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Kin 155 Exercise Physiology > Lecture Exam #1 > Flashcards

Lecture Exam #1 Flashcards

1
Q

6 senses

A 
hearing
seeing
smell
taste
touch
Kinesthetic awareness
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2
Q

responsibility of kinesthetic awareness

A

joint receptors

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3
Q

system responsible for motivational drives and needs

A

Limbic system

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4
Q

functional unit of muscle cell

A

Sarcomer

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5
Q

two roles of calcium during muscle contraction

A

Ca+ in axon termianl causes release of acetycholing

Ca+ binds to regulatory site on troponin removes inhibition between actin and myosin

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6
Q

three roles of ATP during muscle contraction

A

release of energy -> myosin head pulls actin over myosin (powerstroke)
new ATP attaches to myosin head -> seperation of actin and myosin
when nerve impulse stops ATP used to pump Ca+ back to sarcoplasmic reticulum

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7
Q

process that breaks ATP down and moves myosin head

A

myosin ATPase

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8
Q

muscle fiber types

A

Fast twitch Glycholiytic (anaerobic)
Fast twitch Oxidative Glycholytic (intermediate - between aerobic and anerobic capilities)
Slow twitch oxidative (aerobic)

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9
Q

size principle

A

larger cell bodies require greater neural stimulation in order to depolarize (FT muscle fiber)
motor units with smaller cell bodies get recuited first

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10
Q

which muscle fibre type has the largest cell body

A

Fast twitch Glycholytic

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11
Q

what does the max. tension depent on

A

actin-myosin binding

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12
Q

muscle fibre type with highest max. tension

A

fast twitch glycholytic

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13
Q

what does the speed of a contraction depend on

A

size of axon (myelinated)

myosin ATPase

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14
Q

muscle type with lowest endurance

A

slow twitch oxidative

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15
Q

what does the length of a msucle contraction depent on

A

ability to recycle or regnerate ATP (slower endurance)

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16
Q

motor unit

A

one motor neuron and all by it contolled muscle fibres

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17
Q

rest before muscle contraction

A

actin and myosin are seperated
tropomyosin blocks actin binding site
Ca+ stored in Sarcoplasmic Reticulum

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18
Q

steps of muscle contraction

A

release of Ca+ through nerve impulse causes release of acetycholine
ACH attaches to receptors that causes opening of Na+ channels and depolarization
AP causes release of Ca+ from SR
Ca+ binds to troponin receptors and moves tropomyosin away from blocking position
myosin head attaches to actin and pulls it over myosin filament
ATP binds to myosin head and releases it from actin
ATPase causes new attachement and further contraction

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19
Q

power stroke

A

tilting of myosin head and mpulling of actin filament

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20
Q

what causes power stroke

A

stored energy

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21
Q

relaxation after muscle contraction

A

nerve impulse stops
Ca+ released from troponin binding site and transported back to SR
tropomyosin moves into blocking position
myosin head moves back

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22
Q

what system allows Ca+ to travel away and back to the SR

A

Longitudinal Tubules

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23
Q

why does the right side of the brain controls the majority of our bodie´s left side movement

