The loss of muscle force production after muscle stretching is not accompanied by altered corticospinal excitability

Document Type

Journal Article

Publication Title

European Journal of Applied Physiology

ISSN

1439-6327

Volume

119

Issue

10

First Page

2287

Last Page

2299

PubMed ID

31456049

Publisher

Springer

School

School of Medical and Health Sciences / Center for Exercise and Sports Science Research

RAS ID

31042

Funders

ECU International Post Graduate Research Scholarship

Comments

Pulverenti, T. S., Trajano, G. S., Kirk, B. J. C., & Blazevich, A. J. (2019). The loss of muscle force production after muscle stretching is not accompanied by altered corticospinal excitability. European Journal of Applied Physiology, 119(10), 2287-2299.

Available here.

Abstract

PURPOSE: The aim of the present study was to determine whether depression of maximal muscular force and neural drive subsequent to prolonged ( ≥ 60 s) passive muscle stretching is associated with altered corticospinal excitability or intracortical (GABA

METHODS: Fourteen healthy adult males were tested before and after 5 min (5 × 60-s stretches) of intense, passive static stretching of the plantar flexor muscles. Two protocols (A and B) were conducted in a randomized order. Transcranial magnetic stimulation was delivered to the contralateral motor cortex at rest (Protocol A) and during maximal voluntary contractions (Protocol B). Changes in maximal voluntary isometric torque, voluntary surface electromyographic activity of triceps surae muscles (normalized to M-wave; EMG/M), motor-evoked potentials (MEP), and cortical silent period (cSP; Protocol B) in soleus elicited by transcranial magnetic stimulation were examined 10 min after stretch.

RESULTS: In both protocols A and B, significant decreases were observed immediately after stretching in maximal voluntary plantar flexion torque ( - 20.1 ± 15.9%, P = 0.004; and - 17.2 ± 13.5%, P = 0.006) and EMG/M ( - 18.0 ± 18.2%, P = 0.023; and - 13.0 ± 9.3%, P = 0.003). Decreases in torque and EMG/M were highly correlated (r = 0.67-0.85, P < 0.05). However, no changes were observed in MEP amplitudes during rest ( + 29.3 ± 50.0%) or maximum voluntary contraction ( + 1.9 ± 16.8%), or in cSP ( + 2.1 ± 15.1%).

CONCLUSIONS: Impaired neural drive contributed to the stretch-induced force loss; however, changes in corticospinal excitability and intracortical inhibition could not explain the phenomenon.

DOI

10.1007/s00421-019-04212-8

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