The effect of downhill running on Notch signaling in regenerating skeletal muscle.

Notch signaling expression in regenerating muscle following injurious downhill running (DHR) was characterized in male C57BL/J6 mice (3 mo). Hindlimb muscles were harvested from control mice or at 24, 48, 72, 96 or 120 h post-DHR. Muscle injury was observed at 96 h (3.

Mechanical loading and injury induce human myotubes to release neutrophil chemoattractants.

The purpose of this study was to 1) test the hypothesis that skeletal muscle cells (myotubes) after mechanical loading and/or injury are a source of soluble factors that promote neutrophil chemotaxis and superoxide anion (O(2)(-).) production and 2) determine whether mechanical loading and/or injury causes myotubes to release cytokines that are known to influence neutrophil responses [tumor necrosis factor-alpha (TNF-alpha), IL-8, and transforming growth factor-beta1 (TGF-beta1)]. Human myotubes were grown in culture and exposed to either a cyclic strain (0, 5, 10, 20, or 30% strain) or a scrape injury protocol.

Downhill running in rats: influence on neutrophils, macrophages, and MyoD+ cells in skeletal muscle.

The accumulation of neutrophils and macrophages, as well as the activation of satellite cells, are early events following skeletal muscle injury. We examined the temporal relationship between changes in neutrophils, macrophages, and MyoD protein, a marker of satellite cell activation, after injurious exercise. Male rats ( n=47) performed an intermittent downhill (-16% grade) running (17 m/min) protocol and the solei were obtained at 0, 2, 6, 24, 48, or 72 h post-exercise.

Deferoxamine reduces and nitric oxide synthase inhibition increases neutrophil-mediated myotube injury.

We tested the contribution of reactive oxygen species (ROS), reactive nitrogen species (RNS) and the beta 2 integrin CD18 to neutrophil-mediated myotube injury. Human myotubes were cultured with human neutrophils in the presence or absence of inhibitors directed against ROS, RNS, and CD18. Muscle injury was assessed by a (51)Cr release assay.