16/17) *** Cardiovascular Responses to Acute Exercise *** Flashcards
CV responses to Acute Exercise: Resting HR
How does resting heart rate change in response to training?
Highly trained endurance athletes have a Lower Resting HR due to Increased vagal tone with increased training
- Anticiptory response: Initial ↑ in HR prior to exercise mediated by neurotransmitter (NE from SNS and E from adrenal medulla); vagal tone decreases
- Affected by environmental factors (temperature)
FYI: Some resting heart rates:
* Average person → 60 – 80 beats/min
* Below average health 74 – 81 beats/min
* More athletic → lower resting heart rate
* Male 18 – 25: Athletic 49 – 55 beats/min; Highly trained athletes → 28 – 40 beats/min
Resting heart rate increases with age
* FYI: Male 36 – 45: Athletic 50 – 56 beats/min; Below average health 76 – 82 beats/min
Heart’s Conduction System: Intrinsic Control of Heart Rate
What sets Heart Rate?
Sinoatrial node (SAN)
- Cardiac Pacemaker, initiates action potentials
- Sets heart rate
- Automaticity (autorhythmicity)
Nerves and Hormones can adjust HR.
Two types of cardiac muscle cells (myocytes):
* Contractile cells
* Conducting cells (autorhythmic cells)→ initiate and conduct the action potentials responsible for contraction of the contractile myocytes (1% of myocytes)
How do the parasympathetic NS and Sympathetic NS impact HR?
Parasympathetic:
- Vagus Nerve (supplies heart)
- Slows HR by decreasing slope of pacemaker potential (SAN and AVN)
- Dominates at rest
Sympathetic NS:
- Cardiac accelerator nerves
- Increases HR by increasing slope of the pacemaker potential (SAN/AVN)
Intrinsic HR is ~100bpm but is Lower due to parasympathetic system dominating at rest
What is the effect of exercise on Heart Rate?
Heart Rate increases directly in proportion to the increase in exercise intensity
- HR plateaus as exercise workload continues to increase and reaches maximal HR (HRmax)
- HRmax is the highest HR value (beats per 110
minutes) achieved in an all-out effort to the point of volitional fatigue - Normal age-related decline in HRmax
Max HR is based on AGE not on fitness level
Maximum HR
What is HRmax?
How is it calculated?
HRmax is the highest HR value (beats per 110
minutes) achieved in an all-out effort to the point of volitional fatigue
* Normal age-related decline in HRmax
* Predictable ↓ of 1 beat/year starting at 10-15years
Max HR is based on AGE not on fitness level
- Can’t increase HRmax but can improve how long one can exercise at HRmax
- Trained people will take longer to reach HRmax
HRmax = 220-age (years) (less accurate)
HRmax = 208 - (0.7 x age)
What is Steady-state heart rate?
Steady-state heart rate: A heart rate/training rate that is submaximal & maintained at a constant intensity, speed or rate of work
* When exercise is held constant at a submaximal exercise intensity, HR increases fairly rapidly until it plateaus
* Basis of exercise tests
* A higher cardiorespiratory endurance capacity results in a lower steady state HR at each exercise intensity than those who are less fit
IMAGE: Person A has a higher fitness level than person B because:
1) at any given submaximal exercise intensity A has a lower HR
2) extrapolation to age-predicted HRmax yields a higher estimated maximal exercise capacity
Regulation of HR @ onset of exercise
Initial HR increase due to ?
Further HR increases due to ?
Heart rate increases during exercise
Initial increase mainly due to reduction of
parasympathetic activity
* Bring HR up to 100 beats/min by reducing parasympathetic activity
Further increase due to increased stimulation by sympathetic activity
* Increase heart rate above 100 beats/min
Stroke Volume
What is Stroke Volume?
What are three Factors affecting SV?
Stroke volume (SV) → volume of blood ejected from each ventricle during systole
Factors affecting stroke volume:
(1) End-diastolic volume (EDV; preload)
* Preload → tension or load on myocardium before it begins to contract or amount of filling of ventricles at the end of diastole (EDV) (Frank-Starling Mechanism)
* Venous return (VR)
(2) Contractility of the ventricles
* force of contraction @ any EDV
(3) Afterload
* Resistance to ventricles contracting (Hypertension/valve malfunction)
↑filling→ ↑stretch→ ↑alignment of contractile prtns → ↑ force/SV
- Left and right ventricles eject the same volume of blood during contraction; left ventricle does this with more pressure than the right ventricle
- Under normal resting conditions, the ventricles do not eject their entire volume of blood when contracting
Stroke Volume
What is the Frank-Starling Mechanism?
How does it increase SV?
Main determinant of sarcomere length?
