**8. The hypotheses of physical type: The theory of mechanical factors**

The mechanical theory is essentially based on the central role which covers the eccentric contraction in a harmful process. The skeletal muscle may be defined as a flexible biological material, or a material able to sustain elongation which can also go over 5% of its at rest length (Popov, 1990). However, the skeletal muscle is, at the same time, a compound biological material of complex type and, for this exact reason, the study of its components of structural weakness, which can determine the mechanical yielding, appears extremely difficult. As previously implied, the structural damage depending of muscular fiber may be the conse‐ quence, both of a single muscular contraction and of a cumulative series of contractions (Armstrong et al., 1991). During a contraction the muscular fiber may mechanically give way, at the moment in which the tensile stress, to which its structural components are undergone, overtake the maximum production of strength of the same components and goes beyond the said" maximum theoretical stress value" (MTSV). If the tensile stress to which the fiber is subjected, overtakes the MTSV, the structural components give way; in other words an irreversible lesion is produced in the muscular fiber (Figure 5). In a way such as we can see in the course of a monodirectional elongation, such as that described in a stress-strain curve, the muscular structure may give way irreversibly also at the moment in which it undergoes through a stress cutting (i.e. an oblique strength stress), in accordance with what is stated from the "maximum stress-shear theory" said also "maximum distortion-energy theory" (Popov, 1990), in which the acting forces on muscular fiber are considered in a three-dimensional way.

the fiber is exposed, focalizing in such a way on the important aspect of the resistance of biological material to the fatigue phenomena. In this particular investigation we study the answer of the biological material at the moment in which the latter is exposed to a high amount of tension and relaxation, up until its breakpoint. For the materials which present a high degree of flexibility, the relationship between the stress to which it is exposed and the number of tension-relaxation cycles which guide to their breakage, is of exponential type (figure 6). To an increase in stress to which the material is exposed, corresponds a drop in the number of cycles which lead to the structural weakening of the same material (Ashby and Jones, 1988). In accordance with what is stated from the theories of the resistance to the fatigue of the biological materials, the energy absorbed by a muscle in the course of a strong elongation, may be eliminated both under form of heat and plastic deformation, intending the latter term a permanent change in the form and in the dimensions of the structural components of the muscular fiber. A plastic deformation, in a biological structure such as the one represented by muscular fiber, may begin with an initial weakening of one or more of its ultrastructural components, which can lead to perpetual tension-relaxation cycles and to a breakage of the structures exposed to tensile stress. In addition, we must underline that the increase in the rate of development of stress tends to reduce the number of cycles which lead to structural

fiber undergoes.

**Figure 5.** A stress-strain curve, typical of a flexible biological material undergoing tension. The material shows, before the stress which it undergoes surpasses the value of maximum production of strength (VMPF), an elastic type behav‐ ior. Once the MPFV is overtaken, the material undergoes a permanent change in form, in other words it undergoes a "plastic deformation". Once the value of maximum force is reached (MTSV) the material gives way irreversibly. From a traumatological point of view we can therefore indentify three different zones in the stress-strain curve of a muscular fiber undergoing tension in the course of an eccentric contraction. The first is included between the beginning of elongation and the value of MPFV, inside which, despite the lengthening stress, the muscular fiber shows elastic be‐ haviour thus not risking structural damage. The second is included between the value of MPFV and the value of MTSV, inside which the fiber surpasses its elastic limits, in which the fiber doesn't show loss of its structural integrity and un‐ dergoes a plastic deformation. In this zone the fiber doesn't show loss of its structural integrity. And the last an area which goes beyond the value of MTSV, in which the same fiber gives way. In this last case, *we can observe a muscle tear which severity -* first, second or third degree -is directly linked to the magnitude of the tensile stress to which the

Etiology, Biology and Treatment of Muscular Lesions

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13

However, the studies of the mechanisms which may cause structural damage to the muscular fiber, have aimed and still aim, also to the cumulative effect of the mechanical tensions to which

typologies, the first of physical type and the second of metabolic type, even though in many cases these etiological descriptions overlap not allowing, in fact, an unmistakable distinction.

