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Muscle fatigue

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Muscle fatigue, or physical fatigue, is the decline in ability of a muscle 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 - limitations of nerve’s ability to generate a sustained signal and the reduced ability of calcium (Ca2+) to stimulate contraction.

Muscle contraction

Main article: 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.

Nervous 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 barring pathological nervous fatigue, is seldom an issue. For extremely powerful contractions that are close to the upper limit of a muscle's ability to generate force, nervous fatigue can be a limiting factor in untrained individuals. 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 move, often going backwards. As there is insufficient stress on the muscles and tendons, there will often be no delayed onset muscle soreness following the workout. 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. It is this neural training that causes several weeks worth 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 myofibrilar or sarcoplasmic hypertrophy and metabolic fatigue becomes the factor limiting contractile force chode.

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 the reduction of substrates or accumulation of metabolites within the muscle fiber. This can occur through a simple lack of energy to fuel contraction, or interference with the ability of Ca2+ to stimulate actin and myosin to contract.

Metabolites

Metabolites are the substances (generally waste products) produced as a result of muscular contraction. They include 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 from the sarcoplasmic reticulum or reduction of the sensitivity of contractile molecules actin and myosin to calcium.

Chloride

Intracellular chloride inhibits the contraction of muscles, preventing them from contracting due to "false alarms", small stimuli which may cause them to contract (akin to myoclonus). This natural brake helps muscles respond solely to the conscious control or spinal reflexes [citation needed] but also has the effect of reducing the force of conscious contractions.

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.[1]

Lactic acid

It was once believed that lactic acid build-up was the cause of muscle fatigue.[2] The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract. 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 poo increases fatigue through reduced sensitivity of contractile proteins to Ca2+.

Pathology

Muscle weakness may be due to problems with the nerve supply, neuromuscular disease (such as myasthenia gravis) or problems with muscle itself. The latter category includes polymyositis and other muscle disorders

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. [3] [4] [5][6] [7][8]

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). [9][10][11][12]


See also

References

  • Lamb, G.D., Stephenson, D.G., Bangsbo, J. & Juel, C. (2006). Point:Counterpoint: Lactic acid accumulation is an advantage/disadvantage during muscle activity. Journal of Applied Physiology, 100, 1410-1412.
  1. ^ Silverthorn, Dee Unglaub. Human Physiology: An Integrated Approach. Pearsin Benjamin Cummings, 2009, p. 412.
  2. ^ Muscle fatigue and lactic acid accumulation. abstract
  3. ^ Knicker, A. J., Renshaw, I., Oldham, A.R.H., Cairns, S.P. (2011). Interactive processes link the multiple symptoms of fatigue in sport competition. Sports Medicine, 41(4), 307-328.
  4. ^ Montgomery, P. G., Pyne, D.B., Hopkins, W.G., Dorman, J.C., Cook, K., Minahan, C.L. (2008). The effect of recovery strategies on physical performance and cumulative fatigue in competitive basketball. Journal of sports sciences, 26(11), 1135-1145.
  5. ^ Linnamo, V., Hakkinen, K., Komi, P.V. (1998). Neuromuscular fatigue and recovery in maximal compared to explosive strength loading. European journal of applied physiology, 77, 176-181.
  6. ^ Smilios, I., Hakkinen, K., and Tokmakidis, S. (2010) Power output and electrographis activity during and after a moderate load muscular endurance session. Journal of Strength and Conditioning Research. 24(8): 2122-2131
  7. ^ Linnamo, V., Hakkinen, K., Komi, P.V. (1998). Neuromuscular fatigue and recovery in maximal compared to explosive strength loading. European journal of applied physiology, 77, 176-181.
  8. ^ Girard, O., Lattier, G., Micallef, J., and Millet, G. (2006) Changes in exercise characteristics, maximal voluntary contraction, and explosive strength during prolonged tennis playing. British Journal of Sports Medicine. 40:521-526
  9. ^ Carneiro, J. G., Goncalves, E.M., Camata, T.V., Altimari, J.M., Machado, M.V., et al. (2010). Influence of gender on the emg signal of the quadriceps femoris muscles and performance in high intensity short term exercise. Electromyography and clinical neurophysiology, 50, 326-332.
  10. ^ Clark, B. C., Manini, T.M., The, D.J., Doldo, N.A., Ploutz-Snyder, L.L. (2003). Gender differences in skeletal muscle fatigability are related to contraction type and emg spectral compression. Journal of applied physiology, 94, 2263-2272.
  11. ^ Beneka, A. G., Malliou, P.K., Missailidou, V., Chatzinikolaou, A., Fatouros, I., Gourgoulis, V., Georgiadis, E. (2012). Muscle performance following an acute bout of plyometric training combined with low or high intensity weight exercise. Journal of sport sciences, 21, 1-9.
  12. ^ Pincivero, D. M., Aldworth, C., Dickerson, T., Petry, C., Shultz, T. (2000). Quadriceps-hamstring emg activity during functional, closed kinetic chain exercise to fatigue. European journal of applied physiology, 81, 504-509.
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