1 Ventilatory and Cardiovascular Dynamics »Brooks Chapts 13 and 16 Outline Ventilation as limiting factor in aerobic performance Cardiovascular responses to exercise Limits of CV performance VO 2 max criteria CV function and training

2 Ventilation as a Limiting Factor in Aerobic Performance at Sea Level (Chapt 13) Ventilation not thought to limit aerobic performance at sea level.  capacity to  ventilation (35x) with exercise is greater than the capacity to  Cardiac Output (6x)  considerable ventilatory reserve exists to oxygenate blood passing through the lungs

3 Ventilation Perfusion Ratio - V E /CO L inear  in ventilation with  in exercise intensity.  As exercise intensity reaches maximal levels there can be a non-linear increase in ventilation.  Ventilation at rest ~ 5 L/min  Maximal levels ~ 190 L/min (35x)  Linear  in cardiac output with  in exercise intensity.  Cardiac Output at rest ~ 5 L/min  Maximal levels ~ 30 L/min (6x)  Pulmonary minute ventilation (V E ) to Cardiac Output is ~1 at rest and  fold during maximal exercise.  One reason why pulmonary ventilation is not thought to limit aerobic performance.

4 Ventilatory Equivalent V E /VO 2  VO 2 at rest 0.25 L/min, V E /VO 2 = 20  VO 2 max ~ 5 L/min, V E /VO 2 = 35  the ability to  ventilation is greater than the ability to expand oxidative metabolism  V E max vs. MVV during exercise  MVV- maximum voluntary ventilatory capacity  the maximum V E during exercise is less than the MVV  another reason why pulmonary ventilation is not thought to limit aerobic performance

5 P AO 2 (alveolar) and PaO 2 (arterial)  O 2 moves from areas of high conc to areas of low conc  during exercise maintain or  PAO 2  PaO 2 in blood is also well maintained Alveolar surface area is massive (50m 2 ).  only 200ml of blood (4%) is in the pulmonary system during maximal exercise Fatigue of ventilatory muscules.  the diaphragm and ventilatory muscles can fatigue  during MVV test fatigue at end of the test  repeat trials - decreased performance  fatigue yes - is it relevant -NO (ultra endurance)  athletes post ex can raise VE to MVV

6 Pulmonary Limits in Elite Athletes Fig 13-2: decline in PaO 2 with maximal exercise in some elite athletes (individual variability)  may be due to compliance in the ventilatory system  may be due to economy (energy cost of breathing)  athletes may learn to tolerate hypoxemia to  energy cost of breathing during maximal exercise Altitude –experienced climbers breathe more and maintain PaO2 when climbing at altitude

7 Cardiovascular Dynamics During Exercise Brooks, Chapt 16 O 2 to the working muscles  with exercise intensity Principal Cardiovascular Responses to Exercise Increased cardiac output   HR (60 to 200bpm)   SV (80 to 200ml/beat)   O 2 and substrate delivery to muscle  remove CO 2 and metabolites  skin blood flow  regulate temperature

8  blood flow to the kidneys –maintain blood volume  blood flow to viscera –reduced gastrointestinal activity vasoconstriction in the spleen –  blood volume maintain blood flow to the brain  blood flow to coronary arteries of the heart  blood flow to working skeletal muscle

9 Cardiovascular regulation is directed toward maintaining blood pressure. During exercise CV regulation balances the need for more blood to the active tissue with the need to maintain BP and blood flow to the brain and heart. Although maximum CO may limit O 2 transport capacity, maximal exercise may be terminated by the threat of ischemia to the heart (Noakes).

10 Table 16-1: Cardiovascular changes with endurance training. Rest Submax Ex Max Ex HR   NC SV    CONC NC  O 2 up-   SBP   NC TPRNCNC 

11 CV response depends on type and intensity of activity.  dynamic ex: large  in HR, CO, SBP (not diastolic)  volume load on the heart  strength ex: large  in SBP and DBP, mod  in HR, CO  pressure load on the heart

12 Oxygen Consumption Oxygen consumption is proportional to exercise intensity. Determinants:  rate of O 2 transport  O 2 carrying capacity of blood  amount of O 2 extracted VO 2 = [HR x SV] x (a-v)O 2

13 Heart Rate HR accounts for 75% of O 2 uptake at maximal exercise (most important factor)  with intensity, levels off at VO 2 max (Fig 16-1) Range bpm   due to withdrawal of PNS and SNS stimulation  intrinsic HR ~ 100 bpm Estimated max HR = age (+/- 12)  influenced by anxiety, dehydration, temp, altitude, digestion, genetics

14 HR response with strength exercise  lower than endurance training   with muscle mass used  higher with upper body   intrathoracic pressure, smaller muscle mass  less effective muscle pump - venous return Cardiovascular drift  during prolonged exercise HR gradually  at the same work rate   venous return (  blood volume) Rate Pressure Produce - RPP  HR X SBP  rough index of coronary blood flow

15 Stroke Volume SV has major impact on CO (2 x SV; 2 x CO). SV  during exercise to % of max then levels off.  Fig 16-2: SV  from 75ml to 110ml/beat SV  as exercise intensity  toward max (variable). SV is perhaps the most important factor influencing individual differences in VO 2 max.  max SV sedentary 90ml, athlete 180ml Supine exercise:  SV does not increase - starts high  EDV remains unchanged

16 (a-v)O 2 difference Difference increases with exercise intensity  Fig 16-3 : rest max 16 (vol%)  always some oxygenated blood returning to the heart  non active tissue does not extract much O 2  (a-v)O 2 can approach 100% in maximally working muscle

17 Blood Pressure  BP must  during exercise to maintain blood flow to the heart, brain and working muscle (Fig 16-4). TPR  with exercise to 1/3 resting (due to  in CO).  SBP  steadily during exercise ( mmHg).  MAP: 1/3 (systolic-diastolic) + diastolic  DBP is relatively constant

18 Cardiovascular Triage CT: protective mechanisms that prevent coronary and CNS ischemia and maintain central blood volume. During exercise these mechanisms limit blood flow to muscles when the the body cannot meet the needs of the heart and CNS With exercise blood is redistributed from inactive to active tissue  brain and heart spared vasoconstriction  SNS stimulation  steadily with exercise intensity  At altitude the circulatory system appears to protect the heart by  blood flow to the muscles and reduce the work of the heart (Fig 16-5).

