The anatomical sites such as fatigue sites and the related physiological mechanisms involved have long been identified; on an experimental basis, fatigue was differentiated into CENTRAL and PERIPHERAL.
- CENTRAL when it is attributable to mechanisms originating in the central nervous system (CNS), or in all those cortical and subcortical nerve structures whose tasks range from the conception of movement to conduction of the nerve impulse up to the spinal motor neuron.
- PERIPHERAL if the phenomena that determine it occur in the spinal motor neuron, in the motor plaque or in the skeletal fibrocellula.
In long-term sports activities, important metabolic alterations occur such as:
- Blood glucose reduction
- Plasma ammonium accumulation (NH3)
- Increased ratio of aromatic and branched amino acids
which also negatively affects nerve cell function.
The studies so far addressed seem to show that the site most affected by fatigue is the muscle (PERIPHERAL component) excluding the nerve junction. The intense and enduring sporting activity negatively influences the activity of the sarcolemma altering the intra and extracellular ionic distribution with intracellular sodium (Na +) and extracellular potassium (K +) increase. This phenomenon reduces the negativity of the resting potential of the fiber and reduces the amplitude of the action potential as well as the propagation speed. Furthermore, the accumulation of hydrogen ions (H +) in the extracellular environment also seems to contribute to the reduction of the conduction speed of the muscle fiber.
In the fatigued muscle, the alteration of the functionality of the sarcoplasmic transverse-tubular complex plays a decisive role; it compromises the contractile mechanism that is most affected by the availability of adenosine tri phosphate (ATP) and calcium (Ca2 +). It has been shown that the amplitude of the Ca2 + transient decreases with the development of fatigue and is attributable to an inhibition of Ca2 + release and re-uptake channels at the level of the sarcoplasmic reticulum, accompanied by the reduced affinity of the troponin for Ca itself; these phenomena are attributable to the increase in H + and attributed to the increase in lactic acid. Finally, the reduction of the Ca2 + release and reuptake process of the sarcoplasmic reticulum increases the Ca2 + transient duration itself by reducing the contraction rate.
Another factor on which the onset of fatigue depends is undoubtedly the imbalance between the speed of ATP splitting and its synthesis speed. What matters, more than the concentration of this molecule (which rarely falls below 70%), is the concentration of inorganic phosphorus (Pi) which is released by ATP hydrolysis; its increase induces the formation of actino-myosin bridges and hinders the contractile mechanism.
Also noteworthy is the availability of muscle glycogen which, in prolonged exercises in oxygen consumption between 65% and 85% of VO2MAX (recruitment of fast white fibers, oxidative-glycolytic and fatigue-resistant, therefore type IIa), becomes a strongly limiting element; on the contrary, for efforts of lower intensity, the primary substrates are glucose and blood fatty acids; for those of higher intensity, the accumulated lactic acid requires the interruption of the effort BEFORE the exhaustion of the glycogen reserves.
Muscle fatigue is undoubtedly a multifactorial etiology that involves different cellular sites and biochemical mechanisms and that depends on the type of exercise performed, its duration and intensity, therefore the type of fibers involved in the athletic gesture.
