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Muscle fatigue

For reduced ability to generate muscle force as a symptom or that does not improve with rest, see muscle weakness. For the absence of muscle weakness coupled with the feeling that it requires more effort to move the muscle, see asthenia.

Muscle fatigue is when muscles that were initially generating a normal amount of force, then experience a declining ability to generate force. It can be a result of vigorous exercise, but abnormal fatigue may be caused by barriers to or interference with the different stages of muscle contraction. There are two main causes of muscle fatigue: the limitations of a nerve’s ability to generate a sustained signal (neural fatigue); and the reduced ability of the muscle fiber to contract (metabolic fatigue).

Muscle fatigue is not the same as muscle weakness, though weakness is an initial symptom. Despite a normal amount of force being generated at the start of activity, once muscle fatigue has set in and progressively worsens, if the individual persists in the exercise they will eventually lose their hand grip, or become unable to lift or push with their arms or legs, or become unable to maintain an isometric position (such as plank). Other symptoms may accompany such as myalgia (muscle pain), shortness of breath, fasciculations (muscle twitching), myokymia (muscle trembling), and muscle cramps during exercise; muscle soreness may occur afterwards.[1] An inappropriate rapid heart rate response to exercise may be seen, such as in the metabolic myopathy of McArdle disease (GSD-V), where the heart tries to compensate for the deficit of ATP in the skeletal muscle cells (metabolic fatigue) by increasing heart rate to maximize delivery of oxygen and blood borne fuels to the muscles for oxidative phosphorylation.[2] The combination of an inappropriate rapid heart rate response to exercise with heavy or rapid breathing is known as an exaggerated cardiorespiratory response to exercise.[3]

Due to the confusion between muscle fatigue and muscle weakness, there have been instances of abnormal muscle fatigue being described as exercise-induced muscle weakness.[4][5][6]

  1. ^ "Muscle Fatigue". Physiopedia. Retrieved 2023-11-19.
  2. ^ Lucia, Alejandro; Martinuzzi, Andrea; Nogales-Gadea, Gisela; Quinlivan, Ros; Reason, Stacey; Bali, Deeksha; Godfrey, Richard; Haller, Ronald; Kishnani, Priya; Laforêt, Pascal; Løkken, Nicoline; Musumeci, Olimpia; Santalla, Alfredo; Tarnopolsky, Mark; Toscano, Antonio (December 2021). "Clinical practice guidelines for glycogen storage disease V & VII (McArdle disease and Tarui disease) from an international study group". Neuromuscular Disorders. 31 (12): 1296–1310. doi:10.1016/j.nmd.2021.10.006. ISSN 0960-8966.
  3. ^ Noury, Jean-Baptiste; Zagnoli, Fabien; Petit, François; Marcorelles, Pascale; Rannou, Fabrice (2020-05-29). "Exercise efficiency impairment in metabolic myopathies". Scientific Reports. 10 (1): 8765. doi:10.1038/s41598-020-65770-y. ISSN 2045-2322. PMC 7260200. PMID 32472082.
  4. ^ "#254110 - MUSCULAR DYSTROPHY, LIMB-GIRDLE, AUTOSOMAL RECESSIVE 8; LGMDR8". www.omim.org. Retrieved 2023-11-19.
  5. ^ "#300559 - GLYCOGEN STORAGE DISEASE IXd; GSD9D". www.omim.org. Retrieved 2023-11-19.
  6. ^ Das, Anibh M.; Steuerwald, Ulrike; Illsinger, Sabine (2010). "Inborn errors of energy metabolism associated with myopathies". Journal of Biomedicine & Biotechnology. 2010: 340849. doi:10.1155/2010/340849. ISSN 1110-7251. PMC 2877206. PMID 20589068. There are three phenotypes of CPT2 deficiency: the 'classic muscular form' (OMIM 255110) is most frequent and shows onset in childhood or adulthood with exercise-induced muscle weakness and rhabdomyolysis.

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