A

because 90% of pyramidal motor tracts cross

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24
Q

brain area behind the central sulcus

A

sensory cortex

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25
Q

brain area prior to central sulcus

A

primary motor cortex

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26
Q

brain are prior to primary motor cortex

A

pre motor cortex

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27
Q

responsibility of pre motor cortex

A

unconcious, fine tuning, highly skilled

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28
Q

responsibility of primary motor cortex

A

concious, voluntary movement

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29
Q

responsibility of sensory cortex

A

interprets information

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30
Q

pituitary gland

A

controlled by hypothalamus

master gland

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31
Q

basal ganglia

A

grey matter

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32
Q

disease if grey matter is damaged

A

parkinson - lose muscle control

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33
Q

responsibility of cerebellum

A

coordination

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34
Q

A band

A

myosin, overlapping actin

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35
Q

H zone

A

only myosin area

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36
Q

I Band

A

lighter area

actin

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37
Q

z lines

A

attached to sarcolemma

groove for t-tubules to go deep into sarcolemma

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38
Q

where is Acetycholin stored

A

in synaptic vesicles

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39
Q

where is Ca++ within the muscle fibre stored

A

sarcoplasmic reticulum

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40
Q

responsibility of the midbrain

A

visual acuaity

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41
Q

responsibility of the medulla

A

heart rate
blood flow
respiration rate

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42
Q

responsibility of pons

A

respiration rate
facial expression
general eye movement

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43
Q

muscle fiber distribution in untrained people (genetic)

A

almost 50 % FT
50 ST
exceptions exist (some are born with a higher distribtion of one fiber type then others)

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44
Q

difference in gender and fiber type distribution

A

gender does not affect the fiber type distribution

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45
Q

fiber types in location of body

A

each individual has different fiber types in different parts of the body

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46
Q

fiber types within a motor unit

A

only same fiber types within one motor unit

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47
Q

why do motor units operate at “all-or-none” principle

A

because all are the same muscle fiber types - they need the same stimuli to get depolarized

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48
Q

what determines the force production

A

Actin and Myosin Binding
# of fibers within a motor unit
# of motor units activated
size of fiber within an active motor unit
balance between stimulating and inhibitory neurotransmitter

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49
Q

stimulating neurotransmitter

A

Acetycholin (AcH)

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50
Q

inhibitory neurotransmitter

A

gamma amino butyric acis (GABA)

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51
Q

twitch

A

a single muscle fiber contraction

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52
Q

summation

A

new stimuli while muscle fiber is still contracted - next contraction starts at a higher level and is stronger

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53
Q

tetanus

A

max. contraction
muscle cramp
not desrable

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54
Q

what muscle fiber type has more actin and myosin?

A

fast twitch

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55
Q

when is max. tension of a muscle gnerated

A

when length reaches peak tension range

120% of resting muscle

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56
Q

how can max tension of a muscle be increased

A

prestretch before movement

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57
Q

what kind of training can improve prestretch

A

biometric training

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58
Q

what 3 factors additionally affect force production

A

initial length of muscle fiber
angle of pull
architecture of tendon and muscle fiber

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59
Q

angle of pull

A

different angles determine different force production

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60
Q

muscle types

A

Fusiform

Penniform

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61
Q

Fusiform muscles

A

parallel fibers running length of muscle
fibers insert into tendon
greater range of motion
less strangth and resistance to pull - greater risk to insure

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62
Q

Penniform muscles

A

fibers arranged diagonal to the direction of pull
fibers attached to tendon in small spaces
short range of movement
great strength and great resistance to injury

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63
Q

subdivisions of fusiform muscle

A

fusiform
bicipital
triangular

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64
Q

subdivisions of penniform

A

unipennate
bipennate
multipennate

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65
Q

metabolic by-products of muscle fatigue

A

lactic acid

ketone bodies

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66
Q

what causes muscle fatigue

A

metabolic by-products -> decrease of pH -> interference of Ca+ release Actin-Myosin binding & ATP breakdown
depletion (Abbau) of Neurotransmitter (neural fatigue)
depletion of phosphagen (PC & ATP)

67
Q

what leads to an increase in force

A 
hypertrophy (increase in muscle size)
hyperplasia (increase in muscle fiber #)
increase in motor unit recruitment
prestretch
change of fibertype
68
Q

agonist

A

contracting muscle

69
Q

antagonist

A

relaxing muscle

70
Q

high intensity speed training forms what kind of muscle fiber

A

fast twitch, decreases % slow twitch muscle fibers

71
Q

low intensity endurance training forms what kind of muscle fiber

A

slow twitch, decreases % fast twitch muscle fiber

72
Q

what is the most documented muscle fiber conversion due to training

A

SO to FOG

73
Q

what does a reduced neural inhibition lead to

A

increase in motor unit recruitment

74
Q

addition of strength training within endurance training

A

increase time to exhaustion while performing submax workload

75
Q

addition of endurance training to strength program

A

may reduce strength gains from strength training

76
Q

ATP use per day

A

at rest 40 kg

heavy exercise 720 kg

77
Q

phosphagen metabolism

A

highest power
lowest capacity
breakdown of ATP into ADP + Pi + E
extremely low ATP earned