The possible mechanisms of physical type capable of inducing initial structural damage to the muscular fiber, may be divided into two categories. The first includes the hypothesis of mechanical nature, whereas the second includes those induced by change of temperature. The fact that the muscular damage recognizes in an eccentric contraction its "*primum movens*", is a widely spread concept amongst many authors (Armstrong, 1984; Ebbeling and Clarkson, 1989; Stauber, 1989, Kano et al., 2008; Schache et al., 2008, Chang et al., 2009), so for this reason the mechanical theory of the fibrillary damage, underlines the substantial difference, in terms of strength production, between the eccentric and concentric and isometric contraction, whereas the theory which identifies the damage as consequence of a "temperature-dependent" mechanism is based on the hypothesis that, during an eccentric contraction, the local temper‐ ature of the muscle is higher, factor which would predispose the muscular fiber to structural

**8. The hypotheses of physical type: The theory of mechanical factors**

The mechanical theory is essentially based on the central role which covers the eccentric contraction in a harmful process. The skeletal muscle may be defined as a flexible biological material, or a material able to sustain elongation which can also go over 5% of its at rest length (Popov, 1990). However, the skeletal muscle is, at the same time, a compound biological material of complex type and, for this exact reason, the study of its components of structural weakness, which can determine the mechanical yielding, appears extremely difficult. As previously implied, the structural damage depending of muscular fiber may be the conse‐ quence, both of a single muscular contraction and of a cumulative series of contractions (Armstrong et al., 1991). During a contraction the muscular fiber may mechanically give way, at the moment in which the tensile stress, to which its structural components are undergone, overtake the maximum production of strength of the same components and goes beyond the said" maximum theoretical stress value" (MTSV). If the tensile stress to which the fiber is subjected, overtakes the MTSV, the structural components give way; in other words an irreversible lesion is produced in the muscular fiber (Figure 5). In a way such as we can see in the course of a monodirectional elongation, such as that described in a stress-strain curve, the muscular structure may give way irreversibly also at the moment in which it undergoes through a stress cutting (i.e. an oblique strength stress), in accordance with what is stated from the "maximum stress-shear theory" said also "maximum distortion-energy theory" (Popov, 1990), in which the acting forces on muscular fiber are considered in a three-dimensional way. However, the studies of the mechanisms which may cause structural damage to the muscular fiber, have aimed and still aim, also to the cumulative effect of the mechanical tensions to which

**7. The hypotheses of physical type**

12 Muscle Injuries in Sport Medicine

and /or metabolic changes, potentially harmful.

**Figure 5.** A stress-strain curve, typical of a flexible biological material undergoing tension. The material shows, before the stress which it undergoes surpasses the value of maximum production of strength (VMPF), an elastic type behav‐ ior. Once the MPFV is overtaken, the material undergoes a permanent change in form, in other words it undergoes a "plastic deformation". Once the value of maximum force is reached (MTSV) the material gives way irreversibly. From a traumatological point of view we can therefore indentify three different zones in the stress-strain curve of a muscular fiber undergoing tension in the course of an eccentric contraction. The first is included between the beginning of elongation and the value of MPFV, inside which, despite the lengthening stress, the muscular fiber shows elastic be‐ haviour thus not risking structural damage. The second is included between the value of MPFV and the value of MTSV, inside which the fiber surpasses its elastic limits, in which the fiber doesn't show loss of its structural integrity and un‐ dergoes a plastic deformation. In this zone the fiber doesn't show loss of its structural integrity. And the last an area which goes beyond the value of MTSV, in which the same fiber gives way. In this last case, *we can observe a muscle tear which severity -* first, second or third degree -is directly linked to the magnitude of the tensile stress to which the fiber undergoes.

