**2. The definition of muscular lesion**

Few authors have explicitly defined the term "muscular lesion", even though some have attempted to link the concept of lesion to that of the loss of proper muscular function (Brooks et al., 1995). However, identifying muscular lesion with the simple loss of function isn't altogether correct, indeed muscular function may be nullified by events, such as tiredness or atrophy, which have nothing to do with the detrimental mechanism. For these reasons, even though the concept of functionality loss represents one of the main characteristics of the lesion of the muscle, we believe that the correct definition of muscular lesion cannot overlook the concept of "damage" towards the muscular structure. Therefore, a correct definition in this sense could be the following: " muscular lesion is identifiable by the loss of functionality of the muscle caused by damage, more or less severe, on a level of muscular structure or on a level of anatomical sites assigned to transmit strength", intending with the last explanation

© 2013 Bisciotti and Eirale; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

the damage on a level of tendon-muscular passage. This definition clears the concept that in the field of muscular lesion the loss of function cannot be separated from the concept of structural damage.

new systems of focal adhesion, could in fact induce a modification of the transcription and translation processes of mRNA, inducing the muscular cell to raise the proteic synthesis and induce the variation the characteristics of the expressed isoforms from the heavy chain of the

Etiology, Biology and Treatment of Muscular Lesions

http://dx.doi.org/10.5772/56602

5

**Figure 1.** Schematic representation of the adhesion of muscle fiber to extracellular muscular-matrix (ECM). Each fiber contains specific chains of molecules defined integrin and dystrofin, which connect the myofilamentous contractor ap‐ paratus to the ECM through the sarcolemma. The main part of the integrin is located in the neuro-muscular junction. The sarcomeric actin ties itself through several molecules, located on a sarcomeral level, to β1 sub-unit of the trasn‐ membranal muscle specific integrin 7 β1, which is then tied to the ECM protein. The molecules of the dystrofin associ‐ ated complex, are relatively distributed in a homogenous way along the whole sarcolemma, even though they are particularly abundant in the muscle-.tendon junction and the neuro-muscular junction. The actin ties itself to the dys‐

In the end we have to remember the role of dystrofin as a marker of muscular lesion. Some research conducted on animal models show a conspicuous decrease in coloration of the dystrofin in the muscle immediately after an eccentric contraction (Koh and Eswcobedo, 2004; Lovering and Deyne, 2004). In these studies the loss of dystrofin was associated with the decrease of another membrane protein, the beta-spectrin whose role would seem similar to that of the dystrofin in the stabilization of the membrane. On the other hand the role of dystrofin in maintaining membrane integrity as well as its stability is confirmed by the fact that its missing genetics is at the base of the onset of the Duchenne muscular dystrophy

All the same, it is not entirely correct to consider the loss of membrane integrity as a negative event able to compromise muscular homeostasis through the destruction of the barrier which allows the maintenance of an ideal balance between intra and extra cells molecules. In effect a reduced and transitory destruction of the membrane may allow a normal pathway for the

trofin which is in turn associated with three complex proteins: distroglicans, sarcoglicans and sintrofins.

(Hoffman et al., 1987; Zubrycka-Gaarn et al., 1998).

myosin (Lee et al.., 1991).

