PBL 6 - physiological response to exercise Flashcards
what is exercise?
any activity requiring physical effort — requires work my muscles — requires chemicals
what is metabolic rate?
amount of energy liberated per unit time
what happens to metabolic rate during exercise?
- may increase up to 20x basal metabolic rate
- ie. increased demand of fuel and O2 for muscles
what must be tightly regulated?
temp and pH — requires cardio respiratory response
what 3 things does exercise cause?
- increase in blood temp
- increase in O2 demand by skeletal muscles
- increase in metabolic rate
how do muscles respire at the onset of exercise?
anaerobically as oxygen demand is not met
when is a steady state reached during exercise?
once the CO supply has increased to supply necessary O2
what happens at the end of exercise?
ventilation decreases gradually until the O2 debt has been paid off
how is lactic acid removed?
by converting it to glycogen (80%) or by metabolising it to CO2 and water (20%)
what stimulates the removal of lactic acid and how long does it take?
stimulated by increase in protons in the blood and may take up to 90 minutes
what is EPOC?
excess post-exercise oxygen consumption
what is workload proportional to?
the energy produced which is proportional to the oxygen consumption
what must happen to ventilation to accommodate the increased workload?
ventilation must increase
what happens to tidal volume and resp frequency in low intensity exercise?
increase proportionally
what happens to tidal volume and resp frequency in high intensity exercise?
tidal volume plateaus and resp frequency increases to increase ventilation
what is tidal volume limited by?
physical size of the lungs and the strength of the accessory muscles of ventilation
roughly what is resting ventilation? (L/min)
about 5-6 L/min
what must Hb be in order to supply sufficient oxygen to muscles?
fully saturated
what happens to pulmonary capillaries in order to increase blood flow?
increased blood flow is achieved by the recruitment and distension of pulmonary capillaries especially in the upper parts of the lung which are usually less well perfused
why might there be a drop in pO2 in elite athletes at higher work rates?
due to diffusion limitation because the blood flow increases through the pulmonary capillaries so there is less time for diffusion to occur
why is the diffusing capacity higher in trained athletes?
because the physiological dead space is reduced
what does physiological dead space drop from and to?
about 33% to 15%
what is the effect of PO2 dropping in pulmonary capillaries and what does it drop from and to?
40mmHg —> 25mmHg so alveolar-capillary gradient increases
why does PO2 in pulmonary capillaries drop?
because O2 is used up during exercise
what provides resp centres with information about the perfusion status of the muscle?
- neural input from motor cortex
- afferent (proprioceptive) impulses from joints/muscles
why is there an exponential increase in ventilation > 60%?
- because at around 60% the anaerobic threshold has been reached, and lactic acid is starting to be produced
- therefore ventilation increase is triggered by the liberation of CO2 which results from the buffering of lactic acid
where are peripheral chemoreceptors found?
carotid bodies and aortic bodies
what do peripheral chemoreceptors do and result in?
- send info to the resp centre in the brain stem, which detects increases in CO2 (and reduction in O2)
- sympathetic innervation of the heart, lungs and arteries
- results in an increased HR/breathing/constriction of arteries — increase in O2 consumption of the blood
where does Hb give up O2 easily and why?
muscles have used up the O2 so the arterial O2 is much lower therefore Hb gives up some of its O2 easily
what happens to pH in exercising muscles? what is the effect on the saturation curve?
- CO2 and lactic acid are produced — reduced pH of the surrounding interstitial fluid
- shift of curve to RHS
- oxygen is given up more readily
- increased delivery to the muscles
what causes the curve to shift to the RHS?
- increases in temp
- 2,3-diphosphoglycerate
- CO2
- protons
where and when is 2,3-diphosphoglycerate (DPG) produced?
produced by RBCs in glycolysis
what happens to the dissociation curve in the lungs?
shifts to LHS as the blood temp is reduced compared to the muscles — Hb takes up O2 from the alveoli
LHS vs RHS of dissociation curve
LHS = tighter Hb-O2 bond
if curve moves to RHS, O2 is given up more easily
what 2 things reduce the affinity of Hb for O2?