the fiber is exposed, focalizing in such a way on the important aspect of the resistance of biological material to the fatigue phenomena. In this particular investigation we study the answer of the biological material at the moment in which the latter is exposed to a high amount of tension and relaxation, up until its breakpoint. For the materials which present a high degree of flexibility, the relationship between the stress to which it is exposed and the number of tension-relaxation cycles which guide to their breakage, is of exponential type (figure 6). To an increase in stress to which the material is exposed, corresponds a drop in the number of cycles which lead to the structural weakening of the same material (Ashby and Jones, 1988). In accordance with what is stated from the theories of the resistance to the fatigue of the biological materials, the energy absorbed by a muscle in the course of a strong elongation, may be eliminated both under form of heat and plastic deformation, intending the latter term a permanent change in the form and in the dimensions of the structural components of the muscular fiber. A plastic deformation, in a biological structure such as the one represented by muscular fiber, may begin with an initial weakening of one or more of its ultrastructural components, which can lead to perpetual tension-relaxation cycles and to a breakage of the structures exposed to tensile stress. In addition, we must underline that the increase in the rate of development of stress tends to reduce the number of cycles which lead to structural weakening, underlining in this way that the speed of lengthening of muscular fiber may play an important role in the onset of the damage (Armstrong et al., 1991).

literature we may glean some important data regarding the capacity of tensile resistance of the muscular fiber towards the eccentric contraction. The first interesting data is represented by the fact that during an eccentric contraction the strength production may surpass a percentage between 50 and 100% the isometric strength maximum value (P0) of the considered muscle (Woledge et al., 1985), in addition, as previously said, during an eccentric contraction, carried out at a speed of 90 degrees, the strength expressed of the muscular area appears to be three times higher than that produced, at the same speed, during a concentric contraction (Middleton et al., 1994). We must remember that this higher production of force during an eccentric contraction, is mainly due to the elastic capacity of the tail of the myosin, which thanks to its elastic characteristics, allows a substantial increase in the capacity of the force production during the elongating phase of the contraction (Middleton et al., 1994). Another interesting aspect is given by the fact that, during an eccentric contraction, to be able to satisfy the principle of an isovolumetric contraction, the CSA of each fiber drops in function of the degree of lengthening to which the fiber is exposed. From a careful analysis of this data, we may presume that the medium value of tensile stress that a muscular fiber actively lengthened during an eccentric contraction of 130% of its length at rest (L0 ), may be higher from 100 to 160% in comparison to one which appears during an maximum isometric contraction carried out at L0. For this reason regarding the turnover of formation and detachment of the acto-myosinic bridges, it is possible to presume from specific literature some interesting information. The number of acto-myosinic bridges would seem in fact decreasing at the increase of the speed of lengthening of the muscle (McMahon, 1984).This phenomena could involve an increase of the produced force on a level of every single acto-myosinic bridge, predisposing in such a way the contractile proteins of the muscle to the traumatic damage (McMahon,1984). In addition, certain experimental evidence carried out like this would confirm the so far mentioned theories. On preparations of isolated frog sartorious muscle, after only three eccentric con‐ tractions, the rate of development of force drops significantly and we may observe a movement of the length-tension curve of the muscle towards superior muscle lengths. However, these changes appear only following a contraction of certain magnitude, and anyway not before force values exceeding 180% (McCully and Faulkner, 1985; 1986). Even though, in current practice, the majority of muscular lesions would seem to occur in the course of particularly fast eccentric contractions, the degree, in terms of severity, of the structural damage of the fiber is mainly linked to the peak of force expressed during an eccentric contraction and not at its intrinsic speed (McCully and Faulkner, 1986). In addition, it is interesting to note that eccentric contractions of magnitude equal to 85% of P0, are able to cause structural damage to the architecture of the muscular fiber, this does not happen during isometric or concentric contractions of the same leve. This particular mechanical behavior, may be explained by the fact that the same peak of force, during an eccentric contraction, is produced at a superior muscular length in comparison to that of one in the course of an isometric or concentric contraction, a factor which would drop the capacity of tensile resistance of the fiber. In fact, the peak of force during an eccentric contraction is reached at a superior length in comparison to that during an isometric or concentric contraction, or on average at 110% versus the 100% of L0 (McCully and Faulkner, 1986; Newham et al., 1988). Since 1939 (Katz,1939) we could state that the harmful process concerning the skeletal muscle was of "length-dependent" type,

Etiology, Biology and Treatment of Muscular Lesions

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

15

**Figure 6.** A fatigue curve typical of a flexible biological material. At the moment in which the stress applied during a tension relaxation cycle- also defined from a mechanical point of view as a tension-compression cycle- increases, there is a drop in the number of cycles which lead to the structural weakening. In the graph the dotted horizontal line repre‐ sents the limit of resistance of the material, (i.e. the stress value under which the considered biological material can support an infinite number of tension-relaxation cycles without incurring structural damage). The red line represents the behavior of a higher resistant material to fatigue in comparison to that of the behavior represented by the blue line (from Armstrong et al.,1991, modified).