#### **3. The connection of the contractile apparatus to the extra-cellular matrix**

The link of the muscle fibers to the tendon or to the fascia, must have the capacity to resist considerable strength which can go above 1000 kg during maximum type strain (Tidball and Daniel, 1986; Tidball, 1991;). To possess such a great strength, each fiber contains specific molecule chains: integrin and the complex distrofin-glycoprotein (Mayers,2003; Michele and Campbell, 2003). These two complex proteins connect the contractor myofilamentous appa‐ ratus to the extracellular matrix(ECM) through the sarcolemma. (Brown, 1996; Giancotti and Rouslathi,1999; Chiquet, 2003; Chargé and Rudnicki, 2004; Ervasti, 2004; Sunada and Camp‐ bell,1995; Kääriäinen et al., 2000;). It is necessary to remember briefly that ECM is made up of an intricate network of macromolecules formed by fibrous protein included in an gel of polysaccharides, L'ECM, apart from being particularly present on a skeletal muscle level, it also results in abundance in the connective tissue. The integrins are a family of "adhesion molecules" positioned in the cellular membrane, which cover a fundamental role in many biological processes tied related to the tissue survival, at growth and regeneration. In addition, the integrins actively participate in the cellular communication, for example in the case of signal between cell and cell, of interaction between cell and ECM or in the process of translation of the signal inside and outside the cell itself (Giancotti, 1999, Mayer, 2003; Rouslathi, 1996). In a healthy muscular fiber the majority of integrins are positioned on a level with the junction of tendon muscle (MTJs) (Bao et al., 1993; Kääriäinen et al., 2000a; 2000b; Mayer, 2003) and are organized in a structure specifically named "integrin associated-complex" (figure1). In this complex the sarcomerica terminal ties, through different sub-sarcolemmal molecules, to the sub-unit B1 of the transmembral integrin muscle specific x7B1 (Otey et al., 1990; Song et al., 1994; Yao et al., 1996; Kääriäinen et al., 2000a; Mayer, 2003), which in turn connects the intracellular contractor apparatus with the surrounding ECM by means of the link with the proteins ECM (Burkin and Kaufman, 1999) (Figure1). On the contrary what we can observe for the integrin, whose accumulation is met in proximity of the distal of the muscular fiber the molecules of the complex distrofin-glycoprotein(figure1) are relatively distributed along the entire sarcolemma, even though they result more abundant on a level of the MTJs and the neuro-muscular junction (Sunada and Campbell, 1995; Brown,1996; Hoffman,1996; Cohn and Campbell, 2000; Kääriäinen and et al., 2000a; Michele and Campbell, 2003). The terminal actin ties with the distrofin which in turn ties with three proteic complexes: the distroglicans, the sarcoglicans and the sintrofins (Cohn and Campbell, 200; Ground, 1991; Michele and Camp‐ bell, 2003, of these the x-distroglicans tie with the ECM proteins (Michele and Campbell, 2003). The integrins therefore form true " adhesion focal complexes", which form articulated biological systems which show themselves extremely sensitive in comparison with mechanical strengths which stimulate the muscular complex and could, for this reason, perform a key role in the inducing mechanism of hypertrofic phenomena (FLuk et al., 1991). The formation of new systems of focal adhesion, could in fact induce a modification of the transcription and translation processes of mRNA, inducing the muscular cell to raise the proteic synthesis and induce the variation the characteristics of the expressed isoforms from the heavy chain of the myosin (Lee et al.., 1991).

the damage on a level of tendon-muscular passage. This definition clears the concept that in the field of muscular lesion the loss of function cannot be separated from the concept of

