NOVEL METHODS FOR THE TREATMENT OF MUSCLE TRAUMA IN ATHLETES

TECAR® therapy
(CAPACITIVE-RESISTIVE ENERGY TRANSFER THERAPY)

P. Mondardini, R. Tanzi, L. Verardi, S. Briglia, A. Maione, E. Drago

CONI Institute of Sports Medicine, FMSI (Italian Sports Medicine Federation) Bologna
Interuniversitary Sports Medicine Study and Research Centre, Bologna office

ABSTRACT
Over recent years, sports activities, competitive and otherwise, have involved increasingly diverse
age groups, with a consequent increase in those taking part; sports medicine problems have
increased at a similar rate, especially in the field of the prevention and rehabilitation of sports-
related injuries affecting the musculoskeletal apparatus.

The Traumatology–Kinesiology and Rehabilitation Unit at the Institute of Sports Medicine in

Bologna is conducting research and testing new equipment for use as physiotherapy
devices with the purpose of identifying treatment protocols which, in compliance with our
bodies’ physiological repair mechanisms, effectively accelerate musculoskeletal injury
recovery times with minimal invasiveness.

The effects of TECAR® therapy devices have been assessed for the treatment of direct and
indirect acute muscle trauma in athletes, with reference to the technical characteristics of the
device and the theories pertaining to the chemical-biological interactions with tissues.

This paper presents the results of a two year study protocol intended to verify the efficacy
of TECAR® therapy in various grades of muscle lesions in athletes, by means of clinical-
instrumental evaluations (pain, swelling, functional impotence, musculotendinous
ultrasound) before and after one cycle of standardised treatment. 30 subjects (27 males and
3 females) with a mean age of 32 years (max. 58, min. 16), under observation for distractive-
type muscle trauma, have been treated. Each patient has been assessed in terms of clinical
symptomatology, and the diagnosis has been made by means of an ultrasound examination
using a 7.5 MHz probe.

The subjects have been treated at a rate of one session per day, with no more than 5 sessions per
week, at least 72 hours after the trauma, and treatment has been continued until resolution of the
situation as judged by ultrasound (reabsorption of the haematoma, the appearance of fibres in the
lesion area, scar formation), for a maximum of 18 and a minimum of 5 applications in total (mean
of 8). Despite the extent of some of the lesions treated, it has never been necessary to perform
more than 18 treatments, giving an overall duration of 4 weeks of treatment.

The excellent results obtained, in terms of speed of resolution of the clinical-

symptomatological and ultrasound situation, combined with the ease of handling of the
equipment, allow us to recommend TECAR® therapy as a remarkably effective device in the
early non-surgical treatment of muscle lesions.

KEYWORDS

Sports Medicine, traumatology, muscle trauma.

The role of a muscle is to create the force required to stabilise or move a joint. The force produced
by contraction of a muscle depends on numerous factors, but is, in any case, directly proportional
to the cross-sectional area of the muscle1.
It is a common observation that training produces muscle hypertrophy, while immobilisation soon
leads to reduced muscle volume, force, exertion capacity and neuromuscular coordination. Thus, it
is evident that the muscle apparatus is endowed with great plasticity, enabling it to alter its own
structure and, hence, performance in relation to different muscle requirements; the plasticity of
muscle tissue is dependent on the morphological and functional characteristics of the muscle itself.
There are 400 muscles in the human body, representing 40% of body weight in total, and with
lengths varying between 2 mm and 60 cm.

Muscles are surrounded by a connective tissue sheath, the epimysium, with the ends extending
into the tendons or aponeurotic membranes, which are then inserted into the periosteum. Fibrous
layers arising from the epimysium divide the muscle belly into fascicles, surrounded by a layer of
collagen known as the perimysium. Each fascicle contains 10 or more muscle fibres aligned
alongside one another and separated by the endomysium, a network of thin collagen fibres. The
muscle fibre is an elongated, cylindrical, multinucleate cell, ranging in length from a few millimetres
to over ten centimetres, with a diameter varying between 20 and 100 µm.

The muscle fibre is delimited by a membrane known as the sarcolemma, with the interior
composed of:

• sarcoplasm (less than 10% of the cell volume);

• an internal membrane system arranged between the myofibrils and consisting of transverse
tubules (invaginations in the sarcolemma) and sarcoplasmic reticulum;
• hundreds or thousands of myofibrils packed parallel to one another, occupying approximately
90% of the cell volume. Myofibrils are very thin cylinders 1-3 µm in diameter, characterised by
regularly alternating dark A disks (anisotropic disks) and clear I disks (isotropic disks)
responsible for the muscle striations (striated muscle).

