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Exercise Physiology > First Exam > Flashcards

First Exam Flashcards

1
Q

anabolic reations

A

synthesis of molecules

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2
Q

catabolic reactions

A

breakdown of molecules

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3
Q

metabolism

A

sum of all chemical reactions that occur in the body (anabolic and catabolic reactions)

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4
Q

bioenergetics

A

process of converting foodstuffs into usable energy for cell work

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5
Q

endergonic reaction

A

require energy to be added to the reactants, endothermic

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6
Q

exergonic reaction

A

release energy, exothermic

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7
Q

coupled reactions

A

liberation of energy in an exergonic reaction drives an endergonic reaction

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8
Q

Oxidation

A

removing electron (hydrogen atom)

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9
Q

Reduction

A

adding electron

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10
Q

Nicotinamide adenine dinucleotide (NAD)

A

carrier molecule
– Oxidized form: NAD+
– Reduced form: NADH

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11
Q

Flavin adenine dinucleotide (FAD)

A

carrier molecule
– Oxidized form: FAD
– Reduced form: FADH2

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12
Q

enzymes

A

facilitate faster reactions by locking with specific substrates

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13
Q

enzyme activity in blood

A

damaged cells release enzymes into the blood, so the level of enzymes in blood can serve as biomarkers of disease or damage

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14
Q

kinases

A

add phosphate group

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15
Q

dehydrogenase

A

remove hydrogen atoms

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16
Q

oxidases

A

catalyze oxidation-reduction reactions involving oxygen

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17
Q

isomerases

A

rearrangement of structure of molecules

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18
Q

effect of temp on enzymes

A

-small rise in temp increases enzyme activity (warmup)
-large increase in body temp decreases activity

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19
Q

effect of pH on enzymes

A

production of lactic acid and CO2 during exercise lowers pH and decreases enzyme acivity

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20
Q

protein as fuel for exercise

A

-some amino acids can be converted to glucose in the liver (gluconeogenesis)
-others can be converted to metabolic intermediates, contribute as fuel

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21
Q

anaerobic cycles occur in…

A

…cytoplasm

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22
Q

aerobic cycles occur in…

A

…mitochondria

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23
Q

energy system for short, explosive exercise

A

ATP-PC system

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24
Q

energy system for moderate exercise

A

Glycolysis

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25
Q

energy system for prolonged exercise

A

oxidative phosphorylation

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26
Q

ATP-PC system

A

use ATP stored in skeletal muscle and phosphocreatine to create ATP

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27
Q

creatine supplemenation

A

increases performance in short-term, high-intensity exercise

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28
Q

glycolysis

A

-glucose -> 2 pyruvate or 2 lactate
-two phases, energy investment (2 ATP used) and energy generation (4 ATP produced and 2 NADH produced)

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29
Q

blood glucose vs glycogen

A

1 ATP is used to come from glucose vs no energy needed to come from glycogen because free phosphates are used

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30
Q

reason to produce lactic acid

A

to convert NADH to NAD so the energy generation phase in glycolysis can take place and produce ATP

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31
Q

Hydrogens and electrons shuttled to mitochondria

A

for ATP generation, aerobic, slower process

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32
Q

Hydrogens and electrons shuttled to convert…

A

…convert pyruvate to lactate, anaerobic, faster process

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33
Q

two steps of aerobic ATP production

A

citric acid cycle and electron transport chain

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34
Q

steps leading to oxidative phosphorylation

A

glycolysis occurs in cytoplasm breaking glucose into pyruvate and ATP, pyruvate goes through membrane of mitochondria and produces CO2 and becomes 2 acetyl CoA, goes through citric acid cycle, then electron transport chain which produces ATP

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35
Q

primary molecule for energy production

A

acetyl-CoA

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36
Q

beta oxidation

A

process of converting fatty acids to acetyl-CoA
- activated fatty acid (fatty acetyl-CoA) enters mitochondrion where it is broken down into 2 carbon fragments forming acetyl-CoA which is then used as fuel for the citric acid cycle

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37
Q

Electron transport chain

A

electrons are removed from NADH and FADH and are passed along a series of carriers (cytochromes) to produce ATP