**3. The connection of the contractile apparatus to the extra-cellular matrix**

The link of the muscle fibers to the tendon or to the fascia, must have the capacity to resist considerable strength which can go above 1000 kg during maximum type strain (Tidball and Daniel, 1986; Tidball, 1991;). To possess such a great strength, each fiber contains specific molecule chains: integrin and the complex distrofin-glycoprotein (Mayers,2003; Michele and Campbell, 2003). These two complex proteins connect the contractor myofilamentous appa‐ ratus to the extracellular matrix(ECM) through the sarcolemma. (Brown, 1996; Giancotti and Rouslathi,1999; Chiquet, 2003; Chargé and Rudnicki, 2004; Ervasti, 2004; Sunada and Camp‐ bell,1995; Kääriäinen et al., 2000;). It is necessary to remember briefly that ECM is made up of an intricate network of macromolecules formed by fibrous protein included in an gel of polysaccharides, L'ECM, apart from being particularly present on a skeletal muscle level, it also results in abundance in the connective tissue. The integrins are a family of "adhesion molecules" positioned in the cellular membrane, which cover a fundamental role in many biological processes tied related to the tissue survival, at growth and regeneration. In addition, the integrins actively participate in the cellular communication, for example in the case of signal between cell and cell, of interaction between cell and ECM or in the process of translation of the signal inside and outside the cell itself (Giancotti, 1999, Mayer, 2003; Rouslathi, 1996). In a healthy muscular fiber the majority of integrins are positioned on a level with the junction of tendon muscle (MTJs) (Bao et al., 1993; Kääriäinen et al., 2000a; 2000b; Mayer, 2003) and are organized in a structure specifically named "integrin associated-complex" (figure1). In this complex the sarcomerica terminal ties, through different sub-sarcolemmal molecules, to the sub-unit B1 of the transmembral integrin muscle specific x7B1 (Otey et al., 1990; Song et al., 1994; Yao et al., 1996; Kääriäinen et al., 2000a; Mayer, 2003), which in turn connects the intracellular contractor apparatus with the surrounding ECM by means of the link with the proteins ECM (Burkin and Kaufman, 1999) (Figure1). On the contrary what we can observe for the integrin, whose accumulation is met in proximity of the distal of the muscular fiber the molecules of the complex distrofin-glycoprotein(figure1) are relatively distributed along the entire sarcolemma, even though they result more abundant on a level of the MTJs and the neuro-muscular junction (Sunada and Campbell, 1995; Brown,1996; Hoffman,1996; Cohn and Campbell, 2000; Kääriäinen and et al., 2000a; Michele and Campbell, 2003). The terminal actin ties with the distrofin which in turn ties with three proteic complexes: the distroglicans, the sarcoglicans and the sintrofins (Cohn and Campbell, 200; Ground, 1991; Michele and Camp‐ bell, 2003, of these the x-distroglicans tie with the ECM proteins (Michele and Campbell, 2003). The integrins therefore form true " adhesion focal complexes", which form articulated biological systems which show themselves extremely sensitive in comparison with mechanical strengths which stimulate the muscular complex and could, for this reason, perform a key role in the inducing mechanism of hypertrofic phenomena (FLuk et al., 1991). The formation of

structural damage.

4 Muscle Injuries in Sport Medicine

**Figure 1.** Schematic representation of the adhesion of muscle fiber to extracellular muscular-matrix (ECM). Each fiber contains specific chains of molecules defined integrin and dystrofin, which connect the myofilamentous contractor ap‐ paratus to the ECM through the sarcolemma. The main part of the integrin is located in the neuro-muscular junction. The sarcomeric actin ties itself through several molecules, located on a sarcomeral level, to β1 sub-unit of the trasn‐ membranal muscle specific integrin 7 β1, which is then tied to the ECM protein. The molecules of the dystrofin associ‐ ated complex, are relatively distributed in a homogenous way along the whole sarcolemma, even though they are particularly abundant in the muscle-.tendon junction and the neuro-muscular junction. The actin ties itself to the dys‐ trofin which is in turn associated with three complex proteins: distroglicans, sarcoglicans and sintrofins.

In the end we have to remember the role of dystrofin as a marker of muscular lesion. Some research conducted on animal models show a conspicuous decrease in coloration of the dystrofin in the muscle immediately after an eccentric contraction (Koh and Eswcobedo, 2004; Lovering and Deyne, 2004). In these studies the loss of dystrofin was associated with the decrease of another membrane protein, the beta-spectrin whose role would seem similar to that of the dystrofin in the stabilization of the membrane. On the other hand the role of dystrofin in maintaining membrane integrity as well as its stability is confirmed by the fact that its missing genetics is at the base of the onset of the Duchenne muscular dystrophy (Hoffman et al., 1987; Zubrycka-Gaarn et al., 1998).

All the same, it is not entirely correct to consider the loss of membrane integrity as a negative event able to compromise muscular homeostasis through the destruction of the barrier which allows the maintenance of an ideal balance between intra and extra cells molecules. In effect a reduced and transitory destruction of the membrane may allow a normal pathway for the