The analysis of muscular lesions faced through the given perspective of related literature of the science of materials, appears difficult. The first difficulty which we face is represented by the fact that no data regarding the relationship between the entity of tensile or shear forces and the degree of the lesion doesn't exist. Few studies have in fact investigated, from this point of view, the forces directly expressed inside the muscular structure and even if this type of investigation had been done, the derived values always refer to the registration of forces effected on a tendon structure level. It is important to remember that, in this specific case, the values of such calculated forces represent the sum of values of stress of each single structural component, multiplied by their respective section area ( cross-sectional area,CSA). In this way it appears clear that like, from this "global" value, it is difficult, if not impossible, to carry out an analysis of the factors and values of structural weakening for each single component of the considered biological system. A second problem is represented by the fact that individual values of MPSV and of MTSV of the single elements that make up the muscular fiber are, in effect, unknown. A last aspect, problematic in this field, is made up of scarce knowledge of the total capacities of work, in relation to risk lesion, that the skeletal muscle can support during a cycle of eccentric contractions. Above all in this specific field, certain data concerning the loss of percentage of energy absorbed by the muscle and which is dispersed in the form of plastic deformation,. Despite the undoubted conceptual difficulties, from a careful examination of

literature we may glean some important data regarding the capacity of tensile resistance of the muscular fiber towards the eccentric contraction. The first interesting data is represented by the fact that during an eccentric contraction the strength production may surpass a percentage between 50 and 100% the isometric strength maximum value (P0) of the considered muscle (Woledge et al., 1985), in addition, as previously said, during an eccentric contraction, carried out at a speed of 90 degrees, the strength expressed of the muscular area appears to be three times higher than that produced, at the same speed, during a concentric contraction (Middleton et al., 1994). We must remember that this higher production of force during an eccentric contraction, is mainly due to the elastic capacity of the tail of the myosin, which thanks to its elastic characteristics, allows a substantial increase in the capacity of the force production during the elongating phase of the contraction (Middleton et al., 1994). Another interesting aspect is given by the fact that, during an eccentric contraction, to be able to satisfy the principle of an isovolumetric contraction, the CSA of each fiber drops in function of the degree of lengthening to which the fiber is exposed. From a careful analysis of this data, we may presume that the medium value of tensile stress that a muscular fiber actively lengthened during an eccentric contraction of 130% of its length at rest (L0 ), may be higher from 100 to 160% in comparison to one which appears during an maximum isometric contraction carried out at L0. For this reason regarding the turnover of formation and detachment of the acto-myosinic bridges, it is possible to presume from specific literature some interesting information. The number of acto-myosinic bridges would seem in fact decreasing at the increase of the speed of lengthening of the muscle (McMahon, 1984).This phenomena could involve an increase of the produced force on a level of every single acto-myosinic bridge, predisposing in such a way the contractile proteins of the muscle to the traumatic damage (McMahon,1984). In addition, certain experimental evidence carried out like this would confirm the so far mentioned theories. On preparations of isolated frog sartorious muscle, after only three eccentric con‐ tractions, the rate of development of force drops significantly and we may observe a movement of the length-tension curve of the muscle towards superior muscle lengths. However, these changes appear only following a contraction of certain magnitude, and anyway not before force values exceeding 180% (McCully and Faulkner, 1985; 1986). Even though, in current practice, the majority of muscular lesions would seem to occur in the course of particularly fast eccentric contractions, the degree, in terms of severity, of the structural damage of the fiber is mainly linked to the peak of force expressed during an eccentric contraction and not at its intrinsic speed (McCully and Faulkner, 1986). In addition, it is interesting to note that eccentric contractions of magnitude equal to 85% of P0, are able to cause structural damage to the architecture of the muscular fiber, this does not happen during isometric or concentric contractions of the same leve. This particular mechanical behavior, may be explained by the fact that the same peak of force, during an eccentric contraction, is produced at a superior muscular length in comparison to that of one in the course of an isometric or concentric contraction, a factor which would drop the capacity of tensile resistance of the fiber. In fact, the peak of force during an eccentric contraction is reached at a superior length in comparison to that during an isometric or concentric contraction, or on average at 110% versus the 100% of L0 (McCully and Faulkner, 1986; Newham et al., 1988). Since 1939 (Katz,1939) we could state that the harmful process concerning the skeletal muscle was of "length-dependent" type,

weakening, underlining in this way that the speed of lengthening of muscular fiber may play

