Explain the cardiovascular responses to acute exercise
Explain blood pressure and blood flow changes during exercise
Explain the respiratory responses to exercise
Explain adaptations to aerobic training
Outline what is known about responders and non- responders to aerobic exercise training
Increased blood flow to working muscle
Involves altered heart function and peripheral circulatory adaptations:
Heart rate (HR)
Stroke volume (SV)
Cardiac output (Q)
Blood pressure
Blood flow
Blood
Normal ranges
Untrained RHR: 60 to 80 beats/min
Trained RHR: as low as 30 to 40 beats/min
Affected by neural tone, temperature, altitude
Anticipatory response: HR increases above RHR just before the start of exercise
Vagal tone decreases
Noradrenaline, adrenaline increases
Directly proportional to exercise intensity
Maximum HR (HRmax): highest HR achieved in all-out effort
Highly reproducible
Declines with age
Estimated HRmax = 220 - age in years
Better estimated: HRmax = 208 - (0.7 \times age) in years
Steady-state HR: A plateau at a given intensity. HR for meeting circulatory demands at that intensity.
If intensity increases, so does steady-state HR
Adjustment to new intensity takes 2 to 3 min
Steady-state HR basis for simple tests that estimate aerobic fitness and HRmax.
Increases with intensity up to 40 to 60% \dot{V}O_{2max}
Beyond this, SV plateaus to exhaustion (not always in elite athletes)
SV during maximal exercise ≈ double standing SV.
But SV during maximal exercise only slightly higher than supine SV
Supine SV much higher versus standing
Supine EDV > standing EDV
Preload: end-diastolic ventricular stretch
Increase Stretch (i.e., increase EDV), increase contraction strength
Frank-Starling mechanism
Increase Contractility: inherent ventricle property
Increase Noradrenaline or adrenaline, increase contractility
Independent of EDV (increase ejection fraction instead)
Decrease Afterload: aortic resistance (R)
Increase Preload at lower intensities increases SV
Increase Venous return increases EDV increases preload
Muscle and respiratory pumps, venous reserves
Increase in HR decreases filling time, slight decrease in EDV, decrease SV
Increase Contractility at higher intensities, increases SV
Decrease Afterload via vasodilation, increases SV
\dot{Q} = HR \times SV
Increases with intensity, plateaus near \dot{V}O_{2max}
Normal values
Resting \dot{Q} ~5 L/min
Untrained \dot{Q}max ~20 L/min
Trained \dot{Q}max 40 L/min
\dot{Q}max a function of body size and aerobic fitness
Calculation of tissue O2 consumption depends on blood flow, O2 extraction
\dot{V}O{2} = \dot{Q} \times (a-v-)O{2} difference
\dot{V}O{2} = HR \times SV \times (a-v-)O{2} difference
\dot{V}O_{2max} = the size of the engine
During endurance exercise, mean arterial pressure (MAP) increases
Systolic BP increases proportional to exercise intensity
Diastolic BP slight decreases or slight increases (at max exercise)
MAP = \dot{Q} \times total peripheral resistance (TPR)
\dot{Q} increases, TPR decreases slightly
Muscle vasodilation versus sympatholysis
Increased Cardiac output increases available blood flow
Must redirect increased blood flow to areas with greatest metabolic need (exercising muscle)
Sympathetic vasoconstriction shunts blood away from less-active regions:
Splanchnic circulation (liver, pancreas, GI)
Kidneys
Local vasodilation permits additional blood flow in exercising muscle
Local vasodilation triggered by metabolic and endothelial products
As temperature rises, skin vasodilation also occurs
Decreases Sympathetic vasoconstriction, increases sympathetic vasodilation
Permits heat loss through skin
Associated with increased core temperature and dehydration
SV drifts downwards:
Skin blood flow increases
Plasma volume decreases (sweating)
Venous return/preload decreases
HR drifts increases to compensate (\dot{Q} maintained)
Exercise + other demands for blood flow results in competition for \dot{Q}
Exercise (muscles) + eating (splanchnic blood flow)
Exercise (muscles) + heat (skin)
Multiple demands may decrease muscle blood flow
Cardiovascular responses to exercise complex, fast, and finely tuned
First priority: maintenance of blood pressure
Blood flow can be maintained only as long as BP remains stable
Prioritized before other needs (exercise, thermoregulatory, etc.)
