title: Muscular fatigue.
abstract: Although everyone knows fatigue personally, it is a difficult concept to define. For muscular fatigue, one must know the aspect of performance affected. The most obvious demonstrations are decreased maximal force and slowed muscular answer. Fatigue can have a central origin, by reducing cognitive performance or lowering excitation of motoneurons. Various mediators are in question (serotonin, moduline, dopamine). The fatiguing muscular contractions are accompanied by reduced discharges of motoneurons. The neuromuscular junction does not seem to be in question. Cold reduces muscular power, whereas a hot environment limits exercise by a central mechanism, which starts the normal behavioural response to stop the exercise. Fatigue can also be the consequence of overtraining. In the periphery, the electric activity of the membrane's surface is the first possible sign of failure, which explains high-frequency fatigue: the accumulation of potassium outside the cell blocks the sodic channels to block the potentials of action or slow down their propagation. With fatigue, less calcium is released and limits the number of attached actin-myosin bridges connections of actin-myosin. The slowing down of the muscular answer represents a deterioration of the function of actin-myosin bridges. On the metabolic level, the most-often evoked changes are reduced pH and increased intracellular lactate level. However, these variations cannot all describe fatigue, since patients with Mc Ardle disease do not exhibit these variations but very quickly experience tiredness. In fact, an association of small metabolic intracellular variations could explain tiredness. The fast fibres are larger than slow fibres; their metabolic needs are higher and they are thus more sensitive to tiredness. The half time of recovery is within approximately 1 min: normal values of force and power are recovered after 5 to 10 min. During endurance activities, the limiting factors are glycogen reserves and levels of oxidative enzymes. On the whole, mechanisms of fatigue must be explored to completely understand the governing phenomena.
authors.affiliation: Institut Régional de Médecine du Sport, MCU-PH, CHU Côte-de-Nacre, 14033 Caen cedex, France. Sesboue-b@chu-caen.fr
authors.forename: B
authors.initials: B
authors.lastname: Sesboüé
authors.forename: J-Y
authors.initials: JY
authors.lastname: Guincestre
mesh_terms: D000222:Adaptation, Physiological; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D009119:Muscle Contraction / Q000502:physiology; D018763:Muscle Fatigue / Q000502:physiology*; D018482:Muscle, Skeletal / Q000502:physiology / Q000648:ultrastructure; D010807:Physical Endurance / Q000502:physiology
chemical_list: D019344:Lactic Acid