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Anatomy And Physiology > Unit 4 💪🏻 > Flashcards

Unit 4 💪🏻 Flashcards

1
Q

Excitable (functional properties)

A

Can generate an action potential, stimulated by nerves, hormones,local signals

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2
Q

Elastic (functional properties)

A

Can recall when stretched

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3
Q

Extensible (functional properties)

A

. Can stretch/expand

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4
Q

Contractile (functional properties)

A

Shorten w/ force/pull on attachments

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5
Q

Skeletal muscle

A

Voluntary,long, striated, multinucleated, attached to bone (mostly)

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6
Q

Smooth muscle

A

Involuntary, tapered,non-striated, single nucleus, hollow organs, vessels

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7
Q

Cardiac muscle

A

Involuntary, branched,striated, 1-2 nuclei, intercalated discs,🫀 only

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8
Q

Skeletal muscle functions

A

Movement (all locomotion), maintain posture,
Stabilize joints, protection, generate heat

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9
Q

Epimysium (💀 packaging)

A

Outermost dense irregular C.t. Layer (separates muscle from organs), allows independent moves

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10
Q

Perimysium (💀 packaging)

A

C.t. Surrounding fascicles ( bundles of muscle fibers), ‘grain’ of muscles, allow precise movements

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11
Q

Endomysium (💀 packaging)

A

C.t. Around each fiber

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12
Q

Aponeurosis (💀 packaging)

A

Sheet of collagen fibers, connect muscles to other muscles or to bone or skin

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13
Q

What do skeletal muscles contain?

A

Contains lots of blood vessels ( smallest capillaries, highly interconnected) each fiber connects to motor neuron

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14
Q

Myofibril💀

A

Contractile organelle (100s - 1000s per fiber) repeating sarcomere

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15
Q

Sacrolemma💀

A

Plasma membrane, conduct electrical impulses that trigger contraction

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16
Q

Sacroplasmic reticulum💀

A

Smooth Er (regulates ca +), striations due to myofilaments

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17
Q

Actin💀

A

Part of thin filament

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18
Q

Myosin💀

A

Make up thick filament

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19
Q

What does myofibril contain?

A

I band, A band, H zone, m line, sacromere, Z disc

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20
Q

Sacromere💀

A

Functional unit of skeletal muscle,. Thick/thin filaments, repeating unit in my fibril

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21
Q

What does sacromere contain?

A

Actin, troponin +tropomyosin, thick filaments, myosin

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22
Q

I band

A

Thin filaments only (light bond)

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23
Q

A band

A

Thick + thin filaments (dark band)

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24
Q

H zone

A

Thick filaments only W/ in A band

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25
Q

M line

A

Anchor thick filaments, elastic fibers

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26
Q

Z disc

A

Tie everything together, microscopic banding pattern, thin filaments are anchored

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27
Q

Actin

A

Myofilament w/ binding sites for myosin heads, thin filament

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28
Q

Myosin

A

Myofilament ( 300 / filament) w/ heads that bind actin

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29
Q

Troponin+ tropomyosin=

A

Regulatory problems

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30
Q

Sliding filament theory?

A

Actin filaments are pulled closer by myosin, z-discs move closer, h-bands shrink, A bands stay put (contraction, actin and myosin overlap completely)

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31
Q

Crossbridge

A

With Ca + present, ‘cocked’myosin heads bind to actin

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32
Q

Power stroke🌉

A

Myosin pulls actin toward m-line

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33
Q

Cross bridge cycling steps

A

Crossbridge, power stroke, an 300 myosin heads on thick filament, sacromere, myofibril, myosin head detached by ATP, ATP splits and recooks head, form crossbridge, continues until no ATP or Ca

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34
Q

① ATP and muscle contraction

A

Active site on actin exposed as Ca binds to troponin

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35
Q

② ATP and muscle Contraction

A

High energy (adp+p)myosin head binds actin =crossbridge

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36
Q

③ ATP and muscle contraction

A

During power stroke, p released and head pivots forward, ADP released =↓ energy state
(Notice crossbridge still intact)

