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LAB IX
Cardiovascular Response to Exercise
The regulation and integration of cardiovascular and respiratory function is very
important during exercise. This laboratory is designed to demonstrate some of the basic
cardiovascular and respiratory principles that function together to maintain homeostasis during
exercise. Review the underlined words before you come to lab. All of the concepts used in this
lab have been previously taught (Human Physiology and lab and Exercise Physiology) and
should be reviewed again prior to class. Students should also review the previous cardiovascular
lab (especially formulas and components on blood pressure regulation) as well as review
appendix pages 11 and 49 to 53 while reading and completing this lab.
The cardiovascular system plays a critical role in supporting the metabolic needs of the
entire body. In this regard it has several roles including (but not limited to): delivering oxygen to
tissues (especially heart and brain which are very aerobic and exercising skeletal muscle),
clearing carbon dioxide, delivering nutrients, removing metabolic by-products, circulating
signals (hormones), and transferring heat. When metabolic demands are increased during
exercise the delivery system must adjust to meet the demands. There are two major
cardiovascular responses to meet these demands: 1) increase cardiac output, and 2) redistribute
blood flow to the active muscle. In order to meet the metabolic demands placed on them, the
skeletal muscle must also extract more oxygen from the blood delivered to it.
The Central Cardiovascular Response to Exercise: Cardiac Output
The metabolic demands placed on the body during exercise will result in an increase in
cardiac output from 5L/min at rest up to 20-30L/min at maximal exercise in most people. In elite
endurance athletes cardiac output may go as high as 50L/min. On the other hand people with
severe cardiovascular diseases, such as heart failure, may not be able to increase cardiac output
enough to meet the body's metabolic demands. The increase in cardiac output that occurs during
exercise is dependent on both an increase in heart rate and an increase in stroke volume. Heart
rate in healthy college age students will typically increase from a resting value around 65
beats/minute at rest up to a maximal values of around 200 beats/min; a three-fold increase in
heart rate! If cardiac output measurements are not available, one can estimate that cardiac output
increases 5 to 6 Liters for every 1 liter/minute increase in VO2 during exercise.
For most subjects, stroke volume increases during exercise, but will level off (plateau)
around 40 to 60% of VO2max. Therefore, further increases in cardiac output beyond this point
must be attained by increases in heart rate. It is believed that this plateau in stroke volume is
partly due to the high heart rates associated with intense exercise. At high heart rates, diastolic
filling time is significantly shortened, and therefore there is less time to fill the ventricle. On the
other hand, several studies have demonstrated that the stroke volume of elite athletes may not
plateau during intense exercise, even though filling time is shortened, just as it is in normal
subjects. How can elite athletes continue to increase stroke volume when there is reduced time
for ventricular filling? The reason is not completely clear, but a number of possibilities have
been proposed. For example, it has been suggested that these higher stroke volumes could be a
result of any or all of the following: a larger heart, an increase in ventricular compliance
(increased preload, ventricles may be able to stretch more, see preload below) a reduced
peripheral resistance (reduced afterload, see afterload below), an increase in the rate of
ventricular filling, and an increase in the rate of ventricular ejection.
In healthy college age student's stroke volume will typically increase from around
70ml/beat at rest up to values of around 100-120ml/beat. Stroke volumes of over 200ml/beat
have been measured in some elite athletes. On the other hand, a well trained college age student
performing a large muscle mass activity may reach maximal stroke volumes of 140ml/beat. An
Lab IX - 1
increase in stroke volume from 70ml/beat up to 140ml/beat represents a two-fold increase in
stroke volume (usually only well trained or large subjects can increase stroke volume two-fold
above resting values). Thus, in college age students heart rate can increase about three-fold and
stroke volume can increase up to two-fold over resting values in order to increase cardiac output
during acute exercise. This does not by any means suggest that stroke volume is less important
than heart rate. In fact, a great deal of research suggests that most of the increase in VO2max
that occurs with exercise training (chronic exercise) is a result of increases in cardiac output as a
result of increasing stroke volume. In order to increase cardiac output during exercise it is
necessary for blood to be returned to the heart more quickly. Thus the increase in cardiac output
during acute exercise is influenced greatly by venous return.
Venous return is the amount of blood returning to the heart per unit time. During
exercise venous return increases as a result of a number of other physiological events that occur
during exercise. For example, venoconstriction results from an increase in sympathetic nervous
system activity during exercise and will result in a redistribution of blood from the peripheral
circulation to the central circulation. Other physiological changes that increase venous return
during exercise also include an increase in the activity of the respiratory and muscle pumps
which also assist in moving blood from the periphery back to the heart. There is also a cardiac
suction effect that helps to pull blood into the ventricle following ventricular systole. The type
of exercise performed can also affect venous return. For example, there will tend to be a larger
venous return during exercises performed in the supine position compared to exercises
performed in the upright position.
In addition to the effects of venoconstriction, cardiac suction, and the respiratory and
muscle pumps in increasing venous return during acute exercise, other factors, can cause changes
in venous return during chronic exercise (exercise training). For example, blood volume
increases during endurance training and will result in a larger venous return after training. Much
of the increase in stroke volume that occurs with exercise training can be attributed to increases
in venous return. It should be noted, however, that during an acute bout of exercise blood volume
likely decrease due to a reduction in plasma volume, secondary to fluid shifts within the body
and perhaps some loss of plasma due to sweating. Some of these changes can be avoided if one
replenishes fluids during the activity.
