Download Chapter_07_4E - Ironbark (xtelco)

chapter
7
Cardiorespiratory
Responses to
Acute Exercise
Learning Objectives
• Learn about the cardiovascular adjustments to acute
exercise
• Find out how the cardiovascular system responds to
increased demands during exercise
• Examine how the respiratory system functions during
exercise and how it can sometimes limit physical
performance
(continued)
Learning Objectives (continued)
• Learn how the respiratory system maintains acid–
base balance
• Find out why this acid–base balance is important
during exercise
Fick Equation: The Relationship Between
Metabolism and Cardiovascular Function
.
.
VO2 = Q x (a-v)O2diff
.
VO2 = HR x SV x (a-v)O2diff
The Fick principle can be applied to whole body
or regional circulations
Cardiovascular Response
to Acute Exercise
The components of the cardiovascular system must
meet the increased demands for blood flow to the
exercising muscle
• Heart rate (HR)
• Stroke volume (SV)
.
• Cardiac output (Q)
• Blood pressure (BP)
• Blood flow
• Blood
Resting Heart Rate
• Averages 60 to 80 beats per minute (bpm)
• Highly trained athletes: 28-40 bpm (increased vagal
tone)
• RHR is affected by environmental factors (extreme
temperatures and altitude)
• Preexercise heart rate is usually higher than RHR
because of an anticipatory increase in sympathetic
activity
Heart Rate During Exercise
• HR increases in direct proportion to the increase in
exercise intensity
• HR will plateau at a maximum even as workload
continues to increase (HRmax)
• HRmax remains constant day to day and declines ~1
beat per year
• HRmax can be estimated:
HRmax = 220 – age in years
HRmax = 208 – (0.7 x age in years)
Heart Rate vs. Relative Workload
Steady-State Heart Rate
• When workload is constant, HR increases rapidly until it
reaches a plateau (i.e., steady state)
• For each increase in workload, HR will increase to a
new steady-state value in 2-3 minutes
• Exercise training decreases steady-state heart rate for
a given submaximal workload
Heart Rate vs. Increasing Power Output
and Oxygen Uptake in Two Subjects
Reprinted, by permission, from P.O. Åstrand et al., 2003, Textbook of work physiology, 4th ed. (Champaign, IL:
Human Kinetics), 285.
Stroke Volume
SV is the major determinant of cardiorespiratory
endurance capacity
Four factors that determine SV:
1. The volume of venous blood returned to the heart
(preload)
2. Ventricular distensibility
3. Ventricular contractility
4. Aortic or pulmonary artery pressure (afterload)
Stroke Volume Increases
With Exercise
• SV increases with increases in work rate
.
• SV usually plateaus at ~40-60% of VO2max
• SV is influenced by body position due to postural
differences in venous return to the heart
Stroke Volume (SV)
vs. Relative Workload
Postural Influences on Stroke Volume
During Exercise
Reprinted, by permission, from L.R. Poliner et al., 1980, "Left ventricular performance in normal subjects: A
comparison of the responses to exercise in the upright and supine position," Circulation 62: 528-534.
Explanations for the Increase
in Stroke Volume During Exercise
• Frank-Starling Mechanism: an increased volume of
blood enters the ventricle (preload), causing it to
stretch, and consequently it contracts with more force
• Increased ventricular contractility is due to increased
sympathetic stimulation and circulating catecholamines
• Decreased total peripheral resistance (afterload) is due
to increased vasodilation of blood vessels going to
active muscles
Conflicting Research
on Stroke Volume During Exercise
Adapted, by permission, from B. Zhou et al., 2001, “Stroke volume does not plateau during graded exercise in elite
male distance runners,” Medicine and Science in Sports and Exercise 33: 1849-1854.
