12) Coordinated responses of the CVS - gravity & exercise

Question 1

What is orthostasis?

Answer 1

• Standing up

Question 2

What are the effects of orthostasis on the blood flow to the brain?

Answer 2

• During orthostasis the CVS experiences changes due to gravity
• Blood pressure falls at first as we experience postural hypotension causing lack of blood flow to the brain. In cases of extreme hypotension it can result in fainting

Question 3

How does the body counteract postural hypotension caused by orthostasis?

Answer 3

• The fall in BP quickly recovers due to homeostatic mechanisms such as baroreflex
• The baroreflex increases heart rate, force of contraction and total peripheral resistance

Question 4

Describe the effects of orthostasis on blood pressure on different parts of the body

Answer 4

• Blood pressure is lowest at the head and highest at the feet.
• This is due to the force of gravity pulling blood down towards the feet
• This means there is more blood pooling at the feet which applies a greater hydrostatic pressure on the vascular wall

Question 5

How is Bernoulli’s law used to counteract the pooling of blood at the feet during orthostasis?

Answer 5

• There is an increase in potential energy (from heart to feet) and an increase in kinetic energy of ejected blood
• This increases blood flow as a result

Question 6

Why can orthostasis sometimes cause fainting?

Answer 6

• When we stand the blood starts to pool in the legs under the force of gravity
• This causes a fall in central venous pressure (pressure in veins close to the heart)
• As the blood pools at the feet less blood returns to the heart so there is a decrease in end diastolic volume
• Hence there is less filling so less stretch in the heart which means force of contraction would be weaker (Starling’s law) resulting in a decrease in stroke volume (amount of blood released per beat)
• A decrease in stroke volume means a decrease in cardiac output
• So there is poor perfusion of the brain resulting in dizziness and fainting

Question 7

How does lying down/fainting counteract hypotension?

Answer 7

• When laying down in a flat position the blood is evenly distributed in the veins
• This would lead to an increase central venous pressure and so an increased in filling
• This increased filling causes end diastolic volume to increase and increased stretching of vascular muscles.
• This increased stretching leads to increased force of contraction so increases stroke volume
• Increased stoke volume means increased cardiac output and hence better perfusion of the brain

Question 8

What can make postural hypotension worse?

Answer 8

• Alpha-adrenergic blockers, sympathetic blockers or drugs which reduce vascular tone as they inhibit the body’s ability to respond to an increase in vascular tone
• Impairment of varicose veins impairs venous return as more blood will pool in the veins
• Lack of skeletal muscle activity due to paralysis or forced inactivity (e.g. long term bed rest) as normally muscles help pump blood into the heart and so inactivity of these muscles reduces the amount of blood leading to the heart
• Reduced circulating volume: This reduces preload and so baroreceptors are not able to respond to changes (e.g. haemorrhage)
• Increased core temperatures: Peripheral vasodilation reduces the amount of blood going to the heart therefore less stroke volume and cardiac output

Question 9

What are the effects of microgravity (space) on the CVS?

Answer 9

• Initially blood does not pool at the feet. Instead it returns to the heart more easily which increases atrial and ventricular volume resulting in increased cardiac output. This is sensed by cardiac mechanoreceptors which reduce sympathetic activity. This reduces ADH and increases ANP which increases GFR and reduces RAAS. Overall there is a reduction in blood volume
• In the long term there is a lower blood volume as there is reduced stress on the heart. This causes the heart to reduce in muscle mass causing BP to drop.
• When returning to gravity severe postural hypotension can occur due to smaller blood volume and smaller heart . Hence baroreceptors reflex cannot compensate

Question 10

What does the body aim to do when exercising?

Answer 10

• Mechanisms increase blood supply to exercising muscle rather than other tissue
• It is integration of small changes that leads to a larger response to exercise

Question 11

What causes the changes in cardiovascular activity in the body during exercise?

Answer 11

• It is brought about by the central command in the brain in response to stimuli (e.g. anticipation of exercise)
• When exercise starts there is a feedback from muscles through mechanoreceptors and metaboreceptors
• These changes affect sympathetic activity and vagus inhibition

Question 12

What changes do we see in the CVS during exercise?

Answer 12

• Increase lung oxygen uptake: Oxygen is transported around the body to supply exercising muscles. To do this we require an increased HR and increased force of contraction
• Control of BP: By controlling BP we are able to increase cardiac output and protect the heart from excessive damage caused by increased BP (arising from increased HR)
• Co-ordinated dilation/constriction of vascular beds: Which allows us to selectively target areas to which oxygen is delivered

Question 13

How is oxygen uptake into the lungs increased during exercise?

Answer 13

• Increase in heart rate and stroke volume means blood is being pumped around the body at a faster rate causing the oxygen to get used up by respiring tissue more quickly
• Increase difference in arteriovenous oxygen difference. The bigger the difference in oxygen concentration in the arteries and veins the bigger the concentration gradient so faster diffusion.

Question 14

How does arterio-venous oxygen difference change with increasing intensity of exercise?

Answer 14

• During light exercise the arterio-venous oxygen difference is low
• As we go from light to moderate intensity this oxygen difference increases very steeply
• As we go from moderate to heavy the curve is now less steep but still continues to rise
• As we reach heavy exercise the curve starts to plateau

Question 15

How does cardiac output change with increasing intensities of exercise?

Answer 15

• During light exercise we have a very low cardiac output.
• While transitioning from light to medium intensity we see a small increase in cardiac output
• When going from medium to heavy there is a greater increase in cardiac output
• As we reach heavy exercise the cardiac output increases dramatically

Question 16

How does Stroke Volume change with increasing intensities of exercise?

Answer 16

• During light exercise we have a very low stroke volume
• While transitioning from light to medium intensity we see a large increase in stroke volume due to Starling’s law (increased stretching)
• When going from medium to heavy there is a smaller increase in stroke volume as there is a decreased cardiac output when we reach the elastic limit of Starling’s law
• As we reach heavy exercise the stroke volume starts to decrease

Question 17

How does Heart Rate change with increasing intensities of exercise?

Answer 17

• During light exercise we have a very low Heart Rate
• While transitioning from light to medium intensity we see a small increase in HR
• When going from medium to heavy there is a greater increase in HR
• As we reach heavy exercise the HR increases dramatically

Question 18

What is high heart rate called?

Answer 18

• Tachycardia

Question 19

How is tachycardia achieved?

Answer 19

• It is caused by the brain central command
• There is a decrease in the signal down the vagus nerve to the SA and AV nodes and an increase in sympathetic activity to the SA and AV nodes
• This causes the heart rate to increase (tachycardia)

Question 20

How is stroke volume increased?

Answer 20

• Increased end diastolic volume (filling pressure): Increased sympathetic activity and calf muscle pump causes venoconstriction which increases CVP (so Starling’s law increases preload)
• Faster ejection: as increased sympathetic activation of Beta-1 receptors causing inotropic Ca2+ to increase the speed of ejection
• Decreased end-systolic volume (increased ejection): Increased contractility by sympathetic activation of Beta-1 receptors and increases stretching

Question 21

Where does the additional cardiac output go when exercising?

Answer 21

• At the respiring muscle there is local resistance due to metabolic hyperaemia leading to vasodilation.
• There is also a Beta-2 mediated vasodilation through circulating adrenaline binding to Beta-2 receptors
• There is a high concentration of Beta-2 receptors in skeletal muscles and coronary arteries

Question 22

What are the effects of an increase in cardiac output during exercise?

Answer 22

• As we exercise we experience a large increase in CO as we go from light exercise to heavy exercise
• Although we experience areas of vasoconstriction and areas of vasodilation the overall total peripheral resistance decreases as we go from light to heavy exercise. This means blood pressure does not increase by too much
• There is also an increase in systolic and diastolic volumes to increase stroke volume and increase filling

Question 23

What is compensatory vasoconstriction?

Answer 23

• The vasoconstriction/blocking of blood supply to non essential (inactive/unrequired) parts of the body during exercise
• This prevents hypotension as exercise causes decreased TPR so prevents the BP from getting too high/low

Question 24

What are metaboreceptors?

Answer 24

• Small sensory fibres in skeletal muscle

- They are chemosensitive and so are stimulated by K+, H+ and lactate (which increase in exercising muscle)

Question 25

What reflex actions do metaboreceptors cause?

Answer 25

• Tachycardia due to increased sympathetic activity
• Increased blood pressure
• Pressor response to exercise

Question 26

Why are metaboreceptors important?

Answer 26

• During static exercises BP is raised more than in dynamic exercises
• Raised BP maintains blood flow to respiring muscles by forcing blood into these muscles
• Contracted muscles are supplied by dilated resistance vessels due to metabolism (called selective metabolic hyperaemia)