an eccentric contraction is above all ascribable to the main production of registered strength, as opposed to how much happens in the during a concentric or isometric contraction (Stauber, 1989; Garret, 1990). In fact during an eccentric contraction, carried out at the speed of 90 s-1, the strength expressed from the muscle appears to be three times more than that produced, at the same speed, during a concentric contraction (Middleton et al., 1994). This higher strength production during an eccentric contraction, is mainly due to the elastic capacity of the tail of the myosin; in fact from the moment that, during an eccentric contraction the production of strength occurs during the detachment of the acto-myosinic bridges, the fact that the tail of the myosin is capable of resisting the detachment thanks to its elastic characteristics, allows a substantial increase in the capacity of strength production during the course of the eccentric phenomena (Middleton et al., 1994). In addition, during an eccentric contraction, the strength appears higher generated by the passive elements of the connective tissue of the muscle undergoing extension (Elftman, 1966). Above all, with reference to this last data we have to underline that also the purely mechanical phenomena of the extension, may play an important role in the onset of traumatic event, seeing as this latter one may prove, either in an active muscle during the lengthening phase, or in a muscular area which, during the extension phase, is totally passive (Garrett et al., 1987). However, the rate of extension in which the muscle risks its structural integrity is quite broad, being between 75 and 225% of its length at rest (Garret, 1990). This data underlines the fact that the muscular injury, due to elongation, does not appear at an relatively constant extension but may depend on many other factors, for example the level of electric activation of the muscle undergoing elongation, or the structural weakness of the latter following previous structural damage. In any case, it is important to notice the fact that some authors sustain the hypothesis that the length at which the muscle comes under extension represents a key factor in the entity of the possible damage, in that a superior initial muscle length corresponds with a superior extension and, consequently, a possible superior structural damage (Talbot and Morgan, 1998). The fact that at a superior length of extension the muscle may produce superior structural damage could depend on the heterogeneously of the length of the various sarcomeres of minor dimension which compose the muscular fiber. In fact, in superior length of extension the sarcomeres of minor dimension undergo a phe‐ nomena of "overstretching" whose magnitude would be directly linked to the muscle length

Etiology, Biology and Treatment of Muscular Lesions

http://dx.doi.org/10.5772/56602

7

**General term Specific muscle term** Muscular cell Muscular fiber or fiber cell

Endoplasmic reticulum Sarcoplasmic reticulum

Cellular membrane Sarcolemma Cytoplasm Sarcoplasma Mitochondria Sarcosoma

**Table 1.** Equivalent terminology of the principal muscular terms

which triggers the process of elongation(Morgan,1990).

**Figure 2.** Schematic representation of the skeletal muscle

release and for the assumption of some molecules, above all in tissue exposed to repetitive mechanical stress (McNeil and Khakee, 1992). The muscular tissue in effect shows undeniable capacity in repairing quickly minor entity damage dependent on the membrane structure, limiting in such a way the possible negative consequences. A molecule whose pathway depends on a transitory disturbance of the membrane integrity is the Basic Fibroblast growth factor (bFGF), growth factor strongly concerned in tissue repair processes and in adaptation processes of the muscular tissue regarding strenuous physical exercise. In conclusion a transitory and modest loss of the membrane integrity, can be interpreted also as a physiological answer to the muscular tissue in comparison to intense exercise, answer which is seen in function of the release and transfer of essential growth factors for the repair and functional and biological adaptation of the muscle. If the destruction process of the membrane integrity hesitates towards repair and adaptation, or towards cell death it will depend, obviously, on the entity of the detrimental event in itself and from all the other factors which will contribute to the lesion and repair process.

#### **4. Structural damage and contraction types: An overall vision**

The structural damage of muscular fiber may be caused by a singular muscular contraction or by a series of contractions (Armstrong et al., 1991b). In any case the mechanism mainly linked to the possible damage of muscular fiber would be the eccentric contraction (Garret, 1990; Armstrong, 1991b;). The reason of main traumatic incidence on a muscular level, seen during


**Table 1.** Equivalent terminology of the principal muscular terms

release and for the assumption of some molecules, above all in tissue exposed to repetitive mechanical stress (McNeil and Khakee, 1992). The muscular tissue in effect shows undeniable capacity in repairing quickly minor entity damage dependent on the membrane structure, limiting in such a way the possible negative consequences. A molecule whose pathway depends on a transitory disturbance of the membrane integrity is the Basic Fibroblast growth factor (bFGF), growth factor strongly concerned in tissue repair processes and in adaptation processes of the muscular tissue regarding strenuous physical exercise. In conclusion a transitory and modest loss of the membrane integrity, can be interpreted also as a physiological answer to the muscular tissue in comparison to intense exercise, answer which is seen in function of the release and transfer of essential growth factors for the repair and functional and biological adaptation of the muscle. If the destruction process of the membrane integrity hesitates towards repair and adaptation, or towards cell death it will depend, obviously, on the entity of the detrimental event in itself and from all the other factors which will contribute

**4. Structural damage and contraction types: An overall vision**

The structural damage of muscular fiber may be caused by a singular muscular contraction or by a series of contractions (Armstrong et al., 1991b). In any case the mechanism mainly linked to the possible damage of muscular fiber would be the eccentric contraction (Garret, 1990; Armstrong, 1991b;). The reason of main traumatic incidence on a muscular level, seen during

to the lesion and repair process.