**Figure 6.** A fatigue curve typical of a flexible biological material. At the moment in which the stress applied during a tension relaxation cycle- also defined from a mechanical point of view as a tension-compression cycle- increases, there is a drop in the number of cycles which lead to the structural weakening. In the graph the dotted horizontal line repre‐ sents the limit of resistance of the material, (i.e. the stress value under which the considered biological material can support an infinite number of tension-relaxation cycles without incurring structural damage). The red line represents the behavior of a higher resistant material to fatigue in comparison to that of the behavior represented by the blue

The analysis of muscular lesions faced through the given perspective of related literature of the science of materials, appears difficult. The first difficulty which we face is represented by the fact that no data regarding the relationship between the entity of tensile or shear forces and the degree of the lesion doesn't exist. Few studies have in fact investigated, from this point of view, the forces directly expressed inside the muscular structure and even if this type of investigation had been done, the derived values always refer to the registration of forces effected on a tendon structure level. It is important to remember that, in this specific case, the values of such calculated forces represent the sum of values of stress of each single structural component, multiplied by their respective section area ( cross-sectional area,CSA). In this way it appears clear that like, from this "global" value, it is difficult, if not impossible, to carry out an analysis of the factors and values of structural weakening for each single component of the considered biological system. A second problem is represented by the fact that individual values of MPSV and of MTSV of the single elements that make up the muscular fiber are, in effect, unknown. A last aspect, problematic in this field, is made up of scarce knowledge of the total capacities of work, in relation to risk lesion, that the skeletal muscle can support during a cycle of eccentric contractions. Above all in this specific field, certain data concerning the loss of percentage of energy absorbed by the muscle and which is dispersed in the form of plastic deformation,. Despite the undoubted conceptual difficulties, from a careful examination of

an important role in the onset of the damage (Armstrong et al., 1991).

line (from Armstrong et al.,1991, modified).

14 Muscle Injuries in Sport Medicine

meaning by this that the majority of damage to muscular structure happened at the moment in which the eccentric contraction appeared as important muscular lengths and higher than L0; the same data found by Katz was later confirmed by other authors (McCUlly and Faulkner 1985; 1986) So we can affirm that eccentric contractions carried out at higher lengths of L0, cause an excessive tensile stress potentially harmful not only for active elements of the muscular ultrastructure but also for the passive ones, like for example the connective support tissue. In effect this sort of innate structural weakness which the streaked muscle fiber shows during an eccentric contraction, is probably attributable to the fact that, during the amounting of the force peak force in an eccentric contraction The number of active actomyosinic bridges is probably less in comparison to that which we may observe during the peak force fulfillment in an isometric and /or concentric contraction. It is important to underline that in the tensionlength curve of the isolated muscular fiber it is proved, by exceeding lengths of L0, a decrease in active tension, which is compensated by a contextual increase of the expressed tension by the passive elements, which in this case contribute to the production of the level of total force, giving at the same time an idea of how much they are stimulated from a tensile point of view during the lengthening of the muscle. For this reason, during the lengthening phase a muscular complex- intended both in active and passive components – is exposed to the harmful event, not only when is electrically active but also in an electrically silent phase. Many authors have underlined the fact that, for a given level of production of force, the generated stress on a level of passive elements of the muscle, is higher during an eccentric contraction in comparison to an isometric or concentric contraction (McCully and Faulkner, 1986; Faulkner et al., 1989). However, it is also true that during a lengthening carried out at the same speed of a lengthening at which an eccentric contraction is carried out- considered in this case like a sort of active lengthening of the muscle- a harmful event does not occur on a structural level (McCully and Faulkner,1986; Faulkner et al., 1989), this means that despite the fact that structural damage is theoretically possible also in the course of lengthening of an electrically silent muscle, it is also true the fact that the tensile load to which the passive elements of the muscle are exposed is not the same during an active or passive lengthening. In effect, there is not much practical or experimental evidence which witness the fact that the passive elements may be damaged during an eccentric contraction. In fact, in these cases the majority of the passive tension, up to higher sarcomeral lengths of 140-150% of L0, is absorbed by the sarcolemma (Casella,1951; Rapoport,1972; Higuchi and Umazume,1986). Due to the inhomogeneities of the sarcomeral length, in the course of an eccentric contraction, the sarcomeres of minor dimension may sustain an excessive lengthening, even if the change in the muscular belly in full is relatively scarce. (Julian and Morgan, 1979; Colomo et al., 1988). In this particular situation, the sarco‐ meres of minor dimension, due to this undergo a real mechanism of overstretching, they may be harmed or cause a lesion in the nearby sarcomeres. The importance of the sarcomeral integrity, is well illustrated in the diseases associated with of Duchenne muscular dystrophy where we assists in the development in a series of defects on a sarcomeral level. (Bhattacharya et al., 1989) essentially ascribable to a deficiency of dystrofin (Hoffman et al., 1987; Zubrycka-Gaarn, 1988). To this end, some authors (Karpati and Carpenter, 1989) have underlined, for a long time, the fundamental importance of dystrofin for the mechanical stability of plasma‐ lemma, above all what concerns the maintenance of a correct alignment between basal lamina

