Abstract
Resistance exercise triggers a subclinical inflammatory response that plays a pivotal role in skeletal muscle regeneration. Nuclear factor-κB (NF-κB) is a stress signalling transcription factor that regulates acute and chronic states of inflammation. The classical NF-κB pathway regulates the early activation of post-exercise inflammation; however there remains scope for this complex transcription factor to play a more detailed role in post-exercise muscle recovery. Sixteen volunteers completed a bout of lower body resistance exercise with the ingestion of three 400 mg doses of ibuprofen or a placebo control. Muscle biopsy samples were obtained prior to exercise and at 0, 3 and 24 h post-exercise and analysed for key markers of NF-κB activity. Phosphorylated p65 protein expression and p65 inflammatory target genes were elevated immediately post-exercise independent of the two treatments. These changes did not translate to an increase in p65 DNA binding activity. NF-κB p50 protein expression and NF-κB p50 binding activity were lower than pre-exercise at 0 and 3 h post-exercise, but were elevated at 24 h post-exercise. These findings provide novel evidence that two distinct NF-κB pathways are active in skeletal muscle after resistance exercise. The initial wave of activity involving p65 resembles the classical pathway and is associated with the onset of an acute inflammatory response. The second wave of NF-κB activity comprises the p50 subunit, which has been previously shown to resolve an acute inflammatory program. The current study showed no effect of the ibuprofen treatment on markers of the NF-κB pathway, however examination of the within group effects of the exercise protocol suggests that this pathway warrants further research.