Chapter 9: Muscular System Flashcards

(114 cards)

1
Q

Functions of muscular system

A

Movement
Posture
Respiration
Body heat
Communication
Construction of organs and vessels
Contraction of heart

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2
Q

Properties of muscle tissue

A

Contractility
Excitability
Extensibility
Elasticity

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3
Q

Contractubility

A

Ability of muscle to shorten with force

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4
Q

Excitability

A

Capacity of muscle to response to stimulus (usually from nerves)

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5
Q

Exstensibility

A

Muscle can be stretched beyond its normal resting length and still be able to contract

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6
Q

Elasticity

A

Ability if muscle to recoil to original resting length after stretched

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7
Q

Three types of muscles

A

Skeletal - multi nuclei, stations, voluntary, long and cylindrical
Smooth - single, o striations, involuntary, spindle shaped
Cardiac - single, striations, involuntary, cylindrical and branched

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8
Q

Myofiber

A

Long, rod shaped skeletal muscle cell

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9
Q

Sarcolemma

A

Cell membrane, able to carry action potentials

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10
Q

Sarcoplasm

A

Cytoplasm of a muscle cell

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11
Q

Sarcoplasmic reticulum

A

Specialized ER able to store calcium ions needed for contractions — released the Ca due to an action potential in the Sarcolemma

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12
Q

Myofibers are bundled into

A

Fascicles

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13
Q

Endomysium

A

Loose CT within fascicle around Myofibers

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14
Q

Perimysium

A

Denser CT surrounding each fascicle

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15
Q

Epimysium

A

Denser CT that surrounds a whole muscle

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16
Q

Muscle cell to muscle layers

A

Endomysium
Perimysium
Epimysium

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17
Q

Muscular facia

A

Outside of Epimysium, Connective tissue sheet separating or grouping muscles

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18
Q

Motor neurons

A

Cell bodies in brain and spinal cord, innervate muscle for movement

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19
Q

Neuromuscular junction

A

Synapse. A single motor neuron will branch extensively at Perimysium, with each branch synapsing into myofiber at NMJ

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20
Q

Neurotransmitter used st NMJ

A

Acetylcholine

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21
Q

What are Myofibers packed with

A

Myofibrils- rod shaped skeletal

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22
Q

What are packed into myofibrils

A

Myofilaments, the contractile proteins (actin (thin) and myosin (thick))

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23
Q

Sarcomere

A

Highly ordered repeating units of myofilaments - functional contractile unit of muscle

