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11.12.2014

What is muscle fatigue biology, ear ringing after loud noise - Try Out

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Etiology, Biology and Treatment of Muscular LesionsGian Nicola Bisciotti1 and Cristiano Eirale1, 2[1] Qatar Orthopaedic and Sport Medicine Hospital, FIFA Center of Excellence, Doha, Qatar[2] Kinemove Rehabilitation Centers, Pontremoli, Parma, La Spezia, Italy1. Schematic representation of the adhesion of muscle fiber to extracellular muscular-matrix (ECM).
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.
Graphic representation of the force-length relationship in an elongated muscle up to its breakpoint either in passive condition, or in contraction. In a muscle exposed to a series of intense eccentric contractions, a capillary vasoconstriction may happen which can, in itself, be the cause of an intermittent and transitory anoxia inside the muscle belly itself. IntroductionThe detrimental event on a muscular level, founds one of the most recurring traumatic insults in sporting environment.
As is easily recognizable from the graph, the peak of strength of breakage is superior, in the contracted muscle in comparison to the same muscle in relaxed conditions, by a quota equal to only 15%. The injured muscle fiber contract and the gap between the stumps, or the central zone CZ; initially begins to fill with the hematoma. The entity of the lesion can go from simple sprain, often associated with the breakage of small vessels, with appearance of pain and swelling, to complete muscular tear.
However, the tensile energy absorbed by the contracted muscle appears superior to that of the same muscle in relaxed conditions. The muscular fibers are necrotic inside their basal lamina, of a distance which is usually between 1 and 2 millimeters. The reason of main traumatic incidence on a muscular level, seen during 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). The molecules of the dystrofin associated 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. 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 behaviour thus not risking structural damage. Each muscular fiber is innerved, in a single and precise site,by a neuromuscular junction (NMJs, full point in the diagram). 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).
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.3. 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 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. 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.
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.
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 activity entails quite reduced tensile levels, almost all energy due to tensile stress is absorbed in this case by the contractile component.
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. 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). 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. 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. 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.
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 hypotheses of physical typeThe possible mechanisms of physical type capable of inducing initial structural damage to the muscular fiber, may be divided into two categories. 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 consequence, both of a single muscular contraction and of a cumulative series of contractions (Armstrong et al., 1991). 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.
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.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 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. 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. 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. 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. 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.
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).
On preparations of isolated frog sartorious muscle, after only three eccentric contractions, 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.
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. It is important to underline that in the tension-length 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. 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.
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.



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