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Exercise Physiology > Chapter 8 - exam 2 > Flashcards

Chapter 8 - exam 2 Flashcards

1
Q

how is skeletal muscle attached to bone

A

by connective tissue = tendons

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2
Q

What is the origin mean of skeletal muscle

A

end of muscle attached to bone that doesnt move

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3
Q

What is the insertion mean of skeletal muscle

A

opposite end fixed to bone that moves during contraction

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4
Q

Explain the complete breakdown of structures in skeletal muscle down to the smallest unit

A

thin and thick filaments –> myofibrils –> muscle fiber (muscle cells) –> fasicle –> muscle bundle

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5
Q

What is the sarcolemma

A

casing outside muscle fiber that makes up a fasicle

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6
Q

What are the two subpopulations of mitochondria of skeletal muscle fibers

A

1) subsarcolemmal (SS) mitochondrion
2) intermyofibrillar (IMF) mitochondria

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7
Q

What are Subsarcolemmal (SS) mitochondria

A
  • located directly beneath cell membrane (sarcolemma) - effect membrane potential and flow of ions to create potential
  • produce cellular energy needed to maintain active transport of ions across the sarcolemma
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8
Q

What are Intermyofibrillar (IMF) mitochondria

A
  • located near myofibrillar (contractile) proteins
  • provide E needed to sustain muscle contraction
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9
Q

Satellite cells are a type of _______ and are important in what

A

type of myoblast and important in muscle growth/repair
- during muscle growth, satellite cells increase number of nuclei

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10
Q

satellite cells do what with nuclei

A

produce nuclei and transport them to muscle fiber

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11
Q

having more satellite cells allows for what synthesis

A

more satellite cells = more nuclei = greater protein synthesis
- important for muscle growth in response to strength training

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12
Q

on untrained muscle what happens with first training and afterwards with detraining and retraining

A

after first training satellite cells bring more nuclei onto muscle cell –> creating more protein synthesis and causing hypertrophy –> after detraining atrophy is the result and muscle shrinks —> with exercise get back to hypertrophy

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13
Q

What are the 3 functions of skeletal muscle

A

1) force production for locomotion and breathing
2) force production for postural support
3) heat production during cold stress

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14
Q

skeletal muscle produces what in response to contractions

A

produces myokines

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15
Q

What are the three functions of myokines

A

1) stimulate glucose uptake and fatty acid oxidation – b/c during exercise need more glucose in the cells and break down fatty acids
2) promote blood vessel growth in muscle
3) promote liver glucose production and triglyceride breakdown
- ned more glucose in muscles to perform force

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16
Q

What is IL-6

A

immune response
- both proinflammatory and anti-inflammatory
- produced during exercise and promotes anti-inflammatory effect
- increased glucose production in liver w/ exercise

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17
Q

does regular exercise promote anti-inflammatory, pro-inflammatory or no inflammatory environment

A

anti-inflammatory
- reduce chronic inflammation (vasodilate) and reduced risk heart disease, type 2 diabetes and certain cnacers

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18
Q

when is IL-6 hightest

A

during exercise and decreases after

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19
Q

What do flexors do

A

decrease joint angle

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20
Q

what do extensors do

A

increase joint angles

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21
Q

What is static movement

A
  • muscle exerts force w/o changing length
  • pulling against immovable object
    -postural muscles
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22
Q

What are the two types of dynamic movements

A

1) Concentric
2) eccentric

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23
Q

What is Concentric dynamic movement

A

muscle shortens during force production

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24
Q

What is eccentric dynamic movement

A
  • muscle produces force but length increases – resisting
  • associated with muscle fiber injury and soreness “healthy” injury
  • during workout focus on eccentric
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25
Q

What is the central nervous system

A

brain and spinal chord

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26
Q

what is the peripheral nervous system

A

cranial and spinal nerves

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27
Q

What is the direction of movement when starting with activating sensory receptors

A

active sensory receptors –> go to sensory division of PNS –> to CNS –> To the motor division of PNS for response

EITHER
- Somatic Nervous system – skeletal muscle
- Autonomic nervous system – smooth muscle, cardiac muscle, glands

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28
Q

The somatic motor neurons of the PNS are resonsible for what

A

carrying neural messages from spinal chord to skeletal muscles (tissue)

