Exam 1 Flashcards

(33 cards)

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?

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
why is the browning of adipose tissue with exercise beneficial?
brown adipose tissue can increase metabolism, better control glucose metabolism, protect against a high fat diet and decrease body fat
26
why do you think a decrease in cardioprotection after cessation of training is occurring?
downregulation of SOD2 in the mitochondria that causes a decrease in cardioprotection
27
what are key elements of the diseasome as it relates to physical inactivity?
``` cardiovascular disease cancer (breast or colon) type II diabetes depression dementia ```
28
what diseases are linked in some way to chronic low grade inflammation?
``` athlerosclerosis obesity alzhemiers tumors and growth type II diabetes ```
29
how does exercise both acute and chronic alter pro inflammatory mediators?
acute exercise: increase proinflammatory markers | chronic exercise: decreases pro inflammatory markers
30
if obese women exercise train, does their increase in insulin sensitivity depend on weight loss?
no
31
How does TNF alpha influence insulin resistance and fat metabolism?
elevated TNF levels result in : an increased insulin resistance decreased fat metabolism
32
what happens when healthy yound subjects decrease their walking from ~10,000 steps per day to 1,500 steps per day?
``` in 14 days decreased 1.2 kg muscle mass increased insulin resistance 7% increased in visceral fat total fat mass did not change ```
33
what are some common myokines?
IL-6 IL-15 BDNF Irisin