Mod 5: Cardiovascular Function and Regulation During Exercise Flashcards
what are the key components of the cardiovascular system?
what are their key roles?
explain the cardiac conduction system and what it looks like on an ECG
what are the 3 major CV adjustments to acute exercise?
- cardiac ouput(Q) is increased
- Q is redistributed throughout body
- Tissues adjust rate of O2 removal from blood
driving pressure through system must be maintained
-cant have massive vasoldilation bc theres no venous return and BP would drop
-pressure dictates a lot of things during exercise
what are the 4 steps of the cardiac conduction system that gets picked up on an ECG?
- SA node initiates contraction signal
-pacemaker of heart
-signal spreads thru BOTH atria to AV node
- this signals the atria to contract - AV node delays signal from progressing further to maximize ventricular filling (atria fully contract, ensure all of its blood is fully released into ventricles)
-form terminal brahches of R and L bundle branches (spread throughout entire ventricle wall)
-stimulate ventricular contraction - AV bundle relays signal further
-travels along interventricular septum
- R and L bundle branches
-signals toward apex (down) - Purkinje fibres:
-form terminal branches of R and L bundle branches
-spreads throuhgout entire ventricle wall
-stimulate ventricular contraction
systole vs diastole
(what changes?)
systole: contraction phase
diastole: relaxation phase
-changes in pressure and volume
what does the cardiac cycle look like at rest vs during exercise?
HR and cycle (HR/60s)
Rest: Hr=75 BPM
cycle=0.8s
systole: 0.3s (40%)
diastole: 0.5s (60%)
lots of time for filling at rest
Exercise: HR=150 BPM
cycle=0.4s
systole: 0.25s (60%)
diastole: 0.15s (40%)
filling time(relaxation period) reduced
-muscle acts as a second pump for blood
what are the steps of the cardiac cycle:
- ventricular filling
-left V
-diastole(relaxation phase)
-blood goes thru AV valve thru AV valves(open) - Isovolumetric contraction (systole)
-volume doesn’t change
- AV valves closed
-when pressure is high enough in ventricle it forces SL valves open - Ventricular Ejection
- SL forced open, ejection of blood out rhe heart
-once all blood ejected, pressure drops, and enter: - Isovolumetric Relaxation
SL and AV valves shut
what are the volume changes during the cardiac cycle at rest?
EDV, preload, SC, EF
End diastolic volume (EDV)
-volume of blood in ventricles at end of diastole
-at rest for untrained= 100 ml
preload: stretch on ventricles due to filling (create a more powerful ejection)
Stroke volume
-volume of blood ejected from ventricles per beat
- at rest for untrained=60ml (ejection fraction 60/100=60%)
what are the ventricular volume changes during exercise?
EDV increases : less time for filling, but still more blood in the ventricle at end of diastole, heart is more effectively getting blood in
SV increases take advantage of inc diastolic volume and eject MORe blood with every beat, so ESV goes down as well
decrease ESV eject more with each beat(less blood left in heart)
inc venous return EDV, fill vetntrivcles and have greater strength of contraction
how does the muscle pump work?
contraction of skeletal muscles squeezes veins and promotes venous return to heart
what is the Frank Starling Law of the heart?
an increase in EDV causes stroke volume to increase
“force generated by contracting ventricle is greater when muscle is previously stretched (greater filling=stronger subsequent contraction)
fill ventricle more=stretch more=better elastic recoil=increased ejection (SV)
inc EDV=inc stretch on walls = inc force of contraction = inc SV(stroke volume) during exercise
how does cardiac output(Q) change from rest to exercise in untrained vs trained individuals?
