WK 5+6: Cardiovascular responses to exercise Flashcards
What factors need to be controlled within Homeostasis
- Temperature
- Mean arterial blood pressure
- PCO2
- Glucose
- PO2
- pH
What is the aim of the cardiovascular system
- Get blood where its needed quickly
- maximise availability
- maintain homeostasis
What is meant by graded response
- getting the blood to where it is needed as close to the tissues that need it as quickly as possible
- the graded response is linear as exercise intensity increases
- the initial response is anticipatory as it takes place before exercise starts
What sets the limit to the cardiovascular response
- volume of blood
- cardiac output
- number of blood vessels
- ability to redistribute the flow
what is meant by central drive and where does it come from
Central drive causes the anticipatory rise in HR…
Central drive comes from your motor cortex, and is directly linked through to the medulla - your cardiorespiratory control centre
At the medulla you get a withdrawal of parasympathetic outflow and stimulation of the sympathetic outflow
- this causes the anticipatory rise in HR
what does the vagus nerve do
it starts off in the medulla and causes slowing of the heart - a parasympathetic response
what does the sympathetic nerve do
chains down the ganglia and branches off to the heart taking the epinephrine to the SA node to control the beating of the heart
It also controls the secretion of adrenaline from the medulla
what is the difference between the exercise response of a normal HR and the HR response after a heart transplant
after a heart transplant…
The anticipatory rise has gone, the response is flatter because the vagal tone isn’t actually there anymore so you have to wait for adrenaline.
The cardiac nerves have been blunted so there are no nerve interactions with your heart so the response is more gradual and is paced by circulatory factors
Cardiac output values at rest and during exercise
At rest = 3.4/4 litres per minute
During exercise = 25-30 L.min
Describe the cardiac response (supply to demand)
- Non-linear response, get an elevation in SV triggered by gastronomic action on the cardiac muscle itself
- This provides an elevation of calcium current going into each cell of the heart and causes contraction
- More current = stronger contraction
- Also phosphorylation occurring of troponin within the cardiac muscle
- this allows the heart to relax a bit faster
- deeper breaths enhance cardiac return
- … increased pressure in the thorax to hope draw blood back to the heart faster
- contractibility increases causing stimulation of the heart and the atria contracts stronger to preload the ventricles with more blood
Your blood is saturated with oxygen at what level of VO2max
40-50% VO2 max
What causes an increase in HR in the cardiac response
Recruitment of motor cortex and stimulation of the medulla
& the additional component of adrenaline
VO2 max is set by…
Maximal cardiac output = the amount of oxygen you can get to the tissues
arterial - venous = how much of it they can actually use
what is Ficks law/equation
VO2 = Q x (CaO2 - CvO2)
You can determine VO2 by sampling venous and arterial blood so you know what the difference in O2 is
What are the local control factors that determine where oxygenated blood goes to…
- increasing local adenosine
- falling local pH
- elevated local K
- elevated local CO2
- decreased local O2
- increased NO
what are local control factors competing with
Local control factors stimulate dilation, they are in competition with the sympathetic nerve which is secreting adrenaline that activates receptors on the blood vessels causing constriction
what are the adaptions to exercise training on sympathetic vasoconstriction in skeletal muscle
Those who are heavily trained can dilate more so so reduce blood flow further, this is due to:
- more blood vessels and so bigger response
- their blood vessels may be more responsive to sympathetic tone and so improve re-direction
what is NOS and where is is found
- NOS (nitric oxide synthase) is a vasodilator and is secreted during stress
- NOS is commonly found in blood vessel walls, as the endothelium of the walls secretes nitric oxide
What is the process of nNOS signalling
Ca+ release causing contraction can also use the release in NO which causes smooth muscle to relax and therefore vessels to dilate
- Ca+ activates GTP and so protein kinase G is activated which causes the dilation
what is meant by single vs multi limb exercise capacity
VO2 max of one legged exercise is 75-80% of two legged exercise
Higher blood flow can be achieved to the active muscle in one legged exercise
This is because if both legs were dilated to the same extent as during one legged exercise then blood pressure would fall to a level where the individual would lose consciousness as the brain wouldn’t get enough oxygen
What percentage of blood flow goes to skeletal muscles during rest and exercise
at rest 15-20% of blood flow = skeletal muscle
During exercise = 80-85%
what happens to systolic and diastolic BP during exercise
Systolic BP rises to optimise perfusion of the tissue as you need to get more cardiac output out
Diastolic BP should remain the same as it represents the BP in-between the heart beats - you want the difference between the two to increase
Why does systolic BP increase
The baroreceptor thats wrapped around the carotid body stretches with increased blood pressure
This sends signals back to the brain
The rise in BP during exercise is sensitive to what signals
- baroreceptors
- thermosensitive receptors
- mechxnosensitive receptors
- chemosensitive receptors
What is the exercise presser reflex
the change in response to the baroreceptor during exercise, this occurs by…
- changing the set point of the receptor
- where you regulate BP
- changes how sensitive you are to changes in BP
what happens to HR and BP control during exercise
You don’t change the sensitivity of the response - you change the set point
This is set in the medulla for BP
During exercise, you move to a greater range
But you do hit limits
How do you increase venous return
Increasing blood volume:
- contract spleen
- constrict splanchnic supply
- constrict capacitance veins
Increase return:
- contract veins
- constrict supply to other tissues
What is the role of the muscle pump
- The muscles squeeze the veins and therefore cause increased return
- The valves allow movement of blood in one direction but not the other
- Activity increases venous return
- If valves fail it can cause pooling in the veins (varicose veins)
What is the role of the thoracic pump
Negative pressure in the thorax increases venous return
Instigated with deeper/faster breathing of exercise
