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

## TL;DR

This study found no evidence that soleus motor neuron excitability or firing rates contribute to weakness in runners with Achilles tendinopathy.

## Contribution

The study is the first to investigate intrinsic motor neuron excitability as a potential contributor to Achilles tendinopathy-related weakness.

## Key findings

- No significant differences in motor neuron excitability measures were found between runners with and without Achilles tendinopathy.
- Soleus motor neuron excitability or firing rates may not be responsible for plantar flexor weakness in Achilles tendinopathy.
- Future research should explore other neurophysiological factors and the role of the gastrocnemius muscle.

## Abstract

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.

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.

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).

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.