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Exercise physiology, Symp drives increases later in exercise
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Exercise physiology
Graphs and concepts diagrams in squid
- Frank starling law and curves
- Oxyhaemoglobin curve - Bohr and Haldane effect
- Respiratory responses to exercise
Oxyhaemoglobin curve: shows dissociation potential of oxygen - SO2 vs PO2R shift: decrease O2 affinity, release O2 to tissue
L shift: increase O2 affinity, prioritise O2 carriage
- increase in CO2, temperature, 2,3-DPG, [H+] ----> right shift
Haldane effect
Oxygenation of blood in lungs displaced CO2 from Hb, increasing CO2 removal
Oxygenated blood has reduced CO2 affinity
Bohr effect
Relationship between CO2/pH and O2 carriage
CO2 + H2O --> carbonic acid, decrease pH
Curve right shifts --> releases oxygen
Frank starling curves
Family of curves defined by afterload and inotropic state of the heart
Changes in venous return move the ventricle up or down along a single F-S curve; slope defined by preexisting conditions
Baroreflex is a homeostatic mechanism designed to maintain constant BPRapid -ve feedback loop following increased BP that causes HR to decreaseMechanoreceptors located in Bv close to the heart
- detect stretch on vascular walls
- Volume increase - increase stretch - fire
Change parasympathetic outflow to the heart and sympathetic mechanisms directed at the vasculature and heart
Orthostatic/postural hypotensionSudden drop in BP causes syncope
e.g. standing: blood volume directed to legs via gravity
- decrease BP, compromise venous return, lowers CO, lowering of arterial pressure
Respiratory role
- increased ventilation - drive to breath greater
- more oxygen taken in; more CO2 given off
Moderate exercise: blood gas conc = constant
paCO2 must be constant - relationship with blood pH
high paO2 allowing sufficient diffusion gradient from blood --> cell
Driving factor - reduced SvO2 increases activity of respiratory systemPulmonary ventilation = oxygen consumption and CO2 production --> during light, moderate exercise
More intense --> exponential rise
- VT main factor; exponential increase
- increase in resp rate; nonlinear; main contributor @ high intensity
Exponential respiratory rate increase causes PAO2 >100mmHg
- oxygenation of blood faster in alveolar capillaries
CC: Asthma
- chronic inflammation of bronchioles; histamine mediated vasoconstriction increasing resistance
- more work to increase O2 to necessary level; fatigue of resp muscles, breathlessness and tachycardia to compensate
- beta2 agonists dilate airways; relieve r
Cardiac role
- SV = CO x HR increase
- CO can be increased by filling of the ventricles
- Starling law: force of contraction is proportional to volume of blood ejected
Increase CO = major response @ exercise onset
- increase proportional to O2 consumption, max increase: 5-->20L/min
- if healthy, increases arises from tachycardia, not SV increase
- linear increase to 180-200bpm depending on severity of exercise
Elimination of parasymp vagal efferents to SAN and AVN initially drives tachycardia
- via M2 AChR
- HCN channels responsible for cardiac rhythm "funny current" via cAMP rise
EE: vagal inhibition postulated but only confirmed recently
- administer atropine(M-R blocker)
- attenuate initial increase in HR @ exercise
- CO not diminished by prior beta1 antagonists
--> minimal influence of sympathetic activity
Vasculature
- Bv dilation at important sites e.g. heart, lungs, musculature
- Bv constriction at non priority sites e.g. GI tract, kidney
- increase blood supply where needed
Peripheral vasodilation to maintain constant BP in response to increasing COFlow to Sk.m @ rest = 20% of CO; exercise = 80% of CO
- Vasodilator substances e.g. adenosine, K+
- release from Sk.m causes hyperaemia
- trigger relaxation of vascular Sm.m in terminal arterioles
- Vasodilation from increased sympathetic outflow and circulating adrenaline
- act on beta2 Sm.m R
- capillary recruitment 5x SA for gas exchange, 4x flow increase, 2x fall in SO2
- 40x increase in O2 delivery
Flow induced conduit artery dilation
- decrease in arteriole r, increase flow
- decrease shear stress
Renal and splanchnic vasoconstriction
- mediated via sympathetic NA induced alpha1 activation
- shift circulating volume into venous system
- enhance CVP; increase filling pressure
Pulmonary circulation flow
- increased via distension without increase in pulmonary pressure
- decreased SvO2
- 3 fold diffusion capacity
Nervous system
- increased sympathetic drive; increase HR and ventilation/respiration
- pupil dilation, sweating,
- detection of blood composition via peripheral and central chemoreceptors --> central only sensitive to CO2 conc
- peripheral sensitive to CO2, pH, O2,
-
Basic values @ rest 70kg male rest
- HR 60-100bpm
- CO 5L/min
- oxygen usage(VO2) 250ml/min
- VT 5-8L/min
Strenuous exercise
- VO2 x12 ~ 3000ml/min to meet demand
- VT x15 120L/min
- CO increases as SaO2 has limit CO x4
- SvO2 /3 reduction in SvO2 - high partial pressure gradient between capillary and respiring muscle cells
- raised CO2 - increase O2 dissociation and extraction - Bohr effect
Symp drives increases later in exercise
- nerves release NA, adrenal medulla releaes Adr
- protects from xs K+ in circulation: risks hyperkalemia, shortening of cardiac ap, risk of arthymias
- Adr V important in denervation
-
EE: Donald et al, 1968 - Propanolol effect on exercise
- Greyhounds treated has lower CO than control dogs
EE: Chronic cardiac denervated greyhounds
- tachycardia smaller extent and later onset
- beta blockage abolished tachycardia and exhaustion
- Clinical revealing: beta blocker avoided on heart transplant patient - lack autonomic innervation
SV esp. important for cardiac denervated patients
- ejection fraction increase to 80% by symp stimulation of contractility
- increase filling pressure via increased CVP(1mmHg @ moderate exercise)
- accordance to frank starling law
for sudden, maximal exercise rather than sustained
CVP increase via muscle pumping, esp. lower limbs and vasoconstriction