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Reduced neural drive in bilateral exertions: a performance-limiting factor?

Jaap H Van Dieën1, Futoshi Ogita, Arnold De Haan

  • 1Institute for Fundamental and Clinical Human Movement Sciences, Faculty of Human Movement Sciences, Vrije Universiteit Amsterdam, The Netherlands. J_H_van_Dieen@fbw.vu.nl

Medicine and Science in Sports and Exercise
|January 25, 2003
PubMed
Summary

Bilateral movements show significant force deficits, with finger flexion up to 20% lower than unilateral. This reduced neural drive limits performance in tasks requiring simultaneous muscle activation.

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Area of Science:

  • Neuroscience
  • Human Physiology
  • Motor Control

Background:

  • Motor cortex activity in one hemisphere inhibits homologous areas in the opposite hemisphere.
  • This interhemispheric inhibition can reduce maximum voluntary force during concurrent activation of contralateral muscles.

Purpose of the Study:

  • To determine if the bilateral force deficit is substantial enough to limit performance in bilateral exertions.
  • To investigate the neural mechanisms underlying bilateral force deficits.

Main Methods:

  • Comparison of voluntary force production and neural drive during unilateral and bilateral exertions.
  • Experiments included unilateral maximum contractions, synchronous bilateral contractions, and asynchronous bilateral contractions.
  • Muscles studied were finger flexors and knee extensors.

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Main Results:

  • Bilateral knee extension force was 7% lower than unilateral (P < 0.001); finger flexion showed a 20% deficit (P = 0.001).
  • Agonist electromyography (EMG) activity showed corresponding deficits, though not consistently related to force deficits.
  • A 4% deficit in voluntary activation during knee extension (P = 0.003) correlated with force deficits (r = 0.80, P = 0.002).
  • Maximum rate of force development was 13% lower in bilateral knee extensions (P = 0.002).

Conclusions:

  • Bilateral force production deficits are significant and likely limit performance.
  • Reduced neural drive is the probable underlying mechanism for these bilateral deficits.