and the same plasmalemma. Some experiments carried out on frog semitendinosus muscle, show how an important loss of energy at the same time as an increase of the sarcomeral length appears, postulating in such a way that the so dispersed energetic quota may be dispersed under heat form, or in plastic deformation of the sarcolemma, of the sarcoplasmatic reticulum, of the basal lamina or of the cytoskeleton (Tidball and Daniel,1986). Globally from the same data, we may deduct that about 77% of the total energetic dissipation, which happens in the course of a stretching-shortening cycle, is dissipated on a basal membrane level. This same data was confirmed by other experimental studies (Stauber, 1989), which showed histochem‐ istry and immune histochemistry evidence of damage on a basal lamina and endomysium level in a muscle undergoing a eccentric contraction. Also, the theory of the inhomogeneity of the sarcomeral length- and consequently of the phenomena of overstretching to which they were exposed, during an eccentric contraction, the sarcomeres of minor structural length- was later confirmed also by following studies (Morgan, 1990). Morgan also proposed a sequence

Etiology, Biology and Treatment of Muscular Lesions

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17

**a.** The eccentric contraction carries some sarcomeres whose length is minor in comparison

**b.** The over-tensioned sarcomeres are not able to relax conveniently during a contraction-

**c.** Above all, in the course of a cycle of particularly fast eccentric contractions the overtensioned sarcomeres, and for this reason incapable of reaching sufficient relaxation during a succession of contractions, transfer the tensile stress onto the nearby myofibrils.

**d.** Following the transfer of an excessive tensile stress, the sarcolemma and the sarcoplas‐ matic reticulum of the nearby fibers to the over-tensioned sarcomeres it structurally gives

This theory is, at least partially, supported by data supplied by McCully and Faulkner (1986) who showed how there was no evidence of structural damage when the lengthening speed was reduced under a certain limit. In any case, the data supplied from the experimental studies of McCully and Faulkner, give evidence that the structural components of the muscular fiber may meet up with a fatigue phenomena connected to the repetition of an eccentric contraction. Of particular interest is the strong link, shown by the same authors, between the increase in number of the eccentric contractions, the decrease of the peak of maximum eccentric force of the muscle and the increase of the areas of structural weakness inside the same muscle. This data suggests how the degree of lesion may be proportional to the complex amount of eccentric work carried out by muscular fibers. From the data of the work of McCully and Faulkner, we could draw two important conclusions, which have considerable relapses on a practical/

**i.** The muscle would have a maximum limit of eccentric contractions beyond which a

progressive phenomena of structural weakness would start which could lead to

to the average sarcomeral length- to be over-tensioned.

of well defined events in this sense:

time/relaxation-time cycle.

rehabilitative plane and that is:

structural damage.

in.

