Cardiorespiratory
Responses to Acute
Exercise
Cardiovascular Responses
to Acute Exercise
• Increases blood flow to working muscle
• Involves altered heart function, peripheral
circulatory adaptations
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Heart rate
Stroke volume
Cardiac output
Blood pressure
Blood flow
Blood
Cardiovascular Responses:
Resting Heart Rate (RHR)
• 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  above RHR
just before start of exercise
– Vagal tone 
– Norepinephrine, epinephrine 
Cardiovascular Responses:
Heart Rate During Exercise
• Directly proportional to exercise intensity
• Maximum HR (HRmax): highest HR achieved
in all-out effort to volitional fatigue
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Highly reproducible
Declines slightly with age
Estimated HRmax = 220 – age in years
Better estimated HRmax = 208 – (0.7 x age in years)
Accuracy of Predicting Max HR
• All prediction equations have an SEE
• The SEE is a measure of the accuracy of the
prediction
• SEE is based on the normal curve
– There is a 67% probability that the actual value is
within the range of the predicted value ± 1 SEE.
– There is a 95% probability that the actual value is
within the range of the predicted value ± 2 SEE.
Predicting Maximal HR
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HRmax = (220-age) • There is a 67%
probability that true
SEE = 10 beats/min
HRmax is 196 ± 10 or
Age = 24 years
186 – 206.
HRmax = 220-24
• There is a 95%
probability that true
HRmax = 196
HRmax is ± 20 or
176 – 216. This is
the 95% Confidence
Interval.
Cardiovascular Responses:
Heart Rate During Exercise
• Steady-state HR: point of plateau, optimal
HR for meeting circulatory demands at a
given submaximal intensity
– If intensity , so does steady-state HR
– Adjustment to new intensity takes 2 to 3 min
• Steady-state HR basis for simple exercise
tests that estimate aerobic fitness and
HRmax
Figure 8.1
Cardiovascular Responses:
Stroke Volume (SV)
•  With  intensity up to 40 to 60% VO2max
– Beyond this, SV plateaus to exhaustion
– Possible exception: elite endurance 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
Figure 8.3
Cardiovascular Responses:
Factors That Increase Stroke Volume
•  Preload: end-diastolic ventricular stretch
–  Stretch (i.e.,  EDV)   contraction strength
– Frank-Starling mechanism
•  Contractility: inherent ventricle property
–  Norepinephrine or epinephrine   contractility
– Independent of EDV ( ejection fraction instead)
•  Afterload: aortic resistance (R)
Cardiovascular Responses: Stroke
Volume Changes During Exercise
•  Preload at lower intensities   SV
–  Venous return   EDV   preload
– Muscle and respiratory pumps, venous reserves
• Increase in HR   filling time  slight 
in EDV   SV
•  Contractility at higher intensities   SV
•  Afterload via vasodilation   SV
Cardiac Output and Stroke Volume:
Untrained Versus Trained Versus Elite
Cardiovascular Responses:
Cardiac Output (Q)
• Q = HR x SV
•  With  intensity, plateaus near VO2max
• Normal values
– Resting Q ~5 L/min
– Untrained Qmax ~20 L/min
– Trained Qmax 40 L/min
• Qmax a function of body size and aerobic
fitness
Figure 8.5
Cardiovascular Responses:
Fick Principle
• Calculation of tissue O2 consumption
depends on blood flow, O2 extraction
• VO2 = Q x (a-v)O2 difference
• VO2 = HR x SV x (a-v)O2 difference
Cardiovascular Responses:
Blood Pressure
• During endurance exercise, mean arterial
pressure (MAP) increases
– Systolic BP  proportional to exercise intensity
– Diastolic BP slight  or slight  (at max exercise)
• MAP = Q x total peripheral resistance (TPR)
– Q , TPR  slightly
– Muscle vasodilation versus sympatholysis
Figure 8.7
Cardiovascular Responses:
Blood Flow Redistribution
•  Cardiac output   available blood flow
• Must redirect  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
Cardiovascular Responses:
Blood Flow Redistribution
• Local vasodilation permits additional blood
flow in exercising muscle
– Local VD triggered by metabolic, endothelial
products
– Sympathetic vasoconstriction in muscle offset by
sympatholysis
– Local VD > neural VC
• As temperature rises, skin VD also occurs
–  Sympathetic VC,  sympathetic VD
– Permits heat loss through skin
Figure 8.8
Cardiovascular Responses:
Cardiovascular Drift
• Associated with  core temperature and
dehydration
• SV drifts 
– Skin blood flow 
– Plasma volume  (sweating)
– Venous return/preload 
• HR drifts  to compensate (Q maintained)
Figure 8.9
Cardiovascular Responses:
Competition for Blood Supply
• Exercise + other demands for blood flow =
competition for limited Q. Examples:
– Exercise (muscles) + eating (splanchnic blood flow)
– Exercise (muscles) + heat (skin)
• Multiple demands may  muscle blood flow
Cardiovascular Responses:
Blood Oxygen Content
• (a-v)O2 difference (mL O2/100 mL blood)
– Arterial O2 content – mixed venous O2 content
– Resting: ~6 mL O2/100 mL blood
– Max exercise: ~16 to 17 mL O2/100 mL blood
• Mixed venous O2 ≥4 mL O2/100 mL blood
– Venous O2 from active muscle ~0 mL
– Venous O2 from inactive tissue > active muscle
– Increases mixed venous O2 content
Figure 8.10
Central Regulation of
Cardiovascular Responses
• What stimulates rapid changes in HR, Q,
and blood pressure during exercise?
– Precede metabolite buildup in muscle
– HR increases within 1 s of onset of exercise
• Central command
– Higher brain centers
– Coactivates motor and cardiovascular centers
Central Cardiovascular Control
During Exercise
Cardiovascular Responses:
Integration of Exercise Response
• 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.)
Figure 8.12
Respiratory Responses:
Ventilation During Exercise
• Immediate  in ventilation
– Begins before muscle contractions
– Anticipatory response from central command
• Gradual second phase of  in ventilation
– Driven by chemical changes in arterial blood
–  CO2, H+ sensed by chemoreceptors
– Right atrial stretch receptors
Respiratory Responses:
Ventilation During Exercise
• Ventilation increase proportional to
metabolic needs of muscle
– At low-exercise intensity, only tidal volume 
– At high-exercise intensity, rate also 
• Ventilation recovery after exercise delayed
– Recovery takes several minutes
– May be regulated by blood pH, PCO2, temperature
Figure 8.13
Figure 8.14
Respiratory Responses:
Estimating Lactate Threshold
• 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 VE/VO2, VE/VCO2
Respiratory Responses:
Limitations to Performance
• Ventilation normally not limiting factor
– Respiratory muscles account for 10% of VO2, 15%
of 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
Respiratory Responses:
Limitations to Performance
• Exception: elite endurance-trained athletes
exercising at high intensities
– Ventilation may be limiting
– Ventilation-perfusion mismatch
– Exercise-induced arterial hypoxemia (EIAH)
Figure 8.16