During high-load exercise with breath-holding the opposite applies
- this is ‘valsalva manoeuvre’ which also increases the after load and can lead to fainting
What is the relationship with cardiac output and training
Cardiac output increases in both trained and untrained individuals with exercise but trained have a higher peak cardiac output
The pattern is the same for O2 uptake at a given work rate suggesting efficiency is the same but trained athletes have a larger capacity
the untrained athlete plateaus earlier than the trained athlete mean they can work at a higher work rate with a higher cardiac output
what is the relationship between HR and training
Trained = lower resting HR
Linear response between HR and work rate until you reach max HR (same max for both trained and untrained)
The trained person HR is more gradual, meaning at any given work rate they have a lower HR and so can work at higher work rates for longer before max
Training and HR normal values
Untrained max HR ~ 200 bmp
After 4 months endurance training ~ 199 bro
Top endurance athlete ~ 190 bpm
what is the effect of upper vs lower body exercise
larger muscle mass involvement improves venous return and stroke volume during leg exercise
Larger muscle mass involvement and consequent vasodilation means pressure doesn’t rise the same
Thoracic pressure diminishes respiratory pump effect listing venous return
What are the differences between cardiac muscle in trained and untrained athletes
trained have a higher muscle mass - functional mass
posterior wall thickness is larger but you wouldn’t want it higher than 13mm or it can’t contract well
as there is extra muscle and good contractibility you can eject a greater volume
what are signals for change of in cardiac muscle
- cellular load (stretch, tension and calcium)
- growth hormone
- IGF (insulin-like growth factor)
- adrenaline / nor-adrenaline
- angiotensin II
- endothelin
what is the role of plasma growth hormone with exercise
with exercise there is a large change in the % of plasma growth hormone.
an increase in plasma growth factor stimulates insulin like growth receptors
Role of IGF (insulin like growth factors)
Insulin like growth factors act on many cells including cardiac cells.
IGF is often anchored to proteins like distrophine.
Coupled with adrenergic activation - transcription factors
Role of angiotensin
Angiotensin receptors are often found in the heart and lungs.
In the heart angiotensin II can be produced very locally.
The receptors on the heart (angiotensin) can cause fibrosis and remodelling.
It also leads to MEF-2 that causes transcription of new proteins.
why can new proteins be made as a result of angiotensin.
Example of a protein…
The receptors on the heart (angiotensin) lead to MEF-2 that causes transcription of new proteins.
New proteins = myosin - more of the proteins associated with myofibrils can be stuck on the end or in parallel with existing proteins
You can also make more ribosomes - higher capacity to make proteins as transcription occurs at a faster rate.
Ca+ can cause growth of the heart cells
What is physiological hypertrophy
responding to transient stressors
What is pathological hypertrophy
responding to stress - can cause fibrosis and scaring - heart not as efficient
what is normal hypertrophy
normal hypertrophy = desired
- wall stress is proportional to pressure and radius
- even balance between size and thickness
what is concentric hypertrophy
intense weight and aerobic training, large pressure stress
what happens during hypertrophy
at 5% elongation of cardiac myocytes, wall increase volume = 16%
Cells also add sarcomeres in parallel and series - sarcomere length remains constant
- needs to be kept at its peak so contractibility doesn’t become weaker (starling mechanism)
how and why do you want to increase plasma volume
why:
you want to increase plasma volume so you dilate more blood vessels without reducing venous return
How:
as you engage in exercise you get renin activation which is released by the kidneys due to a drop in BP, or because of adrenergic input e.g. adrenaline.
Renin increase triggers angiotensin II - this is a diuretic
You overall get an increased plasma volume
What is blood plasmas response to exercise
plasma volume can increase by 20% - this means blood plasma increases.
A 200-300 ml volume expansion can increase VO2 max by ~4%
Hematocrit is unchanged
what sets the lower resting HR in trained athletes
Vagal tone
- the vagal tone is switched off during exercise
- They also have reduced response to sympathetic tone which may cause the reduced minimum HR
what process can accelerate the time to contract the heart
troponin phosphorylation
what is a benefit of a lower HR
longer to fill
what is the frank starling relationship
- sarcomere length is the same therefore same length tension relationship
- higher pressure in the ventricle = you stretch the myofilaments and elevate the length tension relationship and get more contractibility
how can you eject more blood from the heart
- pack more blood in
- have a bigger heart
- contract harder
- reduce the load its working against
what is peripheral resistance
the resistance against which the heart must work
what increases peripheral resistance
isometric muscle contraction
what are the effects of training on peripheral resistance
with training, vascular responsiveness improves and sympathetic tone withdrawal is improved
how can you improve the exchange of oxygenated blood to the muscle
- increase area for diffusion
- shorten distances
- increase time available
- make more capillaries
what is the effect of shear stress on the capillary wall
- causes release of NO
- this causes dilation and therefore less stress
- it also increases the release of VEGF
what is VEGF
VEGF increases in release as a result of shear stress on the capillary wall
- it causes capillaries to split so you get growth and branching of capillaries
what is the effect of a vasodilation dose in a trained athlete
there can up to 3x the amount of blood flow
meaning they can get a greater delivery of O2
effect of training on capillaries
there is an increase in capillaries with training meaning the distance between the capillary and mitochondria is less
There is greater SA for diffusion
what are the consequences of the training adaptions on capillaries
- muscle can use cardiac output more efficiently
- muscle therefore demands less blood flow at sub-max exercise
- peak blood flow and cardiac output is enhanced
- during sub-max exercise cardiac output can however be the same
what are the advantages of increased cardiac output
- improved lactate removal and lactate threshold
- improved exercise tolerance/resistance to fatigue
- sustained gluconeogenesis
- improved heat tolerance
