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Cardiovascular system > CVS Response to acute exercise - L11 > Flashcards

CVS Response to acute exercise - L11 Flashcards

1
Q

Magnitude of change from rest to strenuous exercise?

A

HR can increase from 70bpm to 200bpm (3 fold)

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2
Q

Aerobic exercise - (dynamic, endurance) what onsets are observed in terms of HR , muscle blood flow, SBP, DBP and MAP and why?

A

Immediate increased HR via parasympathetic withdrawal driven by central command - depends then on what type of intensity of exercise, i.e. the magnitude is dependent on intended effort not recruited mass
There is a small increased MAP via increased HR and not SV (not a chance to consider SV yet) and also due to:
Anticipatory increased muscle blood flow
Increased Systolic Blood Pressure,
Diastolic Blood Pressure change absent or less marked

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3
Q

CVS responses to light to moderate exercise - what is steady state?

A

A condition in which the energy expenditure provided during exercise is balanced with the energy required to perform that exercise and factors responsible for the provision of this energy reach elevated levels of equilibrium

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4
Q

What is RPP - Rate pressure product?
TPR?

A

HR x Systolic Blood Pressure
Summed resistance in circulation

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5
Q

What is CVS drift?

A

The changes in observed cardiovascular variables that occur during prolonged, heavy submaximal exercise without a change in workload

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6
Q

CVS drift - Progressive increase in HR with prolonged
exercise is associated with?
Reason?

A

Decreases SV and MAP, and a maintained cardiac output (Q)

Likely a result of altered sympathetic activity for flow control (CO), and altered distribution of blood (e.g. to skin for cooling- potentially losing fluid volume if we are not replacing)

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7
Q

CV responses to exercise (acute)
1. Change in HR and why?
2. Change in venous return why?

A
  1. HR increases as a result of increased sympathetic and decreased parasympathetic activity to the SA node.
  2. Venous return increases as a result of sympathetically induced venous vasoconstriction and increased activity of the skeletal muscle pump and respiratory pump.
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8
Q

CO distribution changes during exercise - do active tissue of exercise get more O2+nutrients? Explain

A

Active tissue get more O2 and nutrients and organs have increase vasoconstriction to vessels and have more litre of blood for circulation to organs needed for exercise

DON’T FORGET ALL HAPPENS ON BOTH SIDES OF HEART, NOT JUST THE LEFT

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9
Q
  1. What happens to BP that facilitates these changes with CO output during exercise?
  2. Blood to brain does it change?
  3. Change in coronary circulation with exercise increasing?
  4. Skin?
  5. CO distribution to muscles as exercise intensity increases?
  6. 3 main organs that increase in blood during exercise?
A
  1. Increase in systolic pressure, slight decrease/relatively unchanged at diastole as that is due to PR
    Moderate increase in MAP - combination of systolic and diastolic changes BP
  2. Always preserve the blood to the brain despite increase in exercise - same 750ml of blood to the brain as heart rate increases
  3. Coronary circulation increases with exercise intensity
  4. Blood increases to active tissue
  5. CO distribution to the level of the muscle increases as exercise intensity increases
  6. 3 main active organs that has increase in blood: muscles, coronary circulation, skin
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10
Q

What is CO driven by:
Light to moderate exercise?
Moderate to strenuous exercise?

A

Light to moderate exercise: CO driven by HR+SV
60% VO2Max
They contribute equally ^

Moderate to strenuous exercise: 65% upwards CO driven by HR.
After 60% of VO2Max, HR takes over the bulk of the workload and thus SV decreases

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11
Q

Light to moderate exercise - up to 605 VO2 Max
1. What is this often called?
2. Is there more O2 coming in or out?
3. How long can we do this type of exercise for?
4. What would fatigue be due to then if its not ^?
5. How long is this normally done for?
6. What is Q?