Frank-Starling Mechanism
* The ability of the heart to change
its force of contraction and therefore stroke volume in response to changes in venous return
Main determinant of cardiac muscle fiber (sarcomere) length is degree of diastolic filling: preload
* Increase filling → increase EDV → increase cardiac fiber length → greater force during contraction and greater SV
Increasing EDV → Increases fiber length → More accurate alignment of actin and Myosin → Increase Force Generation → Increase SV
Determinants of EDV
End-diastolic volume is dependent on ?
End-Diastolic Volume dependent on venous return of blood to the heart
Venous return increased by:
- Vasoconstriction (SNS activity → constriction of venous sm mm)
- Skeletal MM pump
- Respiratory pump (vol changes in thoracic cavity to increase BF to heart)
Veins = blood reservoir
Skeletal MM Pump:
At rest:
* Proximal and distal valves open, blood
flowing due to (low) pressure in the veins
Muscle contraction:
* Squeezes veins, pushes blood towards the heart. Distal valve closed so blood does not flow backwards
Relaxation:
* Blood pumped through the proximal valve cannot flow backwards as valve is closed. Blood will refill the veins again from the foot.
How does Stroke Volume Change in response to Acute exercise?
SV Increases proportionally with exercise intensity (↑EDV, ↓ESV)
* At 40 – 60% VO2max SV plateaus to exhaustion (remains unchanged until point of exhaustion)
* Exception: Elite endurance athletes: SV increases up until maximal exercise intensities due to adaptations caused by aerobic training ie. increase VR (slope change may occur ~ 70 – 80% VO2max)
SV plateaus in trained and untrained, but NOT in ELITE athletes
- Aerobic adaptions of elite: ↑venous return → ↑EDV → ↑SV (Frank starling mechanism)
Untrained but active individuals (upright; mL/beat):
* Rest ~ 60 - 70mL; intense exercise ~ 110 - 130mL
Elite athletes (upright; mL/beat):
* Rest ~ 80 - 110mL; intense exercise ~ 160 - 200mL
Blood returns more easily to the heart in supine position, with resting SV higher in supine than uptright position (SV starts higher in supine) // GRAVITY
Supine SV @ rest ~= SVmax when upright
Why does SV increase in response to Acute Exercise?
Why is there a plateau?
Rest to exercise: ↑EDV, ↓ESV
- EDV: greater preload ↑EDV by Frank Starling Mechanism
- ESV: increased contractilility results in greater emptying and ↓ESV)
Plateau (or decrease) in EDV at high intensities: increased HR = reduced filling time (less time in diastole)
Stroke volume (SV) increases with increasing intensity of exercise due to:
* Increased venous return (VR): ↑EDV
* Increased contractility: ↓ESV
* Decreased afterload
Contracting harder and emptying more
How is Venous Return regulated to increase stroke volume during exercise?
Increased Venous Return (VR):
- Frank Starling Mech has greatest effect at low exercise intensities (EDV increases as intensity increases from rest to low-intermediate, then plateaus)
- Exercising mm facilitate VR (skeletal mm pump)
- Respiratory Pump
- Redistribution of blood volume from less active tissues
How is contractility regulated to increase stroke volume during exercise?
Increased contractility:
- Intrinsic property of myocardial fibers
- Tension developed and velocity of shortening (the “strength” of contraction) of myocardial fibers at a given preload and afterload
- Increasing Sympathetic nerve stimulation or circulating catecholamines (NE, E) → ↑contractility → ↑ SV (w or w/o an ↑EDV)
- independent of Frank Starling
ESV decreases at high intensity = increase contraction = increase blood volume pumped out
Catecholamines released from adrenal medulla
What is the effect of afterload on Stroke Volume in response to acute exercise?
Decreased Afterload (resistance to BF):
- Total peripheral resistance (TPR) decreases due to vasodilation of blood vessels in exercising muscle
Cardiac Output
CO: How is CO calculated?
CO = HR x SV
SV = EDV - ESV
COmax is a function of body size and endurance training
How Does Cardiac Output Increase in Response to Acute Exercise?
CO: How Does Cardiac Output Increase in Response to Acute Exercise?
CO = HR x SV
- CO increases in direct proportion to increasing exercise intensity
- CO plateaus when maximal exercise intensity is reached
- COmax function of body size (bigger heart) and endurance training
Cardiac Output
Fick’s Principle:
What is the Fick Equation?
