Transcript functional capacity

Regulation and Integration
Integrated Exercise Response:
Before Exercise:
Central command increases HR and myocardial
contractility (suppression of parasympathetic)
As Exercise Continues:
Mechanoreceptors/Chemoreceptors feedback on CV
center (Medulla)
Local metabolic factors (CO2, NO, etc.) dilate blood
vessels, reduce peripheral resistance, increase BF
Centrally mediated vasoconstriction occurs in
vasculature of non-exercising tissue (kidney,
splanchnic region, inactive muscles)
Muscle pump and ventilation ensure venous return and
adequate cardiac output
Regulation and Integration
Orthotopic (Heart) Transplantation:
Sympathetic
nerves stimulate
medulla to
release
epinephrine
Epinephrine via
blood accelerates
SA node and
dilates coronary
vessels
Regulation and Integration
Orthotopic (Heart) Transplantation:
Higher resting HR,
lower HR max prior to
transplantation
Epinephrine via
blood exerts only
control over HR
Exercise response
severely impaired -
-limited CO
-impaired VO2
Functional Capacity of CV
System
Functional Capacity
Cardiac Output (CO):
Amount of blood pumped by the
heart in 1 minute (L/min)
CO = HR x Stroke Volume (SV)
Maximal CO reflects functional
capacity of CV system to meet
physical demand of exercise
Functional Capacity
Calculating Q via Direct Fick Method:
To calculate Q, must know:
1. Average difference between O2
content of arterial blood and venous
blood (a-v O2 difference)
2. O2 consumed in 1 min
Q=
VO2 (mL/min)
a-v O2 difference (mL/100 mL)
X 100
Functional Capacity
Direct Fick Method:
Question:
How much blood
circulates during
each minute to
account for
observed O2
consumption,
given the amount
extracted?
Functional Capacity
I. Cardiac output at rest:
Average values:
5 L/min for 70 kg male (154 lb)
4 L/min for 56 kg female (123 lb)
Untrained:
(Q) 5000 mL/min = (HR) 70 bpm x (SV) 71 mL
Trained:
(Q) 5000 mL/min = (HR) 50 bpm x (SV) 100 mL
Functional Capacity
I. Cardiac output at rest:
Two factors contribute to differences
in trained and untrained:
1. Training increases vagal tone
(parasympathetic) and decreased
sympathetic drive – (Lowers HR)
2. Training increases blood volume,
myocardial contractility, compliance of LV
(Increases SV)
Functional Capacity
II. Cardiac output during exercise:
Blood flow increases directly with
exercise intensity
Untrained - Q increases 4-fold during exercise
(Q) 22,000 mL/min = 195 (HR) x 113 mL (SV)
Trained - Q increases 7-fold during exercise
(Q) 35,000 mL/min = 195 (HR) x 179 mL (SV)
*Trained increase Q solely through increase SV
Functional Capacity
Increased SV accounts for large increase
in Q during exercise
Fig 21.11
Fig 21.10
Functional Capacity
Stroke Volume during exercise:
3 mechanisms increase SV during
exercise:
1. Enhanced diastolic filling
2. Greater systolic emptying
3. Training adaptation – expanded blood
volume and reduced peripheral
resistance
Functional Capacity
1. Enhanced Diastolic Filling:
Increased end diastolic volume (EDV)
occurs when there is increased venous
return or slowing of heart (Preload)
Frank-Starling mechanism – contractile
force increases as resting length of
cardiac fibers increases
Preload (increased EDV) stretches
cardiac fibers and initiates powerful
ejection (increases SV)
Functional Capacity
1. Enhanced Diastolic Filling:
Increased end diastolic volume (EDV)
occurs when there is increased venous
return or slowing of heart
Preload – enhanced ventricular filling
Frank-Starling mechanism – contractile
force increases as resting length of
cardiac fibers increases
Preload stretches cardiac fibers and
initiates powerful ejection (increases SV)
Functional Capacity
2. Systolic Emptying:
Catecholamine release (sympathetic NS)
during exercise increases ventricular
contractile force (facilitates systolic
emptying)
At rest, 40% of EDV remains in left
ventricle after systole
Greater systolic ejection occurs
when there is reduced “Afterload”
(resistance to BF from increased SBP)
Functional Capacity
3. Training Adaptations:
Increased plasma volume
Increased EDV
Higher SBP increases “afterload”
Reduced peripheral resistance
(reduced afterload)
Functional Capacity
3. Training Adaptations:
Increased plasma volume
(chronic
exercise response)
Increases EDV
Reduced peripheral resistance
occurs during exercise
Reduced afterload
(MAP/CO)
Functional Capacity
Heart Rate During Exercise:
HR increases during submaximal “steady
rate” exercise (after ~15 minutes)
Cardiovascular Drift – Increase in HR and
decrease in SV during exercise
Due to:
Plasma volume shift (sweating/cooling)
Decreased Preload
Reduced SV (HR compensation)
Functional Capacity
Heart Rate During Exercise:
Cardiovascular Drift – 2nd explanation
Fig 17.2
*HR increase (not cutaneous BF) reduces SV
during exercise
Functional Capacity
Distribution of Cardiac Output:
Rest –
1/5 of Q to muscle
(4-7 mL/100 g)
Functional Capacity
Distribution of Cardiac Output:
Exercise –
~85% of Q to muscle
(50-75 mL/100 g)
300-400 mL/100 g to
specific portions of muscle
Functional Capacity
Cardiac Hypertrophy (Hypertension):
Heart mass also increase with hypertension NOT a positive adaptation
Heart chronically works against excessive
resistance to blood flow
No "recuperation" periods to induce training
effect (like RT or endurance training)
Constant tension weakens left ventricle
"Hypertrophied" heart becomes enlarged,
distended, and functionally inadequate to
deliver blood to tissues
Cardiovascular Response to Exercise
Aerobic Exercise Training and
Hypertension:
Systolic and diastolic blood pressure decrease by
~6 - 10 mm Hg with aerobic exercise
Exercise training exerts its greatest effect on
patients with mild hypertension
Regular aerobic exercise may control the
tendency for blood pressure to increase over
time (aging)
Cardiovascular Response to Exercise
9 months of aerobic
training significantly
reduced systolic BP
(11 mm Hg) and
diastolic BP (9 mm Hg)
Improved antihypertensive drug
effect
BP began to rise again
after only 1 month of
detraining
Fig. 32.9