Background: Our previous study showed that preconditioned local somatothermal stimulation (LSTS) protected subsequent ischemia-reperfusion injury of the skeletal muscle. The exact mechanisms of LSTS preconditioning remain unknown. The aim of this study was to test the hypothesis stating that heat stimulation induces free radical production, increases enzymatic scavenging activity, and subsequently enhances the expression of heat shock protein 70 (HSP-70) in skeletal muscles.
Materials and methods: After LSTS was applied onto the left quarter ventral abdomen muscle of male Sprague-Dawley rats, the underling muscles were collected at the intervals of baseline, 5-, 15-, 30-, and 60-min after LSTS. The time-dependent profiles of free radical production and enzymatic scavenging activity were measured. The influence of nitric oxide (NO) on HSP-70 expression was evaluated by pretreatment of an NO synthase inhibitor.
Results: The concentrations of reactive oxygen species, NO metabolites, and malondialdehyde increased significantly 5 min after LSTS, whereas the scavenging activity reduced to the lowest level 5 min (dismutase) and 15 min (catalase and glutathione) after LSTS. Expression of HSP-70 was significantly lower in the LSTS with NO synthase inhibitor group than in the LSTS group.
Conclusions: LSTS induces oxidative stress and the scavenging response in the underlying skeletal muscle, which might explain the possible mechanisms of LSTS preconditioning-induced muscle plasticity.
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