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38
Q

How much ATP does NADH and FADH produce

A

NADH: 2.5 ATP
FADH: 1.5 ATP
(called chemiosmotic hypothesis)

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39
Q

Functions of the three pumps in oxidative phosphorylation

A

1.First pump moves H+ into the intermembrane space using NADH (which is converted to NAD)
2. Second pump moves H+ into intermembrane space (FADH is converted to FAD)
3. Third pump moves H+ into intermembrane space (O2 produces H2O with H+)
4. As H+ crosses into the mitochondria through channels, ATP synthase is activated, converting ADP + Pi to create ATP

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40
Q

Free radicals

A
  • molecules with unpaired electron in outer orbital which can be produced by the leakage of e- along electron chain
  • react with and damage other molecules in the cell
  • aerobic exercise promotes the production of free radicals
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41
Q

number of ATP produced by 1 glucose

A

32 ATP

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42
Q

High energy products made by glycolysis

A

2 ATP, 2 NADH
(2 ATP if anaerobic, 7 if aerobic)

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43
Q

high energy products made by converting pyruvate to acetyl-CoA

A

2 NADH

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44
Q

high energy products made by the citric acid cycle

A

2 GTP, 6 NADH, 2 FADH

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45
Q

efficiency of oxidative phosphorylation

A

34% efficiency
66% energy expended as heat

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46
Q

Rate limiting enzyme regulates the rate of metabolic pathways, with what levels of ATP/ADP Pi?

A
  • high levels of ATP inhibit ATP production
  • High levels of ADP+Pi stimulate ATP production
  • calcium stimulates aerobic ATP production (a lot of calcium indicates rapid muscle contraction)
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47
Q

structural organization of skeletal muscle (superficial to deep)

A

tendon connects muscle to bone
- fascia
- epimysium
- perimysium
- endomysium
- sarcolema
–muscle fibers

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48
Q

myosin

A

thick filaments

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49
Q

actin

A

thin filaments

50
Q

satellite cells (muscle growth)

A
  • can increases the number of nuclei in muscle fibers
  • more nuclei allows for greater protein synthesis and more myonuclear domain (the volume of cytoplasm around each nucleus)
51
Q

satellite cells (muscle repair)

A
  • injury to muscle
  • fusion to injured myofiber
  • produce new myofibers
  • regenerated
52
Q

Neuromuscular junction

A

site where motor neuron and muscle cell meet

53
Q

neuromuscular junction (functions)

A

action potential travels to t-tubule which activates calcium storage site in the sarcoplasmic reticulum
(muscle will not do anything until action potential comes down the motor neuron axon)

54
Q

sliding filament (swinging lever-arm) model of muscle contraction

A

reduction in the distance btweem z lines of the sarcomere

55
Q

muscle shortening occurs due to

A

the movement of actin filament over myosin filament

56
Q

power stroke

A

formation of cross-bridges between actin and myosin filaments

57
Q

excitation-contraction coupling

A

depolarization of motor end plate (excitation) is coupled to muscle contraction
- CA++ binds to troponin causing change in tropomyosin, exposing myosin binding sites on actin

58
Q

tropomyosin

A

blocks actin so myosin cannot connect

59
Q

troponin

A

when calcium binds to troponin, tropomyosin unblocks actin

60
Q

cross bridge cycling steps (6)

A
  1. Resting fiber, myosin is not attached to actin (ADP + Pi on myosin head
  2. Myosin head binds to actin and forms cross bridge to actin
  3. Pi is released from myosin head causing conformational change in myosin
  4. Power stroke causes filaments to slide, ADP is released
  5. A new ATP binds to myosin head allowing it to release from actin
  6. ATP is hydrolyzed and Pi binds to myosin causing it to return to its original state
61
Q

muscular fatigue

A

decline in power output due to decrease in force generation and decrease in shortening velocity

62
Q

muscular fatigue in high-intensity exercise

A

due to accumulation of waste products which diminishes cross bridges bound to actin
(lactate & H+, ADP & Pi, free radicals)

