Chapter 10 Flashcards
pulmonary respiration
ventilation (breathing)
refers to the exchange of O2 and CO2 in the lungs
cellular respiration
refers to the O2 utilization and CO2 production by the tissues
purposes of the respiratory system during exercise
gas exchange between environment and the body
regulation of acid-base balance during exercise (regulating blood pH)
ventilation
movement of air due to pressure differences
occurs via bulk flow (from high to low pressure)
inspiration
when the pressure in the lungs < atmospheric pressure
expiration
when the pressure in the lungs > atmospheric pressure
what happens to the diaphragm and volume of the lungs during inspiration
diaphragm pushes down, ribs lift outward
volume of lungs is increased
what happens to diaphragm and volume of lungs during expiration
diaphragm relaxes, ribs pulled inward
volume of lungs decreases
pulmonary ventilation
aka minute ventilation (Ve)
the amount of air moved in or out of the lungs per minute (L/min)
composed of tidal volume and breathing frequency
tidal volume
VT
amount of air moved per breath (L/breath)
breathing frequency
f
number of breaths per minute (breaths/minute)
how to calculate Ve
Ve=VT x f
what happens to Ve as you increase exercise intensity
increases
what happens to tidal volume and breathing frequency during graded exercise
increase as intensity increases
what produces inspiration and expiration at rest
produced by the contraction and relaxation of the diaphragm
what controls ventilation at rest
somatic motor neurons in the spinal cord and the respiratory control center in the medulla oblongata
what are the 2 main forms of input to the respiratory control center
1) neural input
2) humoral chemoreceptors
neural input stems from
motor cortex and skeletal muscle mechanoreceptors
if you stimulate the muscle spindles, golgi tendon organs, and joint pressure receptors, they will all send input to respiratory control center which tells the lungs to increase ventilation due to increased movement in skeletal muscles
if you increase movement in skeletal muscles, you need to deliver more O2 to those tissues
humoral chemoreceptors: 2 kinds
found in the blood and are made up of central and peripheral chemoreceptors
central chemoreceptors
CNS
located in medulla
detect the presence of PCO2 and H+ concentration in the CSF by sensing for changes in partial pressure of CO2 and H+
peripheral chemoreceptors
located in aortic and carotid bodies
detect both what is in CNS (partial pressure of CO2 and H+) but also picks up changes in PO2 and K+
senses changes in PO2, PCO2, [H+], and K+ in blood
primary increase in ventilation during submax exercise is due to
neural input
increase in ventilation during maximal exercise is driven by
humoral chemoreceptors (both central and peripheral)
pulmonary artery receives
mixed venous blood from right ventricle
oxygenated blood is returned to
left atrium via pulmonary vein
after oxygenated blood is returned to LA via pulmonary vein
O2 is not in LV and sends blood out to the rest of the body
how is pulmonary circulation possible
its a low pressure (closed) system with a rate of blood flow = to the systemic circuit
during resting (conditions) such as standing, where is most of blood flow directed to in the pulmonary system
to the bottom (base) of the lungs due to gravity
during upright exercise, what happens to blood flow in the lungs
bloodflow increases at the top of the lungs (apex)
pulmonary arteriole contains
mixed venous blood
pulmonary venule contains
oxygenated blood
key characteristic of pulmonary capillaries
highly vascularized meaning there are lots of blood/blood vessels that have more capillaries as opposed to large vessels
why is it beneficial to have a capillary network around the arterioles
if trying to diffuse O2 into the blood, need to have it as a capillary network to slow down blood flow to allow O2 to diffuse across membranes
ventilation-perfusion ratios
how quickly are we moving air into alveoli and how quickly is blood moving past the alveoli (how well matched is bloodflow to ventilation)
(V/Q)
what is the ideal V/Q
~1.0 (or above if exercising/bloodflow is high)
how to calculate VQ ratio
V(A)/Q
V(A)= volume of air moved into alveoli