**Figure 2.** Schematic representation of the skeletal muscle

6 Muscle Injuries in Sport Medicine

an eccentric contraction is above all ascribable to the main production of registered strength, as opposed to how much happens in the during a concentric or isometric contraction (Stauber, 1989; Garret, 1990). In fact during an eccentric contraction, carried out at the speed of 90 s-1, the strength expressed from the muscle appears to be three times more than that produced, at the same speed, during a concentric contraction (Middleton et al., 1994). This higher strength production during an eccentric contraction, is mainly due to the elastic capacity of the tail of the myosin; in fact from the moment that, during an eccentric contraction the production of strength occurs during the detachment of the acto-myosinic bridges, the fact that the tail of the myosin is capable of resisting the detachment thanks to its elastic characteristics, allows a substantial increase in the capacity of strength production during the course of the eccentric phenomena (Middleton et al., 1994). In addition, during an eccentric contraction, the strength appears higher generated by the passive elements of the connective tissue of the muscle undergoing extension (Elftman, 1966). Above all, with reference to this last data we have to underline that also the purely mechanical phenomena of the extension, may play an important role in the onset of traumatic event, seeing as this latter one may prove, either in an active muscle during the lengthening phase, or in a muscular area which, during the extension phase, is totally passive (Garrett et al., 1987). However, the rate of extension in which the muscle risks its structural integrity is quite broad, being between 75 and 225% of its length at rest (Garret, 1990). This data underlines the fact that the muscular injury, due to elongation, does not appear at an relatively constant extension but may depend on many other factors, for example the level of electric activation of the muscle undergoing elongation, or the structural weakness of the latter following previous structural damage. In any case, it is important to notice the fact that some authors sustain the hypothesis that the length at which the muscle comes under extension represents a key factor in the entity of the possible damage, in that a superior initial muscle length corresponds with a superior extension and, consequently, a possible superior structural damage (Talbot and Morgan, 1998). The fact that at a superior length of extension the muscle may produce superior structural damage could depend on the heterogeneously of the length of the various sarcomeres of minor dimension which compose the muscular fiber. In fact, in superior length of extension the sarcomeres of minor dimension undergo a phe‐ nomena of "overstretching" whose magnitude would be directly linked to the muscle length which triggers the process of elongation(Morgan,1990).

Regarding the level of muscular activation during the course of extension it is important to know that an active muscle is capable of absorbing much more energy- in terms of tensile energy- in comparison to a passive muscle. So the potential energetic absorption of a muscle is increased drastically when the latter contracts actively ( Garret, 1990). This introduces the concept of how a muscle, contracting actively, may put into action a kind of self-blocking strategy following damage due to excessive extension. The capacity of a muscle to resist a lengthening force absorbing energy is represented graphically, in mechanical terms of the underlying area of the stress-strain curve, as shown in figure 3.

**Figure 3.** A biological material such as the skeletal muscle, lengthened over a certain length produces a certain quote of tensile energy which, in the graph that shows the rapport strength-length, is represented by the underlying area of the curve.

activity entails quite reduced tensile levels, almost all energy due to tensile stress is absorbed

**Figure 4.** Graphic representation of the force-length relationship in an elongated muscle up to its breakpoint either in passive condition, or in contraction. As is easily recognizable from the graph, the peak of strength of breakage is supe‐ rior, in the contracted muscle in comparison to the same muscle in relaxed conditions, by a quota equal to only 15%. However, the tensile energy absorbed by the contracted muscle appears superior to that of the same muscle in re‐ laxed conditions. In addition, it is interesting to note that the absorbed energy is superior at low levels of extension

