1. Ventilatory and Cardiovascular Dynamics
Brooks Ch 13 and 16
OUTLINE
Ventilation as limiting factor in aerobic performance
Cardiovascular responses to exercise
Limits of CV performance
anaerobic hypothesis
protection of heart and muscle
CV function and training

2. Ventilation as a limiting Factor to performance
Ventilation not thought to limit aerobic performance at sea level
capacity to inc ventilation with ex
relatively greater than that to inc CO
Ventilation perfusion Ratio - VE/CO
Fig 12-14
linear increase in vent with intensity to vent threshold - then non linear
VE rest 5 L/min - exercise 190 L/min
Fig 13-1
CO rest 5L/min - ex 25 L/min
VE/CO ratio
~1 at rest - inc 5-6 fold to max exercise
Capacity to inc VE much greater
Ventilatory Equivalent VE/VO2
rest 20 (5/.25) ; max 35(190/5)

3. VE max vs. MVV MVV - max voluntary ventilatory capacity
max VE often less than MVV
PAO2(alveolar) and PaO2(arterial)
Fig 11-3 , 12-11
maintain PAO2 - or rises
PaO2 also well maintained
Alveolar surface area - massive
Fatigue of Vent musculature
MVV tests - reduce rate at end of test
repeat trials - decreased performance
fatigue yes - is it relevant -NO
VE does not reach MVV
athletes post ex can raise VE to MVV

4. Elite Athletes
Fig observe decline in PaO2 with maximal exercise in some elite
may see vent response blunted, even with dec in PaO2
may be due to economy
extremely high pulmonary flow, inc cost of breathing, any extra O2 used to maintain this cost
? Rise in PAO2 - was pulmonary vent a limitation, or is it diffusion due to very high CO ?
Altitude
experienced climbers - breathe more - maintain Pa O2 when climbing
Elite - may be more susceptible to impairments at altitude

5. CV Responses to Exercise
Increase flow to active areas
decrease flow to less critical areas
Principle responses
Inc CO - HR, SV
Inc Skin blood flow
dec flow to viscera and liver
vasoconstriction in spleen
maintain brain blood flow
inc coronary blood flow
inc muscle blood flow
Table Rest vs acute exercise
CV response - depends on type and intensity of activity
dynamic - inc systolic BP; not Diastolic
Volume load
strength - in syst and diastolic
Pressure load

6. Cardiovascular System Rest vs Maximal Exercise Table 16
Cardiovascular System Rest vs Maximal Exercise Table (untrained vs trained)
Rest Max Ex
UT T UT T
HR(bpm)
SV (ml/beat)
(a-v)O2(vol%)
CO(L/min)
VO2 ml/kg/min
SBP(mmHg)
Vent(L/min)
Ms BF(A)ml/min
CorBFml/min

7. Oxygen Consumption Determinants VO2 = Q * (a-v)O2
rate of O2 transport
O2 carrying capacity of blood
amount of O2 extracted
VO2 = Q * (a-v)O2
Exercise of increasing intensity
Fig 16-1,2,3
CO and (a-v)O2 increases equally important at low intensities
high intensity HR more important
(a-v)O2 - depends on capacity of mito to use O2 - rate of diffusion-blood flow
O2 carrying capacity - Hb content

8. Heart Rate Most important factor
inc with intensity, levels off at VO2max range bpm
increase due to withdrawal of Psymp and symp stimulation
estimated Max HR 220-age (+/- 12)
influenced by anxiety, dehydration, temp, altitude, digestion
Less HR response with strength exer
increases with muscle mass used
higher with upper body - at same power
inc MAP, peripheral resistance, intrathoracic pressure
less effective muscle pump - venous return

9. HR and Stroke volume Rate Pressure Produce - RPP
HR X Systolic BP
estimate of cardiac load - O2
Stroke Volume
Fig increase with intensity to 25-50% max - levels off
inc EDV (end diastolic volume)
high HR may dec ventricular filling
athletes high Co due to high SV
supine exercise -
SV does not increase - starts high
SV has major impact on CO
same max HR - double the SV and CO

10. (a-v)O2 difference Difference increases with intensity
fig rest max 16
always some oxygenated blood returning to heart - non active tissue
(a-v)O2 can approach 100% in maximally working muscle
Blood Pressure fig 16-4
= CO * peripheral resistance (TPR)
dec TPR with exercise to 1/3 resting
CO rises 5-20 L/min
systolic BP goes up steadily
MAP - mean arterial pressure
1/3 (systolic-diastolic) + diastolic
diastolic relatively constant
rise - associated with CAD
Over 110 mmHg

11. Cardiovascular Triage
With exercise - blood redistributed from inactive to active tissue
brain and heart spared vasoconstriction
symp stim inc with intensity
maintenance of BP priority
working ms can be constricted
protective mechanism - maintain flow to heart and CNS
limits exercise intensity - max CO can be achieved with out resorting to anaerobic metabolism
Eg - easier breathing - inc flow to ms
harder breathing - dec flow to ms
Eg. Altitude study fig 16-5

