Exercise physiology

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

Respiratory role


  • increased ventilation - drive to breath greater
  • more oxygen taken in; more CO2 given off

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

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,

Moderate exercise: blood gas conc = constant


paCO2 must be constant - relationship with blood pH
high paO2 allowing sufficient diffusion gradient from blood --> cell

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

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

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


  1. ejection fraction increase to 80% by symp stimulation of contractility
  2. 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

Graphs and concepts diagrams in squid


  • Frank starling law and curves
  • Oxyhaemoglobin curve - Bohr and Haldane effect
  • Respiratory responses to exercise

Driving factor - reduced SvO2 increases activity of respiratory system


Pulmonary ventilation = oxygen consumption and CO2 production --> during light, moderate exercise
More intense --> exponential rise


  1. VT main factor; exponential increase
  2. 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

Peripheral vasodilation to maintain constant BP in response to increasing CO


Flow to Sk.m @ rest = 20% of CO; exercise = 80% of CO


  1. Vasodilator substances e.g. adenosine, K+
  • release from Sk.m causes hyperaemia
  • trigger relaxation of vascular Sm.m in terminal arterioles
  1. 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

Control of cardiovascular and respiratory responses

Musculature

  • more blood supplied
  • more active - increase in metabolic rate - O2 consumption increase; CO2 production and other waste products increase

Phase 1: Muscle R utilise Peripheral reflex


a. mechanoreceptors(type III/alpha-delta fibres)

  • generate instant tachycardia @ exercise onset via dorsal horn feedback
  • sensitise outflow from midbrain nuclei - inhibit vagus

b. chemoreceptors(type IV/C fibres)

  • sense accumulation of factors released from contracting muscle in 1-2mins
  • K+, lactic acid, ATP, arachidonic acid products, adenosine accumulate @ insufficient perfusion
  • feedback to brainstem via C unmyelinated fibres; increase symp outflow to heart(SAN/myocardium) and vessels

EE: Alam et al, 1937: Pressure cuff experiment


  • BP increase greater in those performing forearm exercises with pressure cuff than those without
  • persisted after exercise stopped until cuff released
  • trapped chemical metabolites unable to escape - increase sympathetic outflow

Phase 1: Central command


  • Brain regions that activate somatic motor overlap with CV and respiratory control areas of the medulla
  • mediate autonomic responses crucial for CV regulation

EE: Krogh et al, 1913: Response to leg cycling


  • within secs of exercise: HR and ventilation increased - too fast for chemical feedback
  • intial ventilation increases ~= to work expected

Recent advancements

  • imagining exercise triggers increased HR
  • central command exaggerated by asking for voluntary contract after partial NMJ block - increased CV response despite contraction equal/lower

Phase 3: Steady state


Fine tuning of steady state ventilation via peripheral sensory feedback


a. Peripheral chemoreceptors detect PaCO2 and PaO2 oscillations which increase in exercise due to increased O2 extraction


b. Baroreceptor reflex ensures feedforward mechanisms don't overshoot
-

Phase 2: Approaching steady state


  • modulation by central command and peripheral receptors
  • ventilation increase correlates with increased K+
  • peripheral chemoreceptors sense K+, lactate, Adr
  • peripheral R denervation = slowed phase 2
  • continuous activation of respiratory neurons in medulla --> short term potentiation; augments responsiveness to continuing stimuli

Interdependence as delivery is product of both with failure of one = inadequate tissue supply

Different:


Separate regulatory centres in brain
Function via different effector pathways

Same:


Central command has similar effect on both in phase I
Muscle and peripheral chemoreceptors both respond to inadequte ventilation

  • lack of O2 - inadequate perfusion causes acidemia and hyperkalemia - both sense
  • muscle cR stimulate CV system
  • peripheral cR stimulate respiratory system

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

Oxyhaemoglobin curve: shows dissociation potential of oxygen - SO2 vs PO2


R 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 BP


Rapid -ve feedback loop following increased BP that causes HR to decrease


Mechanoreceptors 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 hypotension


Sudden 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