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Ventilatory and Cardiovascular Dynamics

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 Vo2 max criteria CV function and training.

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Ventilatory and Cardiovascular Dynamics

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  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 • Vo2 max criteria • 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 ventilation with intensity-to vent threshold - non linear • Fig 13-1 rest 5 L/min - 190 L/min • ~1 at rest - inc 5-6 fold to max exercise • Ventilatory Equivalent VE/VO2 • rest 20 ; max 35

  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 13-2 - 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

  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 kidneys, viscera • vasoconstriction in spleen • maintain brain blood flow • inc coronary blood flow • inc muscle blood flow • Table 16-1 • CV response - depends on type and intensity of activity • dynamic - inc systolic BP; not Diastolic • strength - in syst and diastolic

  6. Oxygen Consumption • Determinants - 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

  7. Heart Rate • Most important factor • inc with intensity, levels off at VO2max range 70 - 200 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

  8. HR and Stroke volume • Rate Pressure Produce - RPP • HR X Systolic BP • estimate of cardiac load - O2 • Stroke Volume • Fig 16-2 - 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

  9. (a-v)O2 difference • Difference increases with intensity • fig 16-3 - rest 5.6 - 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

  10. 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

  11. Coronary blood flow • Large capacity for increase • (260-900ml/min) • due to metabolic regulation • flow occurs mainly during diastole • warm up - facilitates inc in coronary circulation • Limits of CV performance • VO2 max - long considered best measure of capacity of CV system and aerobic performance (fig 16-6) • VO2 max anaerobic hypothesis • = Q max * (a-v)O2 max • VO2 max indicated by point at which O2 consumption fails to rise despite an increased power output or intensity

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

  13. 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

  14. Protection of Heart and Muscle • Noakes (1998) • 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 • suggest peak treadmill velocity as predictor of aerobic performance • high cross bridge cycling and respiratory adaptations • Biochemical factors - mito volume, ox enzyme capacity

  15. Practical Aspects • Primary reg mech of Cardio Resp and neuromuscular systems facilitate intense exercise • until it perceives risk of ischemic injury • prevents muscle from over working • Programs and Techniques for fitness • muscle power output capacity • substrate utilization • thermoregulatory capacity • reduce work of breathing • above reduce load on heart - allows more intense exercise before protection instigated

  16. VO2 max and Performance • General population - VO2 max will predict performance in endurance • elite athletes - not as accurate • world records for marathon • male 69 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 • in general high VO2 max pre req for elite performance - 65-70 ml/kg/min • represents capacity to exercise at high intensity before system limits itself

  17. Changes in CV with Training • Tables 16-1,2 • 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

  18. CV Adaptations • O2 consumption • improvements depend on • 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

  19. CV Adaptations • Stroke volume - cont. • 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

  20. 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

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