The susceptibility to hydrogen embrittlement (HE) of martensitic steels has been examined by means of a delayed-fracture test and hydrogen thermal desorption analysis. The intensity of a desorptionrate peak around 50 ЊC to 200 ЊC increased when the specimen was preloaded and more remarkably so when it was loaded under the presence of hydrogen. The increment appeared initially at the lowtemperature region in the original peak. As hydrogen entry proceeded, the increment then appeared at the high-temperature region, while that in the low-temperature region was reduced. The alteration occurred earlier in steels tempered at lower temperatures, with a higher embrittlement susceptibility. A defect acting as the trap of the desorption in the high-temperature region was assigned to large vacancy clusters that have higher binding energies with hydrogen. Deformation-induced generation of vacancies and their clustering have been considered to be promoted by hydrogen and to play a primary role on the HE susceptibility of high-strength steel.

A cultured C2C12 myotube contraction system was examined for application as a model for acute contraction-induced phenotypes of skeletal muscle. C2C12 myotubes seeded into 4-well rectangular plates were placed in a contraction system equipped with a carbon electrode at each end. The myotubes were stimulated with electric pulses of 50 V at 1 Hz for 3 ms at 997-ms intervals. Approximately 80% of the myotubes were observed to contract microscopically, and the contractions lasted for at least 3 h with electrical stimulation. Calcium ion (Ca2+) transient evoked by the electric pulses was detected fluorescently with Fluo-8. Phosphorylation of protein kinase B/Akt (Akt), 5′ AMP-activated protein kinase (AMPK), p38 mitogen-activated protein kinase (p38), and c-Jun NH2-terminal kinase (JNK)1/2, which are intracellular signaling proteins typically activated in exercised/contracted skeletal muscle, was observed in the electrically stimulated C2C12 myotubes. The contractions induced by the electric pulses increased glucose uptake and depleted glycogen in the C2C12 myotubes. C2C12 myotubes that differentiated after exogenous gene transfection by a lipofection or an electroporation method retained their normal contractile ability by electrical stimulation. These findings show that our C2C12 cell contraction system reproduces the muscle phenotypes that arise in vivo (exercise), in situ (hindlimb muscles in an anesthetized animal), and in vitro (dissected muscle tissues in incubation buffer) by acute muscle contraction, demonstrating that the system is applicable for the analysis of intracellular events evoked by acute muscle contraction.

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