1. 1 Ventilation and Cardiovascular Dynamics Brooks Ch 13 and 16

2. 2 Cardio-Respiratory responses to exercise VO 2 max –Anaerobic hypothesis –Noakes protection hypothesis Limits of Cardio-Respiratory performance Is Ventilation a limiting factor in VO 2 max or aerobic performance? Cardio-respiratory adaptations to training Outline

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4. 4 Increase Respiratory Rate and Depth Increase blood flow to active areas decrease blood flow to less critical areas Principle CV responses –Inc Cardiac Output - Q = 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 Cardio-Respiratory Responses to Exercise

5. 5 Cardio-Respiratory System Rest vs Maximal Exercise Table 16.1 (untrained vs trained) Rest Max Ex UTTUT T HR(bpm) 70 63 185 182 SV(ml/beat) 72 80 90 105 (a-v)O 2 (vol%) 5.6 5.6 16.2 16.5 Q(L/min) 5 5 16.6 19.1 VO 2 ml/kg/min 3.73.7 35.8 42 SBP(mmHg) 120114 200 200 Vent(L/min) 10.2 10.3 129 145 Ms BF(A) ml/min 600 555 13760 16220 CorBFml/min 260250 900 940

6. 6 Cardiovascular Determinants –rate of O 2 transport –amount of O 2 extracted –O 2 carrying capacity of blood VO 2 = Q * (a-v)O 2 Exercise of increasing intensity Oxygen Consumption

7. 7 Ventilatory Response Fig 12-15 - linear increase in ventilation with intensity to about 50-65% VO 2 max - then non linear With training, ventilatory inflection point shifts to right (delay)

8. 8 Exercise of increasing intensity Fig 16-2,3,4 –Q and (a-v)O 2 increases equally important at low intensities –high intensity HR more important –(a-v)O 2 - depends on capacity of mitochondria to use O 2 - rate of diffusion - blood flow O 2 carrying capacity - influenced by Hb content Oxygen Consumption

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10. 10 Most important factor in responding to acute demand inc with intensity due to Sympathetic stimulation and withdrawal of Parasympathetic –estimated Max HR 220-age (+/- 12) –influenced by anxiety, dehydration, temperature, altitude, digestion Steady state - leveling off of heart rate to match oxygen requirement of exercise (+/- 5bpm) –Takes longer as intensity of exercise increases, may not occur at very high intensities Cardiovascular drift - heart rate increases steadily during prolonged exercise due to decreased stroke volume Heart Rate

11. 11 HR response : –Is higher with upper body - at same power requirement Due to : smaller muscle mass, increased intra-thoracic pressure, less effective muscle pump –Is lower in strength training Inc with ms mass used Inc with percentage of MVC (maximum voluntary contraction) estimate the workload on heart, myocardial oxygen consumption, with Rate Pressure Produce - RPP –HR X Systolic BP Heart Rate

12. 12 Stroke Volume - volume of blood per heart beat –Rest - 70 - 80 ml –Max - 80-175 ml Fig 16-2 - increases with intensity to ~ 25-50% max - levels off –inc EDV (end diastolic volume) –high HR may dec ventricular filling –athletes have high Q due to high SV supine exercise - –SV does not increase - starts high SV has major impact on Q when comparing athletes with sedentary –~ same max HR - double the SV and Q for athletes Stroke volume

13. 13 Difference between arterial and venous oxygen content across a capillary bed –(ml O 2 /dl blood -units of %volume also used) (dl = 100ml) Difference increases with intensity –fig 16-4 - rest 5.6 - max 16 (vol %) (ml/100ml) –always some oxygenated blood returning to heart - non active tissue –(a-v) O 2 can approach 100% extraction of in maximally working muscle 20 vol % (a-v)O 2 difference

14. 14 Blood Pressure fig 16-5 –BP = Q * peripheral resistance (TPR) –dec TPR with exercise to 1/3 resting –Q rises from 5 to 25 L/min –systolic BP goes up steadily –MAP - mean arterial pressure 1/3 (systolic-diastolic) + diastolic –diastolic relatively constant Rise of diastolic over 110 mmHg - associated with CAD Blood Pressure

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16. 16 With exercise - blood is redistributed from inactive to active tissue beds - priority for brain and heart maintained –sympathetic stimulation increases with intensity –Causes general vasoconstriction –brain and heart are spared vasoconstriction –Active hyperemia - directs blood to working muscle - adenosine, Nitric oxide - vasodilators Cardiovascular Triage