- increase in CO2
- increase in DPG
how is anaerobic resp favoured at the onset of exercise?
increased sympathetic nervous system activity causes arterial vasoconstriction — reduced O2 delivery to the muscles — favours anaerobic resp
what does a reduction in ATP production lead to?
an accumulation of AMP — diffuses into interstitial space
what leads to arteriolar dilation?
increased CO2, reduction in pH and the subsequent increase in K+ ions diffusing from the cells
equation for resistance?
(length x viscosity of blood) / radius^4
how can a change in the radius affect blood flow?
a small change in the radius will dramatically increase the blood flow — increases blood supply to skeletal muscles
how does dilation of skeletal muscle arteries affect TPR?
causes a reduction in TPR
what is active hyperaemia?
blood moving towards an organ
describe active hyperaemia
- dilation of skeletal muscle arterioles leads to reduction in total peripheral resistance — reduces the mean arterial BP
- baroreceptors respond to reduced stretch in the walls of the carotid artery and send electrical impulses to the medulla oblongata — results in an increased cardiac output and BP
- arterial baroreceptors reflex is reset during exercise in order to maintain the necessary raised BP
- due to the direct effects of local metabolites causing arteriolar dilation, together with the effect of noradrenaline binding to beta-2 receptors on the smooth muscle of arterioles supplying skeletal muscles, the overall peripheral resistance drops and hence diastolic BP drops
- diastolic BP is also reduced due to the reduced filing time of the heart due to the increased HR
what stimulates an increase in CO?
adrenaline release and drop in diastolic BP
how can maximal HR be calculated?
- maximal exercise stress test — put on treadmill then run at increasing speed/inclines until the HR stops going up
- or estimated using Karvonen formula = 220-age
what happens to CO, SV and max HR in trained athletes?
CO is increased by the increased SV, and a maximum HR does not increase after aerobic training
what must happen for CO to increase?
increase blood volume retuning to the heart
how do you achieve an increased venous return?
vasoconstriction in veins
what is the effect of skeletal muscle pump?
leg muscles squeeze the blood back up to the heart when they contract so increase the movement of blood from the peripheral veins
what happens in the spleen to cause more blood to be returned to the heart?
vasoconstriction.
what is the effect of increasing the depth of inspiration during exercise?
causes a reduction in thoracic pressure, drawing blood back into the heart
how does skin blood flow change during exercise?
- initially reduces in order to increase the central BP
- but with increased continuous exercise the temp of the blood increases and therefore the skin blood flwo is increased to lower the temp
what does Starling’s law state?
states that the increase in venous return causes an increase in the load on muscle fibres — increases the stretch in the heart muscle — increases contractility
how does optimal overlap of actin and myosin change from rest compared to with an increased venous return?
- at rest, the EDV of the ventricle does to cause optimal overlap of actin and myosin
- as venous return increases, the ventricular wall is stretched more and comes to a point where there is more optimal degree of overlap between the actin and myosin
- less overlap is best
how does stretching of heart muscle cause a greater number of cross-bridges to form?
stretching of the muscle increases the affinity of troponin C for calcium — causes a grater number of cross-bridges to form
Ca binding to what regulates the contractile state of the cardiomyocyte?
cardiac troponin c
what 2 things account for the increased contractility of the heart during exercise?
- an increase in noradrenaline release from synaptic terminals
- increased stretching of the ventricular muscle
how does actin and myosin overlap change with cardiac muscle stretch? when does optimal degree of overlap occur?
as cardiac muscle stretches, degree of overlap between actin and myosin is reduced — the optimal degree of overlap producing greatest contractile force will therefore occur when there is less overlap between actin and myosin
what results in faster cross-bridge formation?
increase in sympathetic tone — NAdr increases [Ca++]
— more Ca++ inducing a rearrangement in the troponin-tropomyosin complex, exposing a myosin-binding site on actin resulting in cross-bridge formation and shortening of the sarcomere - contraction
where is there an increase in SV despite the reduced filling time?
because HR is increased
what type of LV hypertrophy does aerobic exercise result in?
eccentric LVH — strength of muscle increases, size of LV increases, volume increases
concentric vs eccentric LV hypertrophy
concentric - due to pressure overload, patients with HF, walls of ventricles are thicker and volume acc decreases
eccentric - strength of muscle increases, size of LV increase, volume increases
what is Fick’s equation and what does it state?
