Cardiovascular and respiratory responses to exercise Flashcards
types of exercise
- dynamic or isometric
- aerobic or anearobic
- large muscle mass or small muscle mass
what could everyday tasks be classified as for patients with cardiorespiratory diseases
high-intensity or maximal exercises
VO2
oxygen consumed
VCO2
carbon dioxide produced
how is VO2 and VCO2 determined in exercise
amount of muscle activity
blood flow & ventilation are coupled to metaboliism
what determines method of ATP maintenance?
- metabolic status
- energy requirements
what happens to VO2 during exercise
increases
who will have greatest VO2max
highly trained atheletes
- endurance
tidal volume during exercise
- increases as minute ventilation increases
- increases linearly up to 6 times resting value
- will level off at ~50% vital capacity
what maintains gaseous exchange at all times
residual lung volume
why is there always residual lung volume
to allow for gas exchange
what is residual lung volume
air in the lungs
how are elevated pulmonary ventilations achieved
- linearly increases in tidal volume
- non-linear increases in breathing rate
when does ventilation response to exercise
synchronous with exercise onset
- not a reflex response to altered chemistry
- not feedback mechanism
humoral changes during exercise
- adrenaline released from adrenal medulla
- induces vasoconstriction at viscera
- vasodilation at skeletal muscle
- increases heart rate
- bronchodilator
- glycogenolysis in liver
what happens to K during exercise
K from depolarised muscle cells can increase to levels considered dangerous if muscles were at rest
PaCO2 and PaO2 during exercise
change very little if at all.
- PaO2 may rise a little due to decreased PaCO2 or fall due to limitation in diffusion
- PaCO2 will fall a little at high VO2 as pH increases
One of the most important observations in ventilatory response to exercise
expected rise in PACO2 does not occur with rise in metabolism during exercise
PACO2
partial pressure of alveolar gas
Alveolar are close to arterial blood sample so good measure
PACO2
PaCO2
PACO2 partial pressure alveolar gas
PaCO2 partial pressure arterial gas
4 hypotheses for regulation of respiratory responses to exercise
- central command or feedforward must account for at least fast component of response
- afferent signals from muscles passing up spinal chord my produce feedback control - dog experiments support this but paraplegics don’t
- signals from peripheral chemoreceptors detecting pH changes play some role. Even though PACO2 remains constant, slight oscillations may be detected, or changes in sensitivity. But their removal only mildly alters phase 2
- lactate, potassium and adrenaline all stimulate peripheral chemoreceptors and may play a role
respiratory responses work in
parallel
- if one signal is removed, the others will work to compensate and keep respiration rate constant
change in blood flow during exercise
changes from spending 0.8 seconds in pulmonary capillary at rest to only 0.2 seconds during exercise
- less time to load oxygen
- large reserve usually sufficient to complete oxygenation
changes in cardiac output
cardiocentric
from 5l/min at rest up to 30l/min in intense exercise
cardiac output =
cardiocentric
heart rate x stroke volume
changes in heart rate during exercise
HR often rises with one beat during transition from rest to work = before feedback could do so
- provides evidence for central command or feedforward
- increases rapidly in first 10-20 secs then slowly increase
what provides evidence for feedforward or central command of response to exercise
HR increases within one beat of onset, which is too quick for feedback mechanism
frank-starling’s mechanism showing cardiac output matched to demand
- heart automatically pumps all venous return back to arteries
- dog’s exercise performance was not impaired by cardiac denervation
cardiac output =
tissuecentric
(arterial BP - central venous BP)/ total peripheral resistance
- arterial BP ~90mmHg
- central venous BP ~3mmHg
TPR can be changed to alter CO without changing BP
changes in cardiac output
tissuecentric
total peripheral resistance is altered to change flow/CO without changing BP
precapillary sphincters
- functional unit of the capillary bed with precapillary branching off directly from the arteriole
- important for directing blood to tissue that need it most and reducing blood flow to inactive tissues
- needed ‘cus limited blood
muscle vasodilation during exercise
- resting muscle has a low blood flow and only a few capillaries open at a time
- exercise causes more capillaries to open, higher blood velocity & double the fall in oxygen saturation
- muscle oxygen consumption can increase more than 40 times
- capillary recruitment also reduces diffusion distance
blood flow in resting muscle
- resting muscle has a low blood flow and only a few capillaries open at a time
what changes blood flow in muscle during exerise
vasodilation
changes to muscle capillairies in exercise
- capillary recruitment
- more capillaries open
- higher blood velocity
