Flashcards in Lecture 11 - Cardiovascular responses to exercise Deck (23)
What are the goals of the cardiovascular response to exercise?
Increase )2 supply to skeletal and cardiac muscle
Facilitate Co2 and heat removal
Maintain MAP - so you don't faint - heart is working against gravity to provide blood to brain. MAP is the driving force
VO2 = ___
CO x (CaO2 - CvO2)
CO x TPR
What are the main changes in distribution of CO and blood flow during exercise?
Consider the following areas of circulation
Splanchnic, Renal, Cerebral, Coronary, Muscle, Skin
Muscle receives alot more
Splanchnic bed (liver and gut) is markedly reduced, along with renal blood flow
cerebral blood flow is maintained (rest = maximal exercise)
Coronary - increased, but doesn't need that much (it's very effective)
Skin - increase with light and heavy exercise. but at maximal level drops right down
What is Hyperaemia?
Increase in muscle blood flow
What causes exercise hyperaemia?
metabolic vasodilators from contracting skeletal muscle, endothelium and/or RBC (When the oxygen is released, other factors are as well which cause vasodilation. Also desensitise vasculature to the symp nerves which normally cause vasodilation
Muscle pump - good for maintaining blood flow, key for venous return
"Conducted Vasodilation" - relates to factors in the muscle/capilliaries. Smooth muscle has signalling (through gap junctions) which signal proximal parts of the circulation, the arterioles, to dilate.
Functional sympatholysis - Symp. nerves in muscle vasocontrict so need to turn them off.
What are some of the vasodilator metabolites?
K+ (when muscles contract, they loose potassium), H+ , adenosine, ATP (comes from muscle + RBC)
NO, prostacyclin, Prostaglandin E2
Endothelial derived hyperpolarising factor
ATP released from RBC
Can you just inhibit one of these metabolites for vasodilation and see a reduction in blood flow?
No, there are many (usually a sign of an important physiological function)
would need to block 3/4 before you'll see effects
At a sub-maximal VO2 would you be able to tell the difference between a trained and untrained person based on CO
No, at lower levels they woul dhave the same CO (it's a linear relationship)
How does HR and Stroke volume differ in trained and untrained people?
At a given VO2 - The HR is much lower in the trained athlete, and hence the stroke volume is higher
This would need to be the case as the CO is the same for both, but achieved in different ways
What happens to BP during exercise and is it different between trained/untrained subjects?
not very different b/w trained/untrained
What are the determinants of Mean, systolic, diastolic pressure?
Systolic - When the BP is contracting so mainly influenced by CO
Diastolic is when the heart is relaxing - so is largely determined by peripheral resistance
generally MAP goes __ during exercise
Stroke volume decreases after long duration of exercise becaue...
the distolyic phase doesn't fill the ventricles as much
SO what are the cardiovascular responses to prolonged exericse?
HR rises consistently
TPR rises steadily
blood volume slowly decreases
Arterial blood pressure will drop a little bit
skin blood flow slows
Stroke volume decreaes
What casues the cardiovascular drift during prolonged exercise?
Increased HR and decreased SV
Hyperthermia - as you get hotter the SA node depolaises more rapidly
Increased plasma [adrenaline]
Peripheral displacement of blood volume due to cutaneous vasodilation - as you heat up, blood goes to skin
Where is there feedback in the neural controls of this?
baroreceptors, neurons in the muscle (type 3/4 afferents)
feeedback and say the central command is either appropriate or not
The Vagus nerve to the heart is...
inhibitory - parasympathetic
The rising HR is initially due to withdrawn signalling from the __ and then an increase in _____ activity
The rising HR is initially due to withdrawn signalling from the Vagus and then an increase in Sympathetic activity
Alot of what happens in aging is related to
What happens with cardiovascular adaptations when you train?
COmax goes up
Max HR doesn't cahnge
Stroke volume increases (big benefit)
Why is there an increase in Stroke volume on trained subjects?
Expanded blood volume (Frank-starling mechanism)
Increase heart size
Increase LV mass and chamber size
Increase adrenergic sensitivity