78
Q

enzyme within phosphagen metabolism

A

Myosin ATPase to breakdown ATP

CPK and AK

79
Q

formation of ATP

A

CP + ADP -> ATP + C (use of CPK Enzyme)

ADP +ADP -> ATP +AMP (use of AK Enzyme)

80
Q

when is phosphagen metabolism used

A

0-30 sec

high intensity

81
Q

location of phosphagen metabolism

A

sarcoplasm

82
Q

energy pathway of phosphagen metabolism

A

phosphogen breakdown

83
Q

starting product of phosphagen metabolism

A

ATP and CP

84
Q

location of anaerobic glycolysis

A

sarcoplasm

85
Q

energy pathway of anaerobic glycolysis

A

glycolytic (breakdown of glucose or glycogen)

86
Q

starting product of anaerobic glycolysis

A

carbohydrate (CHO)

87
Q

enzymes of anaerobic glycolysis

A 
H-LDH (phosphorylase)
M-LDH (Hexokinase HK)
PFK (phosphofructokinase)
PK (pyruvate kinase)
A.T. (alanine transaminase)
88
Q

by-product of anaerobic glycolysis

A

pyruvate broken down into lactic acid and alanine to live

89
Q

relationship between lactic acid and pH

A

increase in lactic acid -> decrease in pH

90
Q

earned ATP from anaerobic glycolysis

A

first 2 ATP invested, later 4 earned

Net +2 ATP

91
Q

when is the anaerobic glycolysis used

A

30sec. - 3-4 min

high intensity

92
Q

starting product of aerobic glycolysis/oxydative metabolism

A

pyruvic acid transformed into acetyl CoA

93
Q

location of aerobic glycolysis

A

starts in sarcoplasm, end in mitochondra

94
Q

eneryg pathway of aerobic glycolysis/oxidative metabolism

A

Glycolytic (breakdown of glycogen and glucose) in sarcoplasm

Krebs cycle and Electron Transport System in Mitochondria

95
Q

enzymes of aerobic glycolysis/oxidative metabolism

A

CS (Citrate synthase)
SDH (succinate dehydrogenase)
IDH (isocitrate dehydrogenase)

96
Q

earned ATP with the aerobic glycolysis/oxydative metab.

A

Net in skeletal muscle 36 ATP

Net in cardiac muscle 38 ATP

97
Q

when is oxydative metabilism used

A

3-4 min. - 2-3 h.

moderate intensity

98
Q

by products of oxydative metabolism

A

CO2 and H2O

99
Q

what is beta fat oxidation based on

A

triglycerides = glycerol + 3 fatty acids

100
Q

location of beta (fat) oxidation

A

TG starts in Sarcoplasm

Beta oxidation in mitochondria

101
Q

pathway of beta (fat) oxidation

A

beta oxidation, kreb´s cycle, Electron transport system all in mitochondria

102
Q

starting product of beta (fat) oxidation

A

Acyl CoA

Carnitine - transporter

103
Q

enzymes within the beta (fat) oxidation

A 
lipase (HSL)
thiokinase
thiolase
carnitine fatty acid
transferase
104
Q

by-product of beta (fat) oxidation

A

ketone bodies (decrease in pH)

