exercise and CV disease Flashcards
How does exercise affect homeostasis
1) incr muscular demand for O2
Circulation of O2 with exercise
1) Lung ventilation produces O2
2) goes to LA –> LV
3) incr blood volume, Hb O2 affinity
4) vasodilation of arterioles
5) muscles extract more O2
Factors that affect maximal O2 uptake
1) genetics
2) training
3) age
4) gender- male
5) heat, altitude
peak VO2 vs. VO2 max
peak VO2 = top level of exercise before stop
max VO2 max = max O2 uptake
what is VO2
oxygen consumption (uptake)
what is VO2 related to
1) workload
2) energy req with exercise
shape of VO2 curve with exercise
1) linear incr
2) then plateau at VO2 max (not often reached)
what is VO2 max
plateau (aerobic capacity)
what is Fick’s principle measure
connects respiratory VO2 with O2 delivery (circulatory) and O2 extraction (muscle
Fick’s equation
CO = VO2 / (CaO2 - Cmixed venousO2)
VO2 = CO x a-v O2
Ca or vO2 = [Hgb] x 1.34 x O2 saturation (%)
mixed venous
when all venous blood gets mixed and goes to lung to be oxygenated (USU MAIN PULM ARTERY)
sympathetic nervous system effect on HR and SV
1) incr HR
2) incr contractile strength (incr SV)
effect of PNS on HR
decr HR
based on frank starling, incr contractile strength and stretch, incr ____
EDV
what does frank starling tell you
more LV is filled (LV EDP), more it will contract (SV)
how does incr preload affect SV
increased SV (and CO) for the same inotropic state
circulatory adjustments with exercise
1) incr blood flow (CO, muscle blood flow)
2) redistrib blood flow (from inactive organ to skeletal muscle)
3) maintain blood pressure (supply vital organs and brain)
where is most blood volume?
64% in veins at rest
effect of HR on ventricular filling and contraction
1) incr HR with exercise (decr diastolic time)
2) @ high HR, systolic time decr
what happens to systolic time at high heart rate
systolic time decr
@ rest what controls heart rate
parasympathetic control 60-80 bpm
what is the anticipatory response
just before exercise HR increased
what controls anticipatory response
central command from CNS (sympathetic activity) incr HR
what happens to HR with exercise
1) incr HR proportional to intensity
2) linear response up to near max exercise
Theoretical max HR
220-age = max HR decline after age 15
early exercise (
parasympathetic
moderate to heavy exercise is ___ stim
sympathetic stim
stop exercise –> ____ activated a
parasympathetic
a
a
effect of exercise on stroke volume
1) vasodilation
2) incr venous return
3) venoconstriction
4) preserve ventricular filling
5) incr SV
effect of incr HR at rest on stroke volume
1) decr ventricular filling time 2) decr SV
equation for SV
EDV (filling) - ESV (emptying)
factors influencing SV during Exercise
1) EDV = preload - venous return - ventricular distensibility - pericardial constaint
2) strength of contraction
3) avg aortic or pulm pressure = afterload
components of preload (EDV)
- venous return - ventricular distensibility - pericardial constaint
factors influencing venous return
1) venoconstriction (reflex sympath in venous return)
2) muscle pump (upright exercise)
3) respiratory pump (upright exercise with neg throacic pressure)
effect of preload on SV curve
on steep portion, incr EDV or pressure incr SV
left shift in Starling curve leads to ___
greater SV at same EDV or pressure
which people have left shift of STarling
endurance athletes
what is frank starling law of heart
force of contraction proportional to initi resting length
effect of incr ventricular contractility on SV
1) incr sympath
2) direct innerv and epi + NE
3) incr stretch, incr contractility
SV curve with exercise
SV incr up to 40-60% of max and then plateau
how does SV change with upright exercise in normal vs. endurance athlete
normal: SV doubles endurance: greater resting SV before doubling
compare SV with supine exercise vs upright exercise