Etiology, Biology and Treatment of Muscular Lesions

http://dx.doi.org/10.5772/56602

9

During the eccentric contraction the muscle undergoes an "overstretching" phenomena which, as such, may determine the onset of lesions on a level of tendon insertion, of the muscle – tendon junction, or on a level of a muscular area rendered more fragile by a deficit of vascu‐ larization (Middleton et al., 1994). It is interesting to note how the pluriarticular muscles are the ones mostly exposed to traumatic insult, precisely due to the fact of having to control, through the eccentric contraction, the articular range of one or more articulations (Brewer, 1960). Also the different type of muscular fibers presents a different incidence of harmful event. Fast contraction fibers (FT) are in fact more highly exposed to structural damage in comparison to those of slow contraction(ST), probably due to their superior contractile capacity which translates itself into an increased production of strength and contraction speed, in comparison to fibers type ST (Garret et al., 1984; Friden and Lieber,1992).Furthermore the muscles which present a high percentage of FT, are generally more superficial (Lexell et al., 1983) and are normally interested by two or more articulations, both factors made ready for structural damage ( Brewer, 1960; Garret, 1990). To this we can add several studies (Potvin, 1997), which show how in the course of the eccentric phase of movement, the electromyographic activity

As well as these hypotheses, it is interesting to note several studies, available in bibliography, which ascribe superior susceptibility to structural damage on behalf of the glycolytic fibers to their particular metabolism (Patel et al., 1998). According to this theory the low oxidative

in this case by the contractile component. (Radin et al.,1979)

(from Garret, 1990, modified).

shows a preferential recruitment of FT fibers.

We may consider that inside the biological muscular structure, there are two structural components able to absorb tensile energy: the passive component and the contractile compo‐ nent. The possibilities of energetic absorption on behalf of the passive component don't depend on the muscular activation, but are essentially attributed to the connective tissue which is found inside the muscular belly but also in the "dumping factor" composed of fiber itself and to the connective associated tissue. The muscle shows however an increase of its capacity to absorb tensile energy thanks to its contractile characteristics, which obviously depend on the level of contraction at the time of extension, as we can see represented in the graph in figure 4.

So there could exist conditions able to diminish the contractile capacity of the muscle and thus reduce its capacity to absorb energy during an extension phase. The muscular fatigue and the structural weakness following a previous lesion, could be two determining factors. It is also important to note that an optimal capacity of absorption of extension strength represents an important protection factor, not only for the muscle itself but also as far as articulation and capsule-ligamentous apparatus is concerned (Radin et al., 1979) In addition, it is interesting to observe that at low levels of elongative tension, the energy absorbed by a muscle is almost totally dependent on the contractile component and, since the normal eccentric muscular

Regarding the level of muscular activation during the course of extension it is important to know that an active muscle is capable of absorbing much more energy- in terms of tensile energy- in comparison to a passive muscle. So the potential energetic absorption of a muscle is increased drastically when the latter contracts actively ( Garret, 1990). This introduces the concept of how a muscle, contracting actively, may put into action a kind of self-blocking strategy following damage due to excessive extension. The capacity of a muscle to resist a lengthening force absorbing energy is represented graphically, in mechanical terms of the

**Figure 3.** A biological material such as the skeletal muscle, lengthened over a certain length produces a certain quote of tensile energy which, in the graph that shows the rapport strength-length, is represented by the underlying area of

We may consider that inside the biological muscular structure, there are two structural components able to absorb tensile energy: the passive component and the contractile compo‐ nent. The possibilities of energetic absorption on behalf of the passive component don't depend on the muscular activation, but are essentially attributed to the connective tissue which is found inside the muscular belly but also in the "dumping factor" composed of fiber itself and to the connective associated tissue. The muscle shows however an increase of its capacity to absorb tensile energy thanks to its contractile characteristics, which obviously depend on the level of contraction at the time of extension, as we can see represented in the graph in figure 4.

So there could exist conditions able to diminish the contractile capacity of the muscle and thus reduce its capacity to absorb energy during an extension phase. The muscular fatigue and the structural weakness following a previous lesion, could be two determining factors. It is also important to note that an optimal capacity of absorption of extension strength represents an important protection factor, not only for the muscle itself but also as far as articulation and capsule-ligamentous apparatus is concerned (Radin et al., 1979) In addition, it is interesting to observe that at low levels of elongative tension, the energy absorbed by a muscle is almost totally dependent on the contractile component and, since the normal eccentric muscular

underlying area of the stress-strain curve, as shown in figure 3.

the curve.