Q= bloodflow going past alveoli
Va= rate of ventilation (pulmonary ventilation)
Q= rate of perfusion (cardiac output)
at the base of the lungs what does the V/Q ratio look like and why
less than 1 because ventilation < blood flow at the base of the lung
(overperfused relative to ventilation meaning that blood flow/cardiac output much greater than ventilation or Q>Va)
at the apex of the lungs what does V/Q ratio look like and why
VQ>1 because ventilation > blood flow
(underperfused relative to ventilation meaning that blood flow, or cardiac output, is much less than ventilation or Va>Q)
exercise induced asthma (bronchoconstriction) is caused by
contraction of smooth muscle around the airways (bronchospasms) and mucus in the airways during or after exercise
marked by wheezing sound and labored breathing (dyspnea)
occurs in >10% of elite endurance athletes
if managed correctly, does not impair performance (usually people take vasodilator)
what happens to VQ ratio in asthma
perfusion increased
Va is decreased
V/Q ratio therefore <1
however this can be fixed by the pulmonary arteries themselves to constrict alveoli to help match the decrease in ventilation
by slowing down bloodflow into arteries, can pick up more O2
what happens to V/Q ratio as a result of blood clot
increased ventilation
decreased perfusion
yields a V/Q >1
which can be corrected by pulmonary arteries dilating the arterioles to enhance Va and Q
blot clot travels through bloodstream and lodges itself in pulmonary arteries which prevents blood from being carried from heart to lungs. this impairs the lungs ability to oxygenate blood and decreases O2 in bloodstream. body activates respiratory control centers which leads to an increase in ventilation (hyperventilation) to bring in more O2 and expel high levels of CO2
pulmonary capillary transit time
amount of time it takes RBCs to move past alveoli
what kind of exercise improves V/Q
low to moderate intensity as you increase ventilation and bloodflow
what exercise results in slight V/Q inequality
high intensity
because blood is moving too fast to fully be able to load RBCs with O2 as it passes alveoli, leading to lower partial pressure in arteries
in general is it better for blood to move slower or faster past the arterioles
better to move the blood slower so that you can fully saturate RBCs
99% of O2 transported is bound to
Hb
oxyhemoglobin
Hb bound to O2
deoxyhemoglobin
Hb not bound to O2
the amount of O2 that can be transported per unit volume of blood is dependent on
the Hb concentration
arterial O2 saturation (can’t just have Hb in blood, have to have it as high oxyhemoglobin)
amount dissolved in plasma (minor contribution)- need to be able to diffuse O2 into liquids, so a high enough PO2 will diffuse O2 into plasma
oxyhemoglobin dissociation curve
how we are moving O2 to different parts of the body
oxyhemoglobin dissociation curve equation
deoxyhemoglobin + O2 <—-> Oxyhemoglobin
direction of oxyhemoglobin reaction depends on
1) PO2 of the blood (higher PO2 shifts right)
2) Affinity between Hb and O2
high PO2 results in and where
high PO2 at the lung will promote the formation of oxyhemoglobin, shifting the formula to the right
aka loading
low PO2 results in and where
Low PO2 means there is a decrease in the affinity between Hb and O2, and O2 is being released to the tissues (unloading), driving the formula to the left
increased PO2 drives sigmoidal curve
to the right
decreased PO2 drives sigmoidal curve
to the left
steep portion of sigmoidal curve represents
unloading
flat portion of sigmoidal curve represents
loading
effect of pH on O2-Hb Dissociation curve
decreased pH lowers Hb-O2 affinity which results in a rightward shift of the curve (Bohr effect) and facvors offloading of O2 to the tissues
increase H+ ions which will bind to Hb, Hb goes under conformational change and has less affinity to bind O2, easier to drop off O2
during exercise, what happens to pH
pH decreases as there is an increase in blood H+
H+ ions bind to Hb, which reduces its O2 transport capacity
effects of temperature on O2-Hb Dissociation curve
increased blood temperature lowers Hb-O2 affinity which results in a rightward shift of curve (makes it easier to deliver/offload O2)
