Abstract

Although maximal voluntary contraction (MVC) force is reduced during pain, studies using interpolated twitch show no consistent reduction of voluntary muscle drive. The present study aimed to test if the reduction in MVC force during acute experimental pain could be explained by increased activation of antagonist muscles, weak voluntary activation at baseline, or changes in force direction. Twenty-two healthy volunteers performed maximal voluntary isometric knee extensions before, during, and after the effects of hypertonic (pain) and isotonic (control) saline injections into the infrapatellar fat pad. The MVC force, voluntary activation, electromyographic (EMG) activity of agonist, antagonist, and auxiliary (hip) muscles, and pain cognition and anxiety scores were recorded. MVC force was 9.3% lower during pain than baseline (p < 0.001), but there was no systematic change in voluntary activation. Reduced MVC force during pain was variable between participants (SD: 14%), and was correlated with reduced voluntary activation (r = 0.90), baseline voluntary activation (r = − 0.62), and reduced EMG amplitude of agonist and antagonist muscles (all r > 0.52), but not with changes in force direction, pain or anxiety scores. Hence, reduced MVC force during acute pain was mainly explained by deficits in maximal voluntary drive.

Highlights

  • Musculoskeletal pain is associated with reduced maximal voluntary contraction (MVC) force [1,2]

  • We aimed to determine whether the reduction in maximal voluntary knee extension force during acute experimental pain can be explained by: (i) increased activity of antagonist muscles; (ii) individual differences in baseline levels of maximal voluntary activation; or (iii) modification of force direction

  • We studied whether between-subject variation of MVC force during pain was related to psychological features associated with the pain experience

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Summary

Introduction

Musculoskeletal pain is associated with reduced maximal voluntary contraction (MVC) force [1,2]. Maximal voluntary knee extension force is up to 60% lower in people with knee osteoarthritis [3,4,5,6] and anterior knee pain [7] than healthy controls. This reduction has been attributed to factors such as muscle atrophy [3,8], nociceptive-mediated central inhibition of the motor drive [3,4,7], as well as beliefs and cognition towards pain, such as fear and anxiety [1,9,10]. When the effects of pain are investigated by painful injection of hypertonic saline, studies report smaller (< 20%)

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