Lack of cortical or Ia-afferent spinal pathway involvement in muscle force loss after passive static stretching

This study investigated whether modulation of corticospinal-motoneuronal excitability and/or synaptic transmission of the Ia afferent spinal reflex contributes to decreases in voluntary activation and muscular force after an acute bout of prolonged static muscle stretching. Fifteen men performed five 60-s constant-torque stretches (15-s rest intervals; total duration 5 min) of the plantar flexors on an isokinetic dynamometer and a nonstretching control condition in random order on 2 separate days. Maximum isometric plantar flexor torque and triceps surae muscle electromyographic activity (normalized to M wave; EMG/M) were simultaneously recorded immediately before and after each condition. Motor-evoked potentials (using transcranial magnetic stimulation) and H-reflexes were recorded from soleus during EMG-controlled submaximal contractions (23.4 ± 6.9% EMG maximum). No changes were detected in the control condition. After stretching, however, peak torque (mean ± SD; -14.3 ± 7.0%) and soleus EMG/M (-17.8 ± 6.2%) decreased, and these changes were highly correlated (r = 0.83). No changes were observed after stretching in soleus MEP or H-reflex amplitudes measured during submaximal contractions, and interindividual variability of changes was not correlated with changes in EMG activity or maximum torque. During EMG-controlled submaximal contractions, torque production was significantly decreased after stretching (-22.7 ± 15.0%), indicating a compromised muscular output. These data provide support that changes in the excitability of the corticospinal-motoneuronal and Ia afferent spinal reflex pathways do not contribute to poststretch neural impairment.NEW & NOTEWORTHY This study is the first to specifically examine potential sites underlying the decreases in neural activation of muscle and force production after a bout of muscle stretching. However, no changes were found in either the H-reflex or motor-evoked potential amplitude during submaximal contractions.