XXXX degradation is necessary for skeletal muscle atrophy associated with contractile claudication.

@entity1 @entity3657 @entity63 @entity26 @entity4284 @entity194 @entity121
The arterial blockage in @entity1 with @entity3657 ( @entity3657 ) restricts @entity26 delivery to skeletal muscles distal to the blockage. In advanced-stage @entity3657 @entity1 , this creates a chronic @entity63 in the affected muscles. However, in the majority of @entity3657 @entity1 , the muscles distal to the blockage only become @entity63 during physical activity when the @entity26 demands of these muscles are increased. Therefore, the skeletal muscle of most @entity3657 @entity1 undergoes repeated cycles of low-grade @entity63 -reperfusion each time the @entity1 is active and then rests. This has been speculated to contribute to the biochemical and morphological @entity121 observed in @entity3657 @entity1 . The current study aimed to determine, using a rodent model, whether repeated hind limb muscle contractions during blood flow restriction to the hind limb muscles increases NF-kB activity. We, subsequently, determined whether an increase in NF-kB activity during this condition is required for the increased transcription of specific @entity194 -related genes and muscle fiber @entity194 . We found that hind limb muscle contractions during blood flow restriction to the limb increased NF-kB activity, the transcription of specific @entity194 -related genes, and caused a 35% decrease in muscle fiber cross-sectional area. We further found that inhibition of NF-kB activity, via gene transfer of a dominant-negative inhibitor of kBa (d.n. @entity4284 ), prevented the increase in @entity194 gene expression and muscle fiber @entity194 . These findings demonstrate that when blood flow to skeletal muscle is restricted, repeated cycles of muscle contraction can cause muscle fiber @entity194 that requires NF-kB- @entity4284 signaling.
