Asmussen, E. (1979). Muscle fatigue. Medicine and Science in Sports, 11, 313-321.

Power is concerned with the intensity of exercise that can be sustained while work is concerned with the amount of exercise that can be performed.

The maximum intensity of exercise is determined by physiological factors such as the maximum rate of O2 uptake, maximum heart rate and stroke volume, maximum muscle strength, etc. In the case of maximum work, a time factor is involved. Muscle fatigue is the transient decrease in performance capacity of muscles, usually evidenced by a failure to maintain or develop a certain expected force or power.

Fatigue curves vary between individuals and within individuals depending upon the conditions that exist.

Muscle fatigue can occur in two basic mechanisms: (a) central involves proximal motor neurons (mainly in the brain); and (b) peripheral involves within the motor units (i.e., motor neurons, peripheral nerves, motor endplates, muscle fibers).

In peripheral muscle fatigue there are at least two different sites where repeated contractions may cause impairment: the "transmission mechanism" (neuromuscular junction, muscle membrane, and endoplasmic reticulum), and the "contractile mechanism" (muscle filaments).

As the mechanical response of the individual active muscle fibers decline with fatigue, a certain compensation can be achieved by increasing the innervation frequency and/or the number of active motor units. The reasons for the appearance of peripheral muscle fatigue are local changes in the internal conditions of the muscle. These may be biochemical, depletion of substrates such as glycogen, high energy phosphate compounds in the muscle fibers, and acetylcholine in the terminal motor nerve branches, or they may be due to the accumulation of metabolites, such as lactate or electrolytes liberated from the muscles during activity.

In short-term maximal or near-maximal isometric contractions, it is highly improbable that a general depletion of the energy stores should be the direct cause of exhaustion. The only substances that specifically undergo a significant decrease are the high energy phosphates, especially creatine phosphate (CP). The decrease of high energy phosphates is not due to a depletion of energy stores. It is due to a too low rate of energy transfer from the stores to the ATP and CP. This slowing, presumably of enzymatic processes, might be caused by the concomitant increase in muscle lactic acid, causing a pH decrease. Accordingly, lactic acid might be termed a "fatigue substance." However, there are several other possibilities particularly if transmission fatigue is present. Thus, both the contractile and transmission mechanism may be impaired by continuous muscle activity.

Summary. Peripheral muscle fatigue, defined as a transient decrease in a muscle group's capacity for exercise, can be purely peripheral (i.e., located distally to the motor neurons). The site may be the transmission mechanism, and the cause may be the depletion of some necessary substance(s)) and/or the accumulation of catabolites or other substances set free by the muscle activity.

The "Setchenov phenomenon" (1903): when sawing exhausts the muscles of one arm, they recover faster if the other arm is exercised during the rest pause rather than following rest alone. This was explained as a "recharging with energy" of fatigued nerve centers brought about by afferent nerve impulses from the active non-fatigued arm. The other activity constituted a diverting activity that produced the accelerated recovery of the central mechanism.

It is explained as follows. During muscle fatigue, feedback of nerve impulses from the fatigued muscles impinges on a part of the reticular formation and causes an inhibition of voluntary effort. Diverting activity, on the other hand, produces an increased inflow of impulses from non-fatigued parts of the body to the facilitatory part of the reticular formation, thus shifting the balance between inhibition and facilitation in a facilitatory direction.

Central fatigue is also an expression of lowered arousal. During fatigue studies, EEGs show a gradual appearance of the characteristic alpha-rhythm as fatigue progresses. The introduction of diverting activity makes the alpha-rhythm disappear. Alpha-rhythms are a signal of lowered arousal level in the brain, and usually are found when subjects close their eyes and disappear when the eyes are opened.

Central fatigue is caused by an inhibition elicited by nervous impulses from receptors (probably some kind of chemoreceptors) in the fatigued muscles. The inhibition may act on the motor pathways anywhere from the voluntary centers in the brain to the spinal motor neurons. This kind of fatigue should manifest itself by a decrease in the outflow of motor impulses to the muscles. There are several good reasons for assuming this central component is the result of central inhibition called forth by signals from the fatigued muscles. This inhibition, most likely originating in the reticular formation, may itself be inhibited or counteracted by other signals of peripheral or central nervous origin.

Summary. Peripheral or central fatigue may appear separately or combined, depending on the specific situation. Any one link in the long chain from the voluntary motor centers in the brain to the contractile filaments in the single muscle fibers may be the weaker and thus most direct cause of muscle fatigue. Prevention and treatment of voluntary fatigue must be adapted to these complexities.

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