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Objective <p>Soleus weakness is suggested to contribute to Achilles tendinopathy (AT) in runners. Since muscle force relies on the ability of motor units firing at high frequencies, and intrinsic motor neuron excitability contributes to firing rate modulation, soleus inhibition and hypoexcitability may contribute to AT soleus weakness. This study investigated soleus motor neuron excitability by comparing: (i) estimates of persistent inward currents (Δ<i>f</i> and Δ<i>f</i>/<i>k</i>), which is known to modulate excitability; (ii) brace height, which is related to neuromodulatory input onto motor neurons; (iii) attenuation slopes, which estimate the influence of inhibitory input onto the motor units; and (iv) and motor unit firing rates between runners with and without mid-portion AT.</p> Methods <p>Delta frequency absolute and normalized (Δ<i>F</i> and Δ<i>F</i>/<i>k</i>), brace height, attenuation slope, and peak firing rates were compared between runners with AT (<i>n</i> = 11) and without AT (<i>n</i> = 12). These variables were calculated from ramp triangular-shaped isometric plantar flexor contractions at 20% maximal torque. Soleus motor unit firing rates were assessed using high-density surface electromyography.</p> Results <p>No significant differences were found between groups in soleus Δ<i>F</i> (estimated mean difference: −&#xa0;0.1 pps; 95% CI: −&#xa0;1.3 to 1.0; <i>p</i> = 0.79), Δ<i>F</i>/<i>k</i> (0.2 pps; −&#xa0;0.03 to 0.3; <i>p</i> = 0.09), brace height (−&#xa0;3.9% rTri; −&#xa0;8.3 to 0.4; <i>p</i> = 0.07), attenuation (0.04 pps/% torque; −&#xa0;0.04 to 0.1; <i>p</i> = 0.27), or peak firing rates (−&#xa0;0.4 pps; −&#xa0;1.6 to 0.9; <i>p</i> = 0.55).</p> Conclusion <p>Soleus motor neuron excitability or firing rates may not contribute to plantar flexor weakness in AT. Future studies should investigate other neurophysiological mechanisms and gastrocnemius contributions to AT-related weakness.</p>

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Is soleus intrinsic motor neuron excitability contributing to motor deficits in runners with Achilles tendinopathy?

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月1日

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  • Gabriel L. Fernandes,
  • Lucas B. R. Orssatto,
  • Gabriel S. Trajano

摘要

Objective

Soleus weakness is suggested to contribute to Achilles tendinopathy (AT) in runners. Since muscle force relies on the ability of motor units firing at high frequencies, and intrinsic motor neuron excitability contributes to firing rate modulation, soleus inhibition and hypoexcitability may contribute to AT soleus weakness. This study investigated soleus motor neuron excitability by comparing: (i) estimates of persistent inward currents (Δf and Δf/k), which is known to modulate excitability; (ii) brace height, which is related to neuromodulatory input onto motor neurons; (iii) attenuation slopes, which estimate the influence of inhibitory input onto the motor units; and (iv) and motor unit firing rates between runners with and without mid-portion AT.

Methods

Delta frequency absolute and normalized (ΔF and ΔF/k), brace height, attenuation slope, and peak firing rates were compared between runners with AT (n = 11) and without AT (n = 12). These variables were calculated from ramp triangular-shaped isometric plantar flexor contractions at 20% maximal torque. Soleus motor unit firing rates were assessed using high-density surface electromyography.

Results

No significant differences were found between groups in soleus ΔF (estimated mean difference: − 0.1 pps; 95% CI: − 1.3 to 1.0; p = 0.79), ΔF/k (0.2 pps; − 0.03 to 0.3; p = 0.09), brace height (− 3.9% rTri; − 8.3 to 0.4; p = 0.07), attenuation (0.04 pps/% torque; − 0.04 to 0.1; p = 0.27), or peak firing rates (− 0.4 pps; − 1.6 to 0.9; p = 0.55).

Conclusion

Soleus motor neuron excitability or firing rates may not contribute to plantar flexor weakness in AT. Future studies should investigate other neurophysiological mechanisms and gastrocnemius contributions to AT-related weakness.