The clear I disk is bisected by a darker line, the Z line: the portion of the myofibril contained
between two Z lines is the sarcomere, namely the skeletal muscle contractile unit. In turn, the
sarcomere consists of bundles of filaments regularly intercalated between one another, the
myofilaments.

These are distinguished, according to thickness, as thick filaments, endowed with “cross bridges”
formed by myosin molecules, and thin filaments, formed by actin, tropomyosin and troponin
molecules (Ca++ binding activity).

Shortening of the muscle fibre, with the generation of contractile force, is the result of reciprocal
slippage of the two sets of each half-sarcomere.

A muscle of a given length is formed by a certain number of myofibrils arranged in parallel, with
length equal to that of the muscle itself; in turn, each myofibril is formed by a certain number of
sarcomeres of equal length to one another, arranged one after the other in sequence, i.e. in series.
The force produced by a muscle on contraction is proportional to the number of myofibrils arranged
in parallel, i.e. to the cross-sectional area of the muscle itself; on the other hand, the rate of
shortening of the contracting muscle is proportional to the number of sarcomeres arranged in
series, i.e. the length of the muscle2.

Muscle contraction involves the transformation of chemical energy into mechanical energy.
The chemical energy is provided by the hydrolysis of ATP to give ADP with the release of energy
according to the following formula: ATP+H2O=ADP+H++P+E

Where E represents the energy made available for contraction of the muscle fibres.
However, the pool of ATP inside the fibre is very limited and only sufficient for a few contractions,
thus it is essential that the ATP pool be replenished by means of re-synthesis. This is achieved by
means of three pathways, used in a complementary manner depending on the intensity and
duration of exertion:
1) The anaerobic alactacid pathway: the hydrolysis of muscle phosphocreatine according to the
following reaction: PC+ADP+H+=CR+ATP

2) The anaerobic alactacid pathway: anaerobic glycolysis with the transformation of muscle
glycogen into lactic acid, according to the following reaction: ADP+P+glycogen=ATP+lactate

3) The aerobic pathway (aerobic glycolysis): in the presence of O2, fatty acids, lactate and
pyruvate enter the mitochondrial Krebs cycle which gives rise to the formation of CO2 and H2O
with the release of energy (oxidative phosphorylation according to the reaction: glycogen or
lipids+
+O2+ADP+P=ATP+CO2+H2O)3

Said pathways are differentiated on the basis of the following parameters:

√ power: maximum quantity of energy available per time unit;

√ capacity: total quantity of energy produced by the system;
√ latency: time required to obtain maximum power;
√ replenishment: time necessary for reconstitution of the system.

The functional unit of the muscle is the motor unit, consisting of the motor nerve or motor neuron,
located in the anterior horns of the spinal cord and the muscle fibres, innervated by the axon
(nerve) with its terminal branches.

The stimulus from the motor neuron is transmitted to the neuromuscular plate of the muscle fibre.
Having reached the presynaptic terminal of the nerve, the nerve stimulus releases quanta of
acetylcholine, which cross the synaptic space and depolarise the motor postsynaptic zone.
From here, the depolarisation propagates to the sarcolemma along the entire length of the muscle
fibre4.

Experimental studies5 have shown that the muscle fibres belonging to the same motor unit have
morphological, biochemical and functional characteristics in common, controlled mainly by the
motor neuron itself.

On the basis of these characteristics, muscle fibres are distinguished as:

√ slow-twitch, oxidative, red (high myoglobin content) type 1 fibres, with high fatigue resistance,
innervated by smaller motor neurons;
√ fast-twitch, anaerobic, white (low or zero myoglobin content) type 2B fibres, with low fatigue
resistance, innervated by larger motor neurons;
√ type 2A fibres, with intermediate characteristics compared to the first two.

ACUTE MUSCLE LESIONS DUE TO DIRECT TRAUMA

Lesions resulting from exogenous causes, where the muscle is struck violently by an external
contusive agent.

Clinical and diagnostic aspects

In moderate contusions, the characteristic objective signs include: skin hyperaemia, surface
swelling at the lesion site and ecchymosis (also declivous) several days afterwards. In more
serious forms, hard-elastic swelling appears caused by deeper localised haematoma; in certain
cases, the haematoma is located near the skeletal plane, hence it is difficult to identify by means of
the usual objective findings.