Immediate increases in ventilation
Begins before muscle contractions
Anticipatory response from central command
Gradual second phase increases in ventilation
Driven by chemical changes in arterial blood
Increases in CO2, H+ sensed by chemoreceptors
Right atrial stretch receptors
Ventilation increases proportional to metabolic needs of muscle
At low-exercise intensity, only tidal volume increases
At high-exercise intensity, rate also increases
Ventilation recovery after exercise delayed
Recovery takes several minutes
May be regulated by blood pH, PCO2, temperature
Dyspnea (shortness of breath)
Common with poor aerobic fitness
Caused by inability to adjust to high blood PCO2, H+
Also, fatigue in respiratory muscles despite drive to increase ventilation
Hyperventilation (excessive ventilation)
Anticipation or anxiety about exercise
Increases PCO2 gradient between blood, alveoli
Decreases Blood PCO2, increases blood pH, decreases drive to breathe
Ventilation matches metabolic rate
Ventilatory equivalent for O2
\dot{V}E/\dot{V}O_{2} (L air breathed / L O2 consumed / min)
Index of how well control of breathing matched to body’s demand for oxygen
Ventilatory threshold
Point where L air breathed > L O2 consumed
Associated with lactate threshold and increases in PCO2
Ventilatory threshold as surrogate measure?
Excess lactic acid + sodium bicarbonate
Result: excess sodium lactate, H2O, CO2
Lactic acid, CO2 accumulate simultaneously
Refined to better estimate lactate threshold
Anaerobic threshold
Monitor both \dot{V}E/\dot{V}O{2}, \dot{V}E/\dot{V}CO{2}
Ventilation normally not limiting factor
Respiratory muscles account for 10% of \dot{V}O_{2}, 15% of \dot{Q} during heavy exercise
Respiratory muscles very fatigue resistant
Airway resistance and gas diffusion normally not limiting factors at sea level
Restrictive or obstructive respiratory disorders can be limiting
Exception: elite endurance-trained athletes exercising at high intensities
Ventilation may be limiting
Ventilation-perfusion mismatch
Exercise-induced arterial hypoxemia (EIAH) i.e. pulmonary gas exchange limitations during exercise
Metabolic processes produce H+ which decreases pH
At rest, body slightly alkaline
7.1 to 7.4
Higher pH = alkalosis
During exercise, body slightly acidic
6.6 to 6.9
Lower pH = acidosis
Physiological mechanisms to control pH
Chemical buffers: bicarbonate, phosphates, proteins, hemoglobin
Increase Ventilation helps H+ bind to bicarbonate
Kidneys remove H+ from buffers, excrete H+
Active recovery facilitates pH recovery
Passive recovery: 60 to 120 min
Active recovery: 30 to 60 min
O2 transport system and Fick equation
\dot{V}O{2} = \dot{Q} \times (a-v-)O{2} difference
\dot{V}O{2} = SV \times HR \times (a-v-)O{2} difference
Increase \dot{V}O_{2max} = increase max SV x max HR x increase max (a-v-)O2 difference
Heart size
With training, heart mass and LV volume increases
Cardiac hypertrophy and increase SV
Increase Plasma volume, increase LV volume, increase EDV
SV increases after training
Resting, submax, and max
Plasma volume increases with training increases EDV increases preload
Resting and submaximal HR decreases with training
Increase LV mass with training, increase force of contraction
SV training adaptations decreases with age
Pulmonary ventilation
Decreases At given submaximal intensity
Increases At maximal intensity due to increase tidal volume and respiratory frequency
Pulmonary diffusion
Unchanged during rest and at submaximal intensity
Increases At maximal intensity due to increase lung perfusion
Arterial–venous O2 difference
Increases Due to increase O2 extraction and active muscle blood flow
Increase O2 extraction due to increase oxidative capacity
Fiber type
Increases Size and number of type I fibers (type II to type I)
Type IIx may perform more like type IIa
Capillary supply
Increases capillarization
May be key factor in increases \dot{V}O_{2max}
Myoglobin
Increases Myoglobin content by 75 to 80%
Supports increases oxidative capacity in muscle
Mitochondrial function
Increases Size and number
Magnitude of change depends on training volume
Oxidative enzymes (SDH, citrate synthase)
Increases Activity with training
Continue to increase even after \dot{V}O_{2max} plateaus
Enhanced glycogen sparing
Lactate threshold
Increases To higher percentage of \dot{V}O_{2max}
Increases lactate clearance
Allows higher intensity without lactate accumulation
Respiratory exchange ratio (RER)
Decreases At both absolute and relative submaximal intensities
Increases Dependent on fat, decreases dependent on glucose
HERITAGE family study (n=473)
VO2max responses to endurance training can be explained by ~30 gene RNA expression signature in muscle (prior to training)
Explains ~23% of gains in VO2max
Changes in maximal power (Wmax) after each exercise training period
Values within the shaded area are within measurement error i.e. non-response
Non-response = (1) 69%, (2) 40%, (3) 29%, (4) 0% and (5) 0%
Non-responders respond to a more potent training stimulus!