Fatigue during exercise is a complex phenomenon that results in a temporary and reversible decline in performance. This decline can be attributed to various mechanisms within the central nervous system (CNS) and the muscles themselves. Understanding these mechanisms is crucial for athletes, coaches, and fitness enthusiasts aiming to optimize performance and recovery.​

Central Nervous System (CNS) Fatigue

CNS fatigue refers to a reduction in the neural drive or motor command from the brain to the muscles. It encompasses several mechanisms:​

1. Reductions in Coordination

Fatigue can impair the CNS's ability to coordinate movements, leading to decreased efficiency and disrupted movement patterns.​

2. Reductions in Central Motor Command Generation

Known as supraspinal fatigue, this involves a decreased ability of the motor cortex to generate commands, limiting the recruitment of high-threshold motor units essential for powerful muscle contractions.​

3. Reductions in Central Motor Command Transmission

Over time, the transmission of motor commands down the spinal cord becomes less effective, further reducing the activation of high-threshold motor units.​

These central mechanisms can be influenced by factors such as neurotransmitter levels, motivation, and perceived effort.​

Peripheral Fatigue Mechanisms

Peripheral fatigue originates within the muscles and involves several biochemical and physiological changes:​

1. Reductions in Cell Membrane Excitability

Fatigue can diminish the muscle cell membrane's ability to transmit action potentials, affecting muscle activation.​

2. Excitation-Contraction Coupling Failure (ECCF)

This occurs when the process that links muscle excitation to contraction is disrupted, often due to calcium ion accumulation and subsequent protease activation.​

3. Loss of Calcium Ion Sensitivity

Excessive calcium in the cytoplasm can desensitize actin filaments, reducing their responsiveness and impairing muscle contraction.​

4. Phosphate Accumulation

An increase in phosphate levels within muscle cells can interfere with ATP utilization, hindering energy production and muscle performance.​

5. Acidosis

The buildup of hydrogen ions (leading to acidosis) can slow down the detachment of myosin from actin during muscle contractions, reducing contraction speed without significantly affecting force.​

Conclusion

Fatigue during exercise is a multifaceted phenomenon involving both central and peripheral mechanisms. Central fatigue pertains to the brain and spinal cord's ability to generate and transmit motor commands, while peripheral fatigue involves changes within the muscles themselves. Recognizing and understanding these mechanisms can aid in developing training and recovery strategies to mitigate fatigue and enhance performance.​

References:

  • Davis JM, Bailey SP. Possible mechanisms of central nervous system fatigue during exercise. Med Sci Sports Exerc. 1997 Jan;29(1):45-57. PMID: 9000155

  • Taylor JL, Gandevia SC. A measure of central nervous system fatigue. Clin Neurophysiol. 1993 Apr;89(2):106-17. PMID: 8467889

  • Allen DG, Lamb GD, Westerblad H. Skeletal muscle fatigue: cellular mechanisms. Physiol Rev. 2008 Jan;88(1):287-332. PMID: 18195089

  • Fitts RH. The cross-bridge cycle and skeletal muscle fatigue. J Appl Physiol (1985). 2008 Jan;104(1):551-8. PMID: 18006863

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