Module 4 Flashcards
gas and liquid ting
Henry’s Law of Diffusion
‘When a liquid is in contact with a given gas, that gas will diffuse into solution in proportion to its partial pressure.’
- Gas becomes liquid
what parts of the body does diffusion increase at
Diffusion during exercise?
O2 and CO2 diffusion increases to
- alveolar (lungs)
- capillary (blood)
- tissue (muscle)
PO2 and PCO2diffusion relationship
Large Diffusion Gradient
PO2 muscle can approach 3-0 mmHg during intense exercise (100 arterial blood - 0 muscle = gradient of 100mmHg)
PCO2 muscle can approach 90mmHg (90 muscle - 40 alveolus = gradient of 50 mmHg)
Transport of CO2
transported to lungs by venous blood
what 3 ways does it leave
How does CO2 leave body?
- dissolved in plasma (5%)
- diffuses out of capillaries into alveoli to be exhaled - bount to HB (RBC) (carbamino-haemoglobin)
- CO2 binds to AAs in globin part of HB
- binds easily in muscle (high PCO2)
- CO2 released by HB when PCO2 is low (lungs) –> alveoli –> exhalation - plasma bicarbonate (60-80%)
- CO2 + water = carbonic acid (H2CO3) in muscles
- H2CO3 –> CO2 and H2O –> exhalation
Carbonic Anhydrase
- enzyme within RBC (zinc) that accelerates process
helps convert bicarbonate ions back to carbon dioxide for us to expel
Carbon Dioxide Transport Equation
CO2 + H2O –carbonic anhydrase–> H2CO3 –> H + HCO3
What happens during exercise overall???
When CO2 enters skeletal muscle tissue fluid, carbonic anhydrase catalyses formation of carbonic acid
Increased PCO2 (exercise) = decreased pH = oxyhaemoglobin dissociation
- More O2 liberation into tissues
Better contractions (synergist reaction)
Ventilation at rest and exercise
Rest –> 12 breaths per minute x 0.5 L = 6L/min
Exercise –> 40+ breaths per minute x 2L = 80+L/min
Where does respiratory control occur
In medulla
- neural circuits (info from brain, lungs, etc.)
think about centres and receptors
Ventilation Process (neural factors)
respiratory centres
- afferent/sensory signals to brain centre, efferent/motor signals to effector/target organ
pulmonary stretch receptors
- in airway smooth muscle and responds to lung distension (smooth muscle)
joint and muscle receptors in limbs
- movement stimualtes increase in ventilation
baroreceptor reflexes
- fall in BP = increased ventilation
Inspiratory centre activates
- diaphragm and external intercostals
Expiratory centre activates
- intercostals and abdominal muscles
think about central and peripheral
Ventilation Process (humoral factors)
blood transfer
central chemoreceptors
- medulla (stimulated by CSF)
- pH (increased H+ = increased VE)
- H+ increased by diffusion of CO2 across blood brain barrier
H2O + CO2 <-> H2CO3 <-> H+ + HCO3
peripheral chemoreceptors
- carotid bodies and aortic arch
- PCO2 (increased ventilation)
- pH (increased H+ = increased ventilation due to PCO2)
- arterial PO2 (increased ventilation if PO2 less than 60 mmHg)
Break point of breath hold
increased in arterial PCO2 (50 mmHg)
Hyperventilation
reduces alveolar and arterial PCO2 (e.g. breath hold)
- high PCO2 = stimulus to breathe
Hypoxic Blackout
combo of low PO2 and PCO2 can lose consciousness
how does body regulate this?
Respiratory Regulation
body monitors internal environment via central and peripheral chemoreceptors, stretch receptors in muscle and lungs
think about neural process leading to proper breathing
Respiratory Regulation Process
- info goes to inspiratory centre
- motor signals stimulate inspiratory muscles (external intercostals and diaphragm) increasing thorax volume and lowering diaphragm
- stretch receptors sned messages to expiratory centre (expiration via expiratory muscles)
- decreased thorax volume and raising diaphragm to reduced volume and increased pressure (expiration)
Hypernea
increased ventilation (at start of exercise before any chemical changes)
Corticol Influence
Before Exercise
- neural outflow from motor cortex causing muscle contractions
- stimulate respiratory neurons + phrenic nerve increases ventilation
Peripheral Influence
During Exercise
- proprioreceptive feedback from muscles, tendons and joints
- influence ventilation during exercise
- send signals to brain
- respiratory centre send signals of inspiration/expiratoin to increase TV/BR
Phase 1
0-20s
- initial VE increase before chemical stimulation (corticol and peripheral)
Phase 2
- VE rises exponentially to reach steady state due to neurogenic factors, temp changes and chemical status of blood/muscles
Phase 3
- fine tuning steady state ventilation
- chemoreceptors give feedback to respiratory centre via ventilation needs
what 3 ways is ventilation controlled
Ventilatory control during exercise (controlled by…)
- feed-forward centralc ommand (motor cortex signalling muscles, tendons and joints for feedback)
- peripheral sensory input from joint/muscle receptors
- peripheral and central chemoreceptor activation by changes in H+ and PCO2
Untrained VE Performance
60-85% max voluntary ventilation
- TV rarely exceeds 60% VC
TV = normal breathing
VC = greatest volume of breath expelled after taking longest breath
Untrained Max Exercise
- alovelar PCO2 decreases and PO2 increases
- VE more adequate to maintain diffusion gradients for gas exchange
what happens during this>
Trained Max Exercise
- drop in arterial O2 satuation (SaO2) as complete aeration of blood is not possible in pulmonary in pulmonary capillaries
UNKNOWN
- may be due to ventilation (perfusion mismatch), shunting of blood and capillary due to faster RBC transit time
During high-intensity exercise, the body’s rapid pace can lead to these issues where not all the blood passing through the lungs gets enough oxygen, resulting in a drop in arterial oxygen saturation (SaO2).