The pressure created by the blood flowing into the ventricles of the heart before
contraction starts is called preload and as venous return increases preload is increased. Students
can think of preload as being related to the amount of stretch placed on the myocardium prior to
systole. According to Starling's law of the heart a greater preload will result in a greater strength
of contraction and thus, in a greater stroke volume. Stroke volume is also dependent on the
afterload. The afterload has been defined as the resistance to the ventricular ejection of blood.
Students can think of the afterload as "how hard it is for the heart to pump blood out?"
Remember, blood always travels down a concentration gradient. If arterial pressure is elevated,
such as in hypertension, then the ventricular pressure will need to increase more in order to eject
the same amount of blood. The higher arterial pressure in individuals with hypertension causes a
greater afterload that the heart must overcome in order to eject blood.
Ejection fraction increases slightly during exercise in young healthy subjects from around
60% up to the 70-80% range at maximal exercise depending upon training, type of exercise, and
the method used to determine ejection fraction. It is important to remember EF% = SV/EDV and
SV = EDV-ESV. So, is the increase in SV during exercise more due to increasing EDV or
increasing EF% (which is the same as saying there is a decrease in ESV)? Well, both play a role
in increasing SV during exercise. However , the increase in venous return results in a large
increases in EDV (and thus preload) while the increase in EF% is only slight. The increase in
EF% reflects improvements in contractility; the strength of cardiac contraction for a given EDV,
Lab IX - 2
HR and afterload. For a given EDV, if EF% increases, then ESV must be lower. The increase in
contractility is in part related to stimulation via the sympathetic nervous system and by
circulating catecholamines. Furthermore, the Starling effect of enhanced pre-load on the strength
of cardiac contraction also helps to increase EF% (and decrease ESV). The increase in ejection
fraction during exercise is less in older individuals than in young and is greater in trained than in
untrained (in most studies, in some EF% is so high to begin with that it had no room to
increase!). Whereas changes in the strength of cardiac contraction are referred to as changes in
inotropy, changes in heart rate are referred to as changes in chronotropy. For example, the
parasympathetic nervous system has a negative chronotropic effect and the sympathetic nervous
system has a positive chronotropic and positive inotropic effect.
It may not always be possible to determine stroke volume during exercise (don’t have the
right equipment, cant get accurate readings during intense exercise, etc.), thus methods are
sometimes used to estimate stroke volume during exercise. One way to determine if stroke
volume is increasing or decreasing is by calculating the O2pulse. The O2 pulse is calculated by
dividing the absolute VO2 in ml/min by the heart rate in beats per minute. Increases in O2pulse
are either the result of increases in stroke volume or increases in a-vO2difference.
The Peripheral Cardiovascular Response to Exercise: TPR and the Redistribution of Blood Flow
The demands of exercise are also met by a redistribution of blood flow away from
inactive tissues to the active muscle. This redistribution is accomplished vasoconstriction in the
inactive tissues and vasodilation in the active tissues. The vasoconstriction is primarily a result
of activation of the sympathetic nervous system and an increased secretion of various hormones.
The sympathetic nervous system generally acts in a global type of manner. That is, it is not very
selective, and when it becomes active it will tend to cause widespread vasoconstriction
throughout the body. So, how is the vasodilation in the inactive tissues accomplished? The
vasodilation that occurs in active skeletal muscle during exercise is, for the most part, mediated
locally. This local mediated regulation of blood flow is referred to as autoregulation.
Autoregulation allows the tissue to match its blood flow to its metabolic demands. It is therefore
no surprise that most of the major factors that cause locally mediated vasodilation in active
skeletal muscle are directly related to the metabolic status of the muscle. For example, all of the
following are believed to be important in the locally mediated vasodilation in active skeletal
muscle: a decrease in pO2, an increase in pCO2, a decrease in pH, an increase in ADP, an
increase in potassium, an increase in temperature, and an increased release of nitric oxide (NO,
also called EDRF, which stands for Endothelium Derived Relaxing Factor). This vasodilation in
the active muscles is responsible for the decrease in total peripheral resistance (TPR) that occurs
during aerobic types of exercise.
If a subject were to exercise using a large muscle mass, a greater amount of vasodilation
would be expected than if a small muscle mass were used (there are more blood vessels that can
dilate in a large amount of muscle compared to a small amount of muscle). This vasodilation
will facilitate an increase in blood flow in the active muscle will cause a decrease in total
peripheral resistance. The more blood vessels that dilate, the greater the decrease in TPR. A
large decrease in resistance could potentially be very dangerous for the organism because it
could decrease mean arterial pressure (MAP). If there is a decline in total peripheral resistance,
how can the body maintain mean arterial pressure, or even increase it? The answer lies in the
fact that during exercise, the increase in cardiac output is typically greater than the decline in
TPR. Thus, one normally expects to see an increase in MAP during exercise. In fact MAP is
directly proportional to exercise intensity under normal circumstances. On the other hand, if
people who have heart failure exercise above their heart’s ability to increase cardiac output,
blood pressure can drop (usually the SBP will drop) with an increase in exercise intensity.