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19. 19 maintenance of BP priority –Near maximum, working ms vasculature can be constricted –protective mechanism to maintain flow to heart and CNS –May limit exercise intensity so max Q can be achieved without resorting to anaerobic metabolism in the heart Eg - easier breathing - inc flow to working ms –harder breathing - dec flow to working ms Eg - one leg exercise - muscle blood flow is high –Two leg exercise - muscle blood flow is lower To maintain BP, vasoconstriction overrides the local chemical signals in the active muscle for vasodilation Cardiovascular Triage

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21. 21 Eg. Altitude study fig 16-6 - observe a reduction in maximum HR and Q with altitude even though we know a higher value is possible - illustrates protection is in effect Cardiovascular Triage

22. 22 Large capacity for increase –(260-900ml/min) –due to metabolic regulation –flow occurs mainly during diastole –Increase is proportional to Q warm up - facilitates increase in coronary circulation Coronary blood flow

23. 23 Maximal rate at which individual can consume oxygen - ml/kg/min or L/min long thought to be best measure of CV capacity and endurance performance –Fig 16-7 VO 2 max

24. 24 Criteria for identifying if actual VO 2 max has been reached –Exercise uses minimum 50% of ms mass –Results are independent of motivation or skill –Assessed under standard conditions –Perceived exhaustion (RPE) –R of at least 1.1 –Blood lactate of 8mM (rest ~.5mM) –Peak HR near predicted max VO 2 max

25. 25 Traditional Anaerobic hypothesis for VO 2 max –After max point - anaerobic metabolism is needed to continue exercise - plateau (fig 16-7) –max Q and anaerobic metabolism will limit VO 2 max –this determines fitness and performance Tim Noakes,Phd - South Africa (1998) –Protection hypothesis for VO 2 max –CV regulation and muscle recruitment are regulated by neural and chemical control mechanisms –prevent damage to heart, CNS and muscle –regulate force and power output and controlling tissue blood flow –Still very controversial - not accepted by most scholars What limits VO 2 max ?

26. 26 Q dependant upon and determined by coronary blood flow –Max Q implies cardiac fatigue - ischemia -? Angina pectoris? –this does not occur in most subjects Blood transfusion and O 2 breathing –inc performance - many says this indicates Q limitation –But still no plateau –was it a Q limitation? altitude - observe decrease in Q (fig 16-6) –Yet we know it has greater capacity –This is indicative of a protective mechanism Inconsistencies in Anaerobic hypothesis

27. 27 regulatory mechanisms of Cardio Respiratory 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 / performance by; –muscle power output capacity –substrate utilization –thermoregulatory capacity –reducing work of breathing These changes will reduce load on heart –And allow more intense exercise before protection is instigated CV system will also develop with training Practical Aspects of Noakes Hypothesis

28. 28 Endurance performance - ability to perform in endurance events (10km, marathon, triathlon) General population - VO 2 max will predict endurance performance - due to large range in values elite - ability of VO 2 to predict performance is not as accurate - athletes all have values of 65-70 + ml/kg/min –world record holders for marathon –male 69 ml/kg/min female 73 ml/kg/min - VO 2 max –male ~15 min faster with similar VO 2 max Observe separation of concepts of VO 2 max / performance –Lower VO 2 max for cycling compared to running –Running performance can improve without an increase in VO 2 max –Inc VO 2 max through running does not improve swimming performance VO 2 max versus Endurance Performance

29. 29 other factors that impact endurance performance –Maximal sustained speed (peak treadmill velocity) –ability to continue at high % of maximal capacity –lactate clearance capacity –performance economy –Thermoregulatory capacity –high cross bridge cycling rate –muscle respiratory adaptations mitochondrial volume, oxidative enzyme capacity VO 2 max versus Endurance Performance

30. 30 Relationship between Max O 2 consumption and upper limit for aerobic metabolism is important 1. VO 2 max limited by O 2 transport Q and Arterial content of O 2 2. Endurance performance limited by Respiratory capacity of muscle (mitochondria and enzyme content) Evidence –anemic blood replaced with healthy blood containing red blood cells –immediately raises Hb - and restores VO 2 max to 90% of pre anemic levels –running endurance was not improved VO 2 max versus Endurance Performance