and the same plasmalemma. Some experiments carried out on frog semitendinosus muscle, show how an important loss of energy at the same time as an increase of the sarcomeral length appears, postulating in such a way that the so dispersed energetic quota may be dispersed under heat form, or in plastic deformation of the sarcolemma, of the sarcoplasmatic reticulum, of the basal lamina or of the cytoskeleton (Tidball and Daniel,1986). Globally from the same data, we may deduct that about 77% of the total energetic dissipation, which happens in the course of a stretching-shortening cycle, is dissipated on a basal membrane level. This same data was confirmed by other experimental studies (Stauber, 1989), which showed histochem‐ istry and immune histochemistry evidence of damage on a basal lamina and endomysium level in a muscle undergoing a eccentric contraction. Also, the theory of the inhomogeneity of the sarcomeral length- and consequently of the phenomena of overstretching to which they were exposed, during an eccentric contraction, the sarcomeres of minor structural length- was later confirmed also by following studies (Morgan, 1990). Morgan also proposed a sequence of well defined events in this sense:

meaning by this that the majority of damage to muscular structure happened at the moment in which the eccentric contraction appeared as important muscular lengths and higher than L0; the same data found by Katz was later confirmed by other authors (McCUlly and Faulkner 1985; 1986) So we can affirm that eccentric contractions carried out at higher lengths of L0, cause an excessive tensile stress potentially harmful not only for active elements of the muscular ultrastructure but also for the passive ones, like for example the connective support tissue. In effect this sort of innate structural weakness which the streaked muscle fiber shows during an eccentric contraction, is probably attributable to the fact that, during the amounting of the force peak force in an eccentric contraction The number of active actomyosinic bridges is probably less in comparison to that which we may observe during the peak force fulfillment in an isometric and /or concentric contraction. It is important to underline that in the tensionlength curve of the isolated muscular fiber it is proved, by exceeding lengths of L0, a decrease in active tension, which is compensated by a contextual increase of the expressed tension by the passive elements, which in this case contribute to the production of the level of total force, giving at the same time an idea of how much they are stimulated from a tensile point of view during the lengthening of the muscle. For this reason, during the lengthening phase a muscular complex- intended both in active and passive components – is exposed to the harmful event, not only when is electrically active but also in an electrically silent phase. Many authors have underlined the fact that, for a given level of production of force, the generated stress on a level of passive elements of the muscle, is higher during an eccentric contraction in comparison to an isometric or concentric contraction (McCully and Faulkner, 1986; Faulkner et al., 1989). However, it is also true that during a lengthening carried out at the same speed of a lengthening at which an eccentric contraction is carried out- considered in this case like a sort of active lengthening of the muscle- a harmful event does not occur on a structural level (McCully and Faulkner,1986; Faulkner et al., 1989), this means that despite the fact that structural damage is theoretically possible also in the course of lengthening of an electrically silent muscle, it is also true the fact that the tensile load to which the passive elements of the muscle are exposed is not the same during an active or passive lengthening. In effect, there is not much practical or experimental evidence which witness the fact that the passive elements may be damaged during an eccentric contraction. In fact, in these cases the majority of the passive tension, up to higher sarcomeral lengths of 140-150% of L0, is absorbed by the sarcolemma (Casella,1951; Rapoport,1972; Higuchi and Umazume,1986). Due to the inhomogeneities of the sarcomeral length, in the course of an eccentric contraction, the sarcomeres of minor dimension may sustain an excessive lengthening, even if the change in the muscular belly in full is relatively scarce. (Julian and Morgan, 1979; Colomo et al., 1988). In this particular situation, the sarco‐ meres of minor dimension, due to this undergo a real mechanism of overstretching, they may be harmed or cause a lesion in the nearby sarcomeres. The importance of the sarcomeral integrity, is well illustrated in the diseases associated with of Duchenne muscular dystrophy where we assists in the development in a series of defects on a sarcomeral level. (Bhattacharya et al., 1989) essentially ascribable to a deficiency of dystrofin (Hoffman et al., 1987; Zubrycka-Gaarn, 1988). To this end, some authors (Karpati and Carpenter, 1989) have underlined, for a long time, the fundamental importance of dystrofin for the mechanical stability of plasma‐ lemma, above all what concerns the maintenance of a correct alignment between basal lamina