VO2 = Q(a-v)O2
states that O2 available to muscles increased by increasing CO or muscle’s ability to extract O2 from arterial blood
explain haemoconcentration
- increase in blood flow to muscle capillaries
- increase in hydrostatic pressure across capillary wall — more blood is squeezed out of capillaries into ICS surrounding muscles
- increase oncotic pressure across capillary wall — because metabolites leak out of the muscle into the ICS. helps drive fluid out of the muscle capillaries
- increased conc of RBCs — due to loss of fluid
what is the effect of increased haemoconcentration?
increases conc gradient of O2 from the capillaries to the muscles — speed up diffusion — makes muscles more efficient at extracting O2 from the capillaries
how does myocardium cope with demands of exercise?
- increase HR — compresses LV vasculature
- increased myocardial tension and increased contractile strength — increases O2 demand by a lot
- increase in O2 demand is balanced between the opening of more capillaries are increasing the blood flow to increase the O2 supply
- 5x increase in coronary blood flow
what factors contribute to the increased demand on the heart during exercise?
- the heart’s low capacity for anaerobic exercise
- compression the the LV vasculature
during exercise the coronary flow will increase in response to exercise. this is enabled by the fact that the heart has an increased density of capillaries compared to skeletal muscle
when is VO2 max reached?
when VO2 reminds at a steady state despite an increased workload
what happens to metabolism at the VO2 max?
the individual switches from completely aerobic to anaerobic metabolism and muscle fatigue occurs rapidly
VO2 max changes in athletes vs sedentary people
- little changes in atheletes
- can increase by <90% in sedentary people
what factors limit VO2 max?
- weak resp muscles
- reduced atm O2
- Hb
- CO - increases 20x
- muscle blood flow — limited in severe vascualr disease, increased with aerobic training
- mitochondrial capacity
peripheral vs central theory of VO2 max
peripheral - limited by oxidative enzymes in mitochondria
central - limited by the ability of the cardio respiratory system to release O2 from Hb
what are some adaptations in coronary micro vessels due to training?
- increased arteriolar density / diameter — increased blood flow to myocardium
- increased recruitment of capillaries
what may increased arteriolar density be proportional to?
degree of hypertrophy
what is the effect of shear stress/hypoxia on blood vessels?
NOS = nitric oxide synthase
what does shear stress vary with?
strength of HB, elasticity of arterial walls, blood velocity, age, health and fitness of an individual
what does nitric oxide do to cause vasodilation?
- diffuses into smooth muscle cells
- causes a reduction in IC Ca++
- local relaxation of vascular smooth muscle
how can exposure to shear stress/hypoxia result in angiogenesis?
we get a release of GFs such as metalloproteinases
what are the benefits of aerobic exercise training on the CV system?
- increased efficiency of O2 utilisation by the heart (ie. increased SV but decreased HR)
- decreased peripheral resistance — decreased BP — easier for LV to pump blood so therefore improves the SV
- reduced body fat — less strain on heart
- increased resistance to fatigue (extra energy)
- increased RBC count in some cases — increase a lot of RBC to carry O2
- decelerates arteriosclerosis by preventing degeneration of elastin
what factor affecting VO2 max is most likely to have the largest genetic influence?
mitochondrial capacity
evidence suggests some individuals have more oxidative enzymes in their mitochondria than others, enabling more efficient utilisation of delivered O2
what is the UK physical activity target?
- be active daily: > 150 mins/week
- > 30 mins moderate intensity exercise on >_ 5 days/week OR 75 mins/week vigorous activity
- muscle-strengthening activity on >_ 2 days/week
- balance activity on >_ 2 days/week
- minimise extended sedentary periods
physical activity after MI?
should be physically active for 20-30 mins/day to point of breathlessness or increase activity gradually to increase exercise capacity