12. Coronary blood flow Large capacity for increase
( ml/min)
due to metabolic regulation
flow occurs mainly during diastole
warm up - facilitates inc in coronary circulation

13. CV Performance Limitation
VO2max - long thought to be best measure of CV and endurance capacity
Fig 16-6
VO2 max - maximum capacity for aerobic ATP synthesis
Endurance performance - ability to perform in endurance events
Anaerobic hypothesis
After max point - anaerobic metabolism needed to continue exercise - plateau
max CO and anaerobic metabolism will limit VO2 max
this determine fitness and performance
Tim Noakes - South Africa
re-analyzed data from classic studies
most subjects did not show plateau bringing anaerobic hypothesis into question

14. Inconsistencies with Anaerobic hypothesis
CO dependant upon and determined by coronary blood flow
Max CO implies cardiac fatigue - coronary ischemia -? Angina pectoris?
Blood transfusion and O2 breathing
inc performance - still no plateau
was it a CO limitation?
Blood doping studies
VO2 max improved for longer time period than performance measures
altitude - observe decrease in CO
indicative of protective mechanism

15. VO2 max and Performance
General population - VO2 max will predict endurance performance
high VO2 max for elite performance ml/kg/min
elite - ability of VO2 to predict performance is not as accurate
world records for marathon
male 69ml/kg/min female 73 ml/kg/min
male 15 min faster
other factors in addition to VO2 max
speed
ability to continue at high % of capacity
lactate clearance capacity
performance economy

16. Capacity vs Performance
Local muscle factors more closely related to fatigue than CO limitation
Table 6-3 correlations between ox capacity, VO2 and endurance
Lower VO2 max for cycling compared to running
Running performance can improve without an inc in VO2 max
Inc VO2 max through running does not improve swimming performance
CO depends on coronary blood flow
Max CO implies cardiac fatigue, coronary ischemia and angina pectoris
This does not occur in healthy individuals

17. Protection of Heart and Muscle
Noakes (1998) alternative to anaerobic hypothesis
CV regulation and muscle recruitment are regulated by neural and chemical control mechanisms
prevent damage to heart, CNS and muscle
by regulating force and power output and controlling tissue blood flow
Research suggests peak treadmill velocity as a good predictor of aerobic performance
high cross bridge cycling and respiratory adaptations
Biochemical factors - mito volume, ox enzyme capacity are also good predictors of performance

18. Practical Aspects of Noakes Hypothesis
Primary reg mech of Cardio Resp and neuromuscular systems facilitate intense exercise
until it perceives risk of ischemic injury
Then prevents muscle from over working and potentially damaging these tissues
Therefore, improve fitness by;
muscle power output capacity
substrate utilization
thermoregulatory capacity
reduce work of breathing
These changes will reduce load on heart
allowing more intense exercise before protection instigated
CV system will also develop with training

19. Changes in CV with Training
Tables 16-1,2 - training impacts
Heart - inc ability to pump blood-SV - inc end diastolic volume-EDV
Endurance training
small inc in ventricular mass
triggered by volume load
resistance training
pressure load - larger inc in mass
adaptation is specific to form
swimming improves swimming
Interval training - repeated bouts of short to medium duration
improve speed and CV functioning
combine with overdistance training

20. Cardiovascular Adaptations with Endurance Training Table 16.2
Rest Submax Ex Max Ex
(absolute)
HR   0
SV   
(a-v)O2 0   
CO 0  0  
VO 
SBP 0 0 0
CorBFlow   
Ms Bflow(A) 0 0 
BloodVol 
HeartVol 
0 = no change

21. CV Adaptations O2 consumption improvements depend on Heart Rate
prior fitness, type of training, age
can inc VO2 max ~20%
Performance can improve > than 20%
Heart Rate
training - dec resting and submax HR
inc Psymp tone to SA node
Max HR - dec ~3 bpm with training
progressive overload for continued adaptation
Stroke volume - 20% inc - rest, sub and max with training
slower heart rate - inc filling time
inc volume - inc contractility - SV

22. CV Adaptations Stroke volume - cont. (a-v)O2 difference
EDV also inc with training - inc left vent vol and compliance, blood vol,
Myocardial contractility increased
release and tx of calcium from SR
isoform of myosin ATPase
inc ejection fraction
(a-v)O2 difference
inc slightly with training
right shift of Hb saturation curve
mitochondrial adaptation
Hb and Mb [ ]
muscle capillary density

23. CV Adaptations Blood pressure - dec resting and submax Blood flow
training - dec coronary blood flow rest and submax (slight)
inc SV and dec HR - dec O2 demand
inc coronary flow at max
no inc in myocardial vascularity
inc in muscle vascularity -
dec peripheral resistance - inc CO
dec musc blood flow at sub max
inc extraction - more blood for skin...
Max - 10 % inc in musc flow
no change in skin blood flow