Exercise and the Cardiovascular System Chapter 13: The Physiology of Training 1
CARDIOVASCULAR FITNESS Aerobic fitness measured by VO 2max VO 2max is a product of maximal cardiac output (Q) and arteriovenous difference (a-vo 2 ) VO 2max = HR max x SV max x (a-vo 2 ) max Genetics: 40-66% of baseline VO2max Improvements in VO 2max 50% due to SV 50% due to a-vo 2 2
VO2max Values
CARDIAC OUTPUT AND TRAINING 4
Cardiac Output What is responsible for a higher maximal cardiac output? Qmax = HRmax x SVmax Does HRmax increase with training? Does SVmax increase with training? 5
Heart Rate and Training No difference in HRmax 6
Heart Rate and Recovery 7
Stroke Volume What is responsible for a higher SVmax? Note: SV is higher at all levels of exercise; even at rest. 8
Stroke Volume Increased End Diastolic Volume (Preload) Plasma volume Ventricular volume Filling time and venous return Decreased Total Peripheral Resistance (Afterload) Decrease arterial constriction Increased Contractility
Factors Increasing Stroke Volume 1. Due to a stronger heart 2. Increase blood volume 3. Due to a larger heart 10
Left Ventricular Hypertrophy 11
Blood and Plasma Volume and Training With training, what happens to: Blood Volume? Red Blood Cells? Hematrocrit? Viscosity? 12
Stroke Volume & Heart Rate What affect will a larger SV have on resting HR? What affect will a larger SV have on submaximal exercise HR? What affect will a larger SV have on maximal exercise HR? 13
CV Adaptations 14
a-v O2 DIFFERENCE Changes in what factors would be responsible for increasing the a-v O2 difference? 15
a-vo 2 DIFFERENCE Improved ability of the muscle to extract oxygen from the blood is due to: Capillary density Muscle blood flow Mitochondial number Myoglobin Increased a-vo 2 difference accounts for 50% of increased VO 2max 16
SUMMARY OF INCREASING VO 2max Myoglobin Blood volume Heart Size 17
CARDIOVASCULAR ADAPTATIONS AT VARYING INTENSITY LEVELS VO2 HR Q SV a-v O2 Difference Rest Submax (same intensity) Performance Max 18
Detraining and VO 2max Decrease in VO 2max with cessation of training First: SV max and plasma volume Second: maximal a-vo 2 difference 19
Detraining and VO 2max 20
Detraining and VO 2max About 50% of the increase in mitochondrial content was lost after one week of detraining All of the adaptations were lost after five weeks of detraining It took four weeks of retraining to regain the adaptations lost in the first week of detraining 21
Training/Detraining Mitochondrial Changes 22
IMPROVEMENT IN CARDIOVASCULAR FITNESS Increase in O2 supply Increase cardiac output Increase stroke volume Increase heart size and strength Increase blood volume Increase O2 extraction Capillaries Mitochondria Aerobic system and enzymes Myoglobin 23 Increase in VO2max
Respiration During Exercise Chapter 10 24
Function of the Lungs Ventilation refers to the mechanical process of moving AIR into and out of lungs Respiration is the exchange of gases 1. Pulmonary respiration Exchange of gases (O 2 & CO 2 ) in the lungs 2. Cellular respiration Relates to O 2 utilization and CO 2 production by the tissues 25
Ventilatory Control During Submaximal Exercise 26
Pathway of Air to Alveoli 27
Partial Pressures In room air there is 79% N, 21% O2 and 0.03% CO2 If the total pressure of those gases is 760 mm Hg the partial pressures would be N = 760 x.79 = 600.7 mm Hg O2 = 760 x.21 = 159.0 mm Hg CO2 = 760 x.0003 = 0.3 mm Hg 28
PO2 inside the arterial blood = 40 PO2 inside the alveoli = 100 Therefore, O2 flows from the high pressure (lungs) to the low pressure (blood) PO2 inside the venous blood = 100 29
Respiration PO2 = 100 PCO2 = 40 30
Blood Flow to the Lung When standing, most of the blood flow is to the base of the lung 31
Ventilation-Perfusion Relationships Ventilation/perfusion ratio Indicates matching of blood flow to ventilation Ideal: ~1.0 For example Apex (top) Underperfused (ratio >1.0) Base (bottom) Overperfused (ratio <1.0) 32
Ventilation/Perfusion Ratios Underperfused Overperfused 33
Ventilatory Reponse to Exercise: Trained vs. Untrained Untrained individuals have normal Ventilation/Perfusion ratios In trained individuals, decreases in arterial PO 2 near exhaustion can cause overperfusion This may partially limit their VO2max (maximal aerobic energy production) 34
What is the ventilation breakpoint and what is the cause for the sudden increase in ventilation at that point? When work rate exceeds 55% to 70% VO 2 max, additional energy must come from glycolysis. Glycolysis increases lactic acid levels Buffering of lactic acids leads to an increase in CO 2 : H + HCO3 <---> H20 + CO2 An increase in CO 2 triggers a respiratory response and increased ventilation. The point during intense exercise when ventilation increases disproportionately to (or greater than) oxygen consumption. 35.
Ventilatory Threshold CO2 from Krebs cycle and buffering lactic acid stimulate ventilation even faster CO2 from Krebs cycle stimulates ventilation Aerobic 36 Aerobic and Anaerobic
Ventilatory Threshold The Talk Test can estimate Ventilatory Threshold If you can talk while you exercise, your ventilation is BELOW your anaerobic threshold and you are aerobic. If you have a difficult time talking while you exercise, your ventilation is ABOVE your anaerobic threshold and you are aerobic and anaerobic. If you remain above your AT, acid will accumulate inside your muscle leading to fatigue. 37
Effect of Training on Ventilation Ventilation is lower at same work rate following training May be due to lower blood lactic acid levels Results in less feedback to stimulate breathing 38
Effects of Endurance Training on Ventilation During Exercise 39
Do the Lungs Limit Exercise Performance? Low-to-moderate intensity exercise Pulmonary system not seen as a limitation Diaphragm is very aerobic Maximal exercise Not thought to be a limitation in healthy individuals during moderate exercise at sea level May be limiting in elite endurance athletes New evidence that respiratory muscle fatigue does occur during high intensity exercise 40
Questions?