Medicine:Muscle fatigue

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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.
Short description: Decline in ability of a muscle to generate force


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, muscle twitching, 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 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]

Muscle contraction

Main page: Biology:Muscle contraction

Muscle cells work by detecting a flow of electrical impulses from the brain which signals them to contract through the release of calcium by the sarcoplasmic reticulum. Fatigue (reduced ability to generate force) may occur due to the nerve, or within the muscle cells themselves.[citation needed]

Neural fatigue

Nerves are responsible for controlling the contraction of muscles, determining the number, sequence and force of muscular contraction. Most movements require a force far below what a muscle could potentially generate, and nervous fatigue is seldom an issue. But, during extremely powerful contractions that are close to the upper limit of a muscle's ability to generate force, nervous fatigue (enervation) — in which the nerve signal weakens — can be a limiting factor in untrained individuals.[citation needed]

In novice strength trainers, the muscle's ability to generate force is most strongly limited by nerve’s ability to sustain a high-frequency signal. After a period of maximum contraction, the nerve’s signal reduces in frequency and the force generated by the contraction diminishes. There is no sensation of pain or discomfort, the muscle appears to simply ‘stop listening’ and gradually cease to contract, often going backwards. Often there is insufficient stress on the muscles and tendons to cause delayed onset muscle soreness following the workout.[citation needed]

Part of the process of strength training is increasing the nerve's ability to generate sustained, high frequency signals which allow a muscle to contract with its greatest force. This neural training can cause several weeks of rapid gains in strength, which level off once the nerve is generating maximum contractions and the muscle reaches its physiological limit. Past this point, training effects increase muscular strength through myofibrillar or sarcoplasmic hypertrophy and metabolic fatigue becomes the factor limiting contractile force.[citation needed]

Metabolic fatigue

Though not universally used, ‘metabolic fatigue’ is a common term for the reduction in contractile force due to the direct or indirect effects of two main factors:

  1. Shortage of, or inability to metabolize, fuel (substrates) within the muscle fiber causing a low ATP reservoir.
  2. Accumulation of substances (metabolites) within the muscle fiber, which interfere either with the release of calcium (Ca2+) or with the ability of calcium to stimulate muscle contraction.

Substrates

Substrates within the muscle serve to power muscular contractions. They include molecules such as adenosine triphosphate (ATP), glycogen and creatine phosphate. ATP binds to the myosin head and causes the ‘ratchetting’ that results in contraction according to the sliding filament model. Creatine phosphate stores energy so ATP can be rapidly regenerated within the muscle cells from adenosine diphosphate (ADP) and inorganic phosphate ions, allowing for sustained powerful contractions that last between 5–7 seconds. Glycogen is the intramuscular storage form of glucose, used to generate energy quickly as intramuscular phosphocreatine stores become exhausted, producing lactic acid as a metabolic byproduct.

Substrate shortage is one of the causes of metabolic fatigue. Substrates are depleted during exercise or are unable to be metabolized (e.g. metabolic myopathies), resulting in a lack of intracellular energy sources to fuel contractions. In essence, the muscle stops contracting because it lacks the energy to do so.

Metabolites

Metabolites are the substances (generally waste products) produced as a result of muscular contraction. They include chloride, potassium, lactic acid, ADP, magnesium (Mg2+), reactive oxygen species, and inorganic phosphate. Accumulation of metabolites can directly or indirectly produce metabolic fatigue within muscle fibers through interference with the release of calcium (Ca2+) from the sarcoplasmic reticulum or reduction of the sensitivity of contractile molecules actin and myosin to calcium.

Chloride

Intracellular chloride partially inhibits the contraction of muscles. Namely, it prevents muscles from contracting due to "false alarms", small stimuli which may cause them to contract (akin to myoclonus).

Potassium

High concentrations of potassium (K+) also causes the muscle cells to decrease in efficiency, causing cramping and fatigue. Potassium builds up in the t-tubule system and around the muscle fiber as a result of action potentials. The shift in K+ changes the membrane potential around the muscle fiber. The change in membrane potential causes a decrease in the release of calcium (Ca2+) from the sarcoplasmic reticulum.[7]

Lactic acid

It was once believed that lactic acid build-up was the cause of muscle fatigue.[8] The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract. Though the impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue.