19 Skin blood flow  during submaximal exercise but  to resting values during maximal exercise. Coronary blood flow  during exercise from ml/min  flow occurs mainly during diastole  coronary artery disease may restrict blood flow and cause ischemia  a good warm up facilitates an  in coronary circulation

20 Limits of CV Performance VO 2 max has long been considered the best measure of CV capacity and aerobic performance (Fig 16-6). VO 2 max = [HR max x SV max ] x (a-v)O 2 max VO 2 max is the point at which O 2 consumption fails to rise, despite an  power output or intensity.  VO 2 PEAK

21 VO 2 max Anaerobic Hypothesis After reaching VO 2 max exercise intensity is  by anaerobic metabolism.  max CO and anaerobic metabolism will limit VO2 max  best predictor of performance in endurance sports Tim Noakes - South Africa  re-analyzed data from classic studies  found that most subjects did not plateau

22 Inconsistencies with Anaerobic hypothesis Blood transfusion and O 2 breathing have been shown to  performance.  was it a CO limitation? Blood doping studies  VO 2 max improved for longer time period than performance measures There is a discrepancy between VO 2 max and running performance in elite athletes. At altitude CO   indicative of protective mechanism

23 Lower VO 2 max for cycling compared with running. Running performance can improve without an  in VO 2 max.  VO 2 max through running does not improve swimming. Local muscle factors often appear to be more closely related to fatigue than a limitation in CO. CO is dependant upon and determined by coronary blood flow.  Max CO implies cardiac fatigue, coronary ischemia and angina pectoris?

24 Protection of Heart and Muscle During Exercise 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 by Noakes suggests that peak treadmill velocity is a good predictor of aerobic performance.  high cross bridge cycling and respiratory adaptations  biochemical factors such as mito volume and O 2 enzyme capacity are also good predictors of endurance capacity

25 Practical Basis of the Noakes Hypothesis Primary regulatory mechanism of the CV and neuromuscular systems facilitate intense exercise until it perceives risk of ischemic injury to the heart, CNS and muscles. Fitness should be improved by:  muscle power output capacity  substrate utilization  thermoregulatory capacity  reduce work of breathing The CV system develops at the same time that other adaptations occur from training.

26 Criteria for Measuring VO 2 max Exercise must use at least 50% of the total muscle mass (do not use upper body exercise). The exercise must be continuous and rhythmical and done for at least 10 minutes. The test should try to eliminate motivation and skill. The subject must reach maximum capacity. The measurement must be made in a controlled environment. VO 2 max on a bicycle is usually 10 to 15% less than running on a treadmill.

27 VO 2 max and Performance For the general population VO 2 max will predict performance in an endurance event. For elite athletes VO 2 max is a poor predictor of performance in an endurance event.  male 69, female 73 ml/kg/min: male 15 min faster Other performance factors:  speed  ability to continue at high % of capacity  lactate clearance capacity  performance economy

28 Cardiovascular Adaptations with Endurance Training Rest Submax Ex Max Ex HR   NC SV    (a-v)O 2 NC   CONC NC  VO  SBP   NC CorBF    BloodVol  HeartVol 

29 Changes in CV Parameters with Training Heart  ability to pump blood by  SV (  EDV). Small  in ventricular mass (volume load) with endurance training. Strength training produces a pressure load that will  LV mass. Adaptation to endurance training is sport specific. Interval training –acts as an overload –improve speed and CV functioning –combine with endurance training

30 CV Adaptations Improvements in VO 2 max depend on prior fitness, type of training, age.  can  VO 2 max by ~20% Endurance performance can  by much more than 20% by improving mitochondrial density, speed, running economy, and body composition.

31 Heart Rate Endurance training  resting and submax HR by increasing PNS activity to the SA node.  may  intrinsic HR  athlete 40bpm  may be a genetic influence   resting HR may be due to disease (sick sinus syndrome) Max HR may  ~3 bpm with training.

32 Stroke Volume Endurance training can  resting and submax SV by 20%.  SV due to  in heart volume and contractility.  HR will  SV   HR allows for  filling time (Frank-Starling)  LV compliance allows ventricle to stretch more.  contractility due to  in release and transport of Ca from SR.

33 (a-v)O 2 difference (a-v)O 2  slightly with training difference  right shift of OxyHb dissociation curve  mitochondrial adaptation   Hb and myoglobin conc   muscle capillary density  capillarization around muscle fibres is thought to facilitate diffusion during exercise. Blood Pressure Endurance training  resting and submax SBP, DBP and MAP (no change during max ex).

34 Blood Flow With endurance training coronary blood flow  slightly at rest and during submax exercise.   SV and  HR reduce myocardial O 2 consumption  coronary blood flow  at max ex with training supports higher metabolic requirements with  CO Skeletal muscle vascularity  with endurance training.   peripheral resistance The trained muscle has an  O 2 extraction capacity. There is no change in skin blood flow with training.