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Exercise physiology > Lecture 15 - Pulmonary Physiology of Exercise > Flashcards

Lecture 15 - Pulmonary Physiology of Exercise Flashcards

1
Q

what happens to V’E, V’A, VT and fR when we exercise?
- when we cross Tvent?

A
  • V’E and V’A increase at same rate, with V’E slightly higher than V’A (bc V’A takes into account dead space) –> at ventilatory threshold (TVent), V’E increases a bit more (steeper slope) vs V’A also increases its slope, but less than V’A
  • frequency of breathing follows similar pattern: slow increase. at Tvent, bigger increase
  • VT: pretty big increase au début, and then plateaus once we reach Tvent bc harder to maintain high VT with high fR (which continues increasing) –> so we minimize work of breathing by plateauing VT
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2
Q

what happens to PAO2, PaO2, SaO2, PACO2&PaCO2 when we exercise?
- when we cross Tvent?

A
  • PAO2, PaO2 and SaO2 stay pretty much stable until Tvent
  • At Tvent, PAO2 increases a bit (bc increasing fR will bring more O2 in alveoli), PaO2 stays around the same bc gas exchange is the same) and SaO2 decreases a little bit = Bohr effect (normal response bc natural decrease in pH and increase in body temp –> won’t really limit you)
  • PACO2 and PaCO2 remain same until Tvent
  • At Tvent, decreases a lot bc more O2 in alveolar = more CO2 is exhaled = less CO2 in alveoli/arterioles
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3
Q

what happens to arterial pH and blood lactate as we exercise?
- when we cross Tvent?

A
  • arterial pH and lactate stay the same until Tvent
  • at Tvent, pH decreases bc more hydrogen ions
  • at Tvent, lactate increases very fast!
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4
Q

V’E / V’A ratio increases linearly with what? up to which % of VO2 max?
- after that what happens?

A
  • increases linearly with metabolic rate up to 50-75% of VO2 max (up to ventilatory threshold)
  • after that, V’E/V’A increase disproportionately more than metabolic rate, which increases PAO2 and decrease PACO2&PaCO2
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5
Q

why does V’E/V’A increase a lot (what is it called?) during exercise above Tvent?

A

alveolar hyperventilation
- the excess V’E/V’A during exercise above TVent is related to the increase CO2 (and decrease pH) produced during HCO3- buffering of lactic acid produced by glycolysis during heavy intense exercise

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6
Q

during intense exercise, what happens to cause metabolic acidosis?
- what are the 2 steps after (chemical equations)? where doe they occur?
- what relationship graphically reflects excess CO2 produced?

A
  1. during intense exercise above TVent (or anaerobic threshold), lactic acid (HLa) produced via glycolysis dissociates a La- and H+ ions (H-La –> H+ + La-), thus causing metabolic acidosis
  2. in blood, bicarbonate (HCO3-) combines with H+ to form carbonic acid (H2CO3): H+ + HCO3- –> H2CO3
  3. in lungs, H2CO3 dissociates to CO2 + H2O: H2CO3 –> H2O + CO2
  • increase in slope of V’CO2-V’O2 relationship during strenuous exercise reflects the excess CO2 produced via HCO3- buffering of H+
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7
Q

what happens to concentration of HCO3- after we reach anaerobic threshold/TVent?

A
  • it decreases a lot! bc it buffers the excess hydrogen ions produced by lactic acid dissociation
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8
Q

explain the big colorful schéma that explains the respiratory compensation for metabolic (lactic) acidosis (7 STEPS)

A
  1. glycogen –> pyruvate –> lactic acid –> La- + H+
  2. when you reach/pass ventilatory threshold: increase [H+] and decrease pH
  3. signals chemoreceptors –> increase their activity to send signal to brain (medullary respiratory control center) to tell them blood is now acidic
  4. brain will then increase alveolar ventilation (V’A) as a respiratory compensation for metabolic acidosis –> goal = get rid of CO2
  5. increase V’A will lead to decrease in PACO2 (from formula, while V’CO2 remains the same. bc PACO2 = V’CO2/V’A)
  6. decrease PACO2 = decrease PaCO2 (arterial)
  7. decrease PaCO2 leads to increase PAO2 (bc PAO2 = PiO2 - (PACO2/(V’CO2/V’O2)))
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9
Q

in humans, how is arterial blood [H+] regulated during progressive exercise? particularly at which intensities?