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37
Q

④ ATP and muscle contraction

A

ATP attaches to myosin head, crossbridge detaches

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38
Q

⑤ ATP and muscle contraction

A

Myosin head hydrolizes ATP →adp+p= recocked/high energy

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39
Q

Source of ATP - creatine phosphate

A
  • Stored ATP used up in seconds
  • regenerates ATP for 15 seconds
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40
Q

Sources of ATP - anaerobic respiration

A
  • High demand = rapid ATP delivery
  • glycolysis (breaking glucose) =2 ATP lactic acid (from pyrurate)
  • very rapid, very expensive (only 2 atp/gluccse)
  • about 60 sec., O2 not required
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41
Q

Sources of ATP - aerobic respiration

A
  • Lower demand = O2 can be used
  • 2 ATP from glycolysis +pyruvate sent to mitochondria = 36 ATP per glucose.’
  • hour sustained activity+ resting ATP
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42
Q

Oxygen debt (post exercise excess oxygen consumption)

A
  • Oxygen intake Î after exercise
  • resting ATP, cp, and other fuels restored
  • lactic acid metabolism, cell repair adaption
  • until resting conditions restored (3-40hrs)
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43
Q

Muscle strength

A

Of fibers / muscle does not change, genetically determined

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44
Q

Stress (muscle)

A

Production of more sarcomeres and myofibrils = stronger, losing it=atrophy
Use IT OR lose IT

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45
Q

Muscular dystrophy = inherited disorder

A
  • Muscle fibers degenerate (atrophy) abnormally
  • duchenne muscular dystrophy (dmd ) fatal by early 20’s
  • sarcolemma
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46
Q

Isotonic

A

Muscle moves load (maintain same tone)

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47
Q

Concentric (isotonic)

A

Muscle shortens

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48
Q

Eccentric ( isotonic)

A

Muscle lengthens

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49
Q

Isometric

A

Muscle contracts, but load remains still, often load exceeds strength of muscle

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50
Q

Motor unit

A

-1 motor neuron + all associated muscle fibers
- small (4 fibers) to large (1000’S fiber)
-Small control fine movements (like eyes)- easily excited
-Large units - gross movements

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51
Q

Recruitment

A

Larger motor units ‘recruited’ until goal reached
- small more excitable units recruited 1st
- larger, less excitable units recruited later
- muscles exhibit ‘graded’ response, ex. Matches load

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52
Q

What does fiber length affect?

A

Tension

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53
Q

What do thick and thin filaments have to do to develop tension?

A

Must overlap

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54
Q

80% -120% resting muscle length =

A

Greatest possible tension

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55
Q

Muscle twitch=

A

Single contraction (1 AP)

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56
Q

Latent period (muscle twitch)

A

AP along sarcolemma down tubules

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57
Q

Contraction period (muscle twitch)

A

Ca binding troponin, cross bridges forming

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58
Q

Relaxation period (muscle twitch)

A

Ca pumped back to SR, tropomyosin covering binding site
- last 100 m sec, depending on fiber type

59
Q

Single AP =

A

Twitch

60
Q

Wave summation

A
  • If 2nd AP arrives before end of relaxation period,
  • more ca in sarcaplasm = more active sites exposed = more cross bridges
    -↑ frequency than motor = greater tension per muscle fiber
61
Q

Stimulation frequency, tetanus

A

When max tension achieved

62
Q

Incomplete tetanus

A

Fiber quivers due to relaxation phases

63
Q

Complete tetanus

A

Stimulation frequency ↑ enough

64
Q

Treppe - ‘staircase’ effect

A
  • max stimulation of dormant muscle generates 50% of max tension
  • repeated max stimulus = gradual ↑ to max tension
  • due to heat and extra ca
65
Q

Muscle tone

A

Some fibers are contracting even at ‘rest’

66
Q

What does muscle tone provide?

