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
central chemoreceptors (medulla)
- respond to changes in brain CSF - sensitive to PCO2 via H+
26
an increase in either PCO2 or H+ results in?
central chemoreceptors sending afferent input into the respiratory center to increase ventilation
27
perisperhal chemoreceptors
respond to changes in arterial blod - sensitive to PO2, H+, PCO2
28
carotid bodies are sensitive to
increase in blood potassium levels, NE,, decrease in arterial PO2 and increased body temp
29
location of peripheral chemoreceptors
location in the aortic arch and at the bifurcation of the common carotid artery
30
under normal conditions (sea level) what drives ventilation
CO2
31
exposure to an environment with a barometric pressure much lower than at sea level (high altitude) can cause?
a decreases in arterial PO2 and stimulate carotid bodies which in return signal the respiratory control center to increase ventilation
32
hypoxic indicates low
PO2
33
hypoxic threshold occurs at arterial
PO2 of 60 to 75mmHG
34
the point on the PO?V2 curve where ventilation begins to rise rapidly is called the
hypoxic threshold
35
the chemoreceptors are responsible for the increase in ventilation following expresoure to
low pO2 are the carotid bodies because the aortic and central chemoreceptors in humans do not respond to changes in PO2
36
the initial increase in ventilation during exercise is the
central input
37
peripheral input feeds into the
respiratory control center to fine tune its response
38
chemoreceptors -->
central and peripheral
39
central goes to
nucleus tractus solitarius --> PCO2, H+
40
peripheral goes to
aortic arch and common carotid artery
41
recepistaroy control center can be stimulated by (4)
- higher brain centers - peripheral chemoreceptors - respiratory muscles - skeletal muscles
42
submaximal exercise primary drive
higher brain centers (central command)
43
sub maximal exercise fine tubed by
humoral chemoreceptors and neural feedback from muscle
44
heavy exercise
- 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
ventilation is lower during exercise following training
exercise ventilation's 20 to 30% lower at same sub maximal work rate
46
mechanism for reductio in VE during exercise
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
changes in aerobic capacity of locomotor muscles depends on
- results in less production of H+ - less afferent feedback form muscle to stimulate breathing
48
does pulmonary system limit exercise performance? Low to moderate intensity exercise
pulmonary system does not limit exercise tolerance
49
does pulmonary system limit exercise performance? high intensity exercise
pulmonary ventilation/gas exchange is not a limitation in healthy individuals at sea level at most exercise intensities
50
gas exchange does limit exercise performance in some elite endurance athletes
40 to 50% experience hypoxemia - V/Q mismatch - RB capillary transit time too short