The symptomatology6 is characterised by pain of various degrees at the lesion and perilesion site
which is accentuated by active contraction and passive elongation, in addition to functional
impotence. In the presence of clinical manifestations of this type, ultrasound examination allows
highly precise evaluation of the anatomopathological aspects of the lesion:
• muscle volume expanded locally or diffusely and hypoechogenic due to simple oedematous
inhibition;
• the presence of intramuscular anechogenic areas due to localised bleeding. Sometimes, within
the bleeding, it is possible to recognise small hyperechogenic areas due to necrotic tissue or
coagulation.

DUE TO INDIRECT TRAUMA

Lesions from endogenous causes where the muscle is passively elongated by strong distraction
during contraction, or there is excessively rapid contraction starting from a condition of complete
relaxation.

Predisposing factors
√ Intrinsic: imbalance of force between agonist–antagonist muscles, insufficient or incorrect
muscle state, inadequate warm-up, excessive fatigue.
√ Extrinsic: inappropriate moves (unsuitable movements), unfavourable environmental and
climatic conditions (e.g.: low temperatures).

Clinical and diagnostic aspects

Elongation

Caused by a muscle sprain which does not produce an injury concentration point, since the
intensity is less than the maximum tensile capacity of the muscle7.

The dull, unfocussed pain occurs unexpectedly, often forcing the athlete to interrupt the sports-
related movements. If the pain is not of sufficient intensity to force the athlete to stop, the damage
can be exacerbated by the failure to stop the exercise.

While rest attenuates the pain symptoms, superficial and deep palpation and manipulation against
resistance accentuate the pain. Voluntary guarding is almost constant6.
In such cases, ultrasound shows a hypoechogenic area of muscle due to perifibrillar oedema,
without continuity.

Grade I lesions (distraction-contracture)

The extent of the anatomical-pathological damage is modest since the continuity solution affects
few muscle fibres8. In such cases, the pain, more localised and acute compared to elongation pain,
is accompanied by minimal functional impotence, but almost always forces the athlete to stop
sports activities.

The pain symptoms are accentuated by superficial and deep palpation, active contraction and
passive muscle stretching. By ultrasound, it is possible to observe a small intramuscular
anechogenic area, indicating bleeding and minimal fibrillar continuity.

Grade II lesions (distension-tearing)

The extent of the anatomical-pathological damage is medium, affecting a greater number of

muscle fibres9.
In such cases, the athlete reports intense pain accompanied by varying degrees of functional
impotence.
Aside from the detection of nodular swelling at the site of the lesion by palpation, the objective
characteristics are similar to those of grade I lesions, even though more obvious and more
extensive.
Ultrasound shows the muscle fibres to be interrupted (less than 30% of total muscle cross-
sectional area), in addition to an anechogenic cavity attributable to a haematoma of varying extent.
Grade III lesion (laceration)

The significant number of injured fibres leads to the partial or complete anatomical interruption of
the muscle. This is the most severe acute traumatic muscle pathology, the prognosis for which
should be considered reserved with regard to full recovery of high level sporting activities10.
The pain is very intense and often characteristic: sharp or debilitating spasm (like being struck with
a stick or stone).

The affected limb assumes an antalgic position, with the purpose of keeping the muscle in
positions affording greatest relaxation. The rupture of numerous muscle capillaries causes early
blood infiltration leading to extensive bruising, usually within 48-72 hours.

Objectively, localised hard-elastic swelling is observed while palpation, besides causing sharp
pain, gives the sensation of muscle subsidence due to loss of continuity and retraction of the
injured muscle fibres.

Ultrasound shows an extensive anechogenic area, due to conspicuous bleeding, separating two
hyperechogenic regions corresponding to the retracted muscle heads (“bell clapper”
appearance)11.
Often, when the rupture also involves the bundles surrounding the muscle, the bleeding, in the
form of a transonic area, can appear wedged between the sheaths of adjacent muscles.

PROGRESSION

Regardless of the extent (or grade) of the lesion, the healing process starts very early. The
regularity of progression influences the recovery, with varying efficacy, of the elasticity, stretching
and contractility characteristics typical of the normal tissue7.

In forms with modest severity, cell regeneration phenomena prevail over wound healing:
mononucleate satellite cells (located between the muscle fibrocell cell membranes and the basal
lamina) are activated, proliferate, are transformed into myoblasts and fuse longitudinally to form
myotubules so as to then finally differentiate into mature muscle cells.
On the other hand, in more severe injuries, the healing phenomena are more complex since
regeneration must be accompanied by wound repair tissue formation.

