ERGOMETRY
For evaluation of response of our organism to stress test we can use dynamic, statick, elektric,
farmakologic, cold, hypoxic, psychic tests. In the most cases we use the dynamic test
(exercise).
There are several phases in each dynamic test (ergometry):
• PREPARATORY PHASE: preparation to the test, connecting to equipment
• RESTING PHASE: recording of resting values
• ―WARM UP‖ PHASE: application of low workload in order to increase tissue
perfusion and improve joints mobility
• LOAD PHASE: exposure of examined person to graduated physical work
• ―COOL DOWN PHASE‖: workload of low intensity supporting catabolites removal
(lactic acid), helping heart rate recovery, reducing vertigo and collapses (due to afterwork
hypotension)
• RECOVERY PHASE: follow-up exercise
EXERCISE
STATIC
(IZOMETRIC)
DYNAMIC
(IZOTONIC)
muscle develops
force, but muscle
length does not
change
muscle length varies
continuously, but force
does not change
AUXOTONIC
strength and muscle
length are changing
DYNAMIC
POZITIVE
muscle shortens against
constant or rising
resistance, some of the
energy in the muscle is
converted into kinetic
or potential energy
muscle during contraction
is driven by external force,
the bulk of the energy is
converted into heat
There are some types of „load test―
INDICATIONS FOR EXAMINATION
 Basic medical examination of athletes
 Indication of preventive cardiology
 Indications of differential diagnosis
 Assessment indication
 Pharmacotherapeutic indications
CONTRAINDICATIONS
Absolute contraindications:
 Systolic blood pressure decreases by more than 10 mmHg with increase in work rate,
or drops below baseline in the same position, with other evidence of ischemia
 Increase in nervous system symptoms: Dizziness, ataxia or near syncope
 Moderate to severe anginal pain (above 3 on standard 4-point scale)
 Signs of poor perfusion, e.g. cyanosis or pallor
 Request of the test subject
 Technical difficulties (e.g. difficulties in measuring blood pressure or ECG)
 ST Segment elevation of more than 1 mm in aVR, V1 or non-Q wave leads
 Sustained ventricular tachycardia
Relative indications:
• Systolic blood pressure decreases by more than 10 mmHg with increase in work rate,
or drops below baseline in the same position, without other evidence of ischemia
• ST or QRS segment changes, e.g. more than 2 mm horizontal or downsloping ST
segment depression in non-Q wave leads, or marked axis shift
• Arrhythmias other than sustained ventricular tachycardia e.g. Premature ventricular
contractions, both multifocal or triplet; heart block; supraventricular tachycardia or
bradyarrhythmias
• Intraventricular conduction delay or Bundle branch block or that cannot be
distinguished from ventricular tachycardia
• Hypertensive response (systolic blood pressure > 250 mmHg or diastolic blood
pressure > 115 mmHg)
single stage test continuous incremental steps „ramp― protocolintermittent incremental steps
COMPLICATIONS
• In 0.05% cases - acute myocardial infarction or malignant arrhythmia
• The risk of sudden death in patients is approximately 0.01%
• Another risk is the potential muscle or joint injuries as the result of excessive load
(this risk is particularly high in patients retirement age)
• There may also marginal complications such as dizziness, weakness and persistent
fatigue
BREAK INDICATION OF STRESS TEST
1. Typical symptoms of angina pectoris
2. Dyspnoea
3. Ischemic ECG signs, especially typical ischemic ST depression progressing with
increasing workload
4. Rise of SBP above 240 mmHg or DBP above 120 mmHg
The occurrence of these changes on ECG: various forms of sudden tachycardia, atrial
fibrillation, blockade in connection with the workload
PREPARATION FOR EXAMINATION
It is recommended that at least 3 hours before examination patient does not eat or drink in
large quantities, smoke and at least 12 hours before examination refrains unusual physical
exercise
After consulting with a doctor, it should be discontinued medicines:
• beta-blockers (eg. Vasocardin, Betaloc, Egiloc, Tenormin, Concor, Lokren, Sectral ...)
• nitrates (Cardiket, Isomer, Iso-Mack, Mycor, Nitro-Mack, Mack Mono, Olicard,
Sorbimon, Corvaton, Molsihexal ...)
