Effect of exercise on the heart Flashcards
Summarise the exercise reflex
Reflexive CVS changes in response to contracting skeletal muscle that increase BP
The 3 changes induced by the exercise reflex
Increased respiration (increased motor activity to diaphragm & intercostals)
Increased HR and contractility (increased CO)
Increased sympathetic activity (NA) to GIT, kidneys, skin, all skeletal muscle causing vasoconstriction
What triggers the exercise reflex
metabolites (K+, Pi, adenosine) stimulating metaboreceptors in exercising muscle (+ joint receptors in dynamic exercise)
Which part of the brain is the “exercise integrating area” stimulated on the exercise reflex
subthalamic locomotor region (SLR) in the hypothalamus
Exercise hyperaemia =
local vasodilation in vessels triggered by metabolites
functional sympatholysis =
sympathetic vasoconstriction in exercising muscle is overcome by local vasodilation (exercise hyperaemia)
Overall, what happens to TPR and ABP in static exercise
TPR increases
large increase in ABP
Overall, what happens to TPR and ABP in dynamic exercise
TPR changes little
small increase ABP
how is the vasoconstriction of skin, caused by the exercise reflex, overcome when body temperature increases?
by the thermoregulatory reflex - decreases sympathetic activity causing vasodilation
What metabolites are released from exercising muscles
K+
Pi and adenosine (from ATP hydrolysis)
The mechanical compression of vessels by contracting muscles causes a rhythmic increase in blood flow during dynamic exercise. What does this do to TPR?
overall decreases it
The mechanical compression of vessels by contracting muscles means blood flow may not increase during static exercise, hyperaemia occurs after contraction. What does this do to TPR?
TPR increases during contraction (so ABP does)
Which type of exercise is recommended for people with coronary artery disease and why
Dynamic exercise
Avoid static because it is a greater cardiovascular risk. High ABP during contraction–> aneurysm or stroke. Possibly low ABP after contraction –> postural hypotension
- greater cardiac work so greater coronary vasodilatation required
- O2 delivery to contracting muscle is limited, metabolites accumulate which enhances the exercise reflex causing pain (coronaries limited in how much O2 they can give the heart and an enhanced reflex means the SNS is asking the heart to work harder –>pain)
Characteristics of the alerting/defence response
More SNS/less PSNS activity to heart > higher CO
Increased respiration
Vasoconstriction to GIT, skin, kidneys
Vasodilatation of vessels in skeletal muscle via less SNS activity (less NA binding a1) and more circulating adrenline (binds B2)
Overall: higher ABP, higher HR, increased blood flow to muscle
Habituation
alerting/defence response gets smaller and smaller if the stimulus is repeated several times
Sensitisation
alerting/defence response gets bigger and bigger if the stimulus is repeated several times
What can trigger vasovagal syncope
after the alerting/defence response (occurs in extreme emotional stress)
after strenuous exercise (if you remain standing) or haemorrhage
(these all cause increased contractility of the ventricle on a low EDV - ventricular torsion)
What can trigger the alerting/defence response
emotional/environmental stress
new situations, sound, pain, emotion etc
The effects of vasovagal syncope which lead to fainting
reflexive increase in vagal activity to the heart to decrease HR, and decrease in sympathetic activity to vessels all over -> vasodilatation
ABP drops and faint when brain BP falls
CO at rest does not change with training. What is CO at rest approx?
5L/min-
Training releases growth factors which cause eccentric hypertrophy of the heart. What is the effect of this?
An increased EDV and so an increased SV and CVP
Training increases SV at rest but does not increase CO at rest - how is this?
(CO = SV x HR)
It decreases HR at rest (bradycardia)
How does training cause bradycardia (lower HR) at rest
increased tonic vagal activity
increased local Ach release
decreased pacemaker activity
causes decreased HR so decreased ABP
VO2 max is
the rate of maximum O2 uptake from the air and/or the rate of maximum O2 use by the mitochondria