Determining intracortical, corticospinal and alpha motoneurone excitability in athletes with patellar tendinopathy compared to asymptomatic controls.

Abstract

Lower capacity to generate knee extension maximal voluntary force (MVF) has been observed in individuals affected with patellar tendinopathy (PT) compared to asymptomatic controls. This MVF deficit is hypothesized to emanate from alterations in corticospinal excitability (CSE). The modulation of CSE is intricately linked to the excitability levels at multiple sites, encompassing neurones within the corticospinal tract (CST), intracortical neurones within the primary motor cortex (M1), and the alpha motoneurone. The aim of this investigation was to examine the excitability of intracortical neurones, CST neurones, and the alpha motoneurone, and compare these between volleyball and basketball athletes with PT and matched asymptomatic controls. Nineteen athletes with PT and 18 asymptomatic controls participated in this cross-sectional study. Transcranial magnetic stimulation was utilized to assess CST excitability, corticospinal inhibition (silent period, and short-interval cortical inhibition). Peripheral nerve stimulation was used to evaluate lumbar spine and alpha motoneurone excitability, including the evocation of lumbar-evoked potentials and maximal compound muscle action potential (MMAX ), and CSE with central activation ratio (CAR). Knee extension MVF was also assessed. Athletes with PT exhibited longer silent period duration and greater electrical stimulator output for MMAX , as well as lower MVF, compared to asymptomatic controls (p < 0.05). These findings indicate volleyball and basketball athletes with PT exhibit reduced excitability of the alpha motoneurone or the neuromuscular junction, which may be linked to lower MVF. Subtle alterations at specific sites may represent compensatory changes to excitability aiming to maintain efferent drive to the knee extensors.