A
  • regulated by ventilatory elimination of CO2 from mixed-venous blood during progressive exercise, particularly at intensities above lactic acidosis threshold (LAT) aka ventilatory threshold (TVent) aka anaerobic threshold (AT)
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10
Q

what does ventilatory demand (which variable) depend on? (3)

  • explain physiologically what happens if these variables change ish
A
  • ventilatory demand = V’E
  • V’E = (863 * V’CO2)/(PaCO2 x (1 - VD/VT))
  • depends on:
    1. metabolic requirements (V’CO2)
    2. dead space ventilation (VD/VT)
    3. regulated level of arterial PCO2 (PaCO2)
  • if any of the variables change, it is the ventilatory demand that will change! V’E = compensatory mechanism
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11
Q

what are 2 physiological reasons why your ventilatory demand (V’E) is high (for a given V’CO2) during exercise? ie high V’E/V’CO2 ratio
- happens in which types of populations?

A
  1. increase dead space/tidal ventilation (VD/VT) –> bc of ventilation perfusion mismatching
    - means that you’re breathing less efficiently –> bc higher dead space = less gas exchange
    - happens in people with respiratory disease (ie COPD, asthma)
    - ie to keep same PaCO2 and V’CO2, person with VD/VT of 0.2 needs 70L/min of V’E VS 110L/min if dead space of 0.5
  2. decrease PaCO2 equilibrium point –> respiratory alkalosis or metabolic acidosis
    - ie someone with 40mm Hg PaCO2 and 0.2 dead space needs 90L/min to maintain V’CO2 of 3.0 VS if exhales a lot of CO2 and 30 mmHg PaCO2 (with 0.2 DS), needs 115L/min to maintain 3.0 of V’CO2
    - happens in pregnant women
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12
Q

take home message of physiological determinants of ventilatory demand:
- an abnormally high what ratio during exercise reflects (2)

A

an abnormally high V’E/V’CO2 ratio during exercise reflects
- low PaCO2 “set-point”
and/or
- high physiological dead space (VD/VT)

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13
Q

what happens to your breathing pattern/dynamic operating lung volumes during progressive exercise in healthy human?

A
  • your VT (tidal volume) expands! by increasing end-inspiratory lung volume (EILV) into the available inspiratory reserve volume (IRV) AND decrease EELV into the available ERV
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14
Q

why does the increase in tidal volume during exercise plateaus?
- plateaus at what level?

A
  • bc if we increase it too much, VT will go into the non-compliant zones where more elastic and resistance forces will be needed
  • tidal volume plateaus at around 60% of vital capacity

*Control of dynamic operating lung volumes (increase EILV and decrease EELV) during exercise allow VT to expand within compliant (linear) portion of respiratory systems sigmoid pressure-volume curve where both resistive (bottom) and elastic (top) work of breathing is minimized

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15
Q

does the respiratory system “adapt”/improve during exercise?

A
  • in general exercise training has no demonstrable effect on lung structure or function that would improve pulmonary gas exchange during exercise –> no improvement in lung volumes and capacities, airway structure/function, inspiratory/expiratory muscle strength, # of alveoli or pulmonary capillaries)
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16
Q

is the respiratory system a limiting factor in exercise?
- healthy, untrained vs aerobically trained with VO2 max >65mL/kg/min

A

healthy UNTRAINED
- respiratory system is generally “overbuilt” and exceeds the demand for O2 and CO2 transport in healthy, untrained humans
- limiter would be leg skeletal muscles (vs lungs or heart that are ahead of legs)
TRAINED:
- in aerobically trianed adults, the respiratory system MAY limit exercise performance because, unlike skeletal muscles that adapt super well, the respiratory system DOES NOT ADAPT to exercise training!
- therefore legs and heart are ahead of lungs, which is the limiter

17
Q

what are 2 potentially respiratory limitations to exercise tolerance in trained athletes?
*what are the 2 causes of the first one?

A
  1. exercise-induced arterial hypoxemia (EIAH)
    a) ventilation/perfusion mismatching
    b) pulmonary capillary diffusion disequilibrium
  2. Respiratory muscle “steal” of skeletal (locomotor) muscle blood flow
18
Q

what does EIAH stand for?
1) definition?
2) prevalence?
3) characteristics

A

exercise induced arterial hypoxemia
1) arterial O2 desaturation of > 3-4% resting levels during heavy/maximal exercise
2) 25-50% of endurance trained athletes with a VO2max > 65mL/kg/min
3)
- abnormal decrease in PaO2 (arterial O2 desaturation >4% resting levels)
- causing abnormal widening of alveolar to arterial O2 difference (AaDO2)
–> reflecting incomplete oxygenation of mixed-venous blood in pulmonary capillaries

