Unloaded Speed of Shortening in Voltage-Clamped Intact Skeletal Muscle Fibres from wt, mdx and transgenic Mini-Dystrophin Mice using a novel High-Speed Acquisition System

¹ University of Heidelberg, Institute of Physiology & Pathophysiology
² Dept. of Neurology, University of Washington
³ University of Heidelberg

^* To whom correspondence should be addressed. E-mail: oliver.friedrich{at}physiologie.uni-heidelberg.de.

Submitted on November 27, 2007
Revised on December 21, 2007
Accepted on 8 February 2008

	Abstract

Skeletal muscle unloaded shortening was indirectly determined in the past. Here, we present a novel high-speed optical tracking technique that allows recording of unloaded shortening in single intact, voltage-clamped mammalian skeletal muscle fibers with 2 ms time resolution. L-type Ca²⁺ currents were simultaneously recorded. Time course of shortening was bi-exponential: a fast initial phase, ₁, and a slower successive phase, ₂, with activation energies of 59 kJ/mole and 47 kJ/mole. Maximum unloaded shortening speed, _vu,max, was faster than derived from other techniques, e.g. ~14.0 L₀s^-1 at 30°C. Our technique also allowed direct determination of shortening acceleration. We applied our technique to single fibers from C57 wt, dystrophic mdx and mini-dystrophin expressing mice to test whether unloaded shortening was affected in the pathophysiological mechanism of Duchenne muscular dystrophy. _vu,max and _au,max values were not significantly different in the three strains while ₁ and ₂ were increased in mdx fibers. The results were complemented by myosin heavy (MHC) and light chain (MLC) determinations that showed the same MHC IIA profiles in the interossei muscles from the different strains. In mdx muscle, MLC-1f was significantly increased and MLC-2f and MLC-3f somewhat reduced. Fast initial active shortening seems almost unaffected in mdx muscle.

Key Words: calcium currents, contractility, mdx mouse, skeletal muscle, speed of shortening, unloaded shortening