105
Q

ATP earned by beta (fat) oxidation

A

1 Fatty acid = 100-150 ATP

106
Q

when is the beta (fat) oxidation used

A

during continous low activity

107
Q

factors that determine lactate production

A

oxidative metabolism´s ability to accept pyruvate into krebs cycle
ability of the ETS to accepts NADH+H+ and FADH+H+
ability to form alanine from the breakdown of carbohydrates
ratio of M-LDH (forms lactate) to H-LDH (clears lactate)

108
Q

factors of phosphagen metabilism to increase capacity

A

increase in training
increase in muscle mass
increase in creatine ingestion

109
Q

factors of anaerobic glycolysis to increase capacity

A

increase in muscle mass
increase in alanine transaminase
increase ratio of H-LDH and M-LDH

110
Q

factors of aerobic glycolysis/oxidative metabolism to increase capacity

A

capacity is based on muscle and liver glycogen stores
increase in training
increase in CHO loading
increase in fluid ingestion

111
Q

factors of beta (fat) metabolism to increase capacity

A

increase CHO

112
Q

power

A

speed ATP can be produced and released at

113
Q

what is power of phosphagen metabolism based on

A

enzyme activities

114
Q

what is power of anaerobic glycolysis based on

A

enzyme activities

115
Q

what is power of aerobic glycolysis(oxidative metabolism based on

A

O2 delivery rate

enzyme activity

116
Q

what is power of beta (fat) metabolism based on

A

fat mobilization
enzyme activity
O2 delivery rate

117
Q

H+ and e- carrier within the ETS

A

cytochromes

118
Q

when do NAD carrier take action

A

glycolysis of cardiac muscle, in krebs cylce, beta (fat) oxidation, and conversion of pyruvate to acetyl CoA

119
Q

how many ATP can be earned when NAD dropps of H+

A

3 ATP

120
Q

when do FAD carrier take action

A

in glycolysis of skeletal muscle, krebs cycle, and beta (fat) oxidation

121
Q

molecule for carbohydrates and fat to enter krebs cycle

A

Acetyl CoA

122
Q

how many ATP are in aerobic glycolysis already formed before entering the mitochondria

A

cardiac muscle 2 invested, 10 formed
Net of 8 ATP
skeletal muscle 2 invested, 8 formed
Net of 6 ATP

123
Q

where do NAD and FAD carry H+ and e- to to form ATP

A

Electron Transport System (ETS)

124
Q

Mitchell´s Chemiosmotic Hypothesis

A

electron transfer leads to pumping of protons out of matrix generating proton gradient which leads to phosphorylation of ATP

125
Q

how many ATP are formed in pyruvate oxidation in the Krebs cycle and ETS

A

15 ATP x 2 rounds = 30 ATP

126
Q

Fat metabolism energy yield

A

Fat 9 Kcal/gm
Carbohydrates 4 Kcal/gm
protein 4 Kcal/gm
alcohol 7 Kcal/gm

127
Q

how many carbons are in each fatty acid

A

12-18

128
Q

what does free fatty acid needs to get formed to, to enter the mitochondria in beta oxidation

A

acyl CoA

129
Q

carrier of Acyl CoA into mitochondria

A

carnitine

130
Q

why do energ systems respond in a certain order

A

by- or end-products of energy systems stimulat enzymes of other nergy systems
quick energy systems are often less complex
slower energy systems depend often on intramuscular metabolic factors and other systems likecardiorespiratory and circulatory systems

131
Q

HSL stimulating hormones and fat mobilization

A 
thyroxine
cortisol
glucagon
epinephrine
norepinephrine
132
Q

hormones that inhibit HSL and fat mobilization

A

Insulin

133
Q

what increases stimulating hormone release

A

exercise

134
Q

role of caffein

A

stimulates HSL and fat mobilization

stimulates phosphoralyse in glycolysing and glycogen mobilization

135
Q

what does an increase in carbohydrate loading lead to

A

increases aerobic glycolysis and beta (fat) oxidation capacity due to an increase in muscle glycogen