Ficks Principle: Oxygen consumption of a tissue is dependont on blood flow (dependent on CO) to that tissue and the amount of O2 extracted from the blood by the tissue
- Applied to whole body or regional circulations
VO2 = CO x (a-v)O2 difference
VO2 = HR x SV x (a-v)O2 difference
SV = EDV - ESV
Cardiac Response from Rest to Exercise:
- Heart rate
- Stroke Volume
- Cardiac Output
Heart rate (HR): ↑proportionately w/ ↑exercise intensity
- Initial ↑ due to ↓ parasympathetic (vagal) tone
- Further ↑ due to ↑ sympathetic activity
Stroke Volume (SV): ↑proportionately w/ ↑exercise intensity
- Usually max at 40-60% VO2max
- Highly trained can Increase SV to max intensity
Cardiac Output (CO): ↑ due to ↑ HR and SV
- Must meet needs of exercising muscle
- Redistrubution of BF
- Increase CO @ max intensity is due to ↑SV (trained: stronger heart = stronger contractions)
Untrained: CO increased due to ↑SV & HR
- 40-60% individuals max exercise capacity, SV plateaus (or increases at slower rate)
- Further increases in CO are due to ↑HR
How does blood pressure change with moderate endurance exercise (walking, jogging, swimming, cycling)?
Blood pressure:
- Dilation of blood vessels to active skeletal muscle
- Rhythmic activity forces blood through vessels: return to heart
- Systolic Pressure increases for first few minutes, levels off 140-160 mmHg
- Diastolic pressure remains stable or decreases slightly with higher exercise
Healthy, fit folks: systolic pressure may increase to 200+mmHg
- Increases in direct proportion to increased exercise intensity (b/c ↑CO)
BP: During steady state exercise, systolic pressure may decrease, why?
Systolic pressure may decrease during steady- state exercise but diastolic pressure constant
* Due to increased vasodilation in active muscles which decreases TPR
Diastolic pressure remains constant
BP: How does resistance exercise impact BP?
What is the Valsalva Maneuver?
Resistance Exercise:
- BP increases during weightlifting (as high as 480/350)
- Sustained muscular force compresses peripheral arterioles, increasing Resistance (TPR)
Valsalva Maneuver associated with these high pressures
- breathing patturn for producing max force
- Frequently used in powerlifting
- Can cause eye damage
Myocardial Oxygen utilization
Myocardial Oxygen utilization: What happens to ensure that the heart gets adequate oxygen during exercise?
At rest:
* Myocardium: uses 70 – 80% of the oxygen in blood in coronary vessels
* Most other tissues: use ~ 20% of oxygen
* Increases in coronary blood flow provide the primary means to meet myocardial oxygen demands during exercise
As CO increases → ↑Blood in coronary circulation → ↑Heart oxygen
Heart has LOW Anaerobic Capacity!
Heart’s Energy Supply:
Heart’s energy supply:
* High dependence on aerobic metabolism
* Greater oxidative capacity than skeletal muscle
* Lots mitochondria!
Fuel sources for the heart:
- Glucose
- lactate
- fatty acids from glycolysis in skeletal muscle
* After meal – glucose
* Rest – free fatty acids
During Exercise:
* Moderate – equal fat/CHO
* Prolonged submaximal (low intensity endurance) – 80% fat
* * Intense exercise – lactate (Anaerobic glycolysis)
Pattern same for trained/untrained
* Endurance trained has higher reliance on fat in submaximal exercise (CHO- sparing effect of aerobic training)
Primary driver for the redistribution of Cardiac Output (BF) during Exercise?
CO increases from ~ 5L/min (rest) to ~25-40L/min (exercise)
Primary Driver for redistribution of CO is the increased BF requirement of exercising skeletal mm
Distribution of CO differs at rest and during exercise
* During exercise a greater percentage of the increased
CO is distributed to the skeletal muscle
Rest:
* Kidney and splanchnic circulation: large % CO but only use 10 – 25% of the oxygen in blood at rest
// * Can tolerate reduced blood flow
* Skeletal muscle: 15 – 20% CO
Exercise:
* Kidney and splanchnic circulation: reduced % CO
* Skeletal muscle: 80 – 85% CO
Competition for CO: When might this occur?
Competition for blood supply can occur between:
Skeletal mm and GIT if there is undigested food
- Feeding attenuates the redistribution of blood flow from GIT to the working skeletal mm
Sk mm & Skin:
- CO to skin can increase in hot environment for thermoregulation
What is Cardiovascular Drift?
Cardiovascular drift occurs in response to prolonged submaximal activity (aerobic/aerobic exercise in hot environment)
Describes the time-dependent downward shift in several cardiovascular responses
* SV ↓
* Concomitant heart rate ↑
Other factors:
* CO remains constant
* Arterial blood pressure ↓ (Sweat/loss of plasma volume // decrease preload)
Why does Cardiovascular Drift Happen?
Reduced Stroke Volume:
(1) Progressive ↑ in fraction of CO directed to vasodilated skin for heat loss
- ↓preload (BV to heart) → ↓SV
(2) Loss of blood volume from sweating and shift of plasma across capillary membrane to surrounding tissues (↑[metabolites] draws fluid out of blood)
- Decreased filling pressure→ ↓VR → ↓EDV → ↓SV
- HR ↑ to compensate for ↓SV
Exercise Tachycardia:
- ↑HR → less time to fill ventricles → ↓SV
VR = Venous Return