An inflammatory reaction, with intense localised vasodilatation, appears early in the area
surrounding the lesion, accompanied by migration of polynucleate inflammatory cells and
macrophages towards the necrotic area.
The healing process is promoted by the proliferation of capillary neovessels which carry the O2 and
nutrients required by the tissue repair-regeneration metabolic processes from the periphery
towards the centre10.

Alongside the activation of satellite cells (which develop to form the muscle fibres), fibroblast
proliferation is initiated, causing the formation of granulation tissue, and finally, connective scar
tissue.

Local O2 tension plays a fundamental role during these stages. Indeed, myoblastic regeneration
processes prevail where there is effective neovascularisation and suitable oxygen levels; on the
other hand, scar formation processes prevail with insufficient O2 levels.

Consequently, the initial phases of treatment, which should stimulate capillarisation, are very
important in order to avoid the disordered and excessive formation of fibrous connective tissue
which might compromise muscle function (healing).
INSTRUMENTAL PHYSIOTHERAPY

From the molecular viewpoint, living matter is composed of a collection of unstable molecules in a
continuous state of dynamism. As soon as the molecules are formed, within a very short time, they
have a tendency to decompose into ions, which are mobilised in order to reconstitute
neomolecules (Brownian motion).

Brownian motion causes alterations in the electrochemical balance of matter (ion exchange),
representing the basis of cellular activity in life, but none of this would occur if the cellular
biochemical system did not have available energy.

Energy represents the capacity of physical forces to perform “work”, and can be calculated as the
product of power (Watts) and time (seconds).

In physics, various forms of energy are described: thermal, kinetic, electrical, electromagnetic etc.,
which can be transformed into one another; for example, electrical energy can be transformed into
thermal or mechanical energy and vice versa.

The application of an artificial electromagnetic field, of suitable power, frequency and wavelength,
to a biological tissue, provides energy to the substrate, thus modifying the electrochemical balance
compromised by the pathological event. This is the theory justifying the use of electromagnetic
fields in physiotherapy12.

ELECTROMAGNETIC FIELDS

Put simply, electrical current may be defined as the passage of electrons from one atom in matter
to another (1st type conductors) or as the displacement of ions within a complex liquid (2nd type
conductors).

A current passing through a conductor causes the generation of an array of circular lines of force
therein: said array of force lines constitutes the electromagnetic field. If the conductor is wound to
form a coil (solenoid), the lines of force are arranged in space in accordance with a spherical-
cylindrical course, with “north” and “south” magnetic poles at either end of the field. The position of
said poles depends on the direction of "flow” of the current within the conductor; when this is
inverted then the poles also invert their positions.

With increasing frequency of current inversion, the electromagnetic field expands in space until, at
frequencies greater than 10,000 cycles per second, the lines of force break and are projected into
space, carrying energy (radiation).

We have magnetotherapy at frequencies below 100 Hz, Marconi therapy between 20 and 40 MHz,
RADAR therapy between 2 and 3 GHz, and LASER therapy above 1 THz (billion cycles per
second).

Hence, electromagnetic radiation transfers energy from a source into space.

When a 1st or 2nd type conductor is irradiated by a wave, the energy carried by the wave itself is
dissipated therein.

Living matter behaves as a 2nd type conductor, and the movement of current is achieved through
the physical movement of ions within intracellular and extracellular fluids.

The transfer of energy by means of electromagnetic waves can occur in various ways, depending
on the pulse frequency of the field: • by means of the concatenation of 1st and 2nd type conductors
(Faraday-Neumann’s law); • by means of the antenna effect; • by projection; • by means of
capacitive and resistive contact.
• Magnetotherapy exploits the Faraday-Neumann effect: the region to be treated is inserted
inside an electromagnetic field generated by a solenoid.

The biological-therapeutic effects vary depending on the field applied (magnetic induction,
measured in Gauss) and the duration of treatment:

− physico-chemical state changes (precipitates, opalescence, molecular orientation of

chemical-organic compounds, etc.);
− the action of Lorentz forces on moving charges (e.g.: increased salt flux);
− induced macroscopic (bone surface currents) and microscopic (changes in cell
membrane potential) electrical effects;
− magneto-induced micro-mechanical effects (changes in the shapes of cells and
microstructures).
Hence, the therapeutic effect may be attributed to metabolic stimulation (slight, due
to the limited power), the circulation and structures with slowed metabolism.

