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Related Experiment Video

Updated: Apr 17, 2026

Ex Vivo Assessment of Contractility, Fatigability and Alternans in Isolated Skeletal Muscles

Ex Vivo Assessment of Contractility, Fatigability and Alternans in Isolated Skeletal Muscles

Published on: November 1, 2012

Aberrant post-translational modifications compromise human myosin motor function in old age.

Meishan Li¹, Hannah Ogilvie, Julien Ochala

¹Department of Physiology and Pharmacology, Karolinska Institutet, SE-171 77, Stockholm, Sweden; Department of Clinical Neuroscience, Clinical Neurophysiology, Karolinska Institutet, SE-171 77, Stockholm, Sweden.

|February 4, 2015

Summary

Aging slows human skeletal muscle function by impairing myosin motor proteins. Specific age-related modifications in myosin

Keywords:

aging function myosin post-translational modification skeletal muscle

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Ex Vivo Assessment of Contractility, Fatigability and Alternans in Isolated Skeletal Muscles

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Preparation and Culture of Myogenic Precursor Cells/Primary Myoblasts from Skeletal Muscle of Adult and Aged Humans

Preparation and Culture of Myogenic Precursor Cells/Primary Myoblasts from Skeletal Muscle of Adult and Aged Humans

Published on: February 16, 2017

Area of Science:

Muscle physiology
Molecular biology
Biochemistry

Background:

Aging impairs human skeletal muscle function, affecting motor proteins.
Understanding molecular changes in myosin is crucial for addressing age-related muscle decline.

Purpose of the Study:

To investigate age-related molecular changes in human skeletal muscle myosin.
To identify specific myosin post-translational modifications (PTMs) linked to functional decline.

Main Methods:

Modified single fiber in vitro motility assay.
X-ray diffraction experiments.
Mass spectrometry (MS) analyses.

Main Results:

Old age significantly slowed motility speed of type I and IIa myosin heavy chain (MyHC) isoforms, but not force generation.
X-ray diffraction revealed increased filament disorder in aged muscle.
MS identified eight age-specific myosin PTMs, with motor domain PTMs only in IIx MyHC.

Conclusions:

Age-related PTMs, particularly in the myosin rod region, contribute to filament disorder and slower motility.
Targeting these specific PTMs may reverse age-related myosin dysfunction.