control of ventilation and adaptation to training Flashcards

1
Q

principle 1

A

reason for the abrupt rise at the onset of exercise

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2
Q

principle 1

A

-immediate increase in ventilation begins before muscle contractions
- anticipatory response from central command (cerebral cortex)

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3
Q

f =

A

frequency breathing pattern

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4
Q

Principle 2

A

-TV crees more than the frequency of breathing in moderate exercise
- as exercise intensity increases above lactate threshold, frequency increases

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5
Q

principle 3

A

gradual rise to steady state

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6
Q

principle 3

A
  • gradual 2nd phase of ventilation
  • chemoreceptors
    -mechanorecetpros
  • other receptors
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7
Q

principle 4

A

gradual decrease - recovery from exercise

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8
Q

delayed ventilation reverie after exercise may be regulated by

A

blood pH, PCO2 and temperature

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9
Q

principle 5

A

relationship between VE and VO2

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10
Q

VO2 is

A

how much oxygen consumption

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11
Q

principle 5

A

ventilation increase in proportional to metabolic demand of muscle up to a point (nonlinear increase)

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12
Q

why is there a steeper rise around 70% of VO2max

A

sharper increase could indicate reach of lactate threshold - producing more hydrogen ions and CO2

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13
Q

the repository system pacemaker

A

PreBotzinger complex (PreBoC)

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14
Q

inspiration is

A

active

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15
Q

expiration is

A

passive

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16
Q

the pacemaker is which part of the group

A

inspiratory group of neurons that activate the respiratory muscles

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17
Q

inspiratory muscles

A

diaphragm
- external intercostals

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18
Q

expiratory muscles

A
  • rectus abdominis
  • internal intercostals
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19
Q

a closet of neurons in the ventral respiratory group in the ventrolateral medulla that seems to be key in the generation of the respiratory rhythm

A

pre-botzinger complex

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20
Q

the role of pre-botC with the dorsal respiratory group?

A

sends input via the phrenic nerve to the diaphragm and vita the intercostal nerves to the intercostal muscles

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21
Q

an area in the medulla that receives sensory input forms the peripheral chemoreceptors and mechanoreceptors through the vagus nerve and glossopharyngeal nerves

A

nucleus tractus solitarius

22
Q

which neuron in the prefixal respiratory group appears to be involved in active expiration

A

retro trapezoid neurons

23
Q

pontine respiratory group purpose

A

talks with both the inspiratory and expiratory centers and higher brain centers to coordinate breathing under more active conditions

24
Q

high cardiac output during high intensity exercise result in the rapid movement of RBCs through the lung, which limits?

A

gas equilibrium to be achieved between the lung and blood

25
Q

central chemoreceptors (medulla)

A
  • respond to changes in brain CSF
  • sensitive to PCO2 via H+
26
Q

an increase in either PCO2 or H+ results in?

A

central chemoreceptors sending afferent input into the respiratory center to increase ventilation

27
Q

perisperhal chemoreceptors

A

respond to changes in arterial blod
- sensitive to PO2, H+, PCO2

28
Q

carotid bodies are sensitive to

A

increase in blood potassium levels, NE,, decrease in arterial PO2 and increased body temp

29
Q

location of peripheral chemoreceptors

A

location in the aortic arch and at the bifurcation of the common carotid artery

30
Q

under normal conditions (sea level) what drives ventilation

A

CO2

31
Q

exposure to an environment with a barometric pressure much lower than at sea level (high altitude) can cause?

A

a decreases in arterial PO2 and stimulate carotid bodies which in return signal the respiratory control center to increase ventilation

32
Q

hypoxic indicates low

A

PO2

33
Q

hypoxic threshold occurs at arterial

A

PO2 of 60 to 75mmHG

34
Q

the point on the PO?V2 curve where ventilation begins to rise rapidly is called the

A

hypoxic threshold

35
Q

the chemoreceptors are responsible for the increase in ventilation following expresoure to

A

low pO2 are the carotid bodies because the aortic and central chemoreceptors in humans do not respond to changes in PO2

36
Q

the initial increase in ventilation during exercise is the

A

central input

37
Q

peripheral input feeds into the

A

respiratory control center to fine tune its response

38
Q

chemoreceptors –>

A

central and peripheral

39
Q

central goes to

A

nucleus tractus solitarius –> PCO2, H+

40
Q

peripheral goes to

A

aortic arch and common carotid artery

41
Q

recepistaroy control center can be stimulated by (4)

A
  • higher brain centers
  • peripheral chemoreceptors
  • respiratory muscles
  • skeletal muscles
42
Q

submaximal exercise primary drive

A

higher brain centers (central command)

43
Q

sub maximal exercise fine tubed by

A

humoral chemoreceptors and neural feedback from muscle

44
Q

heavy exercise

A
  • nonlinear rise in VE occurs due to: increasing blood H+ stimulates carotid bodies
  • increase in K++, body temperature, and blood catecholamines may also stimulate breathing
45
Q

ventilation is lower during exercise following training

A

exercise ventilation’s 20 to 30% lower at same sub maximal work rate

46
Q

mechanism for reductio in VE during exercise

A

train does not alter lung structure
- normal lung exceeds demand for gas exchange
- increase respiratory muscle strengh
- changes in aerobic capacity of locomotor muscles

47
Q

changes in aerobic capacity of locomotor muscles depends on

A
  • results in less production of H+
  • less afferent feedback form muscle to stimulate breathing
48
Q

does pulmonary system limit exercise performance? Low to moderate intensity exercise

A

pulmonary system does not limit exercise tolerance

49
Q

does pulmonary system limit exercise performance? high intensity exercise

A

pulmonary ventilation/gas exchange is not a limitation in healthy individuals at sea level at most exercise intensities

50
Q

gas exchange does limit exercise performance in some elite endurance athletes

A

40 to 50% experience hypoxemia
- V/Q mismatch
- RB capillary transit time too short