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Updated: May 12, 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

Impaired mitochondrial function in chronically ischemic human heart.

Nis Stride1, Steen Larsen, Martin Hey-Mogensen

  • 1Xlab, Center for Healthy Aging, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

American Journal of Physiology. Heart and Circulatory Physiology
|April 2, 2013
PubMed
Summary
This summary is machine-generated.

Chronic ischemic heart disease impairs mitochondrial function, reducing energy production and increasing harmful reactive oxygen species (ROS). Studies found no evidence of protective chronic ischemic preconditioning in human heart muscle.

Keywords:
left ventriclemitochondrial respirationreactive oxygen species

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Published on: October 4, 2024

Area of Science:

  • Cardiology
  • Mitochondrial Biology
  • Ischemic Heart Disease

Background:

  • Chronic ischemic heart disease leads to myocardial hypoperfusion and hypoxia.
  • Hypoxia can damage mitochondria, compromising cellular energy and increasing reactive oxygen species (ROS).
  • While acute ischemic preconditioning is protective, chronic effects in humans remain unexplored.

Purpose of the Study:

  • To investigate mitochondrial respiratory capacity in chronic ischemic human myocardium.
  • To assess if ischemic regions exhibit resistance to ex vivo ischemia (chronic preconditioning).
  • To evaluate reactive oxygen species (ROS) production and antioxidant levels in ischemic vs. non-ischemic myocardium.

Main Methods:

  • Biopsies from ischemic and non-ischemic left ventricle regions of nine human subjects were analyzed.
  • Mitochondrial respiration was tested under hyperoxia and hypoxia.
  • ROS production and myocardial antioxidant protein levels were measured.

Main Results:

  • Maximal oxidative phosphorylation capacity was lower in ischemic myocardium.
  • No significant difference in the respiratory control ratio (coupling) was observed.
  • Higher ROS production and lower antioxidant protein expression were found in ischemic myocardium.
  • No evidence of chronic ischemic preconditioning was detected.

Conclusions:

  • Impaired mitochondrial function, characterized by diminished respiration and excessive ROS, is evident in ischemic human heart muscle.
  • Chronic ischemic preconditioning does not appear to confer protection in the studied human myocardium.