Cardiac Output
• Resting value is ~5.0 L/min
• Increases with increasing
exercise intensity up to
~20 to 40 L/min
• Can vary with body size
and endurance training
Changes in (a) Heart Rate, (b) Stroke
Volume, and (c) Cardiac Output With
Changes in Posture
a
b
c
Heart Rate, Stroke Volume,
and Cardiac Output
Key Points
• As exercise intensity increases, HR increases
proportionately, up to maximal
• SV increases proportionately with increasing exercise
intensity. but usually achieves its maximal value at ~4060% of VO2max in untrained individuals
• Highly trained individuals can increase SV up to
maximal exercise intensities
• Increases in HR and SV combine to increase cardiac
output
Blood Pressure Responses
During Dynamic Exercise
• Mean arterial pressure (MAP) increases substantially
during dynamic exercise
• Systolic blood pressure (SBP) increases in proportion
to exercise intensity
• Diastolic blood pressure (DBP) does not change
significantly during dynamic exercise and may
decrease
• Increased MAP facilitates the increase in blood flow
which aids in substrate delivery to working muscles
Blood Pressure Responses
During Dynamic Arm and Leg Exercise
Adapted, by permission, from P.-O. Åstrand et al., 1965, "Intraarterial blood pressure during exercise with different
muscle groups," Journal of Applied Physiology 20: 253-256.
Blood Pressure Responses
During Static Exercise
• BP responses can be exaggerated during static
exercise (as high as 480/350 mmHg)
• Performing the Valsalva maneuver, which increases BP,
is common in these types of exercise (e.g., lifting very
heavy weights)
Redistribution of Blood Flow
During Exercise
• Blood flow is redirected away from areas where
elevated flow is not essential to areas that are active
during exercise
– ↑ Muscle blood flow
– ↑ Skin blood flow (especially in hot environments)
– ↓ Kidney blood flow
– ↓ Splanchnic blood flow (liver, stomach, intestines)
• Redistribution of blood flow is accomplished through
the actions of the sympathetic nervous system
Distribution of Cardiac Output
at Rest and During Exercise
Data from A.J. Vander, J.H. Sherman, and D.S. Luciano, 1985, Human physiology: The mechanisms of body
function, 4th ed. (New York: McGraw-Hill).
Cardiovascular Drift
• With prolonged aerobic exercise and/or exercise in
hot environments, at a constant exercise intensity,
there is a gradual decrease in stroke volume and an
increase in heart rate
• Increase in the fraction of cardiac output directed
toward the skin circulation
• Small decrease in blood volume
Circulatory Responses to Prolonged,
Moderately Intense Exercise,
Illustrating Cardiovascular Drift
Adapted, by permission, from L.B. Rowell, 1986, Human circulation: Regulation during physical stress (Oxford, United
Kingdom: Oxford University Press), 230; adapted from HANDBOOK OF PHYSIOLOGY, SECTION 10, edited by
Peachy, copyright 1983 by American Physiological Society. Used by permission of Oxford University Press, Inc.
Oxygen Content in Blood
• Oxygen content in arterial blood = 20 ml per 100 ml of
blood
• Mixed venous content (at rest) = 14 ml per 100 ml of
blood
• At rest: (a-v)O2 difference = (20 ml – 14 ml) = 6 ml per
100 ml of blood
• (a-v)O2 difference increases with exercise intensity
because of decreasing venous oxygen content
–
Changes in the (a-v)O2 Difference
vs. Oxygen Uptake
Plasma Volume (PV) During Exercise
• Plasma moves from the blood to the interstitial space
• PV is lost through sweat, especially in hot
environments
• 10-15% reduction in PV with prolonged exercise
• PV loss is proportional to intensity with resistance
exercise
• Excessive PV loss can result in impaired performance
• PV loss results in hemoconcentration (a reduction in
the fluid component of the blood)
Filtration of Plasma
From the Microvasculature
Blood Pressure, Blood Flow, and Plasma
Volume Changes With Exercise
Key Points
• MAP increases immediately and in proportion to
exercise intensity
• Endurance exercise:  SBP, ↔ DBP
• Resistance exercise:  SBP,  DBP
• Blood flow is redistributed during exercise from
inactive areas to exercising muscle to meet its
metabolic needs
• Cardiovascular drift is a progressive decrease in SV
and increase in HR during prolonged exercise and/or
exercise in the heat
(continued)
Blood Pressure, Blood Flow, and Plasma
Volume Changes With Exercise (continued)
Key Points
• The (a-v)O2 difference increases as venous oxygen
concentration decreases during exercise
• Plasma volume decreases during exercise through
hydrostatic forces and through sweating
• Hemoconcentration occurs as plasma volume
decreases
Central Regulation of Cardiovascular
Control During Exercise
Adapted, by permission, from S.K.
