Name: Numer: Study group:
This text was supported by project FRMU no. MUNI/FR/1552/2015 (Faculty of Medicine, Masaryk University).
Theoretical part
Ergometry
In order to evaluate how bodies react to stress, we can use dynamic, static, electric,
pharmacological, cold, hypoxic, and mental tests. In most cases we use the dynamic test
(exercise).
Exercise
 Static (isometric) – muscle develops force, but muscle length does not change
 Dynamic (isotonic) - muscle length varies continuously, but force does not change
 Positive - muscle shortens against constant or rising resistance, some of the
energy in the muscle is converted into kinetic or potential energy
 Negative - muscle during contraction is driven by external force, the bulk of
the energy is converted into heat
 Auxotonic - strength and muscle length are changing
There are several phases in each dynamic test (ergometry):
 preparatory phase: preparation for the test, connecting to equipment
 resting phase: recording of resting values
 ―warmup‖ phase: application of low workload in order to increase tissue perfusion and
improve joint mobility
 load phase: exposure of examined person to graduated physical effort
 ―cooldown phase‖: low-intensity workout supporting removal of catabolites (lactic acid),
helping heart rate recovery, reducing vertigo and collapses (due to hypotension following
effort)
 recovery phase: follow-up exercise
Indications for examination
 Basic medical examination of athletes
 Indication of preventive cardiology
 Indications of differential diagnosis
Name: Numer: Study group:
This text was supported by project FRMU no. MUNI/FR/1552/2015 (Faculty of Medicine, Masaryk University).
 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)
Complications
 In 0.05% of cases – acute myocardial infarction or malignant arrhythmia
 The risk of sudden death in patients is approximately 0.01%
 Other risks are potential muscle or joint injuries as the result of excessive load (this
risk is particularly high in patients of retirement age)
 There may also marginal complications such as dizziness, weakness and persistent
fatigue
Break indication of stress test
 Typical symptoms of angina pectoris
 Dyspnoea
 Ischemic ECG signs, especially typical ischemic ST depression progressing with
increasing workload
 Rise of SBP above 240 mmHg or DBP above 120 mmHg
Occurrence of the following changes on ECG: various forms of sudden tachycardia, atrial
fibrillation, blockade in connection with the workload
Name: Numer: Study group:
This text was supported by project FRMU no. MUNI/FR/1552/2015 (Faculty of Medicine, Masaryk University).
Preparation for examination
It is recommended that for at least 3 hours before the examination, the patient does not eat or
drink in large quantities, or smoke, and at least 12 hours before examination the patient should
refrain from unusual physical exercise.
After consulting with a doctor, the following medications should be discontinued:
 beta-blockers (eg. Vasocardin, Betaloc, Egiloc, Tenormin, Concor, Lokren, Sectral,
etc.)
 nitrates (Cardiket, Isomer, Iso-Mack, Mycor, Nitro-Mack, Mack Mono, Olicard,
Sorbimon, Corvaton, Molsihexal, etc.)
Effects of exercise
Changes in ventilation
During exercise, the amount of O2 entering the blood in the lungs increases, 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 increases 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 a 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 incurred.
Ventilation increases abruptly with the onset of exercise, which is followed after 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
Name: Numer: Study group:
This text was supported by project FRMU no. MUNI/FR/1552/2015 (Faculty of Medicine, Masaryk University).
exercise ceases, which is followed after a brief pause by a more gradual decline to preexercise
values. The abrupt increase at the start of exercise is presumably due to mental
stimuli and afferent impulses from proprioceptors in the 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 an increase in body temperature, increase in
the plasma K+
level, or changes of CO2 and O2 in blood.
Figure1: relationship between work load, blood lactate level, and O 2 uptake.
When exercise becomes more vigorous, buffering of the increased amounts of lactic acid that
are produced frees up 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 minutes. The stimulus to ventilation after exercise is not the arterial
Pco2, which is normal or low, nor 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 the heart rate and cardiac
contractility, resulting in increased cardiac output; local factors in the coronary vessels
Name: Numer: Study group:
This text was supported by project FRMU no. MUNI/FR/1552/2015 (Faculty of Medicine, Masaryk University).
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 by 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 delivering 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 of 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.
Name: Numer: Study group:
This text was supported by project FRMU no. MUNI/FR/1552/2015 (Faculty of Medicine, Masaryk University).
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 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).
Name: Numer: Study group:
This text was supported by project FRMU no. MUNI/FR/1552/2015 (Faculty of Medicine, Masaryk University).
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
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 the hypothalamus) provides
information
 anterior hypothalamus – stimulates heat loss
 posterior hypothalamus – stimulates heat conservation
Name: Numer: Study group:
This text was supported by project FRMU no. MUNI/FR/1552/2015 (Faculty of Medicine, Masaryk University).
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)