31. 31 Davies - CH 6 - Correlation's –VO 2 and Endurance Capacity.74 –Muscle Respiratory capacity and Running endurance.92 –Training results in 100% increase in muscle mitochondria and 100 % inc in running endurance –Only 15% increase in VO 2 max –VO 2 changes more persistent with detraining than respiratory capacity of muscle –Again illustrating independence of VO 2 max and endurance VO 2 max versus Endurance Performance

32. 32 Second Davies study - iron deficiency Fig 33-10 restoration of dietary iron –hematocrit and VO 2 max responded rapidly and in parallel –muscle mitochondria and running endurance - improved more slowly, and in parallel VO 2 max versus Endurance Performance

33. 33 Ventilation (VE) does not limit sea level aerobic performance –capacity to increase ventilation is greater than that to inc Q Ventilation perfusion Ratio - VE/Q –VE rest 5 L/min - exercise 190 L/min Fig 13-2 Q rest 5L/min - ex 25 L/min VO 2 /Q ratio ~.2 at rest and max –VE/Q ratio ~1 at rest - inc 5-6 fold to max exercise –Capacity to inc VE much greater Is Ventilation a limiting Factor to performance?

34. 34 Ventilatory Equivalent VE/VO 2 –Fig 12-15 - linear increase in vent with intensity to ventilatory threshold - then non linear VE rest 5 L/min - exercise 190 L/min VO 2.25 L/min - exercise 5 L/min –VE/ VO 2 : rest 20 (5/.25) ; max 35(190/5) Ventilation as a limiting Factor to performance?

35. 35 MVV - maximum voluntary ventilatory capacity 1. VE max often less than MVV 2. PAO 2 (alveolar) and PaO 2 (arterial) –Fig 11-4, 12-12 –maintain PAO 2 - or rises –PaO 2 also well maintained Ventilation as a limiting Factor to performance?

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37. 37 3. Alveolar surface area - is very large 4. Fatigue of Vent musculature –MVV tests - reduce rate at end of test –repeat trials - shows decreased performance –Yes, fatigue is possible in these muscles - is it relevant - NO –VE does not reach MVV during exercise, so fatigue less likely –Further, athletes post exhaustive exercise can still raise VE to MVV, illustrating reserve capacity for ventilation Ventilation as a limiting Factor to performance?

38. 38 Fig 13-3 - observe decline in PaO 2 with maximal exercise in some elite athletes Elite Athletes

39. 39 may see ventilatory response blunted, even with decrease in PaO 2 –may be due to economy –extremely high pulmonary flow, inc cost of breathing, any extra O 2 used to maintain this cost –? Rise in PAO 2 - was pulmonary vent a limitation, or is it diffusion due to very high Q ? Altitude –experienced climbers - breathe more - maintain Pa O 2 when climbing –Elite - may be more susceptible to impairments at altitude Elite Athletes

40. 40 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 heart mass adaptation is specific to form –swimming improves swimming Interval training - repeated short to medium duration bouts –improve speed and CV functioning –combine with over-distance training Changes in CV with Training

41. 41 Cardiovascular Adaptations with Endurance Training Table 16.2 Rest Submax Ex Max Ex (absolute) HR   0 SV    (a-v)O 2 0    Q 0  0   VO 2 0 0  SBP 0  0  0 CorBFlow    Ms Bflow(A)  0  0  BloodVol  HeartVol  0 = no change

42. 42 O 2 consumption improvements depend on –prior fitness, type of training, age –can inc VO 2 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 CV Adaptations

43. 43 Stroke volume - cont. –EDV inc with training - due to inc left vent vol and compliance, inc blood vol, –Myocardial contractility increased Better release and reuptake of calcium at Sarcoplasmic Reticulum Shift in isoform of myosin ATPase –increased ejection fraction (a-v)O 2 difference –inc slightly with training due to ; –right shift of Hb saturation curve –mitochondrial adaptation –Hb and Mb [ ] –muscle capillary density CV Adaptations

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47. 47 Blood pressure - decreased resting and submax BP Blood flow –training - dec coronary blood flow rest and submax (slight) inc SV and dec HR - dec O 2 demand –inc coronary flow at max –no inc in myocardial vascularity inc in muscle vascularity - –dec peripheral resistance - inc Q –dec muscle blood flow at sub max –inc extraction - more blood for skin... –10 % inc in muscle flow at max no change in skin blood flow - though adaptation to exercise in heat does occur CV Adaptations