Powers & E.T. Howley, 2004, Exercise
Physiology: Theory and Application to
Fitness and Performance. New York,
McGraw-Hill, p. 188.
Integration of the Cardiovascular
System’s Response to Exercise
Adapted, by permission,
from E.F. Coyle, 1991,
“Cardiovascular function
during exercise: Neural
control factors,” Sports
Science Exchange 4(34):
1-6. Copyright 1991 by
Gatorade Sports
Science Institute.
Pulmonary Ventilation
During Dynamic Exercise
• With the onset of exercise there is an immediate,
neurally-mediating increase in ventilation
• As exercise progresses, increased metabolism
generates CO2 and H+
– Stimulate the chemoreceptors in the carotid bodies
and the respiratory centers
• Pulmonary ventilation returns to normal at a slower rate
when exercise ceases
The Ventilatory Response to Light,
Moderate, and Heavy Exercise
Breathing Irregularities
During Exercise
Dyspnea: shortness of breath, most often associated
with poor conditioning, is caused by inability to readjust
the blood PCO2 and H+
Hyperventilation: an increase in ventilation that
exceeds the metabolic need for oxygen
Valsalva maneuver: a breathing technique where air is
trapped in the lungs against a closed glottis, and intraabdominal and intrathoracic pressure are increased
Ventilatory Equivalent for Oxygen
•
•
•
•
•
.
.
The ratio between VE and VO2 (i.e., hyperventilation)
Indicates breathing economy
. .
Rest VE/VO2 = 23 to 28 L of air per L O2
. .
Maximal exercise VE/VO2 = 30 L of air L O2
. .
Generally VE/VO2 remains relatively constant over a
wide range of exercise levels
Ventilatory Threshold
• Point during exercise when ventilation increases
disproportionately to oxygen consumption
• At approximately the same point lactate begins to
accumulate in the blood
• Lactic acid is buffered by sodium bicarbonate and
ventilation increases due to increased CO2
stimulating the chemoreceptors
Changes in Pulmonary Ventilation
With Increasing Running Speed
Estimating the Lactate Threshold
. .
Changes in the ventilatory equivalent
for
carbon
dioxide
(V
E/VCO2) and the
. .
ventilatory equivalent for oxygen (VE/VO2) during increasing intensities of
exercise on a cycle ergometer. Note that the breakpoint of the estimated lactate
threshold
at a running velocity of 14.4 km/h (8.9 mph) is evident only in the
. .
VE/VO2 ratio.
Respiratory Limitations
to Performance
• Respiratory muscles consume ~11% of oxygen
consumed during heavy exercise and can receive up to
15% of cardiac output
• Pulmonary ventilation is usually not a limiting factor for
performance in most individuals
• Respiratory muscles have a high oxidative capacity and
are relatively fatigue resistant
(continued)
Respiratory Limitations
to Performance (continued)
• Airway resistance and gas diffusion usually do not limit
performance in healthy individuals, but they can in
people with restrictive or obstructive respiratory
disorders
• Pulmonary ventilation may limit performance in some
highly trained athletes due to exercise-induced arterial
hypoxemia
Respiratory Regulation
of Acid–Base Balance
• H+ + buffer → H-buffer
• Examples of buffers: bicarbonate, phosphate, proteins,
hemoglobin
• Acidosis: H+ concentration above normal
• Alkalosis: H+ concentration below normal
Tolerable Limits of Arterial Blood pH
and Muscle pH at Rest and at Exhaustion
Regulating pH
• Chemical buffers in the blood
• Pulmonary ventilation
• Kidney function
Effects of Active and Passive
Recovery on Blood Lactate Levels
Respiratory Regulation
of Acid–Base Balance
• Excess H+ (decreased pH) impairs muscle contractility
and ATP generation
• The respiratory and renal systems help regulate acid–
base balance
– Respiratory: short-term
– Renal: long-term
• Increased H+ concentrations stimulate respiratory
centers to remove CO2
• Whenever H+ levels begin to rise, from carbon dioxide
or lactate accumulation, bicarbonate ions can buffer the
H+ to prevent acidosis