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Isometric and Eccentric Force Generation Assessment of Skeletal Muscles Isolated from Murine Models of Muscular Dystrophies

Isometric and Eccentric Force Generation Assessment of Skeletal Muscles Isolated from Murine Models of Muscular Dystrophies

Published on: January 31, 2013

Eccentric contractions lead to myofibrillar dysfunction in muscular dystrophy.

Bert Blaauw¹, Lisa Agatea, Luana Toniolo

¹Dept. of Human Anatomy and Physiology, Univ. of Padua, Padua, Italy. bertblaauw@yahoo.com

Journal of Applied Physiology (Bethesda, Md. : 1985)

|November 14, 2009

Summary

Skeletal muscles in muscular dystrophy models like mdx and Sgca-null mice experience greater force loss from eccentric contractions. This enhanced muscle damage is linked to in vivo factors affecting myofibrils, not individual fiber degeneration.

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Area of Science:

Muscle physiology
Skeletal muscle research
Duchenne muscular dystrophy models

Background:

Skeletal muscles in dystrophin-deficient mdx mice are known to be more susceptible to eccentric contraction damage.
The precise downstream mechanisms driving this enhanced force drop are not fully understood and remain debated.

Purpose of the Study:

To investigate the mechanisms underlying the increased force reduction during eccentric contractions in different muscular dystrophy models.
To compare the effects of in vivo versus in vitro eccentric contractions on muscle force generation.

Main Methods:

Eccentric contractions were induced in vivo in the gastrocnemius muscle of wild-type, mdx, alpha-sarcoglycan (Sgca)-null, and collagen 6A1 (Col6a1)-null mice.
Force generation was measured in permeabilized (skinned) muscle fibers following in vivo eccentric contractions.
Force loss was assessed by comparing stimulated fibers to contralateral unstimulated fibers.

Main Results:

mdx and Sgca-null mice showed a 35% force decrease, significantly higher than the 14% in wild-type mice.
Col6a1-null mice exhibited a force drop comparable to wild-type mice.
Force loss in skinned fibers after in vivo eccentric contractions was observed in mdx and Sgca-null mice, but not in wild-type or Col6a1-null mice.
The enhanced force reduction was specific to in vivo contractions; in vitro contractions showed similar effects across all groups.

Conclusions:

The enhanced force loss in mdx and Sgca-null mice is attributed to a myofibrillar impairment present in all muscle fibers, rather than individual fiber degeneration.
The mechanism responsible for the heightened force reduction is active in vivo and is lost upon fiber permeabilization.