An area of a myofibril from one Z disk to an adjacent

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24
Q

Z disk

A

Filamentous network of protein which attaches to the actin myofilament

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25
Arrangement of actin
Double helix Of Fibrous actin or F actin attached at either end of z disk. Had active sites where myosin will bind during contraction
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Function of myosin
Heads grab actin and pull it inward to shrink Sarcomere and thus muscle cell
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Two regular proteins controlling myosin heads
Troponin and tropomyosin
28
Tropomyosin
A long protein winds along the groove of the actin double helix, covering the binding sites at rest
29
Troponin is made of
Made of three subunits: One binds to actin, one binds to tropomyosin, and a third to the calcium ions.
30
Order of power stokes on Sarcomere
Once calcium becomes available, this binds to troponin, pushing tropomyosin off active site, then myosin heads bind to these sits on actin filaments and pull actin inward, shrinking Sarcomere
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Cross bridges
When myosin heads attach to active site on actin molecule
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Structure of myosin
Myosin molecules shaped like golf clubs. Molecules consist of chains wound together to form shaft and heads.
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Myosin head binding sites
Actin and to atp
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Sliding filament model
Actin myofilaments slide over myosin to shorten Sarcomere (active). Relaxation is passive to restore to original resting length.
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Cell membranes are __
Polar: a speratuin of charge Inside more negative - more K Outside more positive- more Na and Ca
36
Resting membrane potential
Difference when cell is at rest. More negative inside with high K and negatively charged proteins. K leak channels but held in with negative proteins. And more positive outside with high Cl and Na.
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Na/k pump ratio
Always working in background. 3 sodium out for every 2 potassium in. Contributes to negativity
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Relationship of resting membrane potential to action potential
Resting polarity must exist bc action potential is created when the charges switch in a little portion of the membrane
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Three major factors affecting RMP
1. Na/K pump working in background 2. Tendency of K to lead down gradient 3. Much lesser tendency of K to re-enter due to charge attraction When 2 and 3 are at equilibrium with 1 working. We reach RMP
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Ion channel openings
Ligand gated - molecules bind to receptor sites Voltage gated- open in response to small voltage changes across plasma membrane
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Two phases of action potential
Depolarization and repolarization
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Depolarization
Due to opening of Na channels and Na comes into the cell Starts when stimulus causes RMP to depolarize to threshhold, then many more Na channels (voltage gated) open
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When does depolarization peak
At 20mv
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Repolarization
Return to RMP due to closing of Na channels and opening of K voltage channels. Brings the charge of the inside back to negative. Action potential ends and resting state is returned when k channels close
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Hyperpolarization
End of repolarization drops lower than original resting potential (below -90mV). Na/K pumps restore to resting potential. Always after an AP, but can be independent
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All or none principle
If stimulus reaches threshold, an action potential will proceed and will be the same every time
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Propagation
APs occur at small area of membrane but propagate down because an AP in one area stimulates one on the next. In a neuron, APs always propagate from cell body to synapse.
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Frequency
Number of APs produced per unit of time. How closely they follow each other down the membrane. Increased stimulus strength increases frequency.
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Synapse between a motor neuron and a muscle
Neuromuscular junction
50
Neuromuscular junction components
Presynaptic terminal (axon terminal with synaptic vescicles) Synaptic cleft (space) Postsynaptic membrane or motor-end plate (Sarcolemma )
51
What contains the neurotransmitter at the NMJ
Synaptic vesicles
52
Neurotransmitter used at NMJ
Acetylcholine
53
Enzyme used to brown down ACh in synaptic cleft
Acetylcholinesterase
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Process of NMJ
1. Action potential opens Voltage gates Ca channels on Presynaptic membrane 2. Ca ions enter terminal and initiate release of ACh by exocytosis 3. ACh diffuses across synaptic cleft and binds to ligand gates Na channels on the postsynaptic membrane 4. Na channels open, causing Na to enter the cell causing the postsynaptic membrane to depolarize 5. If depolarization passes threshold, an action potential is generated along the membrane
55
To stop the process at the NMJ
1. ACh unbinds from ligand gated Na channels, which then close 2. Enzyme Acetylcholinesterase removes acetylcholine by breaking it down into acetic acid and choline 3. Choline is supported with na into the presumptive terminal where it can be recycled to make more ACh. Acetic acid diffuses away from cleft. 4. ACh is reformed with the Presynaptic terminal using acetic acid generated from metabolism and from choline recycled up cleft
56
Excitation- Contraction Coupling
How an action potential causes a muscle fiber contraction. Involves Sarcolemma, transverse tubules, sarcoplasmic reticulum, ca, and troponin
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Transverse tubules
Invaginations of Sarcolemma deep into the muscle cell that carry the action potential to the SR
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Excitation contraction coupling process
AP produced on Sarcolemma AP propagated into t tubules Ca channels on SR terminal cisterae open Calcium leaves SR and binds to troponin Initiates muscle contraction
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Cross bridge movement
Myosin head binds to exposed active site on actin. Energy stores in the myosin head after the power stroke causes ATP to be released. Another ATP is required for the myosin to let go of actin.
60
Muscle relaxation
Ca moves back into SR by active transport. Takes energy. Ca moves moves away from trop-trop complex Complex re establishes position blocking binding site for myosin heads Actin slides back over to original resting length (passive)
61
Muscle twitch
Muscle contraction in response to a stimulus that causes action potential in one or more muscle fibers
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Phases of a muscle contraction
Lag or latent Contraction Relaxation
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Contraction is measured by what force
Tension
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Lag phase
Na channels open causes depolarization and AP in Sarcolemma ACh broken down in synapse Depolarization travels down T tubule Ca is released froM SR Ca binds to troponin and troponin/myosin complex
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Contraction phase
When power stroke occur
66
Relaxation phase
When ca is pumped back into the SR and tropomyosin covers active sites
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Motor unit
Single motor neuron and all the muscle fibers it innervates
68
Motor unit numbers