16 Muscle Injuries in Sport Medicine


This theory is, at least partially, supported by data supplied by McCully and Faulkner (1986) who showed how there was no evidence of structural damage when the lengthening speed was reduced under a certain limit. In any case, the data supplied from the experimental studies of McCully and Faulkner, give evidence that the structural components of the muscular fiber may meet up with a fatigue phenomena connected to the repetition of an eccentric contraction. Of particular interest is the strong link, shown by the same authors, between the increase in number of the eccentric contractions, the decrease of the peak of maximum eccentric force of the muscle and the increase of the areas of structural weakness inside the same muscle. This data suggests how the degree of lesion may be proportional to the complex amount of eccentric work carried out by muscular fibers. From the data of the work of McCully and Faulkner, we could draw two important conclusions, which have considerable relapses on a practical/ rehabilitative plane and that is:

**i.** The muscle would have a maximum limit of eccentric contractions beyond which a progressive phenomena of structural weakness would start which could lead to structural damage.

**ii.** From the time that a progressive increase of the number of eccentric contractions, it would lead to a contextual progressive decrease of the peak of maximum eccentric force, due to the fatigue phenomena, expressed by the muscle, there would exist a limit of the value of eccentric force, below which the muscle would be exposed to the risks of structural damage. According to McCully and Faulkner, such a limit would be between 60 and 80% of the maximum value of eccentric force. In other words when the decrease of the production of eccentric force drops below 20-40% the muscle runs the risk of injury.

the Fenn effect would theoretically foresee a ratio of minor heat during an eccentric contraction, in comparison to the theoretically predictable one in the course of an isometric and concentric contraction. In effect, the theoretic forecast carried out based on the Fenn effect, which would foresee a minor heat production during an eccentric contraction, would be confirmed also in some experimental data (Abbot and Aubert, 1951). All these observations could lead us to consider the highest production of heat observed in the course of negative work, not so much as an increase in the ratio of heat production on behalf of the muscle itself in similar conditions, but as the consequence of the drop of the ratio or heat removal by the muscle, which is registered during an eccentric contraction ( for further information please refer to the specific

Etiology, Biology and Treatment of Muscular Lesions

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

19

The production of metabolic heat and its disposal, may be modeled through a central "heat producer" nucleus, made up of skeletal muscles, bowels, internal organs and the central nervous system, a "means of transport", made up of the circulatory system and of a "cooling surface", made of skin. During an eccentric contraction we can see a transient and intermittent mechanism of vasoconstriction which strongly limits the capacity of transporting heat, produced by the muscular contraction, on the part of the circulatory system. For this reason the highest production of heat during negative work, in comparison to the production of heat during positive work, it is essentially attributable to the reduced ratio of degradation of heat which occurs during negative work, caused by the aforementioned vasoconstriction mecha‐

**10. The metabolic hypotheses: The role of insufficient mitochondrial**

In the course of physical exercise the mitochondrial respiration appears high together with the synthesis and hydrolysis of the ATP. This situation is well balanced from a physiological point of view in the course of moderate exercise in which, the muscular fibers in activity, manage to maintain the concentration of ATP near to the base values (Krisanda et al.,1988). However, in the course of intense and prolonged exercise, a certain reduction in the concentration of energetic phosphates constantly occurs (Krisanda et al.,1988) and the possibility that this event occurs inside some specific compartments of the fiber represents a concrete and reasoned hypothesis which could explain the initial events of the mechanism of muscular lesion. For example, in the case in which a drop in ATP levels occurs near the Ca++ - ATPase on a level of the sarcoplasmatic reticulum or of the sarcolemma, the removal of Ca++ from the cytoplasm could result compromised, causing in such a way an increase in cytosolic Ca++. To this end there exists important experimental evidence which show that, to maintain an optimal state of cellular function, it is of vital importance to maintain an optimal functionality of the Ca++ pump (Duncan, 1987). Also in this field, some studies have shown how a drop in the cellular energetic provision may lead to a release of Ca++ from the sarcoplasmatic reticulum (Duchen

box.)

nism.

**respiration**

**9.1. Eccentric contraction and heat dispersion**

From a practical but above all rehabilitative /preventive point of view, this data underlines the importance of:

