Date of Award


Document Type

Thesis - ECU Access Only


Edith Cowan University

Degree Name

Doctor of Philosophy


School of Medical and Health Sciences

First Supervisor

Professor Anthony Blazevich

Second Supervisor

Dr Gabriel Trajano


Acute bouts of prolonged passive muscle stretching are commonly shown to attenuate maximal force production and negatively affect performance of physical tasks. It has become increasingly apparent that a centrally-mediated impaired voluntary neural drive is the primary factor underpinning stretch-induced force loss. Exacerbated stretching-related sensory feedback could acutely decrease motor cortical excitability and thus impair the level of descending cortical drive reaching muscle. On the other hand, weakened neural drive could stem from changes at the spinal level by alterations in the net excitatory and inhibitory afferent feedback to the spinal motoneurons. However, potential contributions of supraspinal and spinal mechanisms to stretchinduced force loss have not been explicitly studied and this impedes our ability to identify methods to overcome the force decrement after acute muscle stretching. Therefore, the overall aim of this research was to investigate the neurophysiological factors contributing to force loss after acute passive plantar flexor muscle stretching, with particular attention to changes in supraspinal and spinal processes. In Study 1, stretch-induced changes in corticospinal excitability (to soleus) were examined using transcranial magnetic stimulation (TMS) at rest and during maximal muscular contractions. In Study 2, the effect of acute passive muscle stretching on facilitatory Ia afferent spinal reflex pathway and corticospinal excitability were examined using electrically evoked Hoffman reflexes and TMS during submaximal (constant EMG) isometric plantar flexions. Finally, the effect of acute stretching on the sensitivity of tendon tap reflexes and the soleus late response elicited by TMS were examined in an effort to assess potential changes in muscle spindle sensitivity. In each study, significant reductions in both maximum voluntary isometric plantar flexion torque (range: -14.3–20.1%) and triceps surae electromyographic activity (-15.9–18.0%) were found after 5 min of plantar flexor stretching (560-s stretches), and changes in these were highly correlated (r = 0.61–0.85). These data were taken as evidence for a stretch-induced impairment in neural drive underpinning the stretch-induced force loss. However, there were no observable stretch-induced changes in motor-evoked potential amplitude (an indicator of intrinsic corticospinal excitability) or duration of the cortical silent period (an indicator of GABAB-mediated intracortical inhibition), measured at rest or during either submaximal or maximal contractions. In addition, synaptic transmission of the Ia afferent spinal reflex pathway was not significantly affected after stretching as there was a lack of change in the Hoffman reflex amplitude. Of interest was that no changes in tendon reflex responses were detected, but the soleus late response was nearly abolished after stretching and had a similar temporal recovery to reductions in neural drive and force. This may indicate an effect of stretch on a cerebellar-mediated postural response. The present data therefore provide no evidence that alterations in corticospinal excitability, GABAB-mediated intracortical inhibition, Ia reflex pathway or muscle spindle sensitivity contribute to the stretch-induced force loss. Nonetheless, loss (immediately post-stretch) and then recovery of the soleus late response may indicate that cerebellar function mediating postural control may be influenced, and this may speculatively be associated with previous reports of modifications of balance and postural sway.

Access Note

Access to this thesis is restricted to the exegesis.