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Isolation of Mitochondria from Mouse Skeletal Muscle for Respirometric Assays
Published on: February 10, 2022
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A novel method for determining human ex vivo submaximal skeletal muscle mitochondrial function.
Martin Hey-Mogensen1,2, Martin Gram1, Martin Borch Jensen3,4
1Xlab, Center for Healthy Aging - Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
The Journal of Physiology
|June 23, 2015
Summary
Ageing reduces mitochondrial proton leak in skeletal muscle, while training increases hydrogen peroxide emission. These factors influence the metabolic health of aging muscle cells.
Area of Science:
- Mitochondrial Physiology
- Skeletal Muscle Biology
- Aging Research
Background:
- Mitochondrial function alterations with age remain debated.
- Previous studies often lack physiological relevance.
- Novel methods are needed to assess mitochondrial function in situ.
Purpose of the Study:
- Investigate mitochondrial function in human skeletal muscle at submaximal rates.
- Determine the impact of age and training status on mitochondrial parameters.
- Clarify the relationship between aging, physical activity, and muscle mitochondrial health.
Main Methods:
- Cross-sectional study of 64 young and old trained/untrained men.
- Biopsied skeletal muscle for mitochondrial isolation.
- Simultaneous measurement of oxygen consumption, membrane potential, and hydrogen peroxide emission.
Main Results:
- Aging decreased mitochondrial proton leak, independent of training.
- Training increased mitochondrial hydrogen peroxide emission.
- Aging reduced state 3 respiration, an effect mitigated by training.
Conclusions:
- Both aging and physical activity level alter intrinsic skeletal muscle mitochondrial function.
- These intrinsic changes are critical for metabolic health in older adults.
- Understanding these adaptations can inform strategies for healthy aging.