• The antenna effect is used in devices for Marconi and RADAR therapy.
Devices for Marconi therapy consist of an actual radio transmitter for radio transmission. The
energy transferred to the patient, by means of a flat-armed antenna system, is in the order of
400 W at a frequency of between 20 and 40 MHz.

Based on a concept similar to that of Marconi therapy, RADAR therapy makes use of more
modern technology: the much higher operating frequency (2-3 GHz) allows the use of parabolic
antennae projecting energy in a narrow beam. The irradiated area is much more defined and
hence, at the same density (W/cm2), the overall power involved is much less. This favours
better definition of the area to be treated and better control over the effects. These are mainly
represented by macroscopically exothermic vasodilatation, however unfortunately
accompanied by superficial tissue dehydration and mild inflammation.

• At frequencies in excess of 1 THz, the electromagnetic radiation from LASER therapy devices
is propagated by projection.
The main tissue interactions are photochemical, photothermal and photomechanical in nature.
The electromagnetic energy is thus transformed into heat, chemical energy and mechanical
energy.
The therapeutic effects vary depending on the type of LASER, but are mainly:
− interaction with conducting tissues (analgesic); - activation of defensive biochemical
reactions (anti-inflammatory);
− metabolic stimulation.

• TECAR® therapy exploits a different form of electromagnetic interaction which relates to the
physical model of the capacitor: capacitive and resistive contact.

A capacitor is a device consisting of two elements made of conducting material, arranged

facing one another and separated by a thin insulating layer with both elements connected to a
potential difference generator. Due to the reciprocal attraction between opposite charges, there
is increased charge density on the surface of each element closest to the interposing layer of
insulation. As the capacitor accumulates charge the current is reduced, until reaching zero
when the system is charged. At this point, if the polarity of the generator is inverted, current will
flow in the opposite direction and will charge the system with a polarity opposite to that of
before.

Transferring the concept to a biological application, a capacitor is obtained consisting of an

insulated metal electrode (moving electrode) connected to a high frequency generator
(0.5 MHz) and an electrode formed by the biological tissue which, as we have already seen, is
a 2nd type conductor13.
When an insulated electrode is applied, charge movement and concentration develops,
particularly in the soft tissue layer immediately underlying the moving electrode. When a non-
insulated electrode is applied (resistive), at a similar frequency of emission, the concentration
of charges, and hence the biological effect, occurs in the most resistive areas of the tissue
located between the active electrode and a return plate. Said points of most resistance are
represented by bone, tendons, ligaments and muscle-tendon bundles which, on being
subjected to treatment, behave like the insulating material coating the capacitive electrode14.
TECAR® THERAPY

All cell activity is achieved through changes in the electrochemical equilibrium of its components,
whereby any alterations to said equilibrium alter cell activity. Each individual cell participates
towards tissue function through morphological and electrochemical interactions15. When waves or
an electromagnetic field with appropriate characteristics interact with a cellular system, they cause
alterations in system activity. In particular, on the bases of the concepts described above, the
following theory, currently undergoing experimental testing, has been devised.

√ At low energy levels (50-100 W), despite no endothermic dissipation occurring, cellular
ultrastructural stimulation (see magnetotherapy) is obtained, with consequent increase in
energy transformations (ATP production) and O2 consumption. Due to increased tissue
metabolic demand, this leads to indirect activation of arterial and veno-lymphatic
microcirculation without dilation of the major vessels.

√ At medium energy levels (100-200 W), besides the bio-stimulation effect, there is an increase
in endogenous temperature, which is dependent on increased Brownian motion. This increase
in heat stimulates the dilation of larger bore vessels, further increasing blood flow. The thermal
effect is closely related to the displacement currents, which are concentrated, from the more
peripheral areas, in the areas of application, and are directly proportional to their intensity.
Hence, dangerous levels are never reached, unlike the situation that can occur with traditional
radiating systems (RADAR, radio, etc.).

√ At high energy levels (200-300 W), the cell bio-stimulation effect is lower, while on the other
hand, the endothermic effect is greater, with significantly increased haemolymphatic flow.
Finally, thus, stimulation and early re-oxygenation of injured tissues are obtained, along with
the prompt removal of toxic catabolites and faster recovery of normal membrane potentials. In
addition, there is accelerated activation of the defence and repair systems compromised in the
case of pathology:

1) Peripheral pain receptors and nerve fibres: restoration of membrane potential, membrane
hyperpolarisation until conduction blockage due to induced ion exchange.

