Muscle fatigue

By Dr. Francesco Grazzina

The force generated by the skeletal muscle during contraction is the result of a complex series of events, the compromise 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 final common pathway 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", that is by the will of the gesture, by its emotional sphere and by the motivation for the execution of the movement.

On an experimental basis, fatigue has been 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, or rather from those structures whose tasks range from the conception of movement to the conduction of the nerve impulse to the spinal motor neuron. It is defined as "peripheral fatigue" when the phenomena that determine it occur in the spinal motor neuron, in the motor plaque or in the skeletal muscle cell.

Central fatigue is therefore an expression of the decrease in neuronal drive to 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. Thus the central system would play a decisive role in the onset of fatigue.

As far as sports are concerned, it must be said that the central factors, such as psychological motivation, emotional self-control and tolerance of physical discomfort, play a not insignificant role in the complex muscular activity that is the basis of the athletic gesture.

The studies conducted to date seem to suggest that the main site of onset of fatigue is represented by the muscle, and therefore they favor a peripheral localization of fatigue. The anatomical structures that can contribute to the development of localized muscle fatigue are the spinal motor neuron, the neuromuscular junction, 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 utilization of the ATP and its synthesis speed. What really matters is not the total amount of this free energy donor, but rather the amount of Pi that is released by ATP hydrolysis. In fact, it seems that its increase reduces the formation of the astin-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 fatigue-resistant fibers.

For exercises of higher intensity the energy sources are mainly represented by the circulating glucose. Exercises of maximum intensity are interrupted by the increase in lactic acid before the level of muscle glycogen can reach performance-limiting values.