Coordinated cardiovascular responses- Gravity and Exercise

Question 1

What is orthostasis?

Answer 1

→ Standing up

Question 2

What happens to blood pressure in response to orthostasis?

Answer 2

→Blood pressure falls at first
→Postural hypotension - lack of blood flow to the brain
→Quickly recovers - due to homeostatic mechanisms such as baroreflex

Question 3

What three changes does the baroreflex integrate?

Answer 3

→Increase in heart rate
→Increase in heart contractility
→Increase in total peripheral resistance

Question 4

How do we know that blood flows from the heart to the feet?

Answer 4

→ Bernoullis law
→ Blood flow = pressure energy + potential energy + kinetic energy
→ potential energy at heart > feet + increased KE of ejected blood
→Total energy means blood flows from the heart to the feet

Question 5

What is the equation for pressure?

Answer 5

→ ρhg

Question 6

Where is pressure lower?

Answer 6

→ on the venous side

Question 7

How can orthostasis cause fainting?

Answer 7

→ Orthostasis causes a fall in CVP
→ Decreased end diastolic volume--Decreased SV
→ Decreased CO
→ Decreased BP
→ Poor perfusion of the brain
→ dizziness + fainting

Question 8

How does laying down cause increased pulse pressure?

Answer 8

→ Increased CVP
→ Increased EDV
→ Increased SV
→ Increased pulse pressure

Question 9

What is the baroreceptor reflex response to orthostasis?

Answer 9

→ Baroreceptors are unloaded
→ Decrease in afferent fibre activity
→Less NTS switches off inhibitory nerves that go from Caudal ventrolateral medulla (CVLM) to Rostral ventrolateral medulla (RVLM).​
→Results in RVLM being more active sending efferent signals to heart and arterioles.
→ Increased sympathetic drive to SA node and increased HR. Myocardium increased contractility. Vasoconstriction (arterioles, veins) increases TPR.
→Less vagal parasympathetic activity to SA node via NA, overall increase in blood pressure.​

Question 10

What makes postural hypotension worse?

Answer 10

→α-ADRENERGIC BLOCKADE OR GENERALISED SYMPATHETIC BLOCKADE: drugs that reduce vascular tone
Side effect with calcium channel blockers used to treat hypertension, angina. Restrict sympathetic tone
→VARICOSE VEINS: impairs venous return
→ LACK OF SKELETAL MUSCLE ACTIVITY DUE TO PARALYSIS: eg. long term bed rest, soldiers on guard, etc.
→ REDUCED CIRCULATING BLOOD VOLUME: eg. haemorrhage
→INCREASED CORE TEMPERATURE:
peripheral vasodilation, less blood volume available (eg. standing up after a bath

Question 11

What do you need less of to control blood pressure in microgravity?

Answer 11

→less need for ANS, RAAS, ADH, ANP systems

to control blood pressure.

Question 12

What happens to the blood initially in microgravity?

Answer 12

INITIALLY:
→Blood not pooling in feet, it returns to the heart easily so increase in preload
→increase in atria/ventricle volume.
→sensed by mechanoreceptors.
→ Decreased sympathetic nerve activity,
→ reduction in RAAS, ADH
→ increased GFR, ANP and diuresis
→all leading to a 20% reduction in blood volume.

Question 13

What happens long-term to the blood in microgravity?

Answer 13

→Less BV
→ reduced stress on heart
→ heart reduces in muscle mass
→general drop in BP

Question 14

What happens on return to normal gravity?

Answer 14

→Severe postural hypotension
→due to much smaller heart
→Baroreceptor reflex can not compensate

Question 15

What is the difference between static and dynamic exercise?

Answer 15

→static exercise raises the blood pressure more than dynamic exercise.
→Static exercise is the constant contraction of a small number of muscles, so there is a higher load.
→dynamic exercise
→ there is a shortening/lengthening of many muscles, which is a low load

Question 16

What are general CVS responses to exercise?

Answer 16

→ increased lung O2 uptake, which is transported around the body and supplied to exercising muscle

→controlled BP, despite huge changes in CO and TPR
(to protect the heart from excessive afterload)

→increase mechanoreceptor and metaboreceptor stimulation

Question 17

How much can O2 uptake by pulmonary circulation increased by?

Answer 17

10-15 times

Question 18

How can the integration of small adaptations create a big response to exercise?

Answer 18

→increased heart rate (3x)
→increased stroke volume (1.5x)
→increased arteriovenous O2 difference (3x)

→3 x 1.5 x 3 = 13.5 times

Question 19

What happens during exercise induced tachycardia?

Answer 19

→increased stimulation of the brain central command
→increased stimulation of the muscle mechanoreceptors.
→decrease in parasympathetic simulation
→increase in sympathetic stimulation
→ decrease in vagal tone

Question 20

What happens to the stroke volume during exercise?

Answer 20

→increased stroke volume

→ increase in sympathetic activity.

Question 21

Why is there increased end diastolic volume during exercise?

Answer 21

→increased Venous return/CVP through venoconstriction
→increased sympathetic activity + calf muscle pump
→ activates Starling law increasing preload.

Question 22

Why is there faster ejection during exercise?

Answer 22

Increased contractility by sympathetic activation of β1 receptors (inotropic increase in Ca2+).

Question 23

Why is there decreased end-systolic volume during exercise?

Answer 23

(Increased ejection fraction)
Accounts for increase in stroke volume
Increased contractility by sympathetic activation of β1 receptors & Starling’s law,

Question 24

Describe the changes in cardiac output and flow changes during exercise

Answer 24

→fall in local resistance due to metabolic hyperaemia (an excess of blood) vasodilation.
→ increased sympathetic activity
→ β2-mediated vasodilation via the circulating adrenaline.
→[there is a high β2-receptor expression in skeletal muscle and coronary arteries]

→This increases cardiac output and flow changes.

Question 25

What does compensatory vasoconstriction of non-essential circulations during exercise prevent?

Answer 25

→compensatory vasoconstriction of non-essential circulations prevents hypotension due to an exercise-induced decrease in TPR.

Question 26

What does compensatory vasoconstriction of inactive tissues during exercise prevent?

Answer 26

→The compensatory vasoconstrictions of inactive or unrequired tissues (such as in the kidneys, GI tract, inactive muscle) prevents the BP from falling.

Question 27

What are metaboreceptors and what are they stimulated by?

Answer 27

→ small-diameter sensory fibres in skeletal muscle.
→They are chemosensitive
→stimulated by K+, H+ and lactate, which increase in exercising muscle.

Question 28

What are the reflex effects of metaboreceptors?

Answer 28

→tachycardia (via increased sympathetic activity)
→increased blood pressure

Pressor response to exercise

Question 29

When you stand up what happens to blood in the veins?

Answer 29

→ Venous pooling in the legs of about 500ml

Question 30

What is the arterio-venous oxygen difference like during high exercise?

Answer 30

→ Reaches a plateau

Question 31

Why does increasing HR eventually not increase SV?

Answer 31

→ Starling’s law
→ if you have a high HR there is not enough filling time
→ Less preload
→ you can also overfill the heart and get less CO

Question 32

What are the effects of the baroreceptor reflex during orthostasis?

Answer 32

→ Increased Sympathetic drive SA node
→ Increased HR
→ Increased contractility
→Vasoconstriction (arterioles, veins)
→Increased TPR
→ Decrease in vagal parasympathetic activity to SA node
→Together = Increase in BP

Question 33

What is exercise also known as?

Answer 33

→ Extreme form of standing up!

Question 34

What are the defences in blood flow and BP in dynamic and static exercise?

Answer 34

Allow BP to increase. In dynamic exercise, the metabolites are washed away in the blood stream.
In static, there is local high levels at the contraction site.

Especially important during isometric exercise (increased muscle load).
Static exercise raises BP more than dynamic exercise.

Raised BP maintains blood flow to contracted muscle to try to force blood into the contracted muscle.

Contracted muscle supplied by dilated resistance vessels due to metabolism…selective metabolic hyperaemia.

Question 35

Why does static exercise raise BP more than dynamic exercise?

Answer 35

Dynamic:
Constantly shortening and relaxing with lots of different muscle groups involved – lower BP, lower sympathetic tone.

Static:
One specific muscle group is being worked without constant movement – higher BP, local metabolic hyperaemia, local vasodilation. Increased heart rate and BP increases forcing blood into the contracted muscle

Question 36

What happens to blood pressure when cardiac output is increased by 4.5?

Answer 36

BP = CO x TPR
1. Large increase in CO
2. Relatively small
increase in mean BP due to dilated skeletal muscle arterioles decreasing TPR
3. Large decrease in TPR. Some areas are being constricted or dilated.
Decrease means blood pressure doesn’t increase by much

Question 37

How does a fall in local resistance in the legs occur during exercise?

Answer 37

Fall in local resistance due to metabolic hyperaemia vasodilatation by binding to sympathetic nerves directly.
Local sympathetic response and β2-mediated vasodilatation via circulating adrenaline.
β2 receptor expression high in skeletal muscle and coronary artery.

Question 38

How does static exercise stimulate chemoreceptors in muscles?

Answer 38

This reduction in blood flow allows the accumulation​ of acidic metabolic byproducts that stimulate chemoreceptors

Question 39

How is demand for increased oxygen by the lungs met?

Answer 39

Increased heart rate and stroke volume​

Question 40

How is increased O2 transport around the body demand met?

Answer 40

Increased extraction of O2 from blood Bohr shift.

Question 41

Direct the increased O2 supply​ to the exercising muscle… how is this met?

Answer 41

Lower vascular resistance in exercising muscle : metabolic vasodilatation.

Question 42

How is the demand for stabilisation of BP met?

Answer 42

Vasoconstriction in non-exercising and non-required tissue.