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Muscle fatigue refers to the decline in a muscle's ability to maintain the force of contraction after prolonged activity. It primarily stems from changes within muscle fibers. Even before experiencing muscle fatigue, one may feel tired and have the urge to stop the activity. This response, known as central fatigue, occurs due to changes in the central nervous system, namely the brain and spinal cord. While there is no single mechanism that induces fatigue, it may serve as a protective response...
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Updated: May 15, 2026

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
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Published on: January 19, 2017

Metabolic derangements in COPD muscle dysfunction.

Luis Puente-Maestu1, Alberto Lázaro, Blanca Humanes

  • 1Servicio de Neumología, Hospital General Gregorio Marañón, Universidad Complutense de Madrid, Instituto de Investigación Sanitaria Gregorio Marañón, Madrid, Spain. lpuente@separ.es

Journal of Applied Physiology (Bethesda, Md. : 1985)
|January 5, 2013
PubMed
Summary
This summary is machine-generated.

Chronic obstructive pulmonary disease (COPD) patients exhibit mitochondrial dysfunction in skeletal muscles, leading to reduced oxidative capacity and increased oxidative stress. These muscle changes contribute to exercise intolerance and may be linked to comorbidities like diabetes.

Keywords:
bioenergeticselectron transport chainmagnetic resonance spectroscopymitochondriaoxidative enzymespermeability transition porereactive oxygen species

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Last Updated: May 15, 2026

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

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Published on: January 19, 2017

Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry
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Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry

Published on: October 4, 2024

Area of Science:

  • Exercise physiology
  • Mitochondrial biology
  • Pulmonary medicine

Background:

  • Mitochondrial muscle alterations, including decreased oxidative capacity and increased reactive oxygen species (ROS) production, are prevalent in chronic obstructive pulmonary disease (COPD).
  • Reduced mitochondrial content and type I fiber loss in the quadriceps contribute to diminished oxidative capacity, impacting exercise endurance and increasing lactate production.
  • Oxidative stress is evident in both respiratory and peripheral muscles of COPD patients, with potential links to comorbidities like diabetes.

Purpose of the Study:

  • To investigate the specific mitochondrial and metabolic alterations in skeletal muscles of COPD patients.
  • To explore the relationship between muscle changes, exercise intolerance, and potential comorbidities in COPD.

Main Methods:

  • Analysis of mitochondrial content, fiber type distribution, and oxidative capacity in quadriceps muscles.
  • Assessment of reactive oxygen species (ROS) production and oxidative stress markers.
  • Evaluation of amino acid metabolism and gene expression, including peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) mRNA.
  • Examination of muscle cytochrome oxidase gene activation patterns post-training.

Main Results:

  • Significant reduction in mitochondrial content and type I fibers in the quadriceps of COPD patients, correlating with decreased oxidative capacity and exercise intolerance.
  • Elevated ROS production and oxidative stress in both respiratory and peripheral muscles.
  • Altered amino acid metabolism and reduced PGC-1α mRNA expression in COPD quadriceps.
  • Distinct patterns of muscle gene activation after training in COPD patients, suggestive of hypoxic stress.

Conclusions:

  • Skeletal muscle mitochondrial dysfunction and oxidative stress are key features of COPD, contributing to exercise limitation.
  • Muscle alterations in COPD share similarities with those in diabetes, suggesting a role for muscle pathology in comorbidity development.
  • The observed muscle changes, particularly type I fiber loss in the quadriceps, may result from disuse rather than direct respiratory muscle effects.