A

Fiber contraction alternates to provide tone,
-Involuntary, keeps muscles ready for action

67
Q

Hypotonia ( muscle tone)

A

Damage to direct nerves= lack of tone (atrophy)

68
Q

Hypertonia. (Muscle tone)

A

Excessive tone, inhibitory nerve damage = spastic when stretched

69
Q

Types of muscle fibers

A

Speed of ATPases (ATP splitters), ATP forming pathways (oxidative/glycatic), slow oxidant fibers, fast oxidative fibers, fast glycolytic fibers

70
Q

Speed of ATPases (ATP splitters)

A

2 general fiber types = slow and fast (2x faster)

71
Q

ATP forming pathways

A
  • Oxidative fibers - use aerobic respiration
  • glycolic fibers - use anaerobic respiration
72
Q

Slow oxidative fibers (so)- slow ATPases

A
  • Aerobic ATP production - lots o’ mitochondria
  • myoglobin - 02 carrying molecule = dark meat,
  • thin, less tension, fatigue resistant (posture, joint stability)
73
Q

Fast oxidative fibers (fo)- fast ATPase (intermediate fibers)

A
  • aerobic ATP, lots o’ mitochondria
  • little myoglobin, intermediate tension (walking)
74
Q

Fast glycolytic fibers (fg) - fast ATPase

A
  • Anaerobic few mitochondria/myoglobin
  • lots o’ glycogen
75
Q

Endurance exercise = mainly slow fibers

A
  • More mitochondria = more aerobic ATP
  • more myoglobin = extra 02
  • more capillaries = angiogenesis
  • not so much hypertrophy= ↓ blood flow
  • all= greater endurance
76
Q

Resistance exercise = mainly Fg fibers

A

Short term, powerful movements required (anaerobic)
-↑ in my fibril #=↑ in muscle fiber size
-↑ in c.t.
- no significant î in mitochondria or capillaries (02 delivery not critical)
-Hypertrophy= ↑ muscle size

77
Q

Atrophy

A
  • Loss of muscle mass
  • lack of use=atrophy
  • atrophy due to aging= sarcopenia
78
Q

What does cardiac muscle do?

A
  • Pumps blood
  • lots o’ mitochondria + myoglobin (aerobic atp)
  • autorythmic
    -î and ↓ by ANS (autonomic nervous system)
79
Q

Cardiac muscle contraction

A

-Functional synoytium (contracts-like 1 big cell) due to gap junctions.
-Long AP’S due to influx of Ca from extracellalar fluid (long contraction time)
- ca triggers contraction, but most from outside cell

80
Q

Autorhythmic (cardiac)

A

Contractions via self-excitable ‘ pacemaker’ cells

81
Q

Contraction of smooth muscle

A
  • ca enters sarcoplasm (from outside cell + sr)
  • calmodulin activated → myosin kinase activated
  • ATP on myosin heads.→ ADP + p
  • maintain contractions for long periods, ↓power contract., not much ATP
  • some ca in sarcoplasm = maintain tone
  • latch bridges = some intact w/o ca
82
Q

What stimulates smooth muscle contraction?

A

Ca, most stored outside cell, no sr

83
Q

Smooth muscle stimulation

A
  • Natural (ANS) stimulation of smooth MT= neurotransmitters released from varicosites
    -Digestive tract smooth muscle contains pacesetter cells = rhythmic contraction
  • other triggers include hormones and local factors ‘’
84
Q

Single unit (smooth muscle organization)

A
  • Single-unit = smooth muscles linked by gap junctions (aka visceral muscle)
  • most common, 1 cell stimulated causes entire layer to contract
  • often exhibit stretch-relaxation response(for storage stomach/ bladder)
85
Q

Multi-unit (smooth muscle organization)

