Test 3 Flashcards
breathing during exercise
when initially exercising, no diff from rest
as heart beats faster and blood moves quicker, oxygen diffusion rate out of alveoli will be affected (same amount of O2 loading onto hemoglobin)
during exercise, PO2 returning is 2-3 vs 4-5 during rest
affinity for O2
increased affinity means more sticky and vice versa
with increased affinity, saturation occurs with the least PO2
cooperativity for oxygen
steeper slope = greater cooperativity
greater cooperativity = easier to lose oxygen after the first is lost
P50
index where PO2 yields 50% saturation of hemoglobin
when P50 inc, O2 affinity dec
things that cause curve shift
inc in body/blood temp
inc in blood CO2 levels
inc blood acidity (lower pH)
all cause curve shift to the right
bohr effect
explains why O2 affinity declines during exercise
in body fluids where CO2 inc or lower pH, O2 affinity will dec
PO2 levels in the body
cells get rid of CO2 by putting it in blood
in a cell, pCO2 = 46 mmHg
this stays constant in veins
pCO2 in lungs = 40 mmHg
CO2 chemoreceptors
sensing agents that sense when pCO2 gets too high
present on aorta and carotid arteries
when too high, negative feedback loop is initiated to expel CO2
haldane effect
deoxygenated blood is more likely to take CO2
makes sense because pO2 is lowest in the veins
CO2 entering blood
CO2 + H2O => HCO3- + H+
to avoid blood becoming too acidic from H+ buildup, hemoglobin can collect H+ but only when 3/4 oxygen spaces are open
different ways CO2 is moved from cells to atm
- CO2 is dissolved in blood- following partial pressure gradient
- CO2 on hemoglobin- can carry 20+ CO2 molecules
- bicarbonate ions dissolved in blood or RBC- accounts for 90% of CO2
carbonic anhidrase
promote production of bicarbonate ions
quickens chemical reaction
chloride shift
replacing HCO3- with Cl- in RBC
when this happens, pCO2 = 46 mmHg in blood
dissolved CO2 moves toward alveoli first
H+ moves to alveoli on hemoglobin next
HCO3- then moves back into RBC (opposite of chloride shift), interacts with H+ to create CO2 that diffuses out of RBC
normal pH
arterial blood = 7.4
cannot go above 7.7 or below 6.8
outside this range, protein function is interfered with
normal blood pH often varies with body temp in animals that have constant deep body temp (constant relative alkalinity)
alphastat hypothesis
changes in pH are a means of maintaining a constant state of electrical charge on protein molecules
application of alphastat hypothesis
temp changes alter chemical behavior of the buffer groups on protein molecules
dec temps = inc pK1 vales of imidazole groups = tendency to combine with H+ groups inc
this is avoided by dec H+ conc at low temps
concentration of CO2 and acid-base regulation
inc blood acidity = inc lung ventilation = lowering pCO2
dec blood acidity = dec lung ventilation = inc pCO2
H+ concentration regulation
regulated by kidneys (urine release) in humans
in fish, H+ concentration is regulated by gill epithelium (exchanged with env)
HCO3- concentration regulation
dec HCO3- release in urine = H+ is inc removed = alkaline blood
inc release HCO3- = inc H+ concentration in fluid = acidic blood (dec pH)
acidosis
pH is more acidic, below 7.35
respiratory = exhalation of CO2 is dec, inc H+
metabolic = fewer HCO3- in bodily fluids, too much H+