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Fatiguing exercise reduces DNA binding activity of NF-B in skeletal muscle nuclei

¹Pulmonary and Critical Care Medicine Section, Baylor College of Medicine, Houston, Texas 77030; ²Department of Physiology, University of Kentucky, Lexington, Kentucky 40536; ³Metabolism, Shriners Burns Hospital, and Department of Surgery, University of Texas Medical Branch, Galveston, Texas 77555

Submitted 28 January 2004 ; accepted in final form 15 June 2004

This study tested the hypothesis that skeletal muscle contraction activates nuclear factor-B (NF-B), a putative regulator of muscle protein breakdown. Muscle biopsies were obtained from the vastus lateralis of healthy humans before, immediately after, and 1 h after fatiguing resistance exercise of the lower limbs. Biopsies were analyzed for nuclear NF-B DNA binding activity by using electrophoretic mobility shift assay. NF-B activity, measured immediately after exercise, was less than preexercise activity; after 1-h recovery, activity returned to preexercise levels. In follow-up studies in adult mice, basal NF-B activity varied among individual muscles. NF-B activity in diaphragm fiber bundles was decreased after a 10-min bout of fatiguing tetanic contractions in vitro. NF-B activity in soleus was increased by 12 days of unloading by hindlimb suspension; this increase was reversed by 10 min of fatiguing exercise. These data provide no support for our original hypothesis. Instead, acute fatiguing exercise appears to decrease NF-B activity in muscle under a variety of conditions.

signal transduction; muscle contraction; transcription factor; oxidative stress

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