exercise and CV disease Flashcards by A B

How does exercise affect homeostasis

1) incr muscular demand for O2

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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

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Factors that affect maximal O2 uptake

1) genetics
2) training
3) age
4) gender- male
5) heat, altitude

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peak VO2 vs. VO2 max

peak VO2 = top level of exercise before stop

max VO2 max = max O2 uptake

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what is VO2

oxygen consumption (uptake)

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what is VO2 related to

1) workload
2) energy req with exercise

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shape of VO2 curve with exercise

1) linear incr
2) then plateau at VO2 max (not often reached)

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what is VO2 max

plateau (aerobic capacity)

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what is Fick’s principle measure

connects respiratory VO2 with O2 delivery (circulatory) and O2 extraction (muscle

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Fick’s equation

CO = VO2 / (CaO2 - Cmixed venousO2)

VO2 = CO x a-v O2

Ca or vO2 = [Hgb] x 1.34 x O2 saturation (%)

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mixed venous

when all venous blood gets mixed and goes to lung to be oxygenated (USU MAIN PULM ARTERY)

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sympathetic nervous system effect on HR and SV

1) incr HR
2) incr contractile strength (incr SV)

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effect of PNS on HR

decr HR

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based on frank starling, incr contractile strength and stretch, incr ____

EDV

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what does frank starling tell you

more LV is filled (LV EDP), more it will contract (SV)

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how does incr preload affect SV

increased SV (and CO) for the same inotropic state

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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)

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where is most blood volume?

64% in veins at rest

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effect of HR on ventricular filling and contraction

1) incr HR with exercise (decr diastolic time)
2) @ high HR, systolic time decr

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what happens to systolic time at high heart rate

systolic time decr

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@ rest what controls heart rate

parasympathetic control 60-80 bpm

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what is the anticipatory response

just before exercise HR increased

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what controls anticipatory response

central command from CNS (sympathetic activity) incr HR

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what happens to HR with exercise

1) incr HR proportional to intensity
2) linear response up to near max exercise

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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

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

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

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

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