2) Blood and lymph vessels: greatly increased rate of blood macro- and microcirculation and
veno-lymphatic drainage.

3) Muscles: metabolic stimulation results in increased rate of fibrillar damage repair, while the
resolution of any oedema and/or haematoma aids rapid and full functional recovery of the
fibres.

4) Joint capsule, cartilage and bone: rapid absorption of synovial fluid and the return of altered
structures to normality, by means of the aforementioned mechanisms.
From all the above points, it may be deduced that TECAR® therapy seems a rational option for
application, especially in cases in which the main pathological event is altered microcirculation
with tissue damage.

By applying these concepts to the treatment of acute muscle lesions, the effect obtained is:

− an acceleration of the normal recovery processes in low-grade lesions;

− the prevalence of myoblastic regeneration processes and capillarisation over fibrous scar
formation, with improved recovery of function for the injured muscle, in more serious
lesions.
OBJECTIVES

As ever, in the surgical, pharmacological and instrumental fields, therapeutic research activities
pursue the objective of maximum efficacy with minimum invasiveness.

In the physiotherapy sector in particular, this has led to the development of an extensive range of
electromedical devices which have, however, in the past, proved to be of little or no use. The main
reasons for the poor efficacy of instrumental therapy were to be found in the inadequacy of devices
designed and manufactured some time ago and the lack of serious clinical and laboratory
research.

Indeed, the energy sources used and the physico-biological interactions that have been, and
continue to be, exploited are numerous, often in the absence of suitable testing and a proper
therapeutic rationale. For some years, the activities of the Traumatology–Kinesiology and
Rehabilitation Unit at the CONI FMSI Institute of Sports Medicine in Bologna have been
aimed at the testing of novel ultrasound, magnetoelectric and LASER devices with the aim
of identifying the most effective devices and defining the possibilities and methods of
intervention in sports traumatology (Table 1).

Within this context, we have developed a two year protocol to study the use, in physiotherapy, of
a novel magnetoelectric device exploiting Capacitive Resistive Energy Transfer (TECAR® - CRET)
for the treatment of post-traumatic muscle distortions.

MATERIALS AND METHODS

The instrument used by us is a TECAR® therapy device with a peak power of 300 W, adjustable in
10% steps, with an emission frequency of 500,000 Hz.

In this study, we have used the device in the treatment of muscle disorders, using craniocaudal
circular and longitudinal massage as standard treatment methods. The device has a control panel
allowing the energy emitted to be varied, thus allowing the treatment protocol to be adapted
depending on the type of the patient’s response to the increase in heat.

In order to guarantee maximum uniformity of application, sessions have been conducted by

the same operator and the emission characteristics of the device have been tested periodically.
The sample of athletes treated by us in this study consists of 30 cases, represented by 27 males
and 3 females, aged between 16 and 58 (mean of 32), practicing various sporting disciplines,
under observation as a result of distractive type muscle trauma (Table 2).

The diagnosis has been established by ultrasound examination using a 7.5 MHz probe, and each
patient has been evaluated in terms of clinical symptomatology, in particular:

a) pain symptoms by means of evaluation using a visual analogue scale (VAS) from 1 to 10;
b) active and passive muscle-joint function with manoeuvring against resistance.

Serial ultrasound examinations have been performed each week by the same operator and with
the same device, in order to evaluate the organic alterations, induced during the treatment period,
within the region of the muscle lesion.

The subjects have been treated at a rate of one session per day, with no more than 5 sessions per
week, at least 72 hours after the trauma, and treatment has been continued until resolution of the
situation as judged by ultrasound (reabsorption of the haematoma, the appearance of fibres in the
lesion area, scar formation), for a maximum of 18 and a minimum of 5 applications in total (mean
of 8). In the period prior to treatment, patients have not been subjected to any other treatment,
pharmacological or otherwise, except for the application of ice to the zone affected by the lesion.
Each treatment, lasting for 30 minutes overall, has used non-insulated (resistive) and insulated
(capacitive) electrodes, at the maximum power determined by the patient’s sensitivity to tissue
heating.

It should be remembered that application has been conducted using the standard technique, i.e.
circular massage of the muscle affected by the lesion, extending to the muscle-tendon structures
immediately adjacent, in addition to craniocaudal longitudinal massage.