63
Q

muscular fatigue in long duration exercise

A
  • accumulation of free radicals which attack muscles
  • electrolyte imbalance (nerve conduction needs sodium + potassium)
  • glycogen depletion
64
Q

exercise-associated muscle cramps

A

likely due to excessive firing of motor neurons in the spinal cord
- muscle spindle (excitatory) and golgi tendon organ (inhibitory) functions get messed up
- possible relief research with spices,, sending strong inhibitory stimulus to the spinal cord to prevent motor neurons from firing

65
Q

steady state

A

balance between demands on body and response, physiological variable is unchanging but not “normal”

66
Q

biological control system parts

A
  1. sensor or receptor, detects change in variable
  2. control center, assesses input and initiates response
  3. effector, changes internal environment to normal
    (work through negative feedback)
67
Q

positive feedback

A

response increases the original stimulus
ex) childbirth

68
Q

“gain” of a control system

A
  • degree to which a control system maintains homeostasis
  • system with large gain is more capable of maintaining homeostasis than one with a low gain (pulmonary and cardiovascular systems have large gains)
  • gain= correction/error
69
Q

hormesis

A

process where a low to moderate dose of stress (exercise) results in beneficial adaptive response on cell or organ system

70
Q

stress proteins

A

cells synthesize stress proteins when homeostasis is disrupted
ex) heat shock proteins repair damaged proteins in cells

71
Q

increase tension in skeletal muscle by

A
  • increase frequency of stimulation
  • increase strength of stimuli
  • change length of muscle
72
Q

low frequency of neural stimulation of motor unit

A

causes simple twitch

73
Q

three stimuli of motor unit

A

summation

74
Q

continual stimulation motor unit

A

tetanus

75
Q

types of muscle action

A

isometric, isotonic (dynamic), isokinetic

76
Q

isometric muscle action

A

muscle exerts force without changing length

77
Q

isotonic (dynamic) muscle action

A

concentric (muscle shortening)
eccentric (muscle lengthening)

78
Q

isokinetic muscle action

A

movement of labor is constant no matter how much force is exerted

79
Q

how muscle fiber types are observed

A
  • muscle biopsy
  • staining for myosin ATPas isoform
    –immunohisotchemical staiing
    –gel electrophoresis
80
Q

type i fibers

A

slow-twitch fibers
slow-oxidative fibers

81
Q

type iia fibers

A

intermediate fibers
fast-oxidative glycolytic fibers

82
Q

type iix fibers

A

fast-twitch fibers
fast-glycotic fibers

83
Q

oxidative capacity of muscle fiber

A

the number of capillaries, mitochondria and amount of myoglobin (oxygen storage molecule)
(high in slow twitch)

84
Q

type of myosin ATPase isoform of muscle fiber

A

speed of ATP degradation
how fast you contract muscles

85
Q

abundance of contractile protein in muscle fiber

A

actin and myosin
fast twitch fibers contract faster because they have more actin and myosin to exert greater force

86
Q

force-velocity relationship

A

the greatest force production has the lowest velocity and the greatest velocity of shortening is at the lowest force
*slow twitch fibers can exert greater velocity or greater force at the same speed
*the speed of movement is greater in muscles with higher % of fast twitch fibers

87
Q

force-power relationship

A

there is an optimal velocity for the greatest power output
when velocity is low, power is low, and when velocity is too high power goes down

88
Q

sarcopenia

A

age related loss of muscle mass

89
Q

delay age related muscle loss

A

resistance training

90
Q

diabetes and muscle loss

A

muscles become insulin resistant so insulin cannot stimulate muscle to bring glucose or amino acids into cell
aerobic and resistance training are protective

91
Q

muscular distrophy

A

hereditary defects in muscle protein resulting in loss of muscle fibers and weakness

92
Q

cancer and muscle loss

A

cachexia is rapid loss of muscle mass that 50% of cancer patients suffer from
regular exercise and nutrition can counteract

93
Q

energy at rest comes from

A

oxidative phosphorylation, anaerobic, blood lactate levels are low

94
Q

resting oxygen consumption

A

3.5 ml/kg/min (I MET)