- double fall in oxygen saturation
= muscle oxygen consumption increase more than 40 times
muscle oxygen consumption during exercise
can increase more than 40 times
blood flow redistribution during exercise
CO increases with exercise intensity and blood flow is redistributed
- skeletal muscle large proportion
- skin blood flow increases for thermoregulation
changes in blood flow to skin during exercise
rest: 9% 500ml
light exercise 16% 1500ml
heavy exercise: 12% 1900ml
changes in blood flow to skeletal muscle during exercise
rest: 21% 1200ml
light exercise 47% 4500ml
heavy exercise: 71% 12500ml
what exercise types changes BP most
heavy resistance magnifies change in BP more compared to dynamic aerobic
changes in BP and HR in isometric exercise
- hand grip at 30% maximal voluntary contraction
- modest HR increase
- large BP increase
changes in BP and HR in dynamic exercise
- large HR increase to maximal values
- little change in BP
CV control during exercise
controlled by autonomic nerve supply :
- parasympathetic
- sympathetic
- adrenaline
autonomic nerve supply to the heart =
- parasympathetic
- sympathetic
- adrenaline
parasympathetic control of heart during exercise
via vagus nerves, which act via muscarinic acetylcholine receptors
- mainly produce bradycardia
helps to slow the increased HR
sympathetic control of heart during exercise
- via the superior, middle and inferior nerves via beta 1 adrenoreceptors
- produce tachycardia and increased contractility
- releases neurotransmitter noradrenaline
control of circulating adrenaline on heart during exercise
- circulating adrenaline from medulla
- also act of beta 1 adrenoreceptors
- tachycardia and increase contractility
what do afferent signals do to heart during exercise
strong evidence they play a part in feedback control of HR and BP
K+ and H+ are probably sense in the muscle
what does evidence suggests may also play a role in controlling BP and HR
afferent signals from muscle involved in feedback control, most likely from sensing K+ and H+ in muscle
tachycardia
abnormally rapid heart rate
bradycardia
abnormally slow heart rate
summary of CV responses to exercise
- peripheral circulation determines venous return by controlling the perfusion of each tissue
- the heart matches cardiac output to venous return
- blood pressure response depends on the kind, duration and intensity of exercise
- there is evidence for central command, feedforward & humeral mechanisms that are all integrated to regulate responses
variations of VMAX
- generally lower in women than men
- tends to increase up to the of 20
- slowly declines after 20 yrs
- maintaining active lifestyle can delay decrease
- results vary by testing method
- often greater in load bearing exercises
what can VMAX indicate
long-term energy system capacity
method of VMAX measurement
increments exercise test to exhaustion
e.g on a treadmill
method of testing should be tailored to indivual requirement. e.g running for a runner, cycling for a cyclist
what is H+ from exercise buffered by
bicarbonate
glycolysis during exercise causes increases in
lactate and H+
how is H+ buffered
H+ + HCO3 -> H2CO3 -> CO2 + H2O
- needs presence of carbonic anhydrase
when does minute ventilation increase disproportionately to VO2
ventilatory threshold
When lactate and H+ begin to increase and buffered by bicarbonate and CA
what does the ventilatory threshold predict
lactate threshold, from the ventilatory response during incremental exercise
what happens to majority of lactate at lower outputs
pyruvate dehydrogenase and shuttle system enzymes metabolise the majority
what happens lactate at higher power outputs
- ATP demands exceed aerobic provisions
- glycolytic flux must increase
- therefore lactate production is increased
- lactate is increased at greater rate than it can be metabolised
- lactate accumulates in venous blood
= lactate threshold
what is considered a high power output
> 60% VO2max
lactate threshold
when lactate is produced at a greater rate than shuttle system enzymes and pyruvate dehydrogenase can metabolise it. Occurs at high power exercise, when glycolysis used for energy bc ATP provisions are insufficent
what limits exercise
- CV performance is the usual limit not CR
- ventilatory flows are usually lower than highest attainable value
- partial pressure of oxygen; even though muscle mitochondria can work at as low as 0.15kpa, there must be a diffusion gradient from blood to cell
- VMAX corresponds with HR
example VT
3.04L/min
example LT
43.5 ml/kg/min
Effects of training on CR response
- increase total lung capacity to more than 8l e.g endurance divers, wind musicians
- increase VO2max to more than 85ml/kg/min
- decrease resting HR to less than 40bpm
- increase stroke volume from bigger heart, trained muscle!!
how does diffusing capacity for oxygen at rest change with training
doesnt
max stroke volume changes with training
ml
normal: 104
training: 120
olympians: 167
max CO changes with training
ml
normal: 30
training: 23
olympian: 30
VMAX changes with training
l/min
normal: 3
training: 4.2
olympian 5.4
