Evidence of an abnormal intramuscular component of fatigue in multiple sclerosis

Khema R Sharma, J. Kent-Braun, M. A. Mynhier, M. W. Weiner, R. G. Miller

Research output: Contribution to journalArticle

117 Citations (Scopus)

Abstract

The goals of this study were to investigate muscle fatigue in patients with multiple sclerosis (MS), and to determine the relationships between muscle fatigue, clinical status, and perceived fatigue. The fatigability of the anterior tibial muscle was quantitated in patients and controls during 9 min of intermittent stimulation (used to eliminate central sources of muscle fatigue). During exercise, the decline in tetanic force, phosphocreatine, and intracellular pH was greater in patients than in controls. The compound muscle action potential amplitude did not decrease during exercise, indicating that there was no failure of neuromuscular transmission during fatigue. Thus, the excessive fatigue in MS developed from sources beyond the muscle membrane. Following exercise, the recovery of tetanic force was delayed in patients (a pattern that suggests abnormal excitation-contraction coupling), whereas the recovery of metabolites was complete in both groups. Muscular fatigue was correlated with clinical disability but not with perceived fatigue. These results suggests that fatigue in MS has both central (perception, upper motor neuron dysfunction) and peripheral (impaired metabolism and excitation-contraction coupling) components.

Original languageEnglish
Pages (from-to)1403-1411
Number of pages9
JournalMuscle and Nerve
Volume18
Issue number12
DOIs
StatePublished - Dec 5 1995

Fingerprint

Muscle Fatigue
Multiple Sclerosis
Fatigue
Excitation Contraction Coupling
Exercise
Muscles
Phosphocreatine
Motor Neurons
Action Potentials
Skeletal Muscle
Membranes

Keywords

  • excitation-contraction coupling
  • exercise
  • magnetic resonance spectroscopy
  • metabolism

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Evidence of an abnormal intramuscular component of fatigue in multiple sclerosis. / Sharma, Khema R; Kent-Braun, J.; Mynhier, M. A.; Weiner, M. W.; Miller, R. G.

In: Muscle and Nerve, Vol. 18, No. 12, 05.12.1995, p. 1403-1411.

Research output: Contribution to journalArticle

Sharma, KR, Kent-Braun, J, Mynhier, MA, Weiner, MW & Miller, RG 1995, 'Evidence of an abnormal intramuscular component of fatigue in multiple sclerosis', Muscle and Nerve, vol. 18, no. 12, pp. 1403-1411. https://doi.org/10.1002/mus.880181210
Sharma, Khema R ; Kent-Braun, J. ; Mynhier, M. A. ; Weiner, M. W. ; Miller, R. G. / Evidence of an abnormal intramuscular component of fatigue in multiple sclerosis. In: Muscle and Nerve. 1995 ; Vol. 18, No. 12. pp. 1403-1411.
@article{7d7a1769cfa4400685d5b896c6a92a6c,
title = "Evidence of an abnormal intramuscular component of fatigue in multiple sclerosis",
abstract = "The goals of this study were to investigate muscle fatigue in patients with multiple sclerosis (MS), and to determine the relationships between muscle fatigue, clinical status, and perceived fatigue. The fatigability of the anterior tibial muscle was quantitated in patients and controls during 9 min of intermittent stimulation (used to eliminate central sources of muscle fatigue). During exercise, the decline in tetanic force, phosphocreatine, and intracellular pH was greater in patients than in controls. The compound muscle action potential amplitude did not decrease during exercise, indicating that there was no failure of neuromuscular transmission during fatigue. Thus, the excessive fatigue in MS developed from sources beyond the muscle membrane. Following exercise, the recovery of tetanic force was delayed in patients (a pattern that suggests abnormal excitation-contraction coupling), whereas the recovery of metabolites was complete in both groups. Muscular fatigue was correlated with clinical disability but not with perceived fatigue. These results suggests that fatigue in MS has both central (perception, upper motor neuron dysfunction) and peripheral (impaired metabolism and excitation-contraction coupling) components.",
keywords = "excitation-contraction coupling, exercise, magnetic resonance spectroscopy, metabolism",
author = "Sharma, {Khema R} and J. Kent-Braun and Mynhier, {M. A.} and Weiner, {M. W.} and Miller, {R. G.}",
year = "1995",
month = "12",
day = "5",
doi = "10.1002/mus.880181210",
language = "English",
volume = "18",
pages = "1403--1411",
journal = "Muscle and Nerve",
issn = "0148-639X",
publisher = "John Wiley and Sons Inc.",
number = "12",

}

TY - JOUR

T1 - Evidence of an abnormal intramuscular component of fatigue in multiple sclerosis

AU - Sharma, Khema R

AU - Kent-Braun, J.

AU - Mynhier, M. A.

AU - Weiner, M. W.

AU - Miller, R. G.

PY - 1995/12/5

Y1 - 1995/12/5

N2 - The goals of this study were to investigate muscle fatigue in patients with multiple sclerosis (MS), and to determine the relationships between muscle fatigue, clinical status, and perceived fatigue. The fatigability of the anterior tibial muscle was quantitated in patients and controls during 9 min of intermittent stimulation (used to eliminate central sources of muscle fatigue). During exercise, the decline in tetanic force, phosphocreatine, and intracellular pH was greater in patients than in controls. The compound muscle action potential amplitude did not decrease during exercise, indicating that there was no failure of neuromuscular transmission during fatigue. Thus, the excessive fatigue in MS developed from sources beyond the muscle membrane. Following exercise, the recovery of tetanic force was delayed in patients (a pattern that suggests abnormal excitation-contraction coupling), whereas the recovery of metabolites was complete in both groups. Muscular fatigue was correlated with clinical disability but not with perceived fatigue. These results suggests that fatigue in MS has both central (perception, upper motor neuron dysfunction) and peripheral (impaired metabolism and excitation-contraction coupling) components.

AB - The goals of this study were to investigate muscle fatigue in patients with multiple sclerosis (MS), and to determine the relationships between muscle fatigue, clinical status, and perceived fatigue. The fatigability of the anterior tibial muscle was quantitated in patients and controls during 9 min of intermittent stimulation (used to eliminate central sources of muscle fatigue). During exercise, the decline in tetanic force, phosphocreatine, and intracellular pH was greater in patients than in controls. The compound muscle action potential amplitude did not decrease during exercise, indicating that there was no failure of neuromuscular transmission during fatigue. Thus, the excessive fatigue in MS developed from sources beyond the muscle membrane. Following exercise, the recovery of tetanic force was delayed in patients (a pattern that suggests abnormal excitation-contraction coupling), whereas the recovery of metabolites was complete in both groups. Muscular fatigue was correlated with clinical disability but not with perceived fatigue. These results suggests that fatigue in MS has both central (perception, upper motor neuron dysfunction) and peripheral (impaired metabolism and excitation-contraction coupling) components.

KW - excitation-contraction coupling

KW - exercise

KW - magnetic resonance spectroscopy

KW - metabolism

UR - http://www.scopus.com/inward/record.url?scp=0028864415&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028864415&partnerID=8YFLogxK

U2 - 10.1002/mus.880181210

DO - 10.1002/mus.880181210

M3 - Article

C2 - 7477063

AN - SCOPUS:0028864415

VL - 18

SP - 1403

EP - 1411

JO - Muscle and Nerve

JF - Muscle and Nerve

SN - 0148-639X

IS - 12

ER -