PeerJ (Aug 2018)

The influence of residual force enhancement on spinal and supraspinal excitability

  • Caleb T. Sypkes,
  • Benjamin J. Kozlowski,
  • Jordan Grant,
  • Leah R. Bent,
  • Chris J. McNeil,
  • Geoffrey A. Power

DOI
https://doi.org/10.7717/peerj.5421
Journal volume & issue
Vol. 6
p. e5421

Abstract

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Background Following active muscle lengthening, there is an increase in steady-state isometric force as compared with a purely isometric contraction at the same muscle length and level of activation. This fundamental property of skeletal muscle is known as residual force enhancement (RFE). While the basic mechanisms contributing to this increase in steady-state isometric force have been well documented, changes in central nervous system (CNS) excitability for submaximal contractions during RFE are unclear. The purpose of this study was to investigate spinal and supraspinal excitability in the RFE isometric steady-state following active lengthening of the ankle dorsiflexor muscles. Methods A total of 11 male participants (20–28 years) performed dorsiflexions at a constant level of electromyographic activity (40% of maximum). Half of the contractions were purely isometric (8 s at an ankle angle of 130°), and the other half were during the RFE isometric steady-state following active lengthening (2 s isometric at 90°, a 1 s lengthening phase at 40°/s, and 5 s at 130°). Motor evoked potentials (MEPs), cervicomedullary motor evoked potentials (CMEPs), and compound muscle action potentials (M-waves) were recorded from the tibialis anterior during the purely isometric contraction and RFE isometric steady-state. Results Compared to the purely isometric condition, following active lengthening, there was 10% RFE (p 0.05). Discussion These results indicate that spinal excitability is reduced during submaximal voluntary contractions in the RFE state with no change in supraspinal excitability. These findings may have further implications to everyday life offering insight into how the CNS optimizes control of skeletal muscle following submaximal active muscle lengthening.

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