95
Q

oxygen required to burn fat

A

23 O2

96
Q

oxygen required to burn carbohydrates

A

6 O2

97
Q

Respiratory exchange ration (RER or R)

A

R=VCO2/VO2
determines how many calories you burn either using fat or carbs

98
Q

time it takes to reach steady state

A

1-4mins

99
Q

oxygen deficit

A

lag in oxygen uptake at the beginning of exercise
initial ATP comes from anaerobic pathways

100
Q

primary source of fat in low intensity exercise

A

plasma FFA

101
Q

primary source of fat during higher intensity exercise

A

intramuscular triglycerides

102
Q

primary source of carbohydrates during high-intensity exercise

A

muscle glycogen

103
Q

primary source of carbohydrates during long duration exercise

A

blood glucose

104
Q

cardiovascular and muscular adaptations for better aerobic bioenergetic capacity in trained subjects

A
  • higher enzyme activity to raise metabolic functions
  • more capillaries and more mitochondria to transport more oxygen and nutrients to cells
    (results in less production of lactate and H+ and PC)
105
Q

oxygen debt

A

repayment for oxygen deficit at onset of exercise
also called excess post-exercise oxygen consumption (EPOC)
- 20% elevated O2 uptake during recovery to make up for O2 deficit

106
Q

Rapid portion of O2 debt

A
  • first portion
  • resynthesis of PC
  • replenishing muscle and blood O2 stores (myoglobin + hemoglobin)
107
Q

slow portion of O2 debt

A
  • second portion
  • elevated heart rate and breathing = greater energy need
  • elevated body temp = greater enzyme activity = higher metabolic rate
  • elevated epinephrine and norepinephrine = higher metabolic rate
  • conversion of lactic acid to glucose (gluconeogenesis)
108
Q

conversion of lactic acid to glucose

A

gluconeogenesis

109
Q

why is oxygen consumption (EPOC, excess post-exercise oxygen consumption) greater following high intensity exercise?

A
  • higher body temp
  • greater depletion of PC, additional O2 required for resynthesis
  • greater blood concentrations of lactic acid, additional O2 required for greater level of gluconeogenesis
  • higher levels of blood epinephrine and norepinephrine
110
Q

removal of lactic acid following exercise (percentages)

A
  • 70% of lactic acid is oxidized by cells used as a substrate by heart and skeletal muscle
  • 20% is converted to glucose
  • 10% converted to amino acids
111
Q

lactic acid and cooldown

A

light exercise (30-40% VO2 max) during recovery removes lactic acid more rapidly from the blood

112
Q

short term, high intensity exercise first 1-5 seconds metabolic response

A

ATP produced from ATP-PC system

113
Q

short term, high intensity exercise over 5 seconds metabolic response

A

shift ATP production to anaerobic glycolysis

114
Q

short term, high intensity exercise over 45 seconds metabolic response

A

60 seconds, 70% anaerobic/30% aerobic
2 mins, 50% anaerobic/50% aerobic

115
Q

prolonged exercise (over 10mins) metabolic response

A
  • ATP production from aerobic metabolism
  • steady state oxygen uptake can generally be maintained during submaximal exercise (below lactate threshold)
116
Q

cardiovascular drift

A
  • upward drift in oxygen uptake due to increases in body temp and epinephrine and norepinephrine (from prolonged exercise in hot/humid environments or high intensity exercise >75% of VO2 max)
117
Q

metabolic response to incremental exercise

A

oxygen uptake increases linearly until maximal oxygen uptake (VO2 max) is reached, even if work increases there is no further increases in VO2

118
Q

VO2 max

A
  • “physiological ceiling” for delivery of O2 to muscle, affected by genetics and training
  • tight association between VO2 max and endurance performance
119
Q

physiological factors influencing VO2 max

A
  • max ability of cardiorespiratory system to deliver O2 to the muscle
  • ability of muscles to use oxygen and produce ATP aerobically
120
Q

lactate threshold

A

the point at which blood lactic acid rises systematically during incremental/graded exercise

121
Q

sports drinks —

A

maintain blood glucose levels (above 1.5 hour exercise)

Exercise Physiology (4 decks)

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