8 Muscle Injuries in Sport Medicine

**Figure 4.** Graphic representation of the force-length relationship in an elongated muscle up to its breakpoint either in passive condition, or in contraction. As is easily recognizable from the graph, the peak of strength of breakage is supe‐ rior, in the contracted muscle in comparison to the same muscle in relaxed conditions, by a quota equal to only 15%. However, the tensile energy absorbed by the contracted muscle appears superior to that of the same muscle in re‐ laxed conditions. In addition, it is interesting to note that the absorbed energy is superior at low levels of extension (from Garret, 1990, modified).

activity entails quite reduced tensile levels, almost all energy due to tensile stress is absorbed in this case by the contractile component. (Radin et al.,1979)

During the eccentric contraction the muscle undergoes an "overstretching" phenomena which, as such, may determine the onset of lesions on a level of tendon insertion, of the muscle – tendon junction, or on a level of a muscular area rendered more fragile by a deficit of vascu‐ larization (Middleton et al., 1994). It is interesting to note how the pluriarticular muscles are the ones mostly exposed to traumatic insult, precisely due to the fact of having to control, through the eccentric contraction, the articular range of one or more articulations (Brewer, 1960). Also the different type of muscular fibers presents a different incidence of harmful event. Fast contraction fibers (FT) are in fact more highly exposed to structural damage in comparison to those of slow contraction(ST), probably due to their superior contractile capacity which translates itself into an increased production of strength and contraction speed, in comparison to fibers type ST (Garret et al., 1984; Friden and Lieber,1992).Furthermore the muscles which present a high percentage of FT, are generally more superficial (Lexell et al., 1983) and are normally interested by two or more articulations, both factors made ready for structural damage ( Brewer, 1960; Garret, 1990). To this we can add several studies (Potvin, 1997), which show how in the course of the eccentric phase of movement, the electromyographic activity shows a preferential recruitment of FT fibers.

As well as these hypotheses, it is interesting to note several studies, available in bibliography, which ascribe superior susceptibility to structural damage on behalf of the glycolytic fibers to their particular metabolism (Patel et al., 1998). According to this theory the low oxidative potential, typical of glycolytic fibers, would predispose the latter to structural damage in the course of repeated eccentric contractions because of the depletion of the highly energetic phosphates. This situation would cause the formation of actomyosinic bridges in "rigor state" particularly exposed, because of their excessive rigidity, to the potentially induced structural damage from the eccentric contraction. However, this hypothesis even though engaging and not void of rationality, wasn't supported by experimental evidence in the course of ulterior studies conducted by the same author, during which it wasn't possible to show, on an animal model, that a superior oxidative potential of the glycolytic fibers, induced by a specific training plan, could represent a protective factor for the possible damage induced by eccentric con‐ traction. Beyond the undoubted differences of metabolic type between the gylcolytic and oxidative fibers, other theories which attempt to discuss a superior predisposition to the traumatic insult of the FT single out the different contents of the latter regarding the level of some cytoskeletal proteins(Koh,2002). These particular cytoskeletal proteins, which are fewer in glycolytic fibers in comparison to those of oxidative fibers, would provide a kind of structural support for sarcomeres and the cellular membrane, contributing in such a way to maintain the integrity of such anatomical structures towards mechanical stress represented by eccentric contraction. Koh himself moreover identified in other particular proteic molecules, named "heat shock proteins" which would head to a family of "stress proteins", once again contained in superior quantity in oxidative fibers rather than glycolytic ones, substances able to carry out a protective role towards the muscular structure still during the "induced injury contraction" represented by eccentric contraction.

**5. The calcium overload phase**

area.