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29
Q

what is a motor unit

A

motor neuron and and all the fibers it innervates

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30
Q

what is the neuromuscular junction

A

gap between motor neuron and muscle fiber

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31
Q

what is the motor end plate

A

pocket formed around motor neuron by sarcolemma
-in sarcolemma form pocket for motor neuron fiber to fit into

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32
Q

myofibrils can be further subdivided into individual sarcomeres and what are the two major parts to this

A

arrangement of thin (actin, tropomyosin, troponin) and thick (myosin) filaments

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33
Q

Draw out one sarcomere and label the Z line, M lie, I band, A band, and H zone

A

draw and look at drawing

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34
Q

What happens that causes muscle shortening

A

due to movement of thin (actin) filament over the thick (myosin) filament
- form cross-bridges

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35
Q

Do z lines get closer or father away from each other during a contraction

A

get closer during contraction

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36
Q

What is required for muscle contraction

A

myosin ATPase breaks down ATP (already attached) as fiber contracts

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37
Q

What are the two sites on the heads of the myosin

A
  • actin-binding site
  • myosin ATPase site
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38
Q

what do you need ATPase to do that effects a contraction

A

break down ATP to release myosin head from actin filament

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39
Q

what is the source of ATP during muscle contraction

A

ATP-PC system

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40
Q

What are the 5 steps of the excitation-contraction coupling process in muscle contraction

A

1) action potential stimulates acetylcholine (Ach) release from alpha motor neuron at neuromuscular junction
2) Acetylcholine induces an action potential in the muscle fiber. Action potential spreads down sarcolemma and T-tubules
3)Action potential stimulates Ca2+ release from sarcoplasmic reticulum
4) Ca2+ initiates tropomyosin displacement revealing myosin binding site
5) myosin forms cross-bridges w/ actin producing force

41
Q

With an action potential what provides the cellular energy to actively transport Ca2+ across sarcolemma

A

the subsarcolemmal mitochondria

42
Q

List the 7 stages of cross-bridge cycling

A

1) myosin binding sites on actin molecule are covered in resting fibers w/ ADP + Pi attached
2) Action potential releases calcium from sarcoplasmic reticulum
3) Calcium binds to troponin – cause tropomyosin to move revealing the myosin binding site
4) Cross-bridge forms when myosin heads bind to actin
5)myosin head pivots moving actin –> ADP and Pi dissociate from myosin head
6) myosin head releases actin when fresh ATP binds
7) myosin head binds next actin (flagged) –> ATP cleaved to ADP + Pi and cycle repeats

43
Q

if a drug increases Ca2+ release from the SR but does NOT enhance muscle contraction. It is suspected that the drug accidentally bound to the thin filament. Blockage of which structure in the thin filament would prevent Ca2+ binding and skeletal muscle contraction

A

troponin

44
Q

what are muscle cramps

A

-spasmodic involuntary muscle contractions
- often associated with prolonged, high intensity exercise
- electrolyte depletion and dehydration theory: H2O and Na2+ loss via sweat and hot environment

45
Q

Explain the altered neuromuscular control theory

A
  • abnormal spinal reflex activity due to fatigue
  • result: increased excitatory activity of muscle spindles and reduced inhibitory effect of Golgi tendon organ
46
Q

What happens with increased muscle spindle activity

A

muscle spindles detect stretch of muscle (doest want to stretch too much) –> sensory neurons conduct action potential to spinal chord –> sensory neurons synapse with alpha motor neuron –> situation of alpha motor neuron cause muscle to contract and resist stretch (CRAMP)

47
Q

What happens with decreased Golgi tendon organ activity

A

golgi tendon organize detect tension applied to a tendon –> sensory neurons conduct action potentials to the spinal cord –> sensory neuron synapse with inhibitory interneurons that’s an abs with alpha motor neurons –> inhibition of the alpha motor neuron causes muscle relaxation leaving the tension applied to the tendon

48
Q

Activation of Golgi tendon does what?