EFFECTS OF EXERCISE
CHANGES IN VENTILATION
During exercise, the amount of O2 entering the blood in the lungs is increased because the
amount of O2 added to each unit of blood and the pulmonary blood flow per minute are
increased. The Po2 of blood flowing into the
pulmonary capillaries falls from 40 to 25
mmHg or less, so that the alveolar–capillary
Po2 gradient is increased and more O2 enters
the blood. Blood flow per minute is
increased from 5.5 L/min to as much as 20–
35 L/min. The total amount of O2 entering
the blood therefore increases from 250
mL/min at rest to values as high as 4000
mL/min. The amount of CO2 removed from
each unit of blood is increased, and CO2
excretion increases from 200 mL/min to as
much as 8000 mL/min. The increase in O2
uptake is proportional to work load, up to aFigure1: relation between work load,blood
lactate level,and O 2 uptake.
maximum. Above this maximum, O2 consumption levels off and the blood lactate level
continues to rise (Figure 1). The lactate comes from muscles in which aerobic resynthesis of
energy stores cannot keep pace with their utilization, and an oxygen debt is being incurred.
Ventilation increases abruptly with the
onset of exercise, which is followed a
further a brief pause by a further, more
gradual increase (Figure 2). With
moderate exercise, the increase is due
mostly to an increase in the depth of
respiration; this is accompanied by an
increase in the respiratory rate when the
exercise is more strenuous. Ventilation
abruptly decreases when exercise ceases,
which is followed a further a brief pause
by a more gradual decline to preexercise
values. The abrupt increase at the start of
exercise is presumably due to psychic stimuli and afferent impulses from proprioceptors in
muscles, tendons, and joints. The more gradual increase is presumably humoral, even though
arterial pH, P co2, and Po2 remain constant during moderate exercise. The increase in
ventilation is proportional to the increase in O2 consumption, but the mechanisms responsible
for the stimulation of respiration are still the subject of much debate. It can be caused by:
increase in body temperature, increases the plasma K+
level, changes of CO2 and O2 in blood.
When exercise becomes more vigorous, buffering of the increased amounts of lactic acid that
are produced liberates more CO2, and this further increases ventilation. With increased
production of acid, the increases in ventilation and CO2 production remain proportional, so
alveolar and arterial CO2 change relatively little. Because of the hyperventilation, alveolar
Po2 increases. With further accumulation of lactic acid, the increase in ventilation outstrips
CO2 production and alveolar Pco2 falls, as does arterial Pco2. The decline in arterial Pco2
provides respiratory compensation for the metabolic acidosis produced by the additional lactic
acid. The additional increase in ventilation produced by the acidosis is dependent on the
carotid bodies and does not occur if they are removed.
The respiratory rate after exercise does not reach basal levels until the O2 debt is repaid. This
may take as long as 90 min. The stimulus to ventilation after exercise is not the arterial Pco2,
which is normal or low, or the arterial Po2, which is normal or high, but the elevated arterial
H+
concentration due to the lactic acidemia. The magnitude of the O2 debt is the amount by
which O2 consumption exceeds basal consumption from the end of exertion until the O2
consumption has returned to preexercise basal levels. During repayment of the O2 debt, the O2
concentration in muscle myoglobin rises slightly. ATP and phosphorylcreatine are
resynthesized, and lactic acid is removed. Eighty per cent of the lactic acid is converted to
glycogen and 20% is metabolized to CO2 and H2O.
CARDIOVASCULAR SYSTEM IN EXERCISE
Cardiovascular control during exercise involves systemic regulation (cardiovascular centers in
the brain, with their autonomic nervous output to the heart and systemic resistance vessels) in
tandem with local control. Increased sympathetic drive elevates heart rate and cardiac
Figure 2: Diagrammatic representation of changes in
ventilation during exercise
contractility, resulting in increased cardiac output; local factors in the coronary vessels
mediate coronary vasodilation. Increased sympathetic vasoconstrictor tone in the renal and
splanchnic vascular beds, and in inactive muscle, reduces blood flow to these tissues. Blood
flow to these inactive regions can fall 75% if exercise is strenuous. Increased vascular
resistance and decreased blood volume in these tissues helps maintain blood pressure during
dynamic exercise. In contrast to blood flow reductions in the viscera and in inactive muscle,
the brain autoregulates blood flow at constant levels independent of exercise. The skin
remains vasoconstricted only if thermoregulatory demands are absent.