A

-Few gap junctions, each cell requires stimulation
-Much finer control (eyes,respiratory)

86
Q

Origin

A

-Anchoring point, music attachment site does not move

87
Q

Insertion

A

Muscle attachment sites that moves when muscle contracts
- insertion always moves toward origin

88
Q

Prime mover(muscle interactions)

A

(Aka against)- muscle that contributes most to a particular movement
- biceps brachii = prime mover during elbow flexion

89
Q

Synergism (muscle interactions)

A

Muscle that aids/help coordinate desired movement
- brachialis+brachioradialis help prevent undesirable rotation and also assist an elbow flexion

90
Q

Antagonist(muscle interactions)

A
  • Muscle w/ opposite action to prime mover
  • helps maintain position /control rapid movements
91
Q

Fixator (muscle interactions)

A

Type of synergism that keeps joint stable

92
Q

Parallel(non -fusiform) fascicle arrangements

A
  • Flat, fascicles along long axis
93
Q

Parallel-fusiform(fascicle arrangements)

A

Rounded and tapered to tendons(thick middle =belly)
- circular, convergent

94
Q

Unipernate (fascicle arrangements)

A

Like a feather, fascicles angled along on side of tendon

95
Q

Step 1: the neuromuscular junction(excitable contraction)

A

-Each fiber innovated by motor neuron
- connection = neuromuscular junction(NMJ)
- 3 parts= synaptic end bulb (knob),synaptic cleft, motor end plate

96
Q

Synaptic end bulb(knob)

A
  • end of motor neuron, stores acetylcholine (ACH)
97
Q

Synaptic cleft

A
  • gap b/n cells, ACH diffuses across
98
Q

Motor end plate

A
  • sarcoma section, contains ACH receptors
99
Q

Step 2: excitation contraction coupling

A
  • Action potential arrives at synaptic knob
    -Voltage-gated Ca channels open, ca enters knob
  • 3 key paints of ACH and receptors
  • voltage gated Na channels that trigger AP along sarcoma fiber officially excited
  • ACH quickly degraded by acetylcholnesterace = precise control of contraction
100
Q

Key points of excitation contraction coupling

A
  • ACH released via exocytosis from synaptic vesicles
  • ACH diffuses across synaptic cleft, bind w/ACH receptors on motor end plate
  • receptors open and allow Na intosarcoplasm= depolarization
101
Q

Resting membrane potential. (Don’t need for essay) step 3?

A
  • Muscle fibers maintain a voltage across sarcolemma, i.e. Polarized
    If enough Na, voltage gated Na channels open, propagate AP like dominos)
102
Q

Step 4: ap travels ↓ t-tubules

A
  • T-tubule - transverse’ tubule, extension of sarcolemma w/in sarcopiasm
  • terminal cistern-sr surrounding t-tubules,store Ca
103
Q

5th step: contraction phase

A
  • AP ↓ t-tubules stimulate Ca channels on terminal cistern to open
  • Ca floods sarcoplasm
  • ca binds to troponin
  • troponin moves tropomyosin to reveal actin binding sites, contraction!
104
Q

Rhythmic contraction(smooth muscle stimulation

A

Digestive tract smooth muscle contains pacesetter cells = rhythmic contraction

105
Q

Tendons

A

Tough, rope -like structures that connect muscle →bone

106
Q

Sarcoplasm💀

A

Cytoplasm of muscle fibers, contains enzymes and organelles for muscle function

107
Q

Terminal cisternal

A

Large chambers in sr of muscle cells that store ca and release to start contraction

108
Q

Why does skeletal fiber appear striated?

A

Highly organized arrangement of contractile proteins- actin and myosin, w/in their myofibrils, creating bands of light and dark sarcomeres

109
Q

Thick filaments

A
  • Main protein: myosin,
  • function: provide motor protein that generate force for contraction
110
Q

Thin filaments

A
  • Protein: actin
  • function: act as the track along which the myosin heads moving during contraction
111
Q

Neuromuscular junction (Nmj)

A

•Synaptic connection between the terminal end of a motor nerve and a muscle
• synaptic knob, synaptic deft-motor end plate

112
Q

What stimulates ACH release?

