Week 8 - Response to exercise

Question 1

What is a normal resting HR range for trained an untrained populations?
What affects resting HR?

Answer 1

60-80bpm for untrained and as low as 30-40bpm in trained.
Neural tone, temperature and altitude.

Question 2

What is the resting HR screening cut off?

Answer 2

90bpm.
If higher may be sleep deprived or fighting infection.

Question 3

What is the anticipatory rise response?

Answer 3

An increase in HR above resting just before the start of exercise as a result of decreased vagal tone.

Question 4

How does HR change during exercise?

Answer 4

It increases in direct proportion to exercise intensity.
Maximum HR is achieved in an all out effort - to be a max it should be highly reproducible and decline with age.

Question 5

What is steady state HR?

Answer 5

A point of plateau.
The optimal HR for meeting circulatory demands at a given submaximal intensity.
A plateau suggests it is steady state if submaximal, if no plateau not steady state.
If exercise intensity increases, so does steady state HR.
Adjustment to a new intensity takes 2-3 minutes.

Question 6

At what point does SV stop increasing during exercise?

Answer 6

40-60% VO2max.
Plateaus beyond this point until exhaustion.
This is not always the case - in elite endurance athletes SV can continue increasing upwards of 80% VO2max.

Question 7

By how much does SV increase in maximal exercise?

Answer 7

Roughly double standing SV - 2x SV at rest.

Only slightly different during maximal exercise than supine SV - laying down.
Supine EDV>standing EDV due to venous return and skeletal muscle pump. There is a lower volume of blood in the left and right ventricles after filling phase when standing.

Question 8

How does cardiac output change in elite and non-elite during exercise?

Answer 8

Increases due to increases in SV and HR.
Steeper increase in elite as they can increase their SV by a greater amount - increase does not plateau as in non-elite.

Question 9

What are the three factors that increase SV during exercise?

Answer 9

Preload
Contractility
Afterload

Question 10

How does preload affect SV?

Answer 10

Increases stretch –> increased end diastolic volume (volume of blood in ventricle before it contracts) –> increases contraction strength –> frank-Stirling mechanism.

Question 11

How does contractility affect SV?

Answer 11

Increased noradrenaline or adrenaline increases contractility. This is independent of EDV (increased ejection fraction instead - percentage of blood in the ventricle that leaves on contraction).

Question 12

How does afterload affect SV?

Answer 12

Afterload is the pressure the heart must work at to eject the blood.
It decreases due to reduced aortic resistance in trained and elite individuals. (Increases SV).

Question 13

How much of cardiac output is redirected to muscles during maximal intensity exercise?

Answer 13

80%

Question 14

What are the normal values of cardiac output?
Resting, untrained exercise and trained exercise.

Answer 14

5L
20L
40L

Question 15

What is the Fick equation?

Answer 15

VO2 (oxygen consumption) = Cardiac output x (a-v O2 differece)

Question 16

What does the Fick equation show oxygen consumption depends on?

Answer 16

Blood flow (Q) and O2 extraction - this is an adaptation in elite individuals.

Haemoglobin change shape when oxygen is removed – oxygen has a high affinity for haemoglobin but a higher affinity for myoglobin in the muscles. Hence elite trained athletes have more myoglobin to snatch the oxygen from the haemoglobin.

Question 17

How does blood pressure change during endurance exercise?

Answer 17

Mean arterial pressure increases (average of systolic and diastolic blood pressure).
Systolic blood pressure increases
Diastolic blood pressure slightly decreases (increases at max exercise). Main change is systolic blood pressure.

Question 18

What is the equation for mean arterial pressure?
How is it affected during exercise?

Answer 18

Cardiac output (Q) x total peripheral resistance (TPR)

Q increases
TPR decreases due to vasodilation.

Question 19

Blood flow redistribution

Answer 19

Blood flow is redistributed towards the active working muscles (greatest metabolic need).
Sympathetic vasoconstriction decreases blood flow away from less active regions (spanchnic circulation - liver, pancreas, GI and kidneys).

Question 20

Effect of vasodilation during exercise

Answer 20

Local vasodilation permits additional blood flow in exercising muscle - triggered by metabolic endothelial products e.g. lactate.
As temperature rises skin VD allows heat loss through the skin.

Question 21

What is cardiovascular drift?
What is it caused by?

Answer 21

HR continues to increase during exercise despite a decrease in SV, to maintain Q.
Associated with an increased core temperature and dehydration.
Mainly caused by a decrease in venous return.

Question 22

What can affect blood flow redistribution?

Answer 22

Temperature - may force blood towards to skin to reduce core temperature (moves away from the muscles).
Hence marathons are ran in the morning as lowest circadian temperature.

Question 23

How does ventilation change during exercise?

Answer 23

Immediate increase before muscle contractions - anticipatory response.
Second gradual increase in ventilation - driven by chemical changes in arterial blood (increased CO2 and H+ sensed by chemoreceptors)

increase is proportional to metabolic needs of muscle.
At low intensities only tidal volume increases but then rate as intensity increases.

Question 24

What is dyspnea?
What causes it?

Answer 24

Shortness of breath
Poor aerobic fitness, intensive training, unfamiliar workloads.
Inability to adjust to high blood PCO2 and H+.

Question 25

What is hyperventilation?
What causes it?

Answer 25

Rapid breathing - excess ventilation
Increases in PCO2 gradient between blood and alveoli.
Decreases in blood PCO2 - increases in blood pH.

Question 26

What is the ventilatory threshold?

Answer 26

The point where there is an exponential increase in ventilation
The point where L air breathed in > LO2 consumed - cannot process all the oxygen you are breathing in.

Question 27

What is the ventilatory equivalent for O2

Answer 27

V/VO2
L air breathed in/LO2 consumed/min.

How well control of breathing is matched to body’s demand for oxygen.

Question 28

IS ventilation usually a limiting factor to performance?

Answer 28

Not normally.
Respiratory muscles account for 10% of VO2, 15% of Q during heavy exercise.
They are very fatigue resistant, especially the diaphragm.
pectoralis minor and sternocleidomastoid less fatigue resistant.

Question 29

Physiological mechanisms to control pH

Answer 29

Chemical buffers: bicarbonate, phosphates, proteins, haemoglobin

Increased ventilation helps H+ bind to bicarbonate

Kidneys remove H+ from buffers and we excrete H+.

Question 30

How does active recovery (compared to passive recovery) facilitate pH recovery?

Answer 30

Active recovery maintains oxygen delivery quicker as blood pumping more so removes lactate quicker – blood lactate concentration decreases quicker.

Question 31

How does muscle fibre type change in elite?

Answer 31

Increased sixe and number of type 1 fibres (type II –> type II).
Type 2x perform like type 2a.

Question 32

How does capillary supply change in elite?

Answer 32

Increased capillarisation - key factor in increased VO2.

Question 33

How does myoglobin change in elite?

Answer 33

Increased myoglobin content by 75-80%.
Supports increased oxidative capacity in muscle - extracts oxygen from haemoglobin easier.

Question 34

How does mitochondrial function change in elite?

Answer 34

Increased size and number depending on training volume

Question 35

High vs low responders

Answer 35

VO2 max response to endurance training can be explained by roughly 30 gene RNA expressions in muscle - explains roughly 23% of gains in VO2 max.

Question 36

Non-responders

Answer 36

People who under a similar exercise programme don’t see improvements in VO2 max or fitness.
Only respond to a more potent training stimulus.