19
Q

what happens during EIAH in
- PAO2
- PaO2
- AaDO2
- pH
- PaCO2

  • at what point/exercise intensity do these things happen?
A
  • PAO2: increase but doesn’t mean all of it goes into your blood
  • PaO2: decrease bc you’re breathing so fast that there’s no time for gas exchange so O2 stays in alveoli (hence increasing) and there’s less O2 in arterials
  • AaDO2: increase bc PAO2 increase and PaO2 decreases
  • pH: decreases
  • PaCO2: decreases
  • at around 85% of the ultratrained athletes’ VO2max –> around 55 mL/kg/min –> which a normal person practically never reaches
20
Q

what happens to SaO2, PaO2, AaDO2 and PaCO2 to untrained athlete at VO2max vs trained (ultra trained, who can have EIAH) at VO2max? compared to rest

A

SaO2:
- rest = 97%
- untrained: 95% (slight decrease is normal)
- trained: 88% (>4% = very bad)
PaO2:
- rest = 92
- untrained: 90
- trained: 75
AaDO2:
- rest = 10
- untrained: 25
- trained: 40!
PaCO2:
- rest = 40
- untrained: 30
- trained: 35

21
Q

one of the determinants of EIAH is ventilation/perfusion mismatching:
- explain what happens when inflow > outflow vs inverse
- which one has worse effects?

A

LOW V’A(inflow)/Q(outflow):
- compromise pulmonary gas exchange and arterial blood oxygenation –> bc not a lot of O2 coming in = low PAO2 –> big decrease in SaO2
HIGH V’A/Q:
- facilitate pulmonary gas exchange and arterial blood oxygenation –> end up with more than enough PAO2 –> increases SaO2 a bit

  • effect of low V’A/Q on arterial blood oxygenation is greater than equal and opposite effect of high V’A/Q bc of shape of HbO2 dissociation curve (sigmoidal curve, decrease goes lower on the high slope part, vs increase on the almost plateau part)
22
Q

what is the primary contributor to development of EIAH in elite athletes?

A

V’A (inflow)/Q (outflow) mismatching, which increases with increasing exercise intensity

23
Q

what is the other contributor to EIAH, other than ventilation/perfusion mismatching? explain its effects (4 steps ish)

A

pulmonary capillary diffusion disequilibrium
1) during heavy exercise in athletes, pulmonary blood flow (pulmonary O2 outflow) is very high due to increased maximal cardiac output
2) consequently, amount of time RBC spends in pulmonary capillaries may be less than time required for complete O2 equilibration btw lungs and mixed-venous blood (PvO2)
*RBC transit time = pulmonary capillary blood volume/pulmonary blood flow
*higher blood flow = lower transit time to do gas exchange
3) as a result, the AaDO2 widens, while both SaO2 and CaO2 (arterial O2 content) decrease
4) since PaO2 also decreases, less O2 in muscles = EIAH

24
Q

the threshold of EIAH-induced exercise performance limitation occurs at an arterial O2 desaturation of ___% below resting levels (vs what is the normal effect?)
- beyond this threshold, each further 1% decrease in SaO2 = a __-__% decrease/increase in VO2max

A
  • 4% below resting levels VS normal effect = Bohr effect –> body can tolerate it
  • 1% decrease in SaO2 = 1-2% decrease in VO2max
25
Q

what are 3 physiological consequences of exercise-induced respiratory muscle work?

A
  1. respiratory muscles demand a significant amount of blood flow during dynamic exercise (8-10% of max CO in untrained at VO2max vs 15-16% of max CO in endurance trained adults at VO2max)
  2. respiratory muscles are innervated with nerves sensitive to metabolites that project to the respiratory and cardiovascular control centers of the central nervous system
  3. during prolonged heavy intensity exercise (>85% VO2max), respiratory muscles can activate the sympathetic nervous system –> decreasing exercising limb muscle vascular conductance and blood flow (bc vasoconstriction)–> decrease O2 transport to exercising muscles –> negative consequences on metabolic and contractile function –> respiratory limitation to exercise tolerance
26
Q

in normal sedentary males, respiratory muscle V’O2 is around 8-10% of whole body VO2 max vs ___-____ for athletes
- consequence?

A
  • 15-16% of max cardiac output for athletes –> so theory that to more from 8-10% to 15-16%, respiratory muscles “steal” blood flow from working leg muscles (speculatory!)
27
Q

does 30 yo male athlete or 30 yo sedentary male have higher work of breathing/respiratory muscle VO2?
- consequence on legs/other? (figure)

A
  • athlete has higher ventilation, so requires higher work of breathing
  • therefore, effects of respiratory muscle loading (increasing work of breathing) could significantly reduce blood flow to legs (and increase blood flow to “OTHER”) –> so can speculate that respiratory muscles steal blood flow from muscles

Exercise physiology (14 decks)

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