A
  • Neurotransmitter released by motor neurons at NMJ
113
Q

What is action potential?

A
  • Rapid electrical signal that travels along a nerve cell membrane, generated by opening of voltage gated Na, cause rapid depolarization of membrane, propagating signal
114
Q

What is ache, why is it important?

A
  • acetylcholinesterase in NMJ,
    -Immediately breaks down and hydrolyses ACH
115
Q

Triad

A
  • Substructure of SKM that coordinates excitation contraction, made up of 2 terminal cistern of s/r
116
Q

Function of triad

A
  • Translate: action potential from plasma membrane to sr, initiates calcium flow to cytoplasm/ contraction
117
Q

Role of ATP

A

Provide energy needed for myosin head to detach from actin, allowing muscle to relax and prepare for new contraction

118
Q

Why does rigor morris occur?

A

When someone dies, ATP prod. ↓, leading actin and myosin becoming permanently bound tg, causing muscles to stiffen and remain contracted due to lack of energy to detach

119
Q

What causes muscles to relax?

A

When motor protein myosin in sarcomere releases actin

120
Q

Tetanus

A

Serious bacterial infection that affects nervous system and muscle

121
Q

Intercalated disc

A

Correction point between. Individual cardiac cells, allowing ↑ electrical impulses and mechanical fro force through heart

122
Q

Varicosity (smooth)

A

Enlargement of neuron that ↑ neurotransmitter,

123
Q

Dense body (smooth)

A

Anchor thin filaments n sm,

124
Q

Calmodulin

A

Protein that regulates calcium dependent signals

125
Q

Fascicle

A

Bundle of skeletal muscle fibers running parallel to each other, enveloped by perimysium

126
Q

What is role of acetylcholine ( ACH )

A

Stimulate muscle contraction

127
Q

What is a myofibril?

A

Rod - like unit within muscle fibers

128
Q

What structure is responsible for the striated look of a skeletal muscle

A

Sarcomere

129
Q

What protein blocks the myosin-binding site?

A

Tropomyosin

130
Q

What causes muscles to relax?

A

Break ↓ of acetylcholine

131
Q

What are the sources of ATP in skeletal muscle

A

Creative phosphate, glycolysis, and oxidative phosphorylation

132
Q

What is oxygen debt *

A

Amount of oxygen required to oxidize lactic acid and replenish ATP stores after exercise

133
Q

What is a isotonic contraction

A

Contraction where muscle length changes while generating force

134
Q

What is an isometric contraction?

A

Contraction where the muscle length remains constant while generating force

135
Q

How does recruitment help determine overall contraction strength?

A

Increasing the # of of motor units activated

136
Q

How does stimulation frequency affect contraction strength?

A

Higher frequency of stimulation leads to stronger contractions

137
Q

What is wave summation *

A

↑ in muscle contraction strength due to rapid stimulation

138
Q

What is tetanus?

A

Sustained muscle contraction due to rapid stimulation

139
Q

What are the 3 different skeletal muscle fiber types?

A

Slow oxidative, fast oxidative, fa fast glycolytic

140
Q

What determines each category of skeletal muscle finer type?

A

ATPases activity and respiratory pathway

141
Q

What are slow oxidative fibers adapted for?

A

Endurance and continuous contraction

142
Q

What are fast glycolytie fibers adapted for?

A

Short bursts of power and speed

143
Q

How do muscles adapt to resistance exercise?

A

↑ in muscle fiber size and strength

144
Q

What is a variscosity in smooth muscle?

A

Swelling along a nerve finer that releases neurotransmitters

Anatomy And Physiology (4 decks)

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