Muscle fatigue

Edited by Dr. Francesco Grazzina

The force generated by skeletal muscle during contraction is the result of a complex chain of events, the impairment of which, at any level, can contribute to the onset of neuromuscular fatigue.
In order for the muscle fiber to contract, the depolarization impulse must arrive from the spinal motor neuron.

The latter represents the common final path of impulses coming from the motor cortex, from the nuclei of the base and from the cerebellum which, in turn, are influenced by the "activity of the" psyche ", or rather by the will of the gesture, its emotional sphere and the motivation of execution of the movement.
On the experimental basis, fatigue was divided into "central" and "peripheral".

Central fatigue and peripheral fatigue

Fatigue is defined as "central" when it is attributable to mechanisms that originate at the level of the central nervous system, ie from those structures whose tasks range from the idea of ​​movement, to the conduction of the nervous impulse to the spinal motor neuron. It is defined as “peripheral” fatigue when the phenomena that cause it occur in the spinal motor neuron, in the motor plate or in the skeletal muscle fiber cell.
Central fatigue is therefore an expression of the decrease in neuronal "drive" to the skeletal muscles. However, the level of activation of the central nervous system can be increased if the subject is appropriately stimulated with verbal encouragement or feedback of various kinds. Therefore the central system would play a decisive role in the onset of fatigue.
As far as sports practice is concerned, it must be said that the central factors, such as psychological motivation, capacity for emotional self-control and tolerance of physical discomfort, play a not negligible role in the complex muscular activity that is the basis of the athletic gesture.
The studies conducted so far seem to suggest that the main site of the onset of fatigue is represented by the muscle, therefore they tend towards a peripheral localization of fatigue. The anatomical structures that can contribute to the development of localized muscle fatigue are the spinal motor neuron, the junction neuromuscular, the sarcolemma and the T-system of the muscle fiber.
Another factor on which the onset of fatigue depends is the imbalance between the speed of use of ATP and the speed of synthesis of the same. What really matters is not the total amount of this free energy donor, but rather the amount of Pi that is released by the hydrolysis of ATP. In fact, it seems that its increase reduces the formation of the rod-myosin bridges, hindering the contractile mechanism.
The availability of muscle glycogen becomes important for exercises that require an oxygen consumption between 65% and 85% of the maximum oxygen consumption, mainly supported by type II ° fibers resistant to fatigue.
For higher intensity exercises, the energy sources are mainly represented by circulating glucose. Exercises of maximal intensity are stopped due to the increase in lactic acid before the level of muscle glycogen can reach performance-limiting values.