Lab IX - 3
The increase in blood pressure that normally occurs during exercise is not just a biproduct of the increase in cardiac output during exercise; it is the whole reason why we need an
increase in cardiac output during exercise! The increase in MAP that occurs during exercise is
one of the major reasons why there is an increase in blood flow to the active muscle mass.
Recall from Ohm's law that pressure equals flow times resistance, or put another way, flow
equals pressure over resistance. Thus, the combination of an increase in pressure and a decrease
in local resistance is responsible for the huge increase in skeletal muscle blood flow during
dynamic types of exercise.
The cardiopulmonary, aortic and carotid baroreceptors monitor the degree of stretch on
the heart and arteries and therefore allow the central nervous system to maintain the required
blood pressure. At rest blood pressure is normally 120/80. Ohm's law Pressure = Flow x
Resistance, MAP = Q x TPR) can help us understand how blood pressure is regulated.
Additionally, this formula can provide us with an indication of vasomotor control (status of the
blood vessels' vasodilation or vasoconstriction). Using a modification of Ohm's law (see
formulas below) we can calculate total peripheral resistance based on measurements of cardiac
output and mean arterial pressure. TPR at rest is usually around 1500 dyn.s.cm-5 and may
decrease to as low as 300 dyn.s.cm-5 during intense dynamic exercise (a five-fold decrease in
TPR). This large decrease in TPR during aerobic types of exercise indicates that there is a great
deal of vasodilation).
Extraction of Oxygen by the Active Tissues During Exericse: a-vO2difference
The functions of the cardiovascular system discussed above and the normal function of
the respiratory system are integrated in the Fick Equation: VO2 = Q x a-vO2difference. This
formula can help students to visualize the two ways that we can increase oxygen consumption:
pump more blood (increase Q) or extract more oxygen from the blood (a-vO2difference).
Arterio-venous O2 difference (a-vO2difference) is the amount of oxygen being extracted from the
blood per unit of blood delivered to the tissues. The a-vO2difference is usually reported in units
of vols%; one vol% is equal to 1ml of oxygen per 100ml blood (1ml O2 / 100 ml blood). Simply
stated the a-vO2difference is the difference between the O2 content of the arterial blood and the
O2 content of the venous blood. The a-vO2difference can be directly measured if the O2 content
of arterial blood leaving the heart (usually around 20vols%, 20 ml O2 /100 ml blood) and the O2
content of venous blood returned from the body to the right atrium (usually around 15 vols% at
rest) can be determined. The major factors that determine the ability of our blood to carry
oxygen are: the hemoglobin concentration, the oxygen carrying capacity of hemoglobin, and the
percent saturation of hemoglobin:
O2 content (vols%) = [Hb] in g/100ml x 1.39 ml O2 /gHb x Sa O2%
If direct measurements of O2 content of the blood are not available, then the a-v
O2difference can easily be calculated using the Fick equation. Since VO2 = Q x a-vO2difference,
then a-v O2difference equals VO2 / Q. In order to truly understand a-v O2difference one must
first have an understanding of the oxy-hemoglobin dissociation curve (covered in human
physiology and exercise physiology lecture). Oxygen readily diffuses down its concentration
gradient from the oxygen rich blood in the systemic capillaries into the tissues. But why does the
oxygen dissociate from the hemoglobin in the blood?
Hemoglobin concentrations are usually reported in grams of hemoglobin per 100 ml
blood. In humans, hemoglobin concentrations for men are usually in the range of 13.5 to 17.5
g/100ml and are usually in the range of 11.5 to 15.5 g/100ml for women. The hemoglobin
concentration remains roughly the same between arterial and venous blood. The oxygen
carrying capacity of hemoglobin (the amount of oxygen that can be carried by a certain amount
Lab IX - 4
of hemoglobin) remains the same in both arterial and venous blood, about 1.39 ml O2 per gram of
hemoglobin. Thus, the amount of oxygen that is carried in the arterial and venous circulation are
essentially dependent upon the percent saturation of hemoglobin (percent of hemoglobin that is
bound with oxygen). The SaO2, or arterial oxygen saturation, is the percent of arterial blood
bound with oxygen and can be measured easily and non-invasively with a pulse oximeter. SaO2
is usually around 98% in normal healthy subjects (this means that hemoglobin in arterial blood is
carrying almost all of the oxygen that it can possibly carry). What factors determine the percent
saturation of hemoglobin?
In general, the higher the pO2 the greater the affinity hemoglobin has for oxygen. Under
resting conditions the pO2 of the blood returning to the pulmonary circulation is about 40 mmHg
and the pO2 in the alveolar capillaries is around 100 mmHg. Thus, when the red blood cells
(RBCs) reach the alveolar capillaries (where there is a high pO2), oxygen readily binds to the
hemoglobin in these RBCs, and the hemoglobin becomes nearly completely saturated with
oxygen (~98% saturated). The blood is then returned via the pulmonary veins to the left side of
the heart which will pump this oxygen rich blood out into the systemic circulation. The pO2 in
the systemic capillaries is usually around 40 mmHg again. Thus, when the oxygen rich blood
reaches the systemic capillaries, the oxygen readily dissociates from the hemoglobin because of
the lower pO2 (and thus lower affinity of hemoglobin for oxygen). This oxygen will now diffuse
down its concentration gradient from the blood in the systemic capillaries into the tissues. After
some of the oxygen dissociates from the hemoglobin it is less saturated with oxygen. Under
resting conditions about 25% of the oxygen carried by the hemoglobin into the systemic
capillaries is dropped off. Thus, the blood leaving the systemic capillaries is usually 70-75%
saturated with oxygen. This blood is now returned to the heart and eventually to the pulmonary
circulation and the alveolar capillaries where the hemoglobin will again associate with more
oxygen, becoming nearly completely saturated with oxygen again. How do these changes in pO2
relate to a-vO2difference?
