Between channels and tears: aim at ROS to save the membrane of dystrophic fibres

Lengthening during contraction allows muscles to develop force well above the levels reached in isometric conditions. Such enhanced performance has, however, a negative counterpart: damage which is revealed by pain (DOMS), structural and ultra-structural alterations and reduced ability to develop force (Asmussen, 1952). The phenomenon has been demonstrated in vitro and in vivo, in amphibian as well as in mammalian muscles and two main factors have been identified as determinants of eccentric contraction-induced damage: myofibrillar disorganization (Z line streaming and sarcomere length heterogeneity) (Allen, 2001) and calcium homeostasis alteration, possibly related to T tubule disruption (Warren et al. 1993). About 15 years ago Petrof and coworkers showed that mdx dystrophic muscles are highly sensitive to eccentric contraction damage as they showgreater loss of force and cellular damage, indicated by sarcolemmal disruption and procion orange penetration, than wild-type muscles (Petrof et al. 1993). Although only sparse evidence is available, the phenomenon seems to be specific to mdx mice and not present in other murine models of muscular dystrophy (Head et al. 2004).