Muscle blood flow.
A key requirement of cardiovascular function in exercise is to deliver the required oxygen and
other nutrients to the exercising muscles. For this purpose, the muscle blood flow increases
drastically during exercise. Figure 3 shows a recording of muscle blood flow in the calf of a
person for a period of 6 minutes during moderately strong intermittent contractions. Note not
only the great increase in flow—about 13-fold—
but also the flow decrease during each muscle
contraction. Two points can be made from this
study: (1) The actual contractile process itself
temporarily decreases muscle blood flow
because the contracting skeletal muscle
compresses the intramuscular blood vessels;
therefore, strong tonic muscle contractions can
cause rapid muscle fatigue because of lack of
delivery of enough oxygen and other nutrients
during the continuous contraction. (2) The blood
flow to muscles during exercise increases
markedly. The following comparison shows the
maximal increase in blood flow that can occur in
a well-trained athlete.
Thus, muscle blood flow can increase a
maximum of about 25-fold during the most strenuous exercise. Almost one half this increase
in flow results from intramuscular vasodilation caused by the direct effects of increased
muscle metabolism. The remaining increase results from multiple factors, the most important
of which is probably the moderate increase in arterial blood pressure that occurs in exercise,
usually about a 30 per cent increase. The increase in pressure not only forces more blood
through the blood vessels but also stretches the walls of the arterioles and further reduces the
vascular resistance.
Therefore, a 30 per cent increase in blood pressure can often more than double the blood flow;
this multiplies the great increase in flow already caused by the metabolic vasodilation at least
another twofold.
Work output, oxygen consumption, and
cardiac output during exercise.
Figure 4 shows the interrelations among
work output, oxygen consumption, and
cardiac output during exercise. It is not
surprising that all these are directly related
to one another, as shown by the linear
Figure 3:Effects of muscle exercise on blood
flow in the calf of a leg during strong
rhythmical contraction
functions, because the muscle work output increases oxygen consumption, and oxygen
consumption in turn dilates the muscle blood vessels, thus increasing venous return and
cardiac output. Typical cardiac outputs at several levels of exercise are the following:
Thus, the normal untrained person can increase cardiac output a little over fourfold, and the
well-trained athlete can increase output about sixfold (шndividual marathoners have been
clocked at cardiac outputs as great as 35 to 40 L/min, seven to eight times normal resting
output).
Role of stroke volume and heart rate in increasing the cardiac output.
Figure 5 shows the approximate changes
in stroke volume and heart rate as the
cardiac output increases from its resting
level of about 5.5 L/min to 30 L/min in
the marathon runner. The stroke volume
increases from 105 to 162 milliliters, an
increase of about 50 per cent, whereas
the heart rate increases from 50 to 185
beats/min, an increase of 270 per cent.
Therefore, the heart rate increase
accounts by far for a greater proportion
of the increase in cardiac output than
does the increase in stroke volume
during strenuous exercise. The stroke
volume normally reaches its maximum
by the time the cardiac output has
increased only halfway to its maximum. Any further increase in cardiac output must occur by
increasing the heart rate.
BODY HEAT IN EXERCISE
Almost all the energy released by the body’s metabolism of nutrients is eventually converted
into body heat. This applies even to the energy that causes muscle contraction for the
following reasons: First, the maximal efficiency for conversion of nutrient energy into muscle
work, even under the best of conditions, is only 20 to 25 per cent; the remainder of the
nutrient energy is converted into heat during the course of the intracellular chemical reactions.
Second, almost all the energy that does go into creating muscle work still becomes body heat
because all but a small portion of this energy is used for (1) overcoming viscous resistance to
the movement of the muscles and joints, (2) overcoming the friction of the blood flowing
through the blood vessels, and (3) other, similar effects—all of which convert the muscle
contractile energy into heat.
Now, recognizing that the oxygen consumption by the body can increase as much as 20-fold
in the well-trained athlete and that the amount of heat liberated in the body is almost exactly
proportional to the oxygen consumption, one quickly realizes that tremendous amounts of
heat are injected into the internal body tissues when performing endurance athletic events.
