Ingestion of transient receptor potential channel agonists attenuates exercise-induced muscle cramps

Daniel H. Craighead, Sean W. Shank, Jinger S. Gottschall, Dennis H. Passe, Bob Murray, Lacy M. Alexander, W. Larry Kenney

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

Introduction: Exercise-associated muscle cramping (EAMC) is a poorly understood problem that is neuromuscular in origin. Ingestion of transient receptor potential (TRP) channel agonists has been efficacious in attenuating electrically induced muscle cramps. This study examines the effect of TRP agonist ingestion on voluntarily induced EAMC and motor function. Methods: Study 1: Thirty-nine participants completed 2 trials after ingesting TRP agonist-containing active treatment (A), or vehicle (V) control. Cramping in the triceps surae muscle was induced via voluntary isometric contraction. Study 2: After ingesting A or V, 31 participants performed kinematic and psychomotor tests of manual dexterity. Results: A increased precramp contraction duration (A, 36.9 ± 4.1 s; V, 27.8 ± 3.1 s), decreased cramp EMG area under the curve (A, 37.3 ± 7.7 %EMGmax·s; V, 77.2 ± 17.7 %EMGmax·s), increased contraction force to produce the cramp (A, 13.8 ± 1.8 kg; V, 9.9 ± 1.6 kg), and decreased postcramp soreness (A, 4.1 ± 0.3 arbitrary units (a.u.); V, 4.7 ± 0.3 a.u.). Kinematic and psychomotor tests were not affected. Discussion: TRP agonist ingestion attenuated EAMC characteristics without affecting motor function. Muscle Nerve 56: 379–385, 2017.

Original languageEnglish (US)
Pages (from-to)379-385
Number of pages7
JournalMuscle and Nerve
Volume56
Issue number3
DOIs
StatePublished - Sep 2017
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2017 Wiley Periodicals, Inc.

Keywords

  • EMG
  • exercise-associated muscle cramp
  • TRPA1
  • TRPV1
  • α-motor neuron hyperexcitability

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