greater resting SV than upright (20-40% incr) (more blood back to chest)
mechanisms of incr SV in elite athletes
SV continues to rise
1) incr EDV with incr Starling forces at lower workload
2) incr contractility with lower ESV at higher workload
relationship btwn cardiac output and % VO2 max
linear
cardinal rule of CO with exercise
6L/min of CO required for each 1 mL/min incr in O2 uptake above rest
with upright exercise and
HR and SV
with upright exercise and >50% VO2 max, you see changes in __
only HR b/c SV plateaus unless elite athlete
___ difference in resting CO btwn untrained and trained
No
compare trained person and normal at rest SV and HR
trained = greater SV, slower HR
compare trained person and normal at max exercise
trained = similr HR, greater SV
factors affecting blood flow with exercise
1) exercise
2) decr vascular resistance (incr flow NOT BLOOD PRESSURE)
3) sympath nervous system and autoregulation control vesel diameter
is blood viscosity important during exercise
important at rest but NOT with exercise
define mean arterial pressure
avg blood pressure during cardiac cycle rate of flow thru systemic circuit MAP = diastolic BP + (1/3(SBP - DBP))
how do pressures change with exercise
incr systolic P, CO, HR, MAP little change in diastolic P
where does blood redistribut during exercise
incr skeletal muscle and brain decr splanchnic (liver, kidney, GI) decrease
how does blood flow change with exercise in non-exercising vascular beds
1) incr sympath
2) vasoconstriction regul by muscle ergoreceptors and CV control center (medulla)
how does blood flow change with exercise in exercising vascular beds
1) autoregulation –> vasodilation
2) incr capillary recruit for O2 delivery and extraction
where does autoregulation occur
arterioles and small arteries
Metabolic changes with autoregulation
1) decr PO2, incr PCO2
2) NO, K+, acidosis, adenosine
a
a
effect of sympathetic activity with moderate to heavy exercise
1) sympatholysis - vasodilation
2) MAP constant due to vasoconstriction
effect of sympathetic activity with moderate to very high exercise
person usu has large amount of active muscle mass MUSCLE vasodilation > heart pump capacity sympathetic mediated vasoconstriction to preserve MAP (NOT AVERAGE PERSON)
coronary blood flow during exercise
1) incr CO, incr coronary blood flow
2) decr O2 saturation esp coronary compared to mixed venous blood
how does HCT, arterial O2 saturation, and CV O2 sat change with exercise
HCT = incr due to hemoconcentration arterial O2 saturation = no change
CV O2 = coronary venous O2 saturation= decr
how does cardiac and leg blood flow change with VO2 during exercise
incr peak VO2, incr leg flow and CO with CHF and normal patients
equation of O2 delivery
O2 delivery = flow x O2 content Flow = CO, leg blood flow
mechanism to incr O2 availability to exercising muscle
1) incr O2 delivery (supply)
2) incr O2 extraction
3) incr metab efficiency of skeletal muscle
what is PaO2
partial pressure driving force of tissue oxygenation from arteriole –> capill –> tissue –> vein PO2 decr over time so need PaO2
what is CaO2
O2 content quantity of deliverable O2
what is SaO2
relative quantity
how to incr O2 delivery during exercise
1) exercise training
2) blood doping (incr CaO2) with transfusion and EPO
3) high altitude (incr [Hgb])
how does a-v O2 change with exercise
3x incr
how much does blood flow change with exercise
`5x
a
a
factors leading to incr muscle O2 extraction (a-v O2 difference)
1) incr skeletal muscle microcirculation- recruit more capillaries (decr venous O2 sat) 2) incr aerobic activity of skeletal
3) incr size + # mito
4) local vascular and metab improvements
after age 30, ___ decr in max CO for men and women due to decr in max HR____ is not a factor in incr muscle O2 extraction
decr max CO
incr arterial O2 content