The massage duration has been 10 minutes with both the resistive and capacitive electrodes. The
joint segment affected by the lesion was not immobilised and walking was permitted during the
entire treatment period. None of the cases showed side effects of any kind, from the ultrasound or
clinical symptom viewpoints. In fact, patients generally reported improvements in “pain”
symptoms at the first session and reduced functional impotence has been observed.

Each athlete has been subjected to follow-up testing two weeks after the completion of the
treatment, during the active rehabilitation phase, without there being any significant negative
changes to the clinical picture present at the end of treatment examination. Despite the extent of
some of the lesions treated, it has never been necessary to perform more than 18
treatments, giving an overall duration of 4 weeks of treatment (Table 3).
 TABLE 1
NON-SURGICAL TREATMENT OF BONE-MUSCLE-JOINT DISORDERS
PHARMACOLOGICAL MAIN TISSUE INTERACTION MAIN EFFECTS INDICATIONS
THERAPY

Systemic and/or topical anti-
inflammatory agents
Biochemical: alterations in the
biochemical mechanisms of
inflammation
Direct anti-inflammation effect,
with antalgic, antipyretic,
antiedemigenic effects,
depending on the type of drug
Acute soft-tissue pathology,
acute flare-up of chronic
conditions, myofascial pain
syndromes for topical and
systemic treatment

Second level treatment of chronic or acute conditions of moderate to severe extent and for organic pain
syndromes

TREATMENT MAIN TISSUE MAIN EFFECTS INDICATIONS

INTERACTION
Ultrasound therapy Mechanical: high Decalcification, Tendinopathies, chronic
frequency sound waves fibrocalcification of soft degenerative myopathies
with associated heating structures (very slight with fibrosis and/or
effect stimulation of blood and fibrocalcifications
lymph circulation)
Magnetotherapy Weak electromagnetic Biostimulant effect on Muscle injuries, bruises,
with high membrane structures with reduced fractures, chronic
polarity and altered cell metabolism, mild pain degenerative injuries
metabolism relief effect and affecting soft tissues,
stimulation of circulation rachialgia (spinal pain)
Electrotherapy Electromagnetic Pain relief effect in cases Rachialgia and neuritic
interaction with in which nerve and/or and/or muscle-fascial
conducting structures muscle structures are pain
(excitation or depression involved Chronic pain
of conductivity)
TECAR® therapy Thermal type, with Biostimulant effect and Chronic inflammatory
excitation of chemical- stimulation of circulation events, micro and
enzymatic systems with secondary pain macro-circulation
affecting relief and anti- changes, muscle injuries
macrocirculation inflammatory effect
LASER therapy Electromagnetic, Pain relief, anti- Acute and chronic
photochemical, inflammatory and inflammatory events,
photothermal and biostimulant effects, neuritic or myofascial
photomechanical depending on the type of derived pain.
LASER Acute or chronic
arthropathies
 TABLE 2
CLASSIFICATION ACCORDING TO MUSCLE INVOLVED AND GRADE OF LESION
LESION
GRADE I GRADE II GRADE III
Limited reduction in Hypoechogenic area due to Hypoechogenic area due to
echogenicity due to perifibrillar intramuscular haematoma with intramuscular haematoma with
oedema and/or serum- the disappearance of fibrillar the disappearance of fibrillar
haematic effusion structure structure
<30% of thickness <30% of thickness
DESCRIPTION No. OF DESCRIPTION No. OF DESCRIPTION No. OF
CASES CASES CASES
Gastrocnemius 1 Rectal femoral 4 Rectal femoral 2
muscle muscle muscle
Biceps femoral 3 Biceps femoral 3 Biceps femoral 5
muscle muscle muscle
Tibialis anterior 1 Thigh adductor 1 Gastrocnemius 6
muscle muscle muscle
Soleus muscle 2 Intermediate vastus 1
Pectoral muscle 1 muscle
TOTAL 5 11 14

CONCLUSIONS

The excellent results obtained, in terms of speed of resolution of the clinical-symptomatological

and ultrasound situation, combined with the ease of handling of the equipment, allow us to
recommend TECAR® therapy as a remarkably effective device in the early non-surgical treatment
of muscle lesions.

In particular, the focussed action guaranteed by the capacitive-resistive system implies good
specificity of action in the areas affected by the lesion: the ease by which the width of the area
treated can be controlled makes it possible to exclude any particularly delicate tissue areas (skin
continuity, mucosa, etc.). The absence of any side effects detected by the study confirms the
theoretical safety of capacitive-resistive energy transfer.

