control of ventilation and adaptation to training Flashcards
principle 1
reason for the abrupt rise at the onset of exercise
principle 1
-immediate increase in ventilation begins before muscle contractions
- anticipatory response from central command (cerebral cortex)
f =
frequency breathing pattern
Principle 2
-TV crees more than the frequency of breathing in moderate exercise
- as exercise intensity increases above lactate threshold, frequency increases
principle 3
gradual rise to steady state
principle 3
- gradual 2nd phase of ventilation
- chemoreceptors
-mechanorecetpros - other receptors
principle 4
gradual decrease - recovery from exercise
delayed ventilation reverie after exercise may be regulated by
blood pH, PCO2 and temperature
principle 5
relationship between VE and VO2
VO2 is
how much oxygen consumption
principle 5
ventilation increase in proportional to metabolic demand of muscle up to a point (nonlinear increase)
why is there a steeper rise around 70% of VO2max
sharper increase could indicate reach of lactate threshold - producing more hydrogen ions and CO2
the repository system pacemaker
PreBotzinger complex (PreBoC)
inspiration is
active
expiration is
passive
the pacemaker is which part of the group
inspiratory group of neurons that activate the respiratory muscles
inspiratory muscles
diaphragm
- external intercostals
expiratory muscles
- rectus abdominis
- internal intercostals
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
pre-botzinger complex
the role of pre-botC with the dorsal respiratory group?
sends input via the phrenic nerve to the diaphragm and vita the intercostal nerves to the intercostal muscles
an area in the medulla that receives sensory input forms the peripheral chemoreceptors and mechanoreceptors through the vagus nerve and glossopharyngeal nerves
nucleus tractus solitarius
which neuron in the prefixal respiratory group appears to be involved in active expiration
retro trapezoid neurons
pontine respiratory group purpose
talks with both the inspiratory and expiratory centers and higher brain centers to coordinate breathing under more active conditions
high cardiac output during high intensity exercise result in the rapid movement of RBCs through the lung, which limits?
gas equilibrium to be achieved between the lung and blood
central chemoreceptors (medulla)
- respond to changes in brain CSF
- sensitive to PCO2 via H+
an increase in either PCO2 or H+ results in?
central chemoreceptors sending afferent input into the respiratory center to increase ventilation
perisperhal chemoreceptors
respond to changes in arterial blod
- sensitive to PO2, H+, PCO2
carotid bodies are sensitive to
increase in blood potassium levels, NE,, decrease in arterial PO2 and increased body temp
location of peripheral chemoreceptors
location in the aortic arch and at the bifurcation of the common carotid artery
under normal conditions (sea level) what drives ventilation
CO2
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
hypoxic indicates low
PO2
hypoxic threshold occurs at arterial
PO2 of 60 to 75mmHG
the point on the PO?V2 curve where ventilation begins to rise rapidly is called the
hypoxic threshold
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
the initial increase in ventilation during exercise is the
central input
peripheral input feeds into the
respiratory control center to fine tune its response
chemoreceptors –>
central and peripheral
central goes to
nucleus tractus solitarius –> PCO2, H+
peripheral goes to
aortic arch and common carotid artery
recepistaroy control center can be stimulated by (4)
- higher brain centers
- peripheral chemoreceptors
- respiratory muscles
- skeletal muscles
submaximal exercise primary drive
higher brain centers (central command)
sub maximal exercise fine tubed by
humoral chemoreceptors and neural feedback from muscle
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
ventilation is lower during exercise following training
exercise ventilation’s 20 to 30% lower at same sub maximal work rate
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
changes in aerobic capacity of locomotor muscles depends on
- results in less production of H+
- less afferent feedback form muscle to stimulate breathing
does pulmonary system limit exercise performance? Low to moderate intensity exercise
pulmonary system does not limit exercise tolerance
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
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
