NF-kB is the master switch controlling response to exercise.
This is really quite interesting. Somehow, moderate exercise – through the transmission of physical forces in your joints – leads to the inhibition of NF-kappaB. The result is a decrease in inflammation.
However, if instead of being subject to the mechanical stress of moderate exercise, your joints are instead subject to a higher magnitude of physical forces – those physical forces transmitted to the joint (e.g. knee) activate NF-kappaB.
NF-kB is truly the ‘master switch’ of inflammation. It’s even responsible for mediating inflammation or anti-inflammation effects in response to physical forces on the knee.
Signal transduction by mechanical strain in chondrocytes.
Summary of the abstract
PURPOSE OF REVIEW: Exercise and passive motion are beneficial for inflamed joints, whereas excessive mechanical forces initiate cartilage destruction as observed in osteoarthritis.
However, the intracellular mechanisms that convert mechanical signals into biochemical events responsible for cartilage destruction and repair remain paradoxical.
RECENT FINDINGS: Mechanical strain of low magnitude inhibits inflammation by suppressing IL-1beta and TNF-alpha-induced transcription of multiple proinflammatory mediators involved in cartilage degradation.
This also results in the upregulation of proteoglycan and collagen synthesis that is drastically inhibited in inflamed joints.
On the contrary, mechanical strain of high magnitude is proinflammatory and initiates cