CVS responses to acute exercise 2

Question 1

Exercise affects afterload

Answer 1

With exercise/alteration in ventilation: generated by persistent muscle contraction
→ ↑ed arterial compression and subsequent arterial pressure
↑ed intra-thoracic P. & intra-abdominal P. (e.g. Valsalva type manoeuvre)

Compensatory increase in cardiac contractility to maintain CO just to keep enough to keep us functioning
Particularly evident during resistance exercise
As a result adaptations happen to those who exercise like this long term in terms of their heart
Usually higher in males via greater muscle mass

Question 2

What is afterload

Answer 2

Workload that the heart works against
Circulatory resistance to ejection

Question 3

Valsalva Manoeuvre:

Answer 3

Forced expiration against a closed glottis (e.g. during straining)
Valsalva manoeuvre causes a large increase in HR (tachycardia) during the manoeuvre and a decrease in HR (bradycardia) followingthe manoeuvre.

Question 4

Steps of VM:

Answer 4

1. Take a deep breath and pinch your nostrils closed with your friends
2. Close your mouth
3. Blow air out of your nose to regulate the air pressure

Question 5

VM causes:

Answer 5

Increases intrathoracic pressure;
Fall in blood pressure initially and increase in BP at the end of manoeuvre.
Involves the baroreceptor reflex - must maintain MAP at all times

Question 6

VA is forced expiration against a closed glottis or closed airways which increases intrathoracic (intrapleural) pressure - phase 1:

Answer 6

Normally when muscle contracts and the muscle shortens and does the movement but the diaphragm is differnet it is dome shaped when relaxed it is shirter when releaxed and it expands and flattens to icnrease cavity size and pressure decreases when it contracts and when you breathe out it goes back to originial so pressure increases in small space

=>Increased intrathoracic pressure compresses pulmonary vessels impedes venous return
Compression of the aorta also increases aortic pressure
=> Physically compresses blood vessels
=> Resistance has increased and pressure is increasing
=> Spike in systolic pressure

see diagram page 4

Question 7

Phase 2 of VA:

Answer 7

Due to decreased cardiac output, and blood pressure falls, quite quickly over like 10 seconds – reflex tachycardia

Question 8

Upon pressure release phase 3+4 occur explain them:

Answer 8

Phase 3-> Reduction in intrathoracic pressure initially reduces compression on the aorta reducing mean aortic pressure – reflex tachycardia, increase HR
Phase IV -> Increased venous return, increased cardiac output, and HR decreases.

Question 9

Note heart rate changes are caused by:

Answer 9

Activation of baroreceptor reflexes to restore
normal mean aortic pressure

Question 10

Can use VA clinically to determine autonomic nervous system

Question 11

Exercise affects contractility - in addition to Preload & Afterload effects

Answer 11

Dependent on intra-cellular Ca2+ via Calcium Induced Calcium Release
Greater availability of Ca2+ → ↑ ed contractile strength
Impacts on the Frank-Starling mechanism
↑ed contractile strength at same preload

Question 12

Exercise affects contractility and generally increases via?

Answer 12

Generally increased during exercise via:
1. Sympathetic stimulation
2. Circulating catecholamines

Question 13

Summary effects of exercise on contractility

Answer 13

Harder to measure

Contractile state of myocardium
2 ends of spectrum: really fit athlete with higher ventriculAr performance right down to heart failure with lower EDV

Circulating catecholamines
Ionotropic agents can speed up or speed done - figitalis or other agents
pharmacological depressants - slow down heart muscle
Intrinsic mechanisms
Loss of myocardium - after stroke, dead tissue etc
Intrinsic depression
Sympathetic and parasympathetic nerve impulses
Hypoxia Hypercapnia Acidosis
Force of contraction and frequency of contraction
Speed of contraction changes

Question 14

SLIDE 8 - Summary of Cardiac Performance

Answer 14

Cardiac Performance - how much blood can we get out of the heart
Main determinants:
CO - HR+SV
SV- Preload, after-load, contractility and heart rate

HR: Symapthetic+parasympathetic impulses
Catecholamines, Chronotropic drugs

Contractility: Loss of myocardium, Iontropic drugs, pharmacological depressants, force-frequency relation, sympathetic and parasympathetic impulses, Ca^+2 ATPase activity, circulating catecholamines

Afterload: symp+parasymp impulses
Static muscle contraction
Anatomical impedance
Intrathoracic pressure

Preload: CO, Posture, Venous tone, Blood volume, priming by atria, muscle pump, intrathoracic pressure

=> Hardening of arteries with age no matter what

Question 15

Limits to maximal O2 uptake
Ventilatory limits to exercise:

Answer 15

Generally accepted that respiration does not limit VO2max
Exercising VE approaches 65-70% VEmax still have 30% in us at the end
Extra ventilation available if required
VE increases disproportionately to VO2: minute ventilation is VE

Question 16

DIAGRAM TABLE 10 - Changes in Respiratory function during exercise:

Answer 16

We improve O2 capabilities with training

Question 17

Lung blood volume

Answer 17

Blood volume 450ml (approx 9% total blood volume)
70ml in capillaries
Blood can shift from one circulation to another
e.g. in systemic haemorrhage blood shifts from pulmonary as an attempt to compensate
Volume of systemic circulation is 9 times that of pulmonary: shifts affect
pulmonary to a greater extent than systemic

Question 18

Pulmonary artertioles

Answer 18

In systemic circulation, arterioles dilate as PO2
decreases and constrict as PO2
increases.
The opposite occurs in pulmonary circulation
i.e. arterioles dilate as alveolar PO2
increases and constrict as alveolar PO2 decreases.
This aids in ventilation perfusion matching
Opposite is what happens in pulmonary
The only reason the PO2 changes is due to exception of pulmonary veins into right atria - capillaries this is the opposite is what we mean, due to the series of blood through these circulations

Question 19

Pulmonary diffusion capacity

Answer 19

Oxygen diffusing capacity: a measure of the rate at which oxygen can diffuse from the pulmonary alveoli into the blood - at the level of the capillaries
Expressed as mlO2 that will diffuse/min for each mmHg difference between PalvO2 and PO2 in pulmonary blood

Non-athlete at rest: 23ml/min
Non-athlete at max exercise: 48ml/min

Why this difference? Greater pulmonary perfusion therefore greater surface area for diffusion

Elite rower at max exercise: 80ml/min

Why? Training? Naturally large diffusing capacity influences selection of sport?
Following training the increase in diffusion capacity is greater than the increase in ability to deliver blood (i.e CO)

Suggests that the heart (more specifically HR) is the major limit to exercise capacity