Q= HR(beats/min) x SV(ml/beat)
**untrained: Male: HR: 75.SV:80, Q(L/min)=6
Female: HR:75, SV: 60, Q(L/min)=4.5
NORMAL CARDIAC OUTPUT UNDER RESTING CONDITIONS 5L
Trained
Male: HR; 55, SV: 110, Q=6 L/min
Female: HR: 55, SV: 80, Q=4.5 L/min
at rest eject more blood w every beat, due to inc EDV(preload) and ejection fraction
means heart doesnt havw to work as hard (as many times/min)
dec HR, inc SV
how can heart rate be used to prescribe training intensity and determine maximal fitness?
how can we use HR to predict VO2 max(what are some assumptions?)
can be prescribed in different zones of % of Max Heart Rate
1. Recovery Zone: 50% or less
-
Fat Burning zone: 50%-65%
-burn highest relative fat but not absolute - Target Heart Rate Zone: 65%-85%
- Anaerobic Threshold Zone: 85-100%
- HR is directly proportional to exercise intensity
- Maximal HR(HR max): highest HR achieved in an all-out effort to volitional fatigue: slight decline with age
220-age (NOT EVERYONE) but still most common
208-(0.7 x age in years)
Assumptions:
1. linear (direct) relationship bw Hr and workload
2: Hr max= 220-age
Procedure:
1. measure Hr at more than 2 submax workloads
2. extrapolate line to predicted HR max
3. Determine predicted VO2 max
what happens?
Stage 1: 30 W
Stage 2: 60 W
Stage 3: 90 W
HR increases ad workload (W) increases
plot it on graph
more trained = lower Hr at given workload =more fit-higher predicted maximal workload or Vo2 MAX
How does Q(cardiac output) and its variables(HR and SV) change during exercise as VO2 increases?
Q max = HR max x SV max
HR max: fixed, (22-age)
SV max: semi adjustable (genetics and TRAINING)
HR goes up in linear manner as Vo2 increases (BOTH TR AND UT)
SV(Stroke volume); at low intensity SV inc, pletaus around 50% VO2 max, and doesnt increase after that in UNTRAINED.
In trained, inc SV even beyond 50%
Q(cardiac output): sharp inc early on (VV and Hrinc) but beyond 50% VO2 max, goes up a bit( bc SV plateaus and HR still goes up) . TRAINED inc even more due to inc SV
describe why stroke volume increases during exercise:
(how does SV change during exercise?
- increased preload (EDV) ecspecially at lower intensities –> inc SV
- inc venous return –> inc EDV –> inc preload
-muscle pumps promote venous return - inc Left ventricle contractility –> inc SV
- inc epi or norepi –> inc contractility
- independent of EDV (inc EF instead) - dec afterload(aortic pressure) via vasodilation –> inc SV
stroke volume
the volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction.
what are the regulatory factors that control cardiac output?
Q = HR(beats/min) x SV(ml/min)
Intrinsic Factors
chronotropic factors control RATE of contraction (HR)
Inotropic factors control strength of the contraction (SV)
-without any other control, Hr would average 100 BPM!!
Extrinsic Factors:
1. PNS
-AT REST
-vagus N travels from brain stem(medulla oblangata) to heart(SA and AV nodes) not venticles, so no effect on force of contraction
-releases Acetylcholine: MAJOR: dec HR, and minor: can dec force of heart conraction
2. SNS
- cardiac acceleator nerve travels from brainstem to heart(SA and AV nodes and ventricles)
-releases NOREPI (neurotransmitter)
-inc HR (AV and SA nodes) and force of contraction (ventricles)
-also have circulating epi and norepi, i
MECHANORECEPTORS also influence ventricles, inc SV, send more blood back to blood, inc EDV, stretch LV=greater SV/contraction due to inc preload , mediated by mechanoreceptors . enhanced SV
- Hormones
time course as to which SNS or PNS exerct most effect to rise in HR during exercise:
-inc in exercise=inc HR
-PNS at rest (vagal tone)
- anticipatory rise (epi and norepi) inc SA and AV node activity
-increase in HR at beginning of exercise is due to withdrawal of vagal stimulation
how do the regulatory factors that control cardiac output change from rest to exercise to increase cardiac output?
1. Neural
- dec PNS=initial inc in HR (dampening of vagal tone)
-inc SNS = inc HR and SV
2. Hormonal
-inc epi & norepi =inc HR and SV
3. Mechanical
-inc venous return(senses it) and in turn= inc SV
-DOESNT INFLUENCE HR AT ALLL BC ITS MECH
explain the relationship between flow, pressure, and resistance in vasculature
describe the absolute and relative contribution of cardiac output to different tissues at rest and during exercise
pathway of blood thru body
Aorta (2.5 cm)–> arteries (0.5cm)–> arterioles (20microm)(smooth muscle)–> capillaries (6microm)(endothelial cell) –> veins(3cm) –> vena cava (3cm)–> right atrium)
arteries: establish bulk flow and driving pressure
arterioles: regulate flow to specific regions
capillaries regulate Surface Area for exchange
veins/venules regulate flow return(muscle pump)
-pressure highest at left ventricle, gets lower as travels thru ;arge artteies, arterioles, capillaries, venules, large veins,
steepest drop happens in arterioles
**
hemodynamics
-dynamics of blood circulation
–> flow, pressure, resistance
- flow is proportional to change in pressure between ends of a tube
-flow is inversely proportional to the resistance of a tube
FLOW=PRESSURE/RESISTANCE
RESISTANCE = VISCOSITY x LENGTH/(RADIUS)^4
-radius has 16 fold effect
If vessel radius doubles:
resisatnce=1 x 1 /2^4 = 1/16 = 0.0625
flow=p/Res=1/1/16= 16 flow inc by 16 fold just by doubling radius which dec resiatcnce
RAIDIUS MOST IMPT VARIABLE ON INFLUENCING RESIATANCE BLOOD FLOW TO TISSUES
Precapillary Sphincters
blood moves so fast thru capillaries that theres no time for gas exchange (1l / min to 20 L / min during exercise)
-open to inc Surface area(pathways) that blood can take during exercise (controlled by NS) , slows the movement of blood thru capillaries so we can still get required gas exchange
transit time of RBC in capillary for gas exchange : at rest : 0.8 s.
during exercise: 0.4s
muscle blood flow during exercise
- flow to active muscle increases up to 20 fold (like skm)
- due to inc in cardiac output (Q) and local arteriole vasodilation
- more capillaries open –> larger area for exchange (precap sphincters)
-avg speed of RBC thru capillaries only doubles (and transit time reduced by half which is enough time for gas exchange to happen )
muscle blood flow during exercise
- flow to active muscle increases up to 20 fold (like skm)
- due to inc in cardiac output (Q) and local arteriole vasodilation
- more capillaries open –> larger area for exchange (precap sphincters)
-avg speed of RBC thru capillaries only doubles (and transit time reduced by half which is enough time for gas exchange to happen )
muscle blood flow during exercise
- flow to active muscle increases up to 20 fold (like skm)
- due to inc in cardiac output (Q) and local arteriole vasodilation
- more capillaries open –> larger area for exchange (precap sphincters)
-avg speed of RBC thru capillaries only doubles (and transit time reduced by half which is enough time for gas exchange to happen )
muscle blood flow during exercise
- flow to active muscle increases up to 20 fold (like skm)
- due to inc in cardiac output (Q) and local arteriole vasodilation
- more capillaries open –> larger area for exchange (precap sphincters)
-avg speed of RBC thru capillaries only doubles (and transit time reduced by half which is enough time for gas exchange to happen )
explain how the vasculature controls blood flow during exercise through intrinsic and extrinsic regulation
vascular tone=state of tonic vasoconstriction
Extrinsic Control
sympathetic nerve fibers with a high rate of firing=promote vasocontrsiction
sympathetic nerve fibers with a low rate of firing=promote vasodilation
Intrinsic Control
1. Metabolic Regulation
-changes in O2, CO2, H+ causes release of vasodilatory chemicals
2. Endothelium-mediated dilation:
-nitric oxide, acetylcholine, and adenosine cause vasodilation
3. Myogenic response
-increased pressure=constriction
-decreased pressure=dilation
CONTROL DURING EXERCISE
- SNS inc in exercise:
- most nerves –>norepi
-vasoconstriction in most tissues (including muscle)
-especially splanchnic area (viscera or internal organs, especially those of the abdomen)
-reduced flow to less active tissues
-local muscle factors INC in exercise:
local factors released in muscle decrease sensitivity to SNS stimulation (functional sympatholysis)
-dec O2, inc CO2, inc H+, inc temp, inc nitric oxide=compensatory vasodilation (allows vascular beds to inc in size, which dec resiatyance which allows for 20 fold increase in blood flow from rest to exercise)
key points: vascular regulation in exercise
inc SNS= ine norepi release = VASOCONTRCITION in most tissues
-local factors(outweigh vasocontrciton) = vasodilation in active muscle