136
Q

best way for a carbohydrate loading program before a competition

A

1-2 days long hard exercise - exhaustion
2-3 days low carbohydrate diet
2-3 days high carbohydrate diet
competition

137
Q

what can carbohydrate loading be used for

A

to improve endurance performance in events longer than 60-80 min at 65-85% of VO2max or 75-85% of max HR

138
Q

what is understood as a low CHO diet

A

50 % of calories from CHO

4g of CHO per kg of BW

139
Q

high CHO diet

A

70% of calories from CHO

10G of CHO per kg of body weight

140
Q

CHO and fluid during exercise

A

event < 90 minutes -> 4-8 ounces of cold water every 10-15 minutes
event > 90 minutes -> 4-8 ounces of cold water containing 5-10% glucose solution every 10-16 minutes

141
Q

what does the ingestion of caffeine prior to exercise lead to

A

5g/kg of BW 40 min prior to event
improves fat mobilization -> power of fat ocidation
enhance mobilization of muscle glycogen

142
Q

critical aspect of caffeine ingestion prior to event

A

neg. diuretic effect -> dehydration

critical to maintain fluid during exercise

143
Q

how does creatine monohydrate ingestion help prior to an event

A

maintain higher muscle creatine levels
increase phosphocreatine resynthesis -> allows high intensity for longer time
allows to shorten resting time between high intensity exercise
increase phosphagen and anaerobic glycogen capacity

144
Q

how does CHO loading benefits high intensity, short duration athletes

A

increasing work time to exhaustion

145
Q

what needs to be considered as important with CHO loading for sprinters

A

important to not gain BW

146
Q

poitive effects of sodium bicarbonate ingestion

A

buffering of H+ released from lactic acid

increase lactic acid tolerance and capacity of anaerobic glycolysis

147
Q

changes in phosphagen metabolism due to endurance training

A

increase in [ATP], CP, CPK, AK

increase in reaction time -> increase in power

148
Q

changes in oxydative metabolism due to endurance training

A 
increase [myoglobin], O2 delivery
increase in krebs cycle enzyme, ETS cytochrome and beta oxidation enzyme activity
increase in Lipase (HSL) activity
mucle [glycogen]
Triglyceride in muscle
149
Q

oxidative changes in fiber type specificity

A

greater in SO and FOG than in FG

150
Q

glycolytic changes in fiber type specificity

A

greater in FT than in ST

151
Q

phosphagen changes due to endurance training in children

A

increase in [ATP] and [CP], increase in capacity

152
Q

glycolysis changes due to endurance training in children

A

increase in power

153
Q

changes in phosphagen metabolism following strenth training

A

increase ATP and CP level
increased myosin ATPase CPK and AK levels
increased capacity

154
Q

changes in anaerobic glycolysis due to strength training

A

increased enzyme levels

increased power

155
Q

changes in oxidative metabolism due to strength training

A

increase muscle glycogen decreased [mitochondria/fiber volume ratio
increased FT fiber area/ST fiber ratio
muscle hypertrophy

156
Q

when does strength training in children show an effect

A

after puberty

157
Q

peripheral sensory receptors

A

muscle spindles
golgi tendon organs
joint receptors - proprioreceptors

158
Q

muscle spindles

A

operate functional spinal cord level
sense length of muscle fibres
reflex contraction
co-activation of extra- and intrafusal fibers

159
Q

golgi tendon organs

A

reflex inhibition (inhibits muscle to overcome to high force

160
Q

input into motor coretx

A

sensory cortex

limbic system

161
Q

proprioreceptors

A

feedback to sensory cortex = kinesthetic awareness

162
Q

gamma efferent

A

nerves from from spinal cord coming

163
Q

afferent from muscle spindle

A

nerves to spinal cord going
top one primary annulospinal ending
bottom secondary flower spray endind

Kin 155 Exercise Physiology (4 decks)

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