A

inhibits motor neurons in spinal chord, result in muscle relaxationW

49
Q

What are Type I fibers

A
  • slow-twitch fibers
    -slow oxidative fibers
50
Q

What are Type II fibers

A
  • intermediate fibers
    -fast-oxidative glycolytic fibers
51
Q

what are type IIx fibers

A

(less resistant to fatigue)
- fast twitch fibers
-fast glycolytic fibers

52
Q

What effects the oxidative capacity in muscle fiber types

A

number of capillaries (increase blood and O2 to tissues), mitochondria (need O2 to generate ATP - slow fatigue), and amount of myoglobin (increase O2 deliver to tissue)

53
Q

Do each type of muscle fiber types have low/moderate/high number of mitochondria

A
  • Type I: High
  • Type IIa: High/moderate
  • Type IIx: Low
54
Q

Do each type of muscle fiber types have low/moderate/high resistance to fatigue

A
  • Type I: High
  • Type IIa: High/moderate
  • Type IIx: Low
55
Q

what are the predominant energy systems in the muscle fiber types

A
  • Type I: Aerobic
  • Type IIa: Combination
  • Type IIx: Anaerobic
56
Q

The type of myosin ATPase effects what in each muscle fiber type

A

speed of ATP degredation

57
Q

What is the ATPase activity in each muscle fiber type

A
  • Type I: Low
  • Type IIa: High
  • Type IIx: Highest
58
Q

How does the abundance of contractile proteins (actin and myosin) effect the muscle fiber type

A

increased contractile fibers = increased force
– see more in type II than I

59
Q

The speed of shortening (contracting) is greater in what type of fibers

A

in fast fibers
- SR release Ca++ at faster rate
- higher ATPase activity

60
Q

What is the maximal force production per unit of cross-sectional area dependent on
- max force in each tissue:

A
  • NOT more/less fibers
  • same cross-sectional area produce different force
    ** High in Type II and moderate in Type I
61
Q

Why do larger muscle fibers produce more force than smaller fibers

A

because they contain more actin and myosin than small fibers (Type I lowest and type IIx highest max force)

62
Q

Is there a sex or age differences in fiber distribution

A

NO == distribution b/t fiber types not between men and women

63
Q

Do both men and women have same force produces in type I or II fibers

A

YES – only larger cross sectional fiber generates more force

64
Q

How is maximal power output effected by fiber types

A

fast fibers have higher power output than slower

Power = force x shortening velocity

65
Q

How is muscle fiber efficiency differentiated in muscle fiber types

A

lower amount of ATP used to generate force
- high efficiency = Type I
- moderate = Type IIa
- low efficiency = Type IIx

66
Q

what accounts for difference in muscle fiber types

A

genetics, training, hormone production

67
Q

What are the different types of exercise that have more fast fibers vs slow fibers

A

power athlete = fast fiber
endurance = slow fibers

68
Q

What are the three ways force is regulated in the muscle

A

1) types and number of motor units recruited
2) initial muscle length
3) nature of the neutral stimulation of motor units

69
Q

What are the three types of motor units

A
  • Type S (slow): smallest motor neuron and innervate type I muscle fibers == fine control (eyes, hands)
  • Type FR (fast, fatigue resistant): innervate type IIa muscle fibers
  • Type FF (fast, fatigable): largest of motor neurons, innervate type IIx muscle fibers
70
Q

Explain the recruitment pattern during graded exercise

A

Type I recruited first – plateaus and continues sustaining force generation –> right after plateau in type I, Type IIa is recruited if need more force –> reach plateau and continue force generation –> after plateau of Type IIa, recurit IIx if need even more force

71
Q

if you have a high force production how fast is the movement

A

usually slower

72
Q

progressive recruitment of motor units begins with what

A

begin w/ smallest and progress to larger

73
Q

how does initial muscle length effect force regulation

A
  • “ideal” sarcomere length for force generation: to have max # of crossbridges formed over sarcomere
  • increased cross-bridge formation
74
Q

What is the optimal overlap to have with the myosin and actin in order to have the greatest tension produced

A

if there is myosin head overlap and actin is able to move over myosin it is best at the greatest distance without sacrificing cross bridges
- if completely relaxed or fully contracted there isnt as much force

75
Q

How does the nature of the neural stimulation of motor units effect force regulation in muscle

A

effects the frequency of stimulation
- simple switch
-summation
-tetanus

76
Q

normal body movements involve sustained contractions that are NOT _______

A

simple twitches

77
Q

how many action potentials does a single twitch give

A

one action potential == with delay, contraction phase and relaxation phase

78
Q

what are the three phases of a muscle twitch

A
  • 5ms = stimulus –>latent period
    -40ms = twitch and Ca2+ released causing contraction almost at peak remove Ach = more relaxation
  • 50ms = relaxation
79
Q

explain the difference between simple twitch, summation, and tetanus

A

simple twitch: single twitches that increase in force and then decrease
summation: when simple switches summate into higher and higher force – if generate another twitch before relaxation = sum of twitch
tetanus: constant force maintained

