**5. The calcium overload phase**

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

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

contraction" represented by eccentric contraction.

10 Muscle Injuries in Sport Medicine

(Middleton et al., 1994).

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 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 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.