Produced as a by-product of fermentation, lactic acid can increase intracellular acidity of muscles. This can lower the sensitivity of contractile apparatus to Ca2+ but also has the effect of increasing cytoplasmic Ca2+ concentration through an inhibition of the chemical pump that actively transports calcium out of the cell. This counters inhibiting effects of potassium on muscular action potentials. Lactic acid also has a negating effect on the chloride ions in the muscles, reducing their inhibition of contraction and leaving potassium ions as the only restricting influence on muscle contractions, though the effects of potassium are much less than if there were no lactic acid to remove the chloride ions. Ultimately, it is uncertain if lactic acid reduces fatigue through increased intracellular calcium or increases fatigue through reduced sensitivity of contractile proteins to Ca2+.

Lactic acid is now used as a measure of endurance training effectiveness and VO2 max.[9]

Pathology

Muscle fatigue may be due to problems with the nerve supply, neuromuscular disease (such as myasthenia gravis), inborn errors of metabolism (such as metabolic myopathies), or problems with muscle itself. The latter category includes polymyositis and other muscle disorders.

Molecular mechanisms

Muscle fatigue may be due to precise molecular changes that occur in vivo with sustained exercise. It has been found that the ryanodine receptor present in skeletal muscle undergoes a conformational change during exercise, resulting in "leaky" channels that are deficient in calcium release. These "leaky" channels may be a contributor to muscle fatigue and decreased exercise capacity.[10]

Effect on performance

Fatigue has been found to play a big role in limiting performance in just about every individual in every sport. In research studies, participants were found to show reduced voluntary force production in fatigued muscles (measured with concentric, eccentric, and isometric contractions), vertical jump heights, other field tests of lower body power, reduced throwing velocities, reduced kicking power and velocity, less accuracy in throwing and shooting activities, endurance capacity, anaerobic capacity, anaerobic power, mental concentration, and many other performance parameters when sport specific skills are examined.[11][12][13][14][15]

Electromyography

Electromyography is a research technique that allows researchers to look at muscle recruitment in various conditions, by quantifying electrical signals sent to muscle fibers through motor neurons. In general, fatigue protocols have shown increases in EMG data over the course of a fatiguing protocol, but reduced recruitment of muscle fibers in tests of power in fatigued individuals. In most studies, this increase in recruitment during exercise correlated with a decrease in performance (as would be expected in a fatiguing individual).[16][17][18][19]

Median power frequency is often used as a way to track fatigue using EMG. Using the median power frequency, raw EMG data is filtered to reduce noise and then relevant time windows are Fourier Transformed. In the case of fatigue in a 30-second isometric contraction, the first window may be the first second, the second window might be at second 15, and the third window could be the last second of contraction (at second 30). Each window of data is analyzed and the median power frequency is found. Generally, the median power frequency decreases over time, demonstrating fatigue. Some reasons why fatigue is found are due to action potentials of motor units having a similar pattern of repolarization, fast motor units activating and then quickly deactivating while slower motor units remain, and conduction velocities of the nervous system decreasing over time.[20][21][22][23]

See also

References

  1. ↑ "Muscle Fatigue" (in en). https://www.physio-pedia.com/Muscle_Fatigue. 
  2. ↑ Lucia, Alejandro; Martinuzzi, Andrea; Nogales-Gadea, Gisela; Quinlivan, Ros; Reason, Stacey; Bali, Deeksha; Godfrey, Richard; Haller, Ronald et al. (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. PMID 32472082. 
  4. ↑ "#254110 - MUSCULAR DYSTROPHY, LIMB-GIRDLE, AUTOSOMAL RECESSIVE 8; LGMDR8" (in en-us). https://www.omim.org/entry/254110. 
  5. ↑ "#300559 - GLYCOGEN STORAGE DISEASE IXd; GSD9D" (in en-us). https://www.omim.org/entry/300559. 
  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. 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.". 
  7. ↑ Dee Unglaub Silverthorn (2009). Human Physiology: An Integrated Approach (5th ed.). Pearson. p. 412. ISBN 978-0321559807. 
  8. ↑ "Muscle fatigue and lactic acid accumulation". Acta Physiol Scand Suppl 556: 83–91. 1986. PMID 3471061. 
  9. ↑ "Performance Enhancement: What Are the Physiological Limits?". Physiology 30 (4): 282–92. July 2015. doi:10.1152/physiol.00052.2014. PMID 26136542. 
  10. ↑ "Remodeling of ryanodine receptor complex causes "leaky" channels: a molecular mechanism for decreased exercise capacity". Proc. Natl. Acad. Sci. U.S.A. 105 (6): 2198–202. February 2008. doi:10.1073/pnas.0711074105. PMID 18268335. Bibcode: 2008PNAS..105.2198B. 
  11. ↑ "Interactive processes link the multiple symptoms of fatigue in sport competition". Sports Med 41 (4): 307–28. April 2011. doi:10.2165/11586070-000000000-00000. PMID 21425889. https://eprints.qut.edu.au/47248/1/47248_acceptedVersion.pdf. 
  12. ↑ "The effect of recovery strategies on physical performance and cumulative fatigue in competitive basketball". J Sports Sci 26 (11): 1135–45. September 2008. doi:10.1080/02640410802104912. PMID 18608847. 
  13. ↑ "Neuromuscular fatigue and recovery in maximal compared to explosive strength loading". Eur J Appl Physiol Occup Physiol 77 (1–2): 176–81. 1998. doi:10.1007/s004210050317. PMID 9459539. 
  14. ↑ "Power output and electromyographic activity during and after a moderate load muscular endurance session". J Strength Cond Res 24 (8): 2122–31. August 2010. doi:10.1519/JSC.0b013e3181a5bc44. PMID 19834352. 
  15. ↑ "Changes in exercise characteristics, maximal voluntary contraction, and explosive strength during prolonged tennis playing". Br J Sports Med 40 (6): 521–6. June 2006. doi:10.1136/bjsm.2005.023754. PMID 16720888. 
  16. ↑ "Influence of gender on the EMG signal of the quadriceps femoris muscles and performance in high-intensity short-term exercise". Electromyogr Clin Neurophysiol 50 (7–8): 326–32. 2010. PMID 21284370. 
  17. ↑ "Gender differences in skeletal muscle fatigability are related to contraction type and EMG spectral compression". J. Appl. Physiol. 94 (6): 2263–72. June 2003. doi:10.1152/japplphysiol.00926.2002. PMID 12576411. 
  18. ↑ "Muscle performance following an acute bout of plyometric training combined with low or high intensity weight exercise". J Sports Sci 31 (3): 335–43. 2013. doi:10.1080/02640414.2012.733820. PMID 23083331. 
  19. ↑ "Quadriceps-hamstring EMG activity during functional, closed kinetic chain exercise to fatigue". Eur. J. Appl. Physiol. 81 (6): 504–9. April 2000. doi:10.1007/s004210050075. PMID 10774875. 
  20. ↑ "Evaluation of muscle activity during a standardized shoulder resistance training bout in novice individuals". J Strength Cond Res 26 (9): 2515–22. September 2012. doi:10.1519/JSC.0b013e31823f29d9. PMID 22067242. 
  21. ↑ "Muscle activation strategies during strength training with heavy loading vs. repetitions to failure". J Strength Cond Res 26 (7): 1897–903. July 2012. doi:10.1519/JSC.0b013e318239c38e. PMID 21986694. 
  22. ↑ "Back extensor muscle fatigue at submaximal workloads assessed using frequency banding of the electromyographic signal". Clin Biomech (Bristol, Avon) 26 (10): 971–6. December 2011. doi:10.1016/j.clinbiomech.2011.06.001. PMID 21696871. 
  23. ↑ "Does the fast Fourier transformation window length affect the slope of an electromyogram's median frequency plot during a fatiguing isometric contraction?". Gait Posture 38 (1): 161–4. May 2013. doi:10.1016/j.gaitpost.2012.10.028. PMID 23211923. 

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