Biologically appreciable results can be obtained at depth without excessively high energy
projection or concentration. Indeed, due to the effect of capacitive-resistive transfer, there is no
contact current, only movement of charges (ions) due to attraction and repulsion. It has not been
possible to conduct a statistical investigation on recovery times due to the lack of available
literature on the topic.

However, based on our experience, we feel it may be stated that recovery times are very
fast, and rehabilitative options are improved. This is possible thanks to the experimentally
verified therapeutic efficacy of the treatment on the symptoms of pain and functional
impotence, the rapid remission of which allows the early initiation of corrective
rehabilitative techniques.
Figures 1-2 Application of TECAR® therapy with capacitive electrode (left) and resistive
electrode (right).

TABLE 3
NUMBER OF SESSIONS AND ULTRASOUND RESOLUTION TIMES
LESION
PARAMETERS
GRADE I GRADE II Grade III
TOTAL CASES 5 11 14
Max. 10 sessions: 14 days Max. 14 sessions: 21 days Max. 18 sessions: 28 days
Min 4 sessions: 7 days Min 4 sessions: 7 days Min 6 sessions: 14 days
Mean 5.1 sessions: 8 days Mean 8.6 sessions: 14 days Mean 11.7sessions 19 days
:

REFERENCES:

1. COLO A.J., EAGLESTONE M.A.: The benefits of deep heat. Ultrasound and Electromagnetic
Diathermy. Physic Sportsmedicine 1994; 22:77-88
2. GRIBAUDO C.G., ASTEGIANO P., CANALA G.L., GANZIT G.P.: Treatment of acute and
chronic skeletal muscle lesions with resistive and capacitive energy transfer hyperthermy:
preliminary results in Radiation in Medicine: quality and safety. Meeting Proceedings – Health
Physics – No. 1/97 January/March; 379-381
3. MCMEEKEN J.: Electrotherapy in: Zuluaga et el. Eds. Sportphysiotherapy, Applied Science &
practice: Melbourne: Churchill Livingstone 1995, 233-244
4. LEY A., CLADELLAS J.M., DE LAS HERAS P. ET AL.: Capacitive electrical transfer (CET).
Técnica no invasiva de Hipertermia profunda en el tratamiento de los gliomas cerebrales.
Resultados preliminares. Neurochirurgia 1992; 3:118-123
5. CAIOZZO V.J. ET AL. Training induced alterations of the in vivo force-velocity relationship of
human muscle. J. Appl. Physiol. 1981; 51:750-4.
6. FRANKEL V.H. ET AL. Basic Biomechanics of the skeletal system. Philadelphia: Lea and
Febiger. 1980
7. ROTBSTEIN J.M. Muscle biology: clinical considerations. Arch. Phys. Med. Rehab. 1982; 62:
1823-30
8. HUXLEY A. Muscular contraction. Ann. Rev. Physiol. 1988; 50:1-16
9. THORNSTENSSON A. Muscle strength, fibre types and enzyme activities in man. Acta
Physiol. Scand. 1976; (suppl.) 443
10. KIBLER W.B. Clinical aspects of muscle injury. Med. Sci. Sports Exerc. 1990; 4:450
11. LEHTO MUK ET AL. Muscle injuries, their healing process and treatment. Ann. Chir. Gynaecol.
1991; 80:102
12. MOWAT A. Soft tissue injuries. Practitioner. 1992; 236:1068
13. PECINA M. ET AL. Overuse injuries of the musculoskeletal system. CRC Press INC, 1993
14. BENAZZO F. ET AL. Current directions in the pathogenesis, development and treatment of
muscle haematomas in athletes. I J Sports Traumatol 1989; 4:273
15. SANTILLI G. ET AL. Muscle pathology: the role of ultrasound and telethermography. In:
Diagnostica per immagini in Medicina dello Sport. Milan: Ed. Masson, 1989
16. BORG M. J. ET AL. Magnetic fields in physiotherapy. Minerva Med. 1996; 87:495-7
17. ZAUNER A. Introducción a la transferencia eléctrica capacitiva. Barcelona: Jims, 1993:143
18. CALBET J. Tratado de la transferencia eléctrica capacitiva. Barcelona Doyma. 1992
19. MYERSON R.J. ET AL. Principles and practice of radiation oncology. Philadelphia: Lippincott-
Raven Publishers, 1997; 644-6