At rest the tissues usually extraction about 25% of the oxygen associated with
hemoglobin, this corresponds to about 5ml of oxygen for every 100ml of blood delivered to the
tissues. During exercise a-vO2difference increases because the tissues take more oxygen from
the blood, leaving less oxygen in the venous blood. There are several reasons why the tissues
extract more oxygen (and therefore increase a-vO2difference) during exercise: a decrease in
tissue pO2, a rightward shift in the oxy-hemoglobin dissociation curve, the redistribution of
blood flow away from inactive tissues and toward active tissues. One other factor that plays a
minor role in increasing a-vO2difference during exercise is a slight hemoconcentration; an
increase in hemoglobin concentration of the blood.
During exercise there is a drop in pO2 in the tissues as a result of increased aerobic
metabolism. During exercise, temperature increases, pCO2 increases, the pH decreases, and the
amount of 2,3-DPG (2,3-diphosphoglycerate) in the circulation increase. All of these factors
cause a right-shift in the oxy-hemoglobin dissociation curve, which causes more oxygen to
dissociate from the hemoglobin in the systemic capillaries. The effects of pH and pCO2 on the
association and dissociation of hemoglobin from oxygen is called the Bohr Effect. The a-v
O2difference also increases during exercise because a greater proportion of the body's blood flow
is going to the active tissues (which extract a lot of oxygen) and less blood is going to the
inactive tissues (which extract relatively little oxygen). The hemoconcentration that occurs
during exercise is primarily caused by a shift in fluids from the plasma into the active tissues.
All of these factors contribute to the increase in a-vO2difference during exercise. At maximal
exercise, the a-vO2difference may increase to between 14 and 16 vols% (75% of the oxygen
associated with hemoglobin is extracted) in normal individuals and may increase up to 18 vols%
in elite athletes.
Lab IX - 5
Cardiovascular response to aerobic types of exercise (see appendix pages 8 to 12)
Cardiac output increases during all types of exercise. Both trained and untrained subjects
have a resting cardiac output of around 5-6 L/min. However, at maximal exercise, athletes tend
to have higher maximal cardiac output values. For example, untrained male subject’s maximal
cardiac outputs are often in the range of 20-30L/min (representing a 4 to 5-fold increase in
cardiac output above resting values), whereas it is not uncommon for trained subjects to have
maximal cardiac outputs in the range of 30-35L/min (representing a 5 to 7-fold increase in
cardiac output). Maximal cardiac output values of over 40-50 L/min have been recorded in some
elite athletes (over a 7 to 10-fold increase in cardiac output).
In humans, during most types of exercise cardiac output increases as a result of an
increase in both heart rate and stroke volume. Thus, cardiac output during maximal exercise are
determined heart rate maximum and stroke volume during maximal exercise. Individuals of a
similar age usually have roughly equivalent heart rate maximum (HRmax  220-age). The
reason why athletes and trained individuals have greater maximal cardiac outputs is because they
have a greater maximal stroke volume. This greater maximal stroke volume is a result of several
changes that occur with training. For example, training tends to increase blood volume, which,
in turn increases venous return, and thus increases end diastolic volume, and thus increases
stroke volume. Stroke volume increases during exercise for several reasons. Most of the
increase in SV is due to an increase in EDV, which results from an increase in venous return, and
an increase in the strength of ventricular contraction.
The increase in cardiac output during exercise causes an increase in mean arterial blood
pressure. In healthy exercising individuals, more blood is being pumped out during systole, thus
systolic blood pressure increases as a function of the intensity of the exercise (the greater the
intensity, the greater the cardiac output, the greater the systolic blood pressure. However, if the
cardiac muscle is weakened for some reason, such as in individuals with heart failure, the
systolic blood pressure may actually decrease with an increase in intensity. This is very
dangerous, and suggests that blood is not being pumped out efficiently. It may actually represent
a decrease in cardiac output with an increase in intensity. Average values for maximal exercise
SBP have been reported to be 182 mmHg in 18-29 year old males, and to be 155 mmHg in 18-29
year old females.
If cardiac output increases at least 4-fold from rest to maximal exercise, why doesn’t
mean arterial pressure increase at least 4-fold from resting values? Remember, mean arterial
pressure (MAP) is equal to the product of cardiac output (Q) and total peripheral resistance
(TPR). The reason why MAP does not normally increase to the same extent as cardiac output is
because TPR tends to decrease during most types of dynamic exercise (running, cycling, etc.).
TPR tends to decrease as a result of vasodilation of blood vessels in the active muscles.
However, students should realize that because the sympathetic nervous system is highly active
during exercise, blood vessels in nearly all other, non-active, parts of the body will vasoconstrict.
