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Related Concept Videos

Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
Muscle Recovery and Fatigue01:24

Muscle Recovery and Fatigue

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...
Cross-bridge Cycle01:26

Cross-bridge Cycle

As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
The Effect of Aging on Tissues01:19

The Effect of Aging on Tissues

Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
Disorders of the Skeletal Muscle01:28

Disorders of the Skeletal Muscle

The clinical conditions affecting the skeletal muscle tissue are broadly categorized as musculoskeletal and neuromuscular disorders.
Musculoskeletal disorders
Musculoskeletal disorders involve injuries and conditions affecting the skeletal muscles and associated connective tissues. These disorders can arise from acute biomechanical stresses or chronic overuse and can occur across different age groups. Common injuries include sprains, fractures, and muscular strains, often resulting from...

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Related Experiment Video

Updated: Jun 25, 2026

Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry
08:12

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

Published on: October 4, 2024

Aging impairs skeletal muscle mitochondrial bioenergetic function.

Pedro A Figueiredo1, Scott K Powers, Rita M Ferreira

  • 1CIAFEL, University of Porto, Portugal. pfigueiredo@ismai.pt

The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
|February 7, 2009
PubMed
Summary
This summary is machine-generated.

Aging impairs skeletal muscle mitochondrial function, leading to decreased respiratory capacity. This decline is linked to increased mitochondrial oxidative damage in older mice.

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Last Updated: Jun 25, 2026

Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry
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Published on: October 4, 2024

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

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

Published on: January 19, 2017

Area of Science:

  • Mitochondrial biology
  • Skeletal muscle physiology
  • Aging research

Background:

  • Mitochondrial dysfunction is implicated in age-related muscle decline.
  • Understanding age-related changes in skeletal muscle mitochondria is crucial for healthspan research.

Purpose of the Study:

  • To investigate the impact of aging on skeletal muscle mitochondrial function.
  • To determine the relationship between mitochondrial function and oxidative damage in aging.

Main Methods:

  • Isolated mitochondria from young (3-month) and aged (18-month) C57BL/6 mice.
  • Assessed mitochondrial respiration (State 3, State 4, respiratory control ratio) and ADP phosphorylation efficiency.
  • Measured biochemical markers of oxidative damage (aconitase activity, protein carbonyls, sulfhydryl groups, malondialdehyde).
  • Utilized an in vitro repetitive ADP-stimulation test to assess mitochondrial recovery capacity.
  • Quantified mitochondria per suspension using transmission electron microscopy for data normalization.

Main Results:

  • Confirmed an age-associated decline in skeletal muscle mitochondrial respiratory function.
  • Observed a significant correlation between reduced mitochondrial function and increased oxidative damage markers.
  • Demonstrated impaired mitochondrial capacity to reestablish homeostasis after repetitive ADP stimulation in aged mice.

Conclusions:

  • Aging leads to a significant decline in skeletal muscle mitochondrial function.
  • Increased mitochondrial oxidative damage is a key factor contributing to age-related mitochondrial dysfunction in skeletal muscle.