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Nutrition and Exercise > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

is critical power superior to the lactate anaerobic threshold? why?

A

yes. Critical power is a correlate and a DETERMINANT of performance
- lactate anaerobic threshold is only a predictor or correlate not a good determinant

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2
Q

what causes blood lactate to increase during exercise?

A

Ra increases more rapidly than Rd of lactate in the blood

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3
Q

At VO2 max what are the oxygen pressures inside the exercising muscle fibers? Low or zero?

A

low ; 2-3 mmHg

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4
Q

Owels point

A

a critical metabolic level was found below which there was no increase in blood lactate as a result f exercise, although above this level such an increase did occur
- the critical level varies for different subjects and for the same subject for different types of exercise

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5
Q

is the lactate threshold a determinant of athletic performance or it is just related to it? How about critical power?

A
  • lactate threshold- NOT A DETERMINANT just a correlate

- critical power- IS A DETERMINANT of athletic performance

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6
Q

when does lactate begin to accumulate in the blood?

A

lactate increases pre and post training below VO2 max

-it is increasing even at levels with no anaerobiosis

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7
Q

What are the fick equations

A 
VO2= VE(FiO2-FeO2) (sampled from the mouth)
VO2= Q (CaO2-CvO2) (sampled from pulmonary artery
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8
Q

understand the O2 cascade from room air to muscle tissue during exercise? what are the approximate values?

A

from room air to muscle tissue O2 is diffused

150 mmHg room air, 100 mmHg lungs, Resting muscle PO2 ~34 torr, max exercise PO2 ~3 torr

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9
Q

If I am a 102 year old woman, what organ system is likely to fail first? what is the physiological significance?

A
  • Lung will fail first

- Diffusion limitation meaning have the inability to get O2 from the lung into the blood

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10
Q

Is VO2 max determined by the delivery of O2 via the blood or diffusion of blood into muscle tissue

A

diffusion of blood into muscle tissue

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11
Q

In the O2 cascade from room air to muscle tissue what did Professor John B west predict resting Po2 was?

A

~30 torr

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12
Q

what tool did Dr. Richardson use to actually measure resting and max exercise PO2?

A

MRI (magnetic residence spectroscopy)

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13
Q

what is the PO2 in tissue during max exercise? at rest?

A

exercise:~3 torr

at rest: 34 torr

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14
Q

what are some mediators of IR injury?

A 
Oxidants/ROS
calcium
calpain
caspase 3
decreased ATP
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15
Q

what are some mediators of IR injury?

A 
Oxidants/ROS
calcium
calpain
caspase 3
decreased ATP
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16
Q

cardioprotection

A

protecting the heart against IR injury

17
Q

IR injury

A

lack of blood causing a dysfunction in cardiac heart muscle

18
Q

Myokines

A

cytokines and other peptides that are produced, expressed and released by muscle fibers and exert either paracrine or endocrine effects (myokines are produced in muscle cells)

19
Q

give examples of myokines we learned about

A

IL-6
IL15
BDNF
Irisin

20
Q

what exercise intensity gives the greatest cardioprotection? Why is it important for the clinical setting?

A

No differences between 50% and 70% VO2

easier for people to exercise at 50%

21
Q

how long does cardioprotection last after cessation of training?

A

9-18 days

22
Q

what are some potential mechanisms of cardioprotection?

A 
endoplasmic reticulum stress proteins
HSP's
cyclooxygenase
inducible NOS
cytosolic antioxidants (SOD and SOD2)
sarcolemmal K+ channel?
23
Q

how does doxorubicin chemotherapy contribute to the development of heart failure?

A
  • oxidative stress is the key mediator/contributor to heart failure
  • causes an increase in free radical production in mitochondria because heart and skeletal muscle cells have a lot of mitochondria in it making the heart a target
  • increase in radicals results in: damage to DNA, organelle damage, damage to protein, cell death
24
Q

how does doxorubicin chemotherapy contribute to the development of heart failure?

A
  • oxidative stress is the key mediator/contributor to heart failure
  • causes an increase in free radical production in mitochondria because heart and skeletal muscle cells have a lot of mitochondria in it making the heart a target
  • increase in radicals results in: damage to DNA, organelle damage, damage to protein, cell death
25
Q

why is the browning of adipose tissue with exercise beneficial?

A

brown adipose tissue can increase metabolism, better control glucose metabolism, protect against a high fat diet and decrease body fat

26
Q

why do you think a decrease in cardioprotection after cessation of training is occurring?

A

downregulation of SOD2 in the mitochondria that causes a decrease in cardioprotection

27
Q

what are key elements of the diseasome as it relates to physical inactivity?

A 
cardiovascular disease
cancer (breast or colon)
type II diabetes
depression
dementia
28
Q

what diseases are linked in some way to chronic low grade inflammation?

A 
athlerosclerosis
obesity
alzhemiers
tumors and growth
type II diabetes
29
Q

how does exercise both acute and chronic alter pro inflammatory mediators?

A

acute exercise: increase proinflammatory markers

chronic exercise: decreases pro inflammatory markers

30
Q

if obese women exercise train, does their increase in insulin sensitivity depend on weight loss?

A

no

31
Q

How does TNF alpha influence insulin resistance and fat metabolism?

A

elevated TNF levels result in :
an increased insulin resistance
decreased fat metabolism

32
Q

what happens when healthy yound subjects decrease their walking from ~10,000 steps per day to 1,500 steps per day?

A 
in 14 days
decreased 1.2 kg muscle mass
increased insulin resistance
7% increased in visceral fat
total fat mass did not change
33
Q

what are some common myokines?

A

IL-6
IL-15
BDNF
Irisin

Nutrition and Exercise (1 decks)

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