Cardiovascular response to exercise stress enables assessment of cardiovascular reserve. Helps to identify patients with compensated disease with normal resting hemodynamics

1. EXERCISE PHYSIOLOGY
Jayaprakash.K

2. Types of Stress
• Muscular exercise
• Pharmacological stress
• Pacing induced tachycardia

3. Exercise Physiology
• Anticipatory phase
• Hemodynamic changes during exercise
• Post-exercise period

4. Anticipatory changes
• Parasympathetic withdrawalHR
•  alveolar ventilation
• Sympathetic activityvenous return
• Resting CO increase.

5. Response to Exercise
• Heart rate response
• Stroke volume changes
• Systolic function
• Diastolic function.
• Systemic vascular resistance
• Pulmonary vascular resistance

6. Heart Rate Response
• Instant acceleration-due to vagal withdrawal
• Later increase-due to reflex activation of
pulmonary strech receptors(trigger
sympathetic tone & parasympathetic
withdrawal)
• circulating catecholamines.

7. Heart Rate Response(cont’d)
• HR rises rapidly to about 160-180/min
• Rates up to 240/min have been recorded
• HR contributes more to rise in CO than SV
• No further in SV once CO has reached
50% of its maximum- further  in CO by
rise in HR.

8. Stroke Volume Changes
Stroke volume increase by 3 mechanism:
• venous return cardiac filling 
Frank-Starling mechanism.
• Neurohormonal influence (catecholamines)
Positive inotropic effect SV.
• Treppe phenomenon-tachycardia exerts +ve
inotropic effect.

9. TREPPE/ BOWDITCH STAIRCASE PHENOMENON

10. Systemic Vascular Resistance
• Systolic arterial pressure & mean arterial
pressure  linearly in relation to O2
consumption during dynamic exercise.
• Despite rise in arterial pressure, SVR
decreases due to vasodilation in exercising
muscles.

11. Pulmonary Vascular Resistance
• Behaviour of pulmonary circulation differ-
• Mean PA pressure increase proportionate
with CO
• Only slight decrease in PVR

12. LV Systolic Function
Augmentation of LVsystolic function due to:
• Preload(venous return)
• Afterload- due to net fall in SVR
• Contractility- Catecholamines
- Treppe effect

13. LV Diastolic Function
• Diastolic function improves-mechanism:
-Beta adrenergic stimulation
-Progressive acceleration of IVRT.
• Normal subjects- no change or downward
shift in LVD pressure-volume relation.
• In ischemia/LVH, upward shift occur.

14. LV PRESSURE VOLUME LOOP

15. Net effect- CO
• CO by 4-6 fold above basal levels during
strenuous exercise-linear increase with
workload
• Depends on inotropic & chronotropic
reserve
• For each of 100ml/min/m2 of O2
consumption,there is in CO of
600ml/min/m2.

16. Post-exercise changes
• Abrupt in HR & CO- due to removal of
sympathetic drive and reactivation of vagal
axctivity
• SVR remains low for sometime due to
persistent vasodilation in muscles
• Arterial pressure falls often below pre-
exercise levels for up to 12hours of
recovery.

17. Factors Influencing
Hemodynamic Response
• Type of Exercise
• Position-Supine/Erect
• Age
• Drugs

18. TYPES OF EXERCISE

19. Dynamic(Isotonic) Exercise
• Contraction of large muscle groups
resulting in movement
• Primarily induces volume load to heart
• Peripheral vascular resistance falls
• O2 consumption during maximal exercise
(VO2 max) 12 fold in normal individuals
& 18f0ld in trained athletes

20. Dynamic(Isotonic) Exercise(cont’d)
This is met by
• 6fold rise in CO
• 3fold rise in O2 extraction
• Metabolic adaptation:switch from
utilization of FFA at rest to breakdown of
muscle glycogen stores and glucose by
hepatic gluconeogenesis

21. Isometric(Static) Exercise
• Constant contraction of smaller muscle groups
without movement
• Provokes more pressure load to heart
• Lower O2 requirements; VO2 maintained with
smaller  in CO
• Local vasodilation impeded by mechanical
compression of vessels by muscle contrn.To
maintain regional perfusion,pressor response is
evokedrise in BP

22. Isometric Exercise(cont’d)
• in BP without in venous return  SV
decrease
• HR must increase out of proportion to
metabolic needs of active muscle groups,to
maintain higher CO

23. Resistance Exercise
• Combination of isometric & isotonic
exercise
• CV response depends on the extent of
isotonic & isometric components.
• Prototype: weight lifting

24. Respiratory Quotient
• CHO metabolism release more CO2
• RQ= ratio of CO2 production to O2
consumption
• Resting: 0.7-0.8
• Rises to 1 during exercise

25. Exercise index
• EI=Measured CI/Predicted CI
• Normal CO response to exercise- >/=0.8
• Predicted CI=0.0059x + 2.99
(x- O2 consumption in ml/min/m2)

26. Exercise Factor
• in CO(ml/min) / in O2 consumption
(ml/min)
• Normal value- 6

27. Upright vs.Supine Exercise
• Contribution of HR & SV to CO differ
• EDV at rest maximum while supine
• While supine in CO mainly depends on
in HR
• In upright position-LVEDV & SV up to
50% of peak O2 consumption,then platau or
fall.(Frank Starling mechanism blunted by
effect of tachycardia)

28. Relation with Age
• Elderly subjects have d HR reserve and
contractility
• Increased dependence on Frank Starling
mechanism

29. Effect of Betablockers
• Decreased HR reserve
• But no impairment in maximal exercise
capacity(Maximal O2 consumption/CO
response)
• Compensation by:
-Widened AV O2 difference
- SV(due to LVEDV & afterload-BP)

30. Pacing Tachycardia
• Introduced by Sowton et al. in 1967 to
evaluate patients with CAD in cathlab.
• Lead positioned in RA
• Pacing initiated at 20bpm above baseline
rate with 20bpm  every 2 minutes
• End point: Angina,achievement of 85% of
MPHR

31. Hemodynamic Effects-Pacing
• MVO2 due in HR & Myocardial
contractility(Treppe effect)
• Reflex coronary vasodilation Myo
blood flow
• in SV
• No change in venous return,afterload or
circulating catecholamines
• No overall change in CO

32. Exercise vs.Pacing
Exercise Pacing
Preload  -
SV  
Afterload  -
Heart rate  
Contractility  
CO  -
Double product  

33. Pressure Volume Loop in Pacing-
Normal
• P-V relation at baseline,intermediate &
maximum pacing levels
• Progressive leftward & downward shift
• Increased contractility due to treppe effect
• Improved diastolic distensibility

34. Pressure Volume Loop in Pacing-Normal

35. Pressure Volume Loop in Pacing-
CAD
• Initial shift to left followed by rightward shift at
peak pacing
• Initial treppe effect,followed by systolic failure at
peak pacing with increase in ventricular volumes
& Rt shift of end systolic portion of curve.
• Progressive upward shift in the diastolic limb.
• Post pacing rise in LVEDP- most concrete
evidence of pacing induced ischaemia(beats 5-15
after stopping pacing, >5mmHg )

36. Pr.Volume Loop with Pacing in CAD

37. Conclusion
• Cardiovascular response to exercise stress
enables assessment of cardiovascular
reserve.
• Helps to identify patients with compensated
disease with normal resting hemodynamics.