**6. The hypotheses of onset of muscular damage**

Even if the etiology of the event or specific events able to induce damage on skeletal muscle fiber they aren't fully understood, the hypotheses can be, in any case, divided into two

From close examination of international literature it appears clear that, if on the one hand muscular exercise represents a potential source of traumatic events, on the other hand a correct conditioning of the same muscle and its functionality, may reduce considerably the risk of lesion (Ebbeling and Clarkson 1989; Stauber, 1989; Scwane and Armstrong, 1983; Armstrong, 1984). The majority of the studies agrees on the fact that muscular damage is produced, practically in most cases, through an eccentric contraction, during which the muscle elongates at the same time in which it is activated from a contractile point of view (Armstrong et al., 1983b; McCully and Faulkner, 1985; Lieber and Friden, 1988), in addition the muscular damage would seem linked both to the intensity and the duration of exercise (Tiidus and Inauzzo, 1983; McCully and Falukner, 1986).The traumatic event is generally accompanied by a series of clinical and functional problems which are identifiable in : loss of contractile strength, pain, swelling and /or edema, diminution of the contractual capacity, alteration in the proprioceptive muscular pattern and alteration in the strategy of neuro-muscular activation (Davies and White, 1981; Newman et al., 1983; Riden et al., 1983; Armstrong, 1984; Ogilvie et al., 1985; Ebbeling and Clarkson 1989; Darren et al., 1990). The indirect muscular trauma must be visibly distinguished from DOMS (Delayed Onset Muscle Soreness), in fact, if the two biological descriptions present many common points, the DOMS must be anyway understood as a physiological process which poses itself to all effect as a natural forerunner of a process of muscular adaptation aimed at the better functioning of the muscle towards an external load, represented by the training process (Armstrong,1984; Armstrong 1990). The initial detrimental event, drives rapidly to a loss, located inside the injured muscle fiber of the homeostasis of CA ++ which is named "Ca++ overload phase". The muscular cells possess several specific mecha‐ nisms deputed to the regulation of the levels of cytosolic Ca++ (Carafoli, 1985; Klug and Tibbis, 1988); at the moment in which these buffering and translocation mechanisms are inhibited by the excessive intracellular level of Ca++, caused by the breakage of the sarcoplasmatic reticulum following the injury, we may assist with the activation of numerous pathways of degradation inside the muscular fiber of the injured area. In such a way it activates, on the injured area, a mechanism of autogenetic degradation which includes the activation of the phosfolipase A2 (PLA2) with consequent production of arachidonic acid, prostaglandin, leukotrien, Ca++ dependent proteases and lysomial proteases. In addition, the increase of intracellular Ca++ levels, apart from provoking a sarcomeral contraction reflex ( i.e. not interposed from the SNC), may inhibit, or even suppress, the normal mitochondrial breathing. This series of autogenetic factors inside the damaged fiber comes about before the invasion, inside the injured fiber of the macrophages and continues, anyway, also after the appearance of the latter on the damaged

Etiology, Biology and Treatment of Muscular Lesions

http://dx.doi.org/10.5772/56602

11

Another risk factor is represented by the heterogeneity of the sarcomeral length. The sarcomers of minor length represent in fact, the "weak point of the chain" during the eccentric over‐ stretching phenomena (Morgan,1990). To this end it's important to remember that after a muscular lesion we can note, in an animal model, an increase of the heterogeneity of the sarcomeral length (Patel et al.,), this could, at least in part, explain why, a previously damaged muscle, presents a higher risk of traumatic recurrence. In addition, it is interesting to note how the traumatic event is mainly located on a muscle-tendon junction level, witnessing the fact that in this area, just as in the rest of the final portion of muscle fiber, appears the most mechanical stress (Garrett et al., 1987; Garrett,1990; Lieber etal., 1991). Even though to this end we have to remember that some studies (Huxley and Peachey, 1961) show how muscle fiber, in proximity of the muscle-tendon junction, shows a minor lengthening during an eccentric phase, in comparison to the one in its central area. This data could lead us to the hypothesis that the following damage in an eccentric contraction, on a muscle-tendon level, is not so attributable to the size of elongation as such, but to the application of forces of tangential type on a less vascularized area, and thus structurally more fragile. We need to underline the particular metabolic aspect connected to the eccentric type of contraction. During this type of contraction, since the muscular perfusion is drastically diminished with consequential functional deficit of the aerobic mechanism, the physiological activity is mainly anaerobic type; this determines, either an increase in local temperature, or acidosis, in addition to a marked cellular anoxia. These metabolic events translate themselves into an increased muscular fragility and into a possible cellular necrosis, both on a muscular level as on connective tissue (Middleton et al., 1994).