79
Q

increasing the frequency of the stimulus results in what

A

summation of the twitches and finally tetanus

79
Q

Why is the force production additive in relation to Ca2+ availablility

A

after calcium is released from sarcoplasmic reticulum onto the sarcomeres == calcium used and released and using ATP, Ca2+ is pumped back into the sarcoplasmic reticulum

79
Q

Explain DOMS

A

delayed onset muscle soreness
- appear 24-48 hours after strenuous exercise
- due to microscopic tear in muscle fiber or connective tissue
- eccentric exercise (downhill running) causes more damage than concentric exercise (cycling)

79
Q

Explain why there is no physiological evidence that lactate production causes muscle soreness

A

= lactate removal is rapid (w/i 60 min) following exercise
= w/ continuous exercise produce same lactate - not always sore though

80
Q

What are the three types of exercise induced muscle injury

A

1) sarcomere damage (hours to days) = tearing
2) immune cell infiltration (days) = response to initial damage: inflammatory response
3) satellite cell activation (days to weeks) = important in muscle cell hypertrophy – build muscles

81
Q

explain the breakdown of what happens during DOMS

A

1) structural damage to muscle fibers
2) membrane damage
3) Ca2+ leaks out of the sarcoplasmic reticulum
4) Protease activation == result in breakdown of cellular proteins - cellular apoptosis
5) inflammatory response
6) edema and pain

82
Q

How do muscle fibers repair themselves

A

use resident satellite cell populations == ***** myogenic precursor cells

83
Q

What happens to force production with DOMS

A

force production decreases because there is increased sarcomere (force producing unit) damage = force loss – high chance of injury
- ability to send signal = inhibited
- impair ability for high intensity exercise

84
Q

What two substances are found in muscle that hints towards muscle damage (only in muscle not blood)

A
  • myoglobin
    = creatine kinase (high at 48 hours and super high at 4 days): immediate E production===== delayed response = Doms and high muscle damage at 4 days
85
Q

What are the three consequences of DOMS

A

E-C coupling failure, contractile protein loss, physical disruption

86
Q

What is the repeated bout effect

A

bout of unfamiliar exercise results in DOMS
- another bout of same exercise results in minimal injury

initial bout of exercise –> muscle damage or injury –> adaptation –>

Neural Theory: change in Nervous System
Connective Tissue Theory: increased intramuscular connective tissue
Cellular Theory: cellular changes that strengthen and protect muscle fibers –> repeated bout of exercise

–> less muscle damage == more adaptation
- slowly begin specific exercise over 5-10 sessions to avoid DOMS and do eccentric submax exercise

87
Q

What parts of the sarcomere change width during a concentric contraction

A

A band: does not change
H- zone: width decreases
I-band: width decreases
sarcomere: width decreases
thick filament: does not change
thin filament: does not change

88
Q

myoglobin delivers O2 to where

A

to the mitochondria = increase oxidative fibers and decreases fatigure

89
Q

What is the difference in BP and Hr with arm vs. leg exercises

A

at same O2 uptake arm work results in higher:

  • BP b/c of vasoconstriction of large inactive muscle mass
  • HR due to higher sympathetic stimulation
90
Q

with intermittent exercise what effects HR and BP

A
  • fitness level
    -temperature and humitidity
  • duration and intensity of exercise : lower intensity = less drift
91
Q

During prolonged exercise how is Q, SV, and HR effected

A

Q maintained, gradual decrease in SV because of a higher HR and dehydration, increase in HR b/c of heat – cardiovascular drift

92
Q

Why does cardiac output stay the same when HR and SV are effected

A

b/c wth the equation no change in Q = increase in HR * decrease in sV

93
Q

Explain the effects of cardiovascular drift

A

increase in HR and decrease in SV

  • to prevent maintain hydration and decrease intensity in cooler environment
94
Q

explain the transition from exercise to recovery and how HR, SV, and Q are effected

A

decrease HR, SV, and Q towards resting

Depends on: duration and intensity and training state

  • in the EPOC all decrease over time

Exercise Physiology (8 decks)

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