Next, with a vast rate of heat flow into the body, on a very hot and humid day so that the
Figure 5: approximate stroke volume output and heart rate
at different levels of cardiac output in a marathon athlete
sweating mechanism cannot eliminate the heat, an intolerable and even lethal condition called
heatstroke can easily develop in the athlete.
THERMOREGULATION AND EXERCISE
Mean body temperature
Tbody = (0.6 x Tcore) + (0.4 x Tskin)
This equation gives the average body temperature at any given time such that:
- 60% is accounted for by the core
- 40% is accounted for by the skin
What regulates body temperature?
• Hypothalamus:
– contains the central coordinating center for temperature regulation
– receives input from:
• thermal receptors in the skin provide information
• temperature of the blood (as it flows by hypothalamus) provides
information
– anterior hypothalamus – stimulates heat loss
– posterior hypothalamus – stimulates heat conservation
Mechanisms of temperature regulation
When it is hot: (need for heat loss)
– there is vasodilation of subcutaneous blood vessels; more sweating (↑ heat loss)
– there is decreased muscle activity; decreased secretion of thyroxine and epinephrine (↓ heat
production)
When it is cold: (need for heat retention)
– there is vasoconstriction of skin blood vessels; also curling up to stay warm (↓ heat loss)
– shivering and increased voluntary muscle activity; increased secretion of thyroxine and
epinephrine (↑ heat production)
Heat Loss Mechanisms
• Radiation – emission of electromagnetic heat waves
• Conduction – direct transfer of heat through a liquid, solid, or gas (direct contact)
• Convection – transfer of heat via air currents over surface of skin
• Evaporation – vaporization of water from respiratory passages or surface of skin (2-4
million sweat glands)
Factors affecting heat loss
• Increased ambient temperature (reduces effectiveness of heat loss particularly by radiation,
conduction, and convection)
• Increased relative humidity (reduces effectiveness of heat loss by evaporation)
• Decreased wind velocity (reduces both convective and evaporative effectiveness)
• Reduced surface exposed to environment (reduces effectiveness of all heat loss mechanisms)
ERGOMETRIE
Bicycle ergometry + continuous incremental steps protocol + 2-lead ECG
PROCEDURE:
The experimental person takes a seat on the bicycle ergometer. Place five ECG electrodes on
the chest (scheme near PC). Connect the electrodes and PowerLab recording system using
ECG cables.
Start up the program called ERGOMETRY by double-clicking the icon. Set the amplifier
sensitivity for ECG registration in channel 1 and 2. Upper two channels represent the ECG
curve obtained from 2-lead ECG, lower two channels represents the heart rate calculated from
the RR intervals of corresponding ECG leads.
Record continuous ECG during all 5 phases of the exercise.
1. Resting period – record resting ECG for 1 minute
2. Warm-up period – set 20W on the ergometer, the experimental person is cycling at the
constant speed (60 turns/minute) for 1 minute.
3. Stress testing
Stage 1: set 1 W/kg on the ergometer (weight of the person x 1W), the person is cycling for 3
minutes with the constant speed;
Stage 2: set 2 W/kg on the ergometer (weight of person x 2 W), the person is cycling for 3
minutes with the constant speed;
Stage 3: set 3 W/kg on the ergometer (weight of the person x 3 W), the person is cycling for 3
minutes with the constant speed;
4. Cool-down period: set 20 W on the ergometer, the person is cycling for 1 minute with the
constant speed.
5. Recovery period: the person is just sitting on ergometer without pedaling for 9 minutes;
subsequently stop the ECG recording, insert comments about particular phases, and save the
recording as ―Ergometry XY‖ into the computer memory.
Evaluation:
In the 3rd
or 4th
channel (that represent heart rate calculated from the 1st
and 2nd
ECG
channels, respectively) choose last 30 seconds of each phase ( resting period, warm-up period,
3 endurance stages, cool-down period and recovery period at the end of the 3rd
,6th
and 9th
minute);the value of the heart rate will appear in mini-window.
Use the obtained data to construct a graph of heart rate (axis y) dependence on time and work
(axis x). Interpolate a line among points representing the endurance phases and estimate work
at the heart rate 170/minute (index W170). Compare your value with physiological values.
Protocol:
Conclusion: …………………………………………………………………………………
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person rest 20W 1W/kg 2W/kg 3W/kg 20W 3.min 6.min 9.min
heartrate/minute
Time,min