**16. The lysosomal protease**

above all if the latter stays high inside the specific compartments of the fiber - different degradation mechanisms start inside the injured muscle fiber which are represented by:

The loss of the homeostasis of the Ca++ involves an uncontrollable contractionreflex (or not through the SNC) by the sarcomeres inside the injured area (Ogilvie et al., 1988). We need however to specify that the myofibrillar contraction reflex phenomena, does not have to be necessarily understood as a degradation phenomena in the strict meaning, like for example the enzymatic pathway could be. Even if some authors have put forward the hypothesis that this zone of concentration may make up a sort of barrier apt to block the degradation processes preventing the latter to extend to the sarcomeres adjacent to the injured zone (Carpenter and Karpati, 1989), we need to consider that this uncontrolled state of contraction of the sarcomeres may have serious consequences in the field of aggravation of structural damage. The first negative effect is represented by the local depletion of ATP following the endurance of the contraction itself, which would give origin to a vicious circle, and so, capable of auto sustain‐ ment, identifiable in "depletion of ATP- increase in levels of Ca++" and vice versa (Goodman, 1987). The second negative outcome of the mechanism of myofibrillar contraction reflex is made up of the fact that such a phenomena produces mechanical forces, inside the fibers able to damage further both the membrane and the same contractile components, contributing in

such a way to further deterioration of the clinical situation (Armstrong et al., 1991).

The mitochondria inside the muscular fiber have, among their tasks, also that which to react to "buffer", or to tampon mechanism, regarding the increase of the concentration of cytosolic Ca++. However the hypothesis is generally creditable that the uptake of Ca++ on a mitochondrial level is quite modest, and in any case insufficient to be able to consider as fundamental, or at least important, the role taken on the mitochondria itself in the field of the mechanism of relaxation of the muscular fiber. Even though we need to remember that the mitochondria, in particular pathologic situations, are capable of accumulating a large quantity of ions (Gillis, 1985). Between all the types of fibers, the oxidative ones show marked capacity of mitochon‐ drial buffering regarding the Ca++ which can exceed the registered ones by 2-3 times on a

**14. The phenomena of mitochondrial Ca++ overload**

**•** The mechanism of the myofibrillar reflex contraction

**•** The mechanism of activation of the dependent Ca++ protease

phospholipase

**13. The mechanism of the reflex myofibrillar contraction**

**•** The phenomena of mitochondrial Ca++ overload

**•** The lysosomal protease

26 Muscle Injuries in Sport Medicine

**•** The pathway of the A2

Since the myofibrillar protein may be degraded by the proteolytic enzymes contained in the lysosomes of the muscular fibre (Schwartz and Bird,1977), it is reasonable to suppose that the lysosomial protease plays an important role in the field of the successive autogenic phase to the muscular damage. This supposition is corroborated by the evidence of a strong increase in the lysosomal protease, following exhaustive exercise in an animal model (Vinko et al., 1978). There is also evidence of the fact that the lysosomal enzymes are activated by the increase of the level of intracellular Ca++ (Rodemann et al., 1982).