A
  1. Considered steady state
  2. Enough O2 coming in to reach demands, more O2 available than CO2
  3. We could continue working like this indefinitely as we have enough O2
  4. Fatigue is then due to other factors such as food, as long as you have food you can stay at this level
  5. 10-15 mins of exercise
  6. CO = Q = Cardiac Output
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12
Q

Normal O2 consumption at rest:

A

Approx 250mL/min

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13
Q

O2 consumption under maximal conditions:
Untrained
Trained athlete
Marathon runner

A

Untrained: 3600ml/min
Trained athlete: 4000ml/min
Marathon runner: 5100ml/min

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14
Q

VO2 max defined as?
What is a test of?
How much O2 we take in what relevance does that to how much O2 is in our muscles?
What is this measured in?
What is O2 uptake measured in?

A

The rate of oxygen usage under maximal aerobic metabolism
Test of fitness: cardiac respiratory fit - measures whole body oxidative capacity
give or take +/- 10% we take in and out during this test is how much we have in our muscles
Measured in L/min
O2 uptake measured in mL/min or mL/min/kg body weight

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15
Q

Flow is determined by BP/Resistance
What happens to these during light to moderate exercise?

A

Resistance decreases need to make sure BP gradient stays the same during exercise which is why BP increases during exercise
Slight decrease in diastolic
Slight increase: 2-3mmHg max can be seen for diastolic
If they increase in diastolic terminate exercise as that shows pathological conditions

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16
Q

RPP = Rate pressure product - what is it?

A

Indicator of how hard the heart muscle is working

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17
Q

CVS responses to moderate to strenuous exercise?
How long?
How much VO2 max?
SV?
HR?
The greater the EDV - what happens to myocytes?
Do myocytes fire better when stretched or unstretched?
What effect does this have on contractility and SV with this?
Do we still see CVS drift at natural ambient temperature?

A

60 mins of exercise in diagram
Have not reached VO2 max
Probably at 80-85% VO2max

SV increases - then plateaus - then finally declines
HR increases - then plateaus and then drifts upwards - more than SV - as SV declines, HR increases

EDV: end of refill - volume in ventricles ready for ejection
The greater the EDV - the bigger the stretch of myocytes and myocytes fire better when stretched, they like to be stretched and this increases contractility and contract greater which increases SV

Yes at Natural ambient temp - we see CVS drift

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18
Q

Interval exercise VS steady state exercise
Take home message about BP in regards to HIT Interval training?

A

52 years old males

HIT interval training

1 min on 270 W and 1 min off 120 W
15 minutes for other one
CVS responses similar patterns in both steady state and interval
Reduction in TPR, Increased HR, etc

=> Take home message: Do not be worried about BP about HIT interval training - does not make much changes
1999 Paper- older papers good core texts too

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19
Q

Why measure VO2 Max?

A

How physically fit is a person
Medically - exercise is integration of all systems in the body particularly CVS and respiratory
O2 in and getting to active tissue so many places this can be affected
once O2 gets delivered to tissue - hopefully tissue is healthy enough to take it - can get an indicator to individual’s health from this

Acts as a prognostic marker of all cosmortality
lower vO2max the more likely they are to have poor quality of life and death

Depends on age, gender, etc

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20
Q

Exercise efficiency: correalting VO2 Max with power output
Similar VO2 Max but 1 athlete is considerably more efficient why?

A

Can have same VO2 max and different power output
but one can have a greater efficiency -
2 very well trained athletes
Does this determine who wins a race?
Huge amount of stuff that can contribute to this:
genetics - the more type 1 the more fibre muscles the better
Subtle differences in: antagonist and postural muscular actions
Antagonist - how an individual is their head straight while running?
Technique - wind resistance, friction, drag, running/swimming style, aerodynamics/hydrodynamics
Body composition
Manipulation of ventilatory rhythm
Cytosol - intracellular component to oxidative
Lower VO2max resistance training compared to aerobic
Complete sedentary goes back slower than someone who was fit as a child then sedentary due to muscle memory
Muscle memory doesn’t affect vO2max

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21
Q

CVS drift - not fully understood

A

CVS drift influenced by many factors

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22
Q

TABLE 10-5 EXAM Q Slide 10

A

Talk about 3 of those points
Need table

ACUTE: Asked to discuss CVS response to chronic exercise
Talk about: long term exercised training -> period of time of training NOT ACUTE

Acute = sudden onset: 1 bolt of exercise even if its 1 hour 30 mins - still acute if its just once

Q COULD BE Asked to discuss acute and chronic BP changes

Be aware of Blood flow
Be able to talk about arteriolar vasodilation, -presphincter offloading etc capillaries feeding into venoules taking O2 away and moving back to

All about thermoregulation: protect HEART, lung, brains

-> Increase in CO2 causes blood vessel to respond
Increase in O2 then vasoconstriction if we have enough
Extrinsic and intrinsic control factors

23
Q

Maximal O2 uptake predicts performance?

A

If VO2max predicted performance then a lab test could decide a contest. In general, a high VO2max is a prerequisite for elite endurance performance
VO2max predicts performance better in events lasting between 10-30 min
=> NO

10-30 mins
Aerobic measure

U shaped graph for elite athletes such as ultramarathons point of bad compared to highly trained resistance

24
Q
  1. Minimal values for elite running and skiing in men and women
  2. Minimal values for elite swimming and cycling.
A
  1. 65 ml.kg-1 .min-1 for women
    70 ml.kg-1 .min-1 for men
  2. 55 ml.kg-1 .min-1 for women
    65 ml.kg-1.min-1 for men
25
Q
A

Dot is v important - it means the rate of the volume of O2
In formula slide 15

26
Q

Provides 4 factors which may potentially limit VO2max

A
  1. Cardiac Performance (i.e. cardiac output)
  2. Respiration/Ventilation (i.e. arterial oxygen carrying capacity) - RULE IT OUT as for regular healthy person it tends to rectify itself even though you try to control breathing, we can’t override it
  3. Pulmonary diffusion capacity (i.e. oxygen uptake capacity)
  4. Skeletal muscle characteristics (i.e. tissue extraction - avO2 difference)
27
Q

Cardiac performance is determined by 4 factors:

A

1) Heart Rate (i.e. speed of beating)

2) Stroke volume (i.e. volume of blood ejected with each beat)
- Preload (i.e. ventricular stretch on filling – related to EDV)
- Frank-Starling mechanism
- Provides “flow” work of the heart: blood flowing in, filling and leaving the heart

3) Afterload (i.e. circulatory resistance to ejection)
- Most often considered to be aortic resistance
- Provides “ pressure ” work of the heart
- Pressure coming outside of heart
- Often overlooked
- Systemic
- Damage of increased afterload does to the ventricles can cause increased chamber sizes and cardiac remodelling and now always in a good way

4) Contractility (i.e. ventricular performance)
- Ventricular contractile strength
- Due to Frank Sterling Mechanism and increased length tension relationship but also have increased calcium which can contract more efficiently

=> components you need to talk about
Can only return to heart when blood has been ejected

28
Q

Aerobic exercise - dynamic, endurance with onset
What is magnitude dependent on?

A

Dependent on intended effort but not recruited mass
-> The body anticipates its about to exercise so it increases blood flow to active tissues but does not know how much it actually needs but it still prepares for what is coming next

29
Q

When we are at rest what system is predominant?

A

When we are at rest, the parasympathetic nervous system is predominant

30
Q

During CVS drift -
What happens do power output?
What happens to SV?
What happens to HR?
If the intensity stays the same, do we still see the drift?
What happens to DBP, if this change did not happen what would happen to SBP+MAP, what conditions we observe?

A

Power output is the same
After 30 mins SV goes down and HR drifts upwards
The intensity stays the same we still see HR drift
Would expect to see slight decrease in DBP
If we didn’t have DBP decrease than SBP and MAP would increase more-> pathological

31
Q
  1. What can CVS drift be altered by?
  2. Why is there a TPR reduction during CVS drift?
  3. Why do we see fluid shifting during 2-5 mins of exercise during CVS drift?
  4. Can this initial fluid shift be changed at all?
  5. Do blood volumes change during CVS drift during moderate to strenuous exercise and if so why?
  6. Not hydrating during this exercise - impact on heart?
A
  1. Heat contribution, fitness, etc
  2. Have to offload heat building up: vasodilation - drives blood to skin gives greater TPR reduction
  3. 2-5 mins of exercise: have fluid shifts and a reduction in SV just extracellular fluids shifting, there’s no loss of blood volume and that stabilises after 5 mins
  4. That can be offset in trained individuals
  5. Blood volumes have also changed due to sweating and if you’re not hydrating
  6. Places heart in more strain and less blood available, the heart works harder
32
Q

The body needs fluids, especially during exercise why?

A

NEED FLUIDS
SV -> Reduction in blood volume, reduction in how much is being returned to the blood, reduction in ED pressures and reduction in pre load, reduction in how much can be ejected

33
Q

CV responses to exercise (acute)
1. Change in SV and why?
2. Change in CO and why?

A
  1. SV increases - both as a result of increased venous return by means of the Frank-Sterling Mechanism (unless diastolic fIlling time is significantly reduced by a high HR) and due to sympathetically induced increase in myocardial contractility.
  2. CO increases due to increases in both HR + SV
34
Q

CV responses to exercise (acute)
1. Change in Blood flow to active skeletal muscles and heart muscle and why?
2. Change in blood flow to the brain and why?

A
  1. Increases as a result of locally controlled arteriolar vasodilation, which is reinforced by the vasodilatory effects of adrenaline and overpowers the weaker sympathetic vasoconstrictor effect
  2. Unchanged as sympathetic stimulation has no effect on brain arterioles, local control mechanism maintain constant cerebral blood flow whatever the circumstances.
35
Q

CV responses to exercise (acute)
1. Change in blood flow to the skin and why?
2. Change in blood flow to the digestive systems, kidneys and other organs and why?

A
  1. Increases because the hypothalamic temperature control centre induces vasodilation of skin arterioles, increased skin blood flow brings heat produced by exercising muscles to the body surface where the heat can be lost to the external environment.
  2. Decreases as a result of generalised sympathetically induced arteriolar vasoconstriction.
36
Q

CV responses to exercise (acute)
1. Change in TPR and why?
2. Change in MAP and why?

A
  1. Decreases because resistance in the skeletal muscles, heart, and skin decreases to a greater extent than resistance in the other organs increases.
  2. Increases (modest) because CO increases to a greater extent than TPR decreases.
37
Q

What happens to Peripheral resistance as CO increases?

A

Peripheral resistance decreases as CO increases

38
Q

MAP ? normally and more mathematically

A

MAP = CO X SV: not mathematical - just variables that govern this but you can put values to it and get change
120/80 comes from diastolic pressure + 1/3 Pulse pressure

MAP = Diastolic + 1/3 pulse pressure

39
Q

Rate of VO2 max formula to define VO2 max?

A

VO2 max = Q max (a-v)O2 max
Dots on V and Q to indicate Rate

Q max = maximal cardiac output
(a-v)O2max = maximum arterio-venous O2 difference

40
Q

What limits your Maximal Oxygen Uptake (VO2max) and
what improvements occur with training?

A

Cardiac output: what is being delivered and what is being extracted and utilised
Highly dependent on the level of muscle activity
difference between O2 content in arterial blood and venous blood - how much O2 has been taken
out
The greater the avO2 difference the greater we are extracting

avO2 difference normally 5mL of oxygen and with exercise around 15mL

41
Q

Exercise affects HR -

A

HR is a major determinant of CO at intensities > 50%
i.e. moderate to maximal intensities

42
Q

Output from left ventricle to systemic circulation
What is preload and after-load?

A

Preload: Input
End diastolic volume
Relates to venous return
Increases in hypervolaemia
Afterload: Affects output
Reistance the ventricle must
overcome to eject stroke
volume
Increases in hypertension
Increases workload of ventricle

43
Q
A

don’t forget about CO2 impact

44
Q

control of SV

A

Preload - we want greatest amount of blood returned
Contractility - how efficiently heart can pump blood in and out
After-load - extrinsic mechanism what actually gets to leave the heart

45
Q

Exercise affects preload via

A

Cardiac Output, which equals Venous Return
Over a few beats an increase in CO, increases VR
NB: most of the ↑ed CO during exercise is via ↑ed HR rather than ↑ed SV

Blood volume
↓ BV → ↓ Preload (less blood available for delivery
to the heart)
e.g. dehydration during exercise in the heat
(is this why cardiovascular drift occurs ie trying to
maximise use of a decreased BV?)

Posture
EDV remains relatively constant during supine
exercise (e.g. swimming) ->as we are flat and gravity is out of the occasion, different types of fitnesses
EDV increases during upright exercise to ~50%
maximum after which CO overtakes such as a jog so different fitness, can take less pressure off heart to make sure CO is achieved
Skeletal muscle pump is affected by upright
Also why swimmers have higher VO2max as they’re working harder than land trainers
After which high HR’s limit preload
In static upright postures, reduced skeletal muscle
pump activity contributes to
→ gravitational venous pooling
→ reduced brain perfusion pressure
→ fainting response (<40mmHg)
Because huge pressure from gravity pushing pressure downwards on you and bringing blood downwards

Pumps (skeletal & thoracic)
The alternating increase and decrease of intra-abdominal and thoracic
pressure assists in return of blood to the heart, also
Venous compression via limb muscle contractile activity

Heart Size
Determined primarily by training status
Endurance training → enlarged chamber size
Resistance training → enlarged wall thickness
Untrained: maximal SV = 90-100 ml
Elite X-country Skier: maximal SV = 170-200 ml
SV = EDV - ESV

Venous Tone
65% of blood volume stored in major veins
Mobilised during exercise via sympathetic venoconstriction

Other factors
Ventricular compliance (i.e. sensitivity to filling pressures)
Filling pressure (i.e. atrial pressure) - elevated in some athletes

46
Q

Effect of gravity on haemodynamics slide 23

A

Blood is pulled down from effect of gravity in the body
Pressure is constant across the board
Look how it changes for a period of standing
Greatest pressure at feet especially when standing

47
Q

What is after-load? What is it primarily?

A

Pressure against which the left ventricle works
Primarily aortic pressure: resistance to outflow

48
Q

Preload - Frank Sterling law of heart what does increase EDV do?

A

Stretch muscle fibres closer to optimum length gives a greater strength of contraction and thus increases SV

optimal length for muscle fibres to contract

49
Q
A

Upon immediate onset of exercise: reduction of blood volume but though to be more fluid shifts and this stabilises within 5 minutes
We do have slight changes in blood volume with training
This decrease from both means decrease in blood volume still
If we continue to lose fluid then problems arise such as dehydration as we must maintain CT at all costs so we must dissipate heat via water in sweat
If we lose lots of fluid during exercise perhaps this is what causes cardiac drift

50
Q
A

Fainting brings homeostasis back to normal - is a good thing

51
Q

Compliancy - how willing they are to stretch

A
52
Q

Slide 24

A

Keep going up and down on the feet to keep blood flowing

If you have constant pooling downwards and then do movement, but continue to stand for longer then pressure will always win out and veins become varsocisity and bulging - wear compression stockings
Athletes do after to promote venius return of metabolites

53
Q

Summary of effects of exercise on Preload

A

We want to increase EDV as then the greater capacity the ventricle has to eject more blood
Increasing stretch ion myocytes: myocardium and breaking them t optimal tension to give optimal contraction which evolves around the Frank Sterling Mechanism Law

Venous tone affects stretching of myocardium
May way it happens is via skeletal muscle pump

Body position also affect this stretch and intrathoracic pressure not so much a role but they do help
Respiratory pump it comes from
This pressure comes more into play with resistance exercise

What are the factors that can maximise

Cardiovascular system (13 decks)

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