Large muscles have motor units with many fibers Small muscles with delicate movements contain units with few muscle fibers
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Muscle fibers of a motor unit contact in
An all or nothing fashion.
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How do whole muscles contract
In a graded fashion; the strength of the contraction is determined by the strength of the stimuli
71
To increase the strength of a contraction, muscle cells perform
Recruitment
72
Multiple motor unit summation
Strength of contraction depends on recruitment of motor units
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Submaximal stimulus
No motor unit
74
Maximal stimulus
All motor units of a muscle are firing
75
Supramaximal stimulus
Stimulus beyond maximal that yields no further effect
76
What are bodybuilders actually gaining when increasing the strength of a muscle
Increasing actin and myosin to increase number of cross bridges. NOT an increase to motor units.
77
Multiple wave summation
Increase in frequency of stimulus. As the frequency of APs increases, the contraction force increases.
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Incomplete and complete tetanus
Incomplete is when muscle fibers partially relax between contraction Complete is no relaxation; causing a sustained muscle contraction as opposed to a twitch
80
Muscle contractions
Isometric - no change in length but tension increases (ex: pushing palms together)- postural muscles Isotonic - length changes but tension remains relatively constant, as in lifting something Most contractions are a combination of the two
81
Muscle tone
Constant tension by muscles for long periods of time. Depends on a few motor units contracting at any given point so that some tension in the muscle remains constant. These tense and firm muscles.
82
The greatest amount of force of contractions comes from
When you form the most cross bridges
83
Stretched muscle (too long)
Not enough cross bridging
84
Crumped muscle (too short)
Myofilaments crumple and cross bridges can’t contract
85
Muscle fatigue
Decreased capacity to work and reduced efficiency of performance
86
Types of muscle fatigue
Psychological - depends on emotional state. Can be overcome. Muscular- results from ATP depletion Synaptic- occurs in NMJ due to lack of ACh. Least common
87
Physiological contracture
State of fatigue where due to lack of ATP, neither contraction or relaxation can occur
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Rigor Mortis
Development of rigid muscles several hours after death. Ca leaks into sarcoplasm and attaches to myosin heads and cross bridges form. Lack of ATP means myosin heads cannot release actin filaments.
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ATP produced by three ways
Creatine phosphate Aerobic respiration Anaerobic respiration
90
When is creatine phosphate (CrPO4) built up?
During resting conditions
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What happens during exercise?
ATP is broken down into ADP, increasing the ADP levels in the body
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What reacts with ADP to make ATP?
The PO4 in Creatine phosphate is added to ADP to make ATP
93
How useful is Creatine phosphate in ATP production
Used up very quickly and used by muscles adapted for short, quick bursts of energy/muscle contraction. Yieleds only 1 ATP per molecule of CrPO4
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Cellular respiration for muscle contraction
Glucose is broken down through glycolysis to produce 2 pyruvic acids and 2 ATP. Second step determined by oxygen availability
95
Anaerobic respiration for muscle contraction
Occurs in the cytoplasm. 2 pyruvic acids and 2 ATP result in 2 lactic acids (the burn during a workout) (later to be sent to liver and converted back to glucose) and 2 ATP. Used by same muscles as CrPO4
96
Aerobic respiration
2 pyruvic acids are taken into the mitochondria and completely broken (Krebs) down into CO2+ H2O + and 34 ATP result. Results in 36 ATP, water and CO2. Used for more endurance muscles
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Two types of muscle fibers
Slow and fast twitch
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Slow twitch
-More mitochondria -Contract slower but last longer-(endurance) -smaller diameter -better blood supply -use aerobic respiration -large amts of myoglobin (o2 reservoir) -ATP broken down slower -use lipids and carbs for energy Ex: postural muscles, more in lower than upper limbs
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Fast twitch fibers
-respond rapidly and break down ATP faster -less blood supply -less mitochondria -densely packed Myofibers - powerful -fatigue quickly -use anaerobic respiration and CrPO4 -specialized for quick powerful burrs -hypertrophy with training Ex: lower limbs in sprinters, upper limbs of most people
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Distribution of fast twitch and slow twitch
Most muscles have both but varies Some have higher percentage than other Arm muscles are fast, lower limbs are slow You cannot switch from one to the other but do certain exercises to accentuate one type (swimming for ST)
102
Effects of exercise:
Change in size of muscle fibers- Hypertrophy is an increase in size from increase in myofibrils. Increased strength due to better coordination, increase in metabolic enzymes, better circulation Atrophy is a decrease in muscle size
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Smooth muscle compared to skeletal
Fewer actin and myosin Actin/myosin complexes not as organized (not striated) No t tubules
104
Actin/myosin connection in smooth muscle
No true Sarcomere, but have actin/myosin complexes attached to dense bodies scattered around the cell and joined with intermediate fibers. Dense bodies act like Z disks. Like a loose netting covering the cell. When contracted, the muscle shortens and gets fatter.
105
Calcium ls relationship with smooth muscle contraction
Still required but can come from inside or outside of the cell
106
Flow of calcium in smooth muscle contraction
Calcium enters cytoplasm from SR to bind with calmodulin— this activates the enzyme Myosin Kinase, which transfer a phosphate from ATP to the myosin heads, initiating the power stroke. Relaxation occurs when myosin phosphatase removes phosphate group from myosin heads
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Types of smooth muscle
Visceral or unitary Multi unit
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Electrophysiology of smooth muscle
-does not follow all or nothing -stimuli can summary to create action potential (GI tract, uterus) -slow to contract, slow to relax (bc resting potential is not as negative as skeletal) -can be autorhythmic (need pacemaker) -cells can be stretched and still contract to same degree -controlled by nervous system (autonomic), hormones and autorhythmic
109
Slow wave of depolarization in smooth muscle
Result of slow influx of na and ca through leaky channels. Once it reaches threshold, depolarization and AP occurs.
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Benefit of smooth muscle for lining hollow organs
As the volume of organs increase, only a small increase develops in the tension applied by the surrounding muscle to the contents of the structure
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Cardiac
-found in heart -striated with one nucleus -has intercalated disks and gap junctions (allow for wave of contraction rhythmically) -autorhymic - pacemaker is the SA node in right upper atrium -action potentials of longer duration and longer refractory period -Ca2+ regulates contraction
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Visceral smooth muscle
most common, occurs in sheets, in digestive, reproductive, and UT. Numerous gap junctions so they create waves of contraction. Often autorhythmic
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Multi unit smooth muscle
less common, fewer gap junctions, act more like individual units. Sheets (blood vessels), bundels (arrector pili and iris), or single (spleen capsule)