This study investigated intercellular adhesion molecule-1 (ICAM-1), a membrane protein that mediates cell-to-cell adhesion and communication, as a mechanism through which the inflammatory response facilitates muscle regeneration after injury. Toxin-induced muscle injury to tibialis anterior muscles of wild-type mice caused ICAM-1 to be expressed by a population of satellite cells/myoblasts and myofibers. Myogenic cell expression of ICAM-1 contributed to the restoration of muscle structure after injury, as regenerating myofibers were more abundant and myofiber size was larger for wild-type compared with Icam1 À/À mice during 28 days of recovery. Contrastingly, restoration of muscle function after injury was similar between the genotypes. ICAM-1 facilitated the restoration of muscle structure after injury through mechanisms involving the regulation of myofiber branching, protein synthesis, and the organization of nuclei within myofibers after myogenic cell fusion. These findings provide support for a paradigm in which ICAM-1 expressed by myogenic cells after muscle injury augments their adhesive and fusogenic properties, which, in turn, facilitates regenerative and hypertrophic processes that restore structure to injured muscle.

Gender-related differences in maximal leg muscle power were examined in 496 females and 426 males aged 8 to 20 years. Cycling peak power (CPP, including the force required to accelerate the flywheel of the cycle ergometer) was measured during three sprints. Optimal velocity (Vopt, velocity at CPP) was also determined. No gender-differences were observed in anthropometric characteristics and cycling performance between 8- and 14-year-old. From age 14, however, males showed a higher CPP than females, but also a higher lean leg volume (LLV, assessed by anthropometry). Allometric relationship between CPP and LLV (CPP = a . LLV ( b)) showed a clear gender-differentiation between 14- and 16-year-old: LLV exponent (b) was 1.05 in males vs. 0.74 in females. From 16 years onwards, analysis of covariance (ANCOVA) showed that the slopes of the CPP-LLV relationship were similar in both genders, but the intercepts differed. In other words, for a similar LLV, males showed greater CPP than females. It was suggested that this sex-related difference was due to total body fat increase, and more specifically lower-limb fat increase during puberty in girls, whilst the boys experienced increased lean body mass. Considering that the same gender-related difference was observed for optimal velocity adjusted for leg length, other factors such as fibre type variability or (and) neuromuscular activation might also be partly responsible for the higher peak muscle performance observed in males.

The overall objective of the study was to identify mechanisms through which intercellular adhesion molecule-1 (ICAM-1) augments the adhesive and fusogenic properties of myogenic cells. Hypotheses were tested using cultured myoblasts and fibroblasts, which do not constitutively express ICAM-1, and myoblasts and fibroblasts forced to express full length ICAM-1 or a truncated form lacking the cytoplasmic domain of ICAM-1. ICAM-1 mediated myoblast adhesion and fusion were quantified using novel assays and cell mixing experiments. We report that ICAM-1 augments myoblast adhesion to myoblasts and myotubes through homophilic trans-interactions. Such adhesive interactions enhanced levels of active Rac in adherent and fusing myoblasts, as well as triggered lamellipodia, spreading, and fusion of myoblasts through the signaling function of the cytoplasmic domain of ICAM-1. Rac inhibition negated ICAM-1 mediated lamellipodia, spreading, and fusion of myoblasts. The fusogenic property of ICAM-1-ICAM-1 interactions was restricted to myogenic cells, as forced expression of ICAM-1 by fibroblasts did not augment their fusion to ICAM-1+ myoblasts/myotubes. We conclude that ICAM-1 augments myoblast adhesion and fusion through its ability to self-associate and initiate Rac-mediated remodeling of the actin cytoskeleton.

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