If there is a large amount of vasodilation and if there is a substantial decrease in TPR, it is not
uncommon to see a decrease in DBP during exercise. In 18-29 year old individuals, average
maximal exercise DBP values have been reported to be 69mmHg in men and 67 mmHg in
women. However, in older subjects or in individuals with peripheral vascular disease (PVD), the
blood vessels do not dilate as well as in younger subjects. Thus, in older subjects and in subjects
with PVD, DBP may not decrease during exercise, and may even increase slightly.
The duration of the exercise bout also has the potential to influence the cardiovascular
response to exercise, even with a constant intensity. It has been known for a long time that heart
rate tends to increase over time (“drift up”) and that as this occurs there is a decrease in stroke
volume (“drifting down), such that for exercise < 1 hour, cardiac output is usually somewhat
maintained. This phenomenon is referred to as cardiovascular drift (sometimes cardiac drift).
Lab IX - 6
The observed drift in HR and SV are greater in hot environments and become greater as duration
of exercise increases. Fluid ingestion tends to prevent some of the observed drift. A portion of
the decrease in SV is attributed to a decrease in blood volume over time and also partly to the
increases in HR, which are partly due to the progressive increase in body temperature. Increases
in HR decrease ventricular filling time and thus have the potential to compromise SV. Thus, in
order to maintain performance of a given intensity, which requires a certain cardiac output, it is
very important to prevent dehydration.
After exercise, cardiac output returns to resting levels faster than TPR. That is, TPR
remains low longer than Q remains high. As a result, following exercise there is usually a period
of time when blood pressures are lower than at rest. This is referred to as post-exercise
hypotension (PEH). PEH can last up to several hours and appears more pronounced in
hypertensive subjects than normotensive subjects and is greater in the standing than the supine
position. Following a 20-60 minute exercise bout a decrease of 5-10mmHg could be expected in
normal subjects. There are several possible causes of PEH including reduced sympathetic
outflow to the muscles and enhanced local vasodilator activity. PEH has been observed
following both aerobic and resistance exercise.
Cardiovascular response to isometric and resistance types of exercise (see appendix p. 8 to 12)
During isometric and resistance types of exercise (as with aerobic types of exercise),
cardiac output, and thus SBP increase as a function of intensity. However, these types of
exercise are associated with strong muscular contractions that can compress the blood vessels
that supply the muscle. The blood vessels in the active muscle are trying to dilate, but because
they are compressed by the contracting muscle (this is not the same as vasoconstriction, which is
due to contraction of the smooth muscle lining the blood vessel) they can not dilate during these
strong contractions. Therefore, there is a greater resistance to blood flow to the active muscle
and there is usually also an increase in TPR. As a result, the DBP typically goes up during
isometric and resistance types of exercise. Additionally, MAP and SBP tend to go up to a much
greater extent during these types of exercise, when compared to aerobic exercise.
An additional concern during isometric and resistance exercise is whether or not the
subject is performing a valsalva maneuver. When one performs a valsalva maneuver, the
pressure in the thoracic cavity is increased. This pressure is transmitted to the aorta, which goes
through the thoracic cavity. Because the aorta is continuous with our arterial circulation, arterial
blood pressure is typically elevated during a valsalva maneuver. However, when thoracic cavity
pressure is high, venous return is impaired, and heart rate may actually decrease as a result.
Whereas a valsalva maneuver may actually play some beneficial roles in elite power lifters, in
older individuals or individuals with increased cardiovascular risk it may result in a dangerously
high blood pressure. Thus, it is best to instruct most individuals to breathe when performing
resistance types of exercise.
Lab IX - 7
Q = cardiac output
FORMULAS & ABBREVIATIONS
SV = stroke volume
VR = venous return
MAP = mean arterial pressure
TPR = total peripheral resistance
SaO2 = percent saturation of Hemoglobin with O2
Q = VR
Q = SV x HR
SV (ml/bt) = Q (ml/min) / HR (bt/min)
MAP (mmHg) = (SYSTOLIC + (2 x DIASTOLIC)) / 3 or = 1/3PP + DBP
TPR (dyn/sec.cm5) = (MAP x 1333) / Q ml/s where (Q L/m x 1000 / 60 = Q ml/s)
TPR can then be estimated as: TPR = (MAP/Q) x 80
a-vO2 diff (ml/100ml or vols%) = VO2 (L/min) x 1000 (ml/L) / Q (L/min) x 10 (100ml/L)
a-v O2diff can then be estimated as: a-vO2diff = (VO2/Q) x 100
O2pulse (ml O2/beat) = VO2 (ml/min)/ HR (bt/min)
Arterial oxygen content = [g hemoglobin / 100ml blood] x 1.39ml/gHb x SaO2
Venous oxygen content = arterial oxygen content – a-vO2difference
Rate Pressure Product = HR x SBP
% ventricular systole = ventricular systole (sec) / RR interval (sec)
% ventricular diastole = ventricular diastole (sec) / RR interval (sec)
LABORATORY PROCEDURES
I.
