximal stimulus is the strongest that causes all the muscle’s motor units to be recruited

  6. because some acts don’t require that much force like muscles that maintain posture

  7. Size principle :

    1. Larger motor units require larger stimulus due to higher threshold stimuli

    2. Smaller motor units are recruited first then the larger then the largest

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  1. How does the body prevent fatigue with the recruitment characteristic

  1. Different motor units are activated at different times and not at the same time with different muscle fibers in the same muscle belonging to different motor units

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  1. What helps muscles be ready for contraction quickly

  2. What is it exactly

  3. what causes it

  4. what are its benifits

  1. Muscle tone

  2. Muscles are always slightly contracted but doesn’t produce active movements

  3. spinal reflexes which activate some motor units then another continuously

  4. 4

    1. helps maintain muscles healthy

    2. ready to respond to stimulation

    3. stabilize joints

    4. maintain posture

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  1. What are the types of contractions

    1. What are the differences between them

      1. what is the subdivisions of one

        1. What are their differences

        2. One example on each

        3. which one is stronger

      2. Why is two important and where it is used

  2. On what does the classification depend

  1. Types:

    1. Isotonic : generates enough force (more than the load) to shorten (thin filaments move)

      1. Concentric:

        1. Shorten and does work like picking up a book

      2. Eccentric:

        1. Generation of force when it is lengthening like walking down a steep hill

        2. Eccentric is stronger by 50 %

    2. Isometric : generates force but doesn’t shorten or lengthen because the load needs more force than the muscle can generate (no movement of thin filaments)

      1. Isometric is important for maintaining posture and holding joints stationary while movement occurs at other joints

  2. Classification depends if muscle changes length or not

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  1. Where does energy come from initially and how long does it last?

  2. What is the condition for the contraction to continue

  3. what are the sources of regeneration

    1. How do they work

    2. Speed

    3. how long do they last

  1. hydrolysis of stored ATP which lasts for only 4- 6 seconds

  2. ATP hydrolysis should be = to ATP regeneration

  3. Regeneration occurs by :

    1. Direct phosphorylation of ADP by creatine phosphate

      1. Creatine phosphate transfers a phosphate group to ADP to form ATP

      2. Fast

      3. 10 seconds (2 to 3 times more than ATP)

      4. Enzyme is creatine kinase

    2. Anaerobic pathway :

      1. Glycolysis occurs to break down glucose without the presence of oxygen to 2 pyruvate molecules to produce 2 ATP and if there is no oxygen the pyruvate is converted to lactic acid

      2. Fast

      3. Lactic acid diffuses to blood stream into liver so that it can be converted to energy by liver and kidneys

      4. lasts for 30-40 seconds

    3. Aerobic respiration :

      1. Glucose is broken down to pyruvate which is then broken down to CO2 and Water and 30 ATP

      2. really slow

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  1. What is the legnth of time the muscle can continue to contract using aerobic pathways called

  2. at which point does muscles convert to anaerobic metabolism

  1. aerobic endurance

  2. Anaerobic threshold (when ATP is needed quickly and aerobic respiration cannot provide enough in that time)

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What metabolic processes do those activities rely on :

  1. Lifting a 200 kg bench press for 3 sets

  2. lifting 30 Kg bench press for 30 sets

  3. lifting a 200 kg bench press for 12 sets

  1. Creatine phosphate

  2. Aerobic damn u gettin a pump

  3. anaerobic (u will never do it anyway)

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  1. What is muscle fatigue

  2. why does it happen

  3. what causes it to happen

    1. What happens because of that cause

  4. what is assumed as a cause but isnt

  5. what types of activities cause fatigue at what speed and healing at what speed

  1. when the muscle is unable to contract even though the muscle is still receiving a stimulus

  2. preventative mechanisms stop contraction in order not to cause complete depletion (rigor mortis and muscle death)

  3. many causes but include :

