"Motor Neuron Pool Excitability of the Lower Leg Muscles After Acute Lateral Ankle Sprain"- Klykken et al, JAT 6-11.
I'm really impressed at the quality of the research in the Journal of Athletic Training in the last decade or so. This was a good one. The researchers took 10 athletes with recently sprained ankles, placed them in a relaxed prone position, then measured the motor neuron pool excitability of the soleus, anterior tib, & peroneus longus. The soleus was facilitated, the anterior tibialis inhibited, & no difference in the peroneus longus.
The authors go on to explain the reasons for the results. Included was the possibility the CNS was re-organizing to compensate for the loss of posterior talar glide, ie loss of dorsiflexion in the ankle. In running & gait, remember the soleus is a knee extensor. So in this scenario it is helping to limit the degree of knee excursion to control the degree of ankle dorsiflexion at the ankle joint.
A thought: What if this loss of dorsiflexion is not restored? Could the facilitated soleus persist? Could the articular complications resulting from an unresolved ankle sprain(s) be a culprit in chronic calf cramping in middle age runners?