during exercise, how does an increase in body temperature affect the O2-Hb curve
an increase in temperature weakens the bond between O2 and Hb, which assists unloading of O2 to working muscle, shifts curve to the right
effects of 2-3 DPG (or BPG) on O2-Hb curve
BPG is a byproduct of RBC glycolysis (since RBCs do not have nucleus or mitochondria, they rely on glycolysis to produce energy)
an increase in BPG may result in a rightward shift on the curve only at altitude exposure, and is NOT a major cause of rightward shift during sea level exercise
if you are dropping off more O2 to the tissues, what happens to (a-v)O2 difference and VO2
increases (a-v)O2 difference (due to decreased venous return) which will increase VO2
how is O2 transported in muscle
via myoglobin
myoglobin
shuttles O2 from the cell membrane to the mitochondria of skeletal and cardiac muscle fibers
what type of skeletal muscle fiber contains high Mb content
type 1 fibers
low in type IIx fibers
what has a higher affinity for O2 : Mb or Hb
Mb because it binds O2 at a very low PO2
when Hb is unloading on the dissociation curve what is happening with Mb
loading
Mb O2 stores serve as an ___ from rest to exercise
“O2 reserve” during transition periods from rest to exercise
after exercise, Mb O2 stores must be
replenished and this O2 consumption above rest contributes to O2 debt (EPOC)
how is CO2 transported in blood
10% dissolved CO2 in plasma
20% bound to Hb
70% as bicarb (HCO3-)
bicarb buffering reaction
CO2 + H2O = H2CO3 = HCO3- + H+
CO2 transport in the blood
CO2 produced in high concentrations from Krebs cycle
CO2 dissolved in plasma (10%)
CO2 combines with Hb (20%)
CO2 bound to Hb converted to carbonic acid which turns into bicarb. for the reaction to continue, need to shuttle bicarb out and chloride in to drive the formula to the left
pulmonary ventilation does what to bicarb rxn
removes H+ from blood by HCO3- reaction and exhales out CO2 (rxn driven to the left)
increased ventilation results in
CO2 exhalation which reduces the PCO2 and H+ concentration to increase pH via hyperventilation
decreased ventilation results in
buildup of CO2 via increases in PCO2 and H+ concentration which decreases pH and activates respiratory control centers
at the onset of submaximal, steady state exercise what happens to PO2, PCO2, and ventilation
PO2 and PCO2 remain unchanged
Ventilation increases rapidly then a slower, steady rise towards steady state in order to expire more CO2 and bring in more O2
what happens to PCO2 and ventilation during prolonged exercise in a hot environment
little change is observed but ventilation is still increased due moving anatomical dead space, NOT the increase in PCO2
ventilation tends to drift upward b/c increased blood temp activates respiratory control center for thermoregulation
VT
inflection point where Ve increases exponentially
increase in ventilation is to meet the bodies needs to exhale excess CO2 to help balance the change in CO2 or H+ ions
is the pulmonary system a limitation during submax exercise
no because we can maintain arterial PCO2 throughout submax exercise to max exercise
arterial PO2 is maintained within
10-12 mmHg of resting value
does the pulmonary system limit performance in a trained subject during during graded exercise
pulmonary system may limit performance in highly trained elite endurance athletes during maximal exercise due to
mechanical limitations of the lung (if maintaining a high ventilation during max exercise= increase respiratory muscle fatigue or shuttling too much blood flow to respiratory lungs/muscles which will limit performance by taking O2 away from legs)
respiratory muscle fatigue during prolonged (>120min), high intensity (90-100% VO2 max) exercise
40-50% athletes experience exercise induced arterial hypoxemia
why do elite athletes experience a decrease in arterial PO2 during high intensity exercise
blood flowing too quickly across the lungs (pulmonary capillary transit time) - less than 0.25 sec
typical Ve value at rest and at max exercise
rest- 7.5 L/min
max- 120-175 L/min
typical f value at rest and max exercise
rest- 15 breaths/min
max- 40-50 breaths/min
typical Vt value at rest and max exercise
rest- 0.5 L/breath
max- 3-3.5 L/breath