    1. Ionic imbalances : no more K+ in and too many Na+ in cause no AP to happen

    2. increased organic pi caused by ATP and CP breakdown : interferes with Release of other pi from Myosin heads and release of Ca2+ from SR

    3. Decreased ATP more Mg2+ : Mg2+ normally binds to ATP but with low ATP they bind to voltage sensitive proteins of T-tubules which cause Ca2+ release to decrease

    4. Decreased glycogen : no more energy

  4. Lactic acid is assumed as a major cause but it isn’t it just causes pain

  5. two types of activities :

    1. Strenuous but fast : fatigue fast : heal fast

    2. Slow developing fatigue : fatigue slow : heal slow

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52
  1. what happens after the activity is done

    1. What are it’s events

  2. what is it also called

  1. Excess postexercise oxygen consumption returns muscle chemistry back

    1. Muscle’s myoglobin are reoxygenated

    2. muscle’s glycogen stores are refilled

    3. lactic acid is reconverted to pyruvate by liver

    4. ATP and CP reserves are resynthesized

  2. also called paying back the debt to muscles for their huge favor (oxygen debt)

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53
  1. What does the force of a muscle contraction depend on

  2. what is hypertrophy and what causes it

  1. Depends on number of myosin cross bridges that are attached to actin which is affected by:

    1. Frequency of stimulation : more = temporal summation = stronger

    2. number of muscle fibers recruited

    3. size of muscle fibers

    4. degree of muscle stretch in picture:

      1. More stretch = too far away from myosin heads to cause force

      2. Less stretch = no where for actin filaments to go in center

  2. Hypertrophy is caused by resistance exercises which causes enlargement of muscles

<ol><li><p>Depends on number of myosin cross bridges that are attached to actin which is affected by: </p><ol><li><p>Frequency of stimulation : more = temporal summation = stronger</p></li><li><p>number of muscle fibers recruited</p></li><li><p>size of muscle fibers</p></li><li><p>degree of muscle stretch in picture:</p><ol><li><p>More stretch = too far away from myosin heads to cause force</p></li><li><p>Less stretch = no where for actin filaments to go in center</p></li></ol></li></ol></li><li><p>Hypertrophy is caused by resistance exercises which causes enlargement of muscles</p></li></ol>
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54

on what does the velocity and duration of contraction depend on

  1. Muscle fiber type

  2. size of the load

  3. recruitment

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55

What does the classification of fiber types depend on :

  1. Speed of contraction :

    1. How fast does ATPase of myosin break down ATP

    2. How quickly Ca2+ moves from cytosol to SR

    3. it also show which pathway is used for generating ATP

  2. Major pathways of forming ATP :

    1. Glycolysis and CP or aerobic or both

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56
  1. What are the different types of muscle fibers

  2. Compare them in

    1. Speed of contraction

    2. Myosin ATPase activity

    3. primary pathway for ATP synthesis

    4. Myoglobin content

    5. glycogen stores

    6. recruitment order

    7. rate of fatigue

    8. best suited activities

    9. fiber diameter

    10. mitochondria

    11. capillaries

    12. color

In the picture

<p>In the picture </p>
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57
  1. What type of muscle fibers do muscles have mainly

  2. what type of muscle does a motor unit have

  1. they have a mixture between all three types but they depend on the person’s activity

  2. they only have 1 muscle type

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58
  1. What are the different types of exercise

    1. What do these exercises do to the body

  1. Aerobic exercise (running to Qatar) :

    1. More capillaries

    2. More mitochondria

    3. More myoglobin

    4. in general they turn convert fast glycolytic to fast oxidative fibers

  2. Resistance exercise (500kg / 3 sets) :

    1. Fast oxidative to fast glycolytic

    2. causes hypertrophy

    3. return back to normal if stopped

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59
  1. What happens if muscles are not used

  1. disuse atrophy (degeneration of muscles)

  2. muscle fibers are replaced by fibrous connective tissue

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