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how is o2 tranported in blood
98.5% to Hb
1.5 % plasma
How is CO2 transported in the blood?
7-10% plasma
20-23% carbaminohemoglobin
70% bicarbonate
what chemical factors influence the rate and depth of breathing
hypercapnia and hypoxia
central chemoreceptors
Receptors in the central nervous system that monitor the PCO2 pH of CSF to help regulate ventilation rate.
peripheral chemoreceptors
Receptors in the carotid arteries and the aorta that monitor blood pH to help regulate ventilation rate.
how does training influence VE during exercise
- increased VE efficiency
- higher tolerance for high CO2 levels
- better adaptation
Organs involved in acid production and regulation
lungs, kidneys, liver
O2-Hb disassociation with decreased pH
right shift, weakened bonds (Bohr effect)
O2-Hb disassociation with decreased temp
right shift, weakened bonds
CO2 transport in blood
1. Dissolves in plasma
2. Combines with Hb
3. Combines with water, releasing H+ and HCO3-, which exits RBC, and Cl- enters to balance charge
how is Co2 released at lungs
1. Diffuses from plasma
2. Carbaminohb dissociates and CO2 diffuses
3. HCO3- reenters and forms Co2 is formed, diffusing out
what happens to pulmonary ventilation in rest to work transition
increases abruptly, then rises gradually to SS
what happens to arterial pressures of O2 and CO2 in rest to work transition
PO2 slightly decreases, PCO slightly increases, but remain relatively unchanged
what happens to pulmonary ventilation in incremental exercise
linear increase with O2 uptake to 50-75% Vo2max, beyond this point is Tvent
difference between untrained and trainer person's change in pulmonary ventilation in incremental exercise
trained increases more gradually and Tvent is at a higher threshold
what happens to arterial PO2 in incremental exercise untrained
maintain arterial Po2 within 10-12 mmHg of normal
what happens to arterial PO2 in incremental exercise trained
drop in arterial PO2 of 30-40mmHg
exericse induced hypoxemia
location of respiratory control center
medulla oblongata
preBotzinger complex
sets basic rhythm of breathing
Retrotrapezoid nucleus (RTN)
site of integration of central command and exercise pressor reflex signals that increase ventilation during exercise
parafacial respiratory group
Group of neurons within the ventral respiratory group important for generation of active contraction of abdominal muscles
Pons function in breathing
fine tune breathing
Types of Input to Respiratory Control Center
- neural (higher brain centers, afferent signal from mechanoreceptors)
- humoral (blood borne stimuli, chemoreceptors)
pFRG/RTN central chemoreceptors respond to what
increased PCO2, and H+ in CSF
aortic peripheral chemoreceptors respond to what
pH, PCO2
carotid peripheral chemoreceptors respond to what
PH, PCO2, PO2
a 1 mmHG rise in arterial PCO2 can increase ventilation by
2L/min
what happens to VE following training
lower VE at similar relative intensities due to enhanced efficiency of bioenergetic pathways
afferent feedback to respiratory center
mechanoreceptors in muscles and joints
what is the fine tuning mechanism of ventilation during exercise
afferent feedback from muscles and chemoreceptors
what causes the alinear rise in ventialtion associated with lactate threshold
rising H+ levels from lactic acid
3 main contributors to muscle acidosis
1. production of CO2/carbonic acid
2. production of lactic acid
3. ATP breakdown, releasing H+
4 types of intracellular buffers
1. cellular proteins
2. histidine dipeptide (carnosine)
3. phosphate groups
4. bicarbonate
3 extracellular buffers
1. bicarbonate
2. Hb
3. Blood proteins
2 main H+ transporters on the sarcolemma
sodium hydrogen exchanger (NHE)
MCT1 & MCT4
what muscle fiber type has a higher buffering capacity
fast twitch T2
Effect of Exercise Training on Buffering Capacity
increases muscle buffering capacity, and level of carnosine and MCT transporters
Henderson-Hasselbalch equation
pH = pKa + log [base]/[acid]
What % of H+ is buffered by each intracellular buffer type
60% cellular proteins
20-30% bicarbonate
10-20% phosphate groups
muscle and blood pH during exercise
- muscle and blood pH decrease, muscle pH is 0.4-0.6 units lower than blood pH
factors influencing H+ production
- exercise intensity
- amount of muscle mass involved
- duration
what happens when supplementing with sodium citrate
improved extracellular buffering capacity and high intensity exercise performance
what happens when supplementing with beta alanine (precursor to carnosine)
intracellular buffer, buffer and increase time to exhaustion
Do the lungs adapt to exercise training?
not really: lung structure and pulmonary function remain relatively unchanged, and pulmonary gas exchange does not improve.
why is the lung "overbuilt"
it's capacity for gas exchange is far greater than the needs for O2 and CO2 during exercise.
exercise induced hypoxemia
is probably caused by a red blood cell transit time through the pulmonary circuit that is too fast to allow for adequate diffusion and the achievement of gas equilibrium.
does the pulmonary system limit exercise performance
no at prolonged submax exercise, put potentially near VO2max
how does breathing low density air (heliox) affect exercise performance
can improve exercise performance by reducing WOB
what are the mechanical components of breathing that implicate WOB
elastic and resistive properties
do females have a greater or lower WOB
greater
how does breathing through a smaller tube during exercise affect WOB
increases SCM EMG activity, and metabolic demand, increasing overall WOB and VO2 needs
considering WOB is particularily important when working with what type of demographic
people with COPD, since they will have increased expiratory flow resistance
what V/Q ratio is considered ideal and why
1 because it means that the ventilation into the lungs is equally to the blood being perfused, no extra air or flow.
How do kidneys play a role in long term acid base balance
only contribute at rest because they talk a long time to exert their effects:
regualte bicarb concentration in blood