Cardiovascular & pulmonary response to exercise (Demo)
a. The first part of today’s lab will be a demonstration that will involve one subject and
a number of students will be needed to take blood pressures, take SaO2, record HR,
SV, run the metabolic cart, enter data, and perform calculations.
b. Determine the subject’s hemoglobin concentration using one of two methods. In our
labs we routinely use two different methods for determining hemoglobin
concentrations: the Tallquist Method and the Cyanmethemoglobin method. Each of
these methods has pro’s and cons. The Tallquist method is fast and inexpensive but
lacks precession. The Cyanmethemoglobin method is more expensive and time
consuming, but is very precise. Depending on time and equipment availablility you
will use one of the following methods to determine hemoglobin concentration.
i. The Tallquist Method uses a book of special Tallquist blotting papers and
a color comparison chart having different intensities of red. These
intensities correspond to different concentrations of hemoglobin found in
human blood.
ii. The cyanmethemoglobin method is an accurate colorimetric method for
the determination of hemoglobin concentration. This test is based on the
reaction of hemoglobin with a solution (Drabkin’s solution) containing
potassium cyanide (KCN) , which together form cyanmethemoglobin, a
colored compound. The concentration of this compound can be
determined using a spectrophotometer once one has prepared a standard
Lab IX - 8
c.
d.
e.
f.
g.
h.
i.
j.
k.
curve to reflect the relationship between light absorbance and hemoglobin
concentration.
Prepare the subject’s skin for an EKG using limb lead II. We will use the exercise
electrode placement scheme with the right arm electrode (negative) placed in the
subclavicular fossa on the right mid-clavicle and the left leg electrode (positive)
placed in the lowest intercostal space on the left at the mid-clavicular line. The EKG
will be used to determine heart rate using the RR interval. Students are reminded that
HR = 60/RRinterval.
Prepare the subject’s skin and place two strip impedance electrodes on the back of the
neck (one at bottom of the neck, one an inch above. Then place two strip impedance
electrodes at the bottom of the Thorax – the upper of the two electrodes should be on
the back at the level of the xyphoid process and the lower electrode an inch below.
Impedance cardiography will provide us with changes in impedance of the thoracic
cavity over time (dz/dt) which reflect aortic flow. The amount of blood flow in the
aorta per beat reflects stroke volume and the amount of flow in the aorta per minute
reflects cardiac output. For our purposes we will determine SV and HR and Q can
then be calculated. In this course Doppler ultrasound technology can be used to
determine cardiac output also by looking at the velocity of blood flow in the aorta.
Prepare the subject’s skin and place the phonocardiogram on the fourth, left
intercostals space at the sterna border (roughly over the tricuspid valve). This will
allow us to monitor the heart sounds. S1 is the first heart sound and reflects closing of
the AV valves and S2 is the second heart sound and reflects closing of the semilunar
valves. If the third and/or fourth heart sounds are observed they are associated with
filling of the ventricles.
The heart sounds (from the phonocardiogram), the EKG, and the impedance tracing
(aortic flow) will give us cues from which to measure time periods of the cardiac
cycle.
Hook the subject up to the metabolic cart so that absolute VO2 and VE can be
reported.
Put a blood pressure cuff on the subject and get a sphygmomanometer and
stethoscope ready for determining blood pressure.
Finally, SaO2, arterial oxygen saturation, will be determined using a pulse oximiter,
which will be placed on the subejct’s finger.
Everyone who is not assigned a job will get a calculator ready and calculate the
following according to the formulas provided earlier: RPP, Q, TPR, O2 pulse, a-vO2
difference, arterial O2 content, venous O2 content, % of cardiac cycle spend in
ventricular systole and diastole.
Measure time periods of the cardiac cycle for the ventricles:
i. Ventricular systole lasts from the peak of the QRS complex to S2
ii. Ventricular diastole lasts from S2 until the peak of the next QRS
iii. Ventricular systole can be further broken down:
1. Isovolumetric ventricular contraction, measure from S1 to the beginning of the
increase in aortic flow
2. Ventricular ejection period/left ventricular ejection time (LVET), measure from
the beginning of the increase in aortic flow until S2
l. Review your results and answer the questions in your lab manual.
Lab IX - 9
II. Heart Rate and Blood Pressure response to Exercise
a. Each group will be assigned one or two of the following sets of exercises:
Group 1: Aerobic exercise, effects of intensity and size of active muscle mass
Group 2: Effects of type of exercise (aerobic vs. isometric) and exercise intensity
Group 3: Resistance exercise, effects of intensity and size of active muscle mass
Group 4: Effects of type of exercise (resistance vs. isometric) and exercise intensity
Group 5: Aerobic exercise, effects of duration
Group 6 Aerobic exercise, effects of thermal stress.
Resting and post-exercise Heart rates and blood pressures should be taken in roughly the
same posture as during exercise (e.g. standing for treadmill exercise, seated for cycle
exercise).
b. Post exercise heart rates and blood pressures would ideally be obtained at least 20-30 min
post-exercise. However, due to time constraints you may need to take them 10-20 min
post. Additionally, if the same subject is used for both sets of data (groups 1-4) only take
post-exercise measurements after the final bout of exercise.
c. For blood pressure measurements during all exercise bouts, make sure that you isolate the
arm well and pump the cuff up above the systolic BP before beginning measurements.
d. For aerobic exercise bouts for groups 1, 2, and 6 each bout of exercise will be 5 minutes.
Take heart rates and blood pressures throughout for practice. Record the heart rate and
blood pressure data obtained during the last minute of each 5 min exercise bout. The
subject can go immediately from one intensity to the next without a break. The high
intensity bout should be of sufficient intensity that the subject could not maintain the
intensity for much more than 5 minutes.
e. For the isometric exercises (groups 2 and 4), the high intensity exercise bout should be of
sufficient intensity that the subject can only maintain the contraction for a minute, or
perhaps a little longer. Intensities of 20-25%, 40-50%, and 60-75% of maximum will
probably give you reasonably good data. Determine the heart rate and blood pressure
during the final 30 seconds of each bout (begin pumping up pressure in the cuff 20-25
seconds into each bout. During arm exercises, carotid pulses can be taken from behind the
subject. If the subject is unable to estimate their maximum, it is suggested that the
perceived moderate intensity exercise be performed first; if it feels hard call it the heavy
exercise bout and if it feels to easy call it the easy/light bout.
f. For the resistance exercises (groups 3 & 4), the high intensity exercise bout should be of
sufficient intensity that the subject can only do 10-12 repetitions. Intensities of 20-25%,
40-50%, and 60-75% of maximum will probably give you reasonably good data. In order
to get data within this time frame, repetitions should be performed somewhat slowly and
the cuff should be rapidly inflated during the first few reps. Ideally blood pressure and
heart rate should be determined in the same number of reps.
Lab IX - 10
Data Sheet
I. Cardiovascular & pulmonary response to exercise data & calculations
rest
Stage
1
Stage
2
Stage
3
Intensity
[Hb]
VO2
VE
RR interval
HR
SV
SaO2
SBP
DBP
Ventricular
Systole
Isovol Vent
Contr
Ejection
Period
Ventricular
Diastole
Calculations:
MAP
RPP
Q
TPR
O2pulse
a-v O2diff
Arterial O2
content
Venous O2
Content
% v sytole
% v diastole
Lab IX - 11
Stage
4
Stage
5
Stage
6
Stage
7
Stage
8
Questions about the data
1. Did stroke volume plateau? If so, at what percent of their peak VO2 did it plateau?
2. What factors contribute to the increase in SV during exercise?
3. What happened to the percent of the cardiac cycle spent in ventricular diastole and
ventricular systole as the subject went from rest to max exercise?
4. How might the above finding relate to the plateau in SV (if observed)?
5. Using the SV values that we collected, calculate estimated EDV and ESV at rest, during
the 3rd exercise intensity (moderate), and at maximal exercise assuming EF% were 60%,
65%, and 70% at these intensities, respectively.
Rest:
SV = ________
est. EF% = 60%
EDV = ______
ESV= ______
Moderate: SV = ________
est. EF% = 60%
EDV = ______
ESV= ______
Max:
est. EF% = 60%
EDV = ______
ESV= ______
SV = ________
Based on these estimates, does the increase in SV during exercise appear to be due more
to increases in EDV or decreases in ESV?
6. What happens to EDV during exercise? Why? What happens to ESV during exercise?
Why?
7. In what ways might training influence the SV response to exercise considering the
following: left ventricular volume, blood volume, ejection time, filling time?
Lab IX - 12
8. If determined pre- and post- exercise, what happened to [Hb] during exercise? If it
changed, what likely caused this change? How might this influence SV, a-vO2difference,
and VO2?
9. What factors contribute to the increase in a-vO2difference during exercise?
10. What factors contribute to the increase in a-vO2difference during exercise?
11. Was the increase in a-vO2difference mostly due to an increase in arterial O2 content or a
decrease in venous O2 content?
12. What factors affect the arterial O2 content and venous O2 content during exercise?
13. Do the changes in O2pulse seem to make sense? Write in the formulas that demonstrate
the relationship between O2pulse and HR, SV, VO2, and a-vO2difference.
14. What factors contribute to the decrease in TPR during exercise?
15. How would the following have been different if we had used arm crank ergometry
instead? Why?
a. heart rate
b. stroke volume
c. cardiac output
d. TPR
e. Systolic blood pressure
f. Diastolic blood pressure
g. mean arterial pressures
h. a-vO2difference
Lab IX - 13
16. What variables do you think would be different if a subject performed blood doping with
erythropoietin?
17. What are normal values for the following variables at rest and at maximal exercise for
normal individuals and elite athletes: HR, SV, Q, SBP, DBP, A-vO2diff, VO2, TPR,
MAP.
18. How would the following have been different if we had the subject performing isometric
or resistance exercises with the legs? Why?
a. Systolic blood pressure
b. Diastolic blood pressure
c. mean arterial pressures
d. TPR
19. Draw response of the following cardiovascular variables to aerobic exercise.
SV
Rest
easy
moderate
TPR
hard
Rest
easy
easy
moderate
hard
Rest
easy
Arterial O2 content
Rest
easy
moderate
hard
a-vO2difference
O2pulse
Rest
moderate
moderate
hard
Venous O2 content
hard
Rest
easy
Lab IX - 14
moderate
hard
II. Heart Rate and Blood Pressure response to Exercise *
* please enter group data into computer
Group 1: Aerobic exercise, effects of intensity and size of active muscle mass
HR
SBP
DBP
PP
MAP
cycle
rest
low
moderate
heavy
RPP
post-exercise
arm crank
rest
low
moderate
heavy
post-exercise
How was the cardiovascular response to exercise simmilar/different between the exercise bouts?
Explain your answer.
Group 2: Effects of type of exercise (aerobic vs isometric) and exercise intensity
HR
SBP
DBP
PP
MAP
cycle
rest
low
moderate
heavy
post-exercise
isometric knee extension
rest
low
moderate
heavy
post-exercise
RPP
How was the cardiovascular response to exercise simmilar/different between the exercise bouts?
Explain your answer.
Lab IX - 15
Group 3: Resistance exercise, effects of intensity and size of active muscle mass
HR
SBP
DBP PP
MAP
RPP
dynamic knee extensions
rest
low
moderate
heavy
post-exercise
dynamic dumbell curls
rest
low
moderate
heavy
post-exercise
How was the cardiovascular response to exercise simmilar/different between the exercise
bouts? Explain your answer.
Group 4: Effects of type of exercise (resistance vs isometric) and exercise intensity
HR
SBP
DBP PP
MAP
RPP
dynamic dumbell curls
rest
low
moderate
heavy
post-exercise
isometric dumbell curls
rest
low
moderate
heavy
post-exercise
How was the cardiovascular response to exercise simmilar/different between the exercise
bouts? Explain your answer.
Group 5: Aerobic exercise, effects of duration
HR
treadmill or cycle
rest
1min
2 min
5 min
10 min
15-20 min
20-30 min
post-exercise
SBP
DBP
PP
Expalin how/why duration influenced the cardiovascular response to exercise?
Lab IX - 16
MAP
RPP
Group 6: Effects of Thermal Stress during aerobic types of activity
HR
SBP
DBP
PP
normal
rest
low
moderate
heavy
post-exercise
Thermal stress
rest
low
MAP
RPP
moderate
heavy
post-exercise
How was the cardiovascular response to exercise simmilar/different between the exercise bouts?
Explain your answer.
1. Regarding the data from all of the groups, how/why are resistance/isometric exercise
different from aerobic types of exercise?
2. Regarding the data from all of the groups, how/why does intensity influence SBP, DBP,
PP, MAP?
3. Regarding the data from all of the groups, how/why does a large muscle mass influence
the cardiovascular response to aerobic exercise? How about resistance/isometric
exercise?
4. Rearding the long duration exercise bout, was there any evidence of cardiac drift? If so
what? What is cardiac drift and why does it happen?
5. Rearding the thermal stress experiment, how did thermal stress influence the
cardiovascular response to exercise
Lab IX - 17
Study questions
1. If a subject stops moving immediately following maximal exercise sometimes become
light-headed or pass out. Why ?
2. Name several factors which are believed to play a role in autoregulation in active muscle.
3. Upper and lower body exercise use very different muscle masses and vascular segments.
Would you expect them to produce the same cardiovascular responses? What differences
would you expect?
4. Name several factors that increase stroke volume by affecting EDV, and several factors
that affect stroke volume by affecting ESV.
5. What differences were observed when our subject was doing isometric actions instead of
dynamic (cycling) muscle actions?
6. How does the combination of increased sympathetic nervous system activity and
autoregulation create optimal conditions for delivery of oxygen to the active tissues?
7. In your own words what is A-vO2 difference? How is it related to the oxygen
association-dissociation curve?
8. What factors cause A-vO2 difference to increase during exercise? How do each of these
factors cause an increase in A-vO2 difference?
Lab IX - 18
9. What are the major possible limiting factors for VO2max? What factors are most likely
responsible for the difference in VO2max observed between trained and untrained
subjects?
10. If exercise intensity is constant, would you expect heart rate to remain constant? Explain
why/why not?
11. Although heart rate is not directly proportional to blood pressure, the relationship
between heart rate and blood pressure is demonstrated by what two formulas? What
formulas define the relationship between Heart Rate and VO2?
12. Why/how does respiration (the mechanics of moving air in and out of the lungs) directly
affect the cardiovascular system?
13. Explain the changes in blood pressure (systolic, diastolic, pulse, and mean) and heart rate
in response to the aerobic exercise and resistance exercise, and how are they influenced
by exercise intensity? (What happens and why?) Also, how are aerobic and resistance
exercise similar or different?
14. What are the major factors that influence the systolic and diastolic blood pressure
responses to exercise?
15. How does the size of the active muscle mass affect the systolic and diastolic blood
pressure response to aerobic exercise? How about to isometric exercise?
Lab IX - 19
16. What happens to heart rate and blood pressure post exercise? Why? What are possible
clinical implications of these findings?
17. What role does posture (e.g. supine vs standing) play in determining heart rate and blood
pressure? What adjustments are made to accomplish these changes and what causes these
adjustments to occur? How do you think posture would affect HR and BP response to
exercise?
18. What are normal resting and maximal values for HR, Q, SV, EF%, a-vO2difference,
SBP, DBP? Are there different values between trained and untrained subjects?
19. How did we measure the duration of the cardiac cycle, ventricular systole, isovolumetric
ventricular contraction, ejection period, ventricular diastole?
20. What happened to the duration of the cardiac cycle, ventricular systole, isovolumetric
ventricular contraction, ejection period, ventricular diastole during the exercise bout, and
what is the relevance of this information?
21. If we combined the thermal stress experiment and the prolonged duration experiment,
what might happen to the following: HR, SV, Q, MAP, TPR, skin blood flow, muscle
blood flow, plasma volume, and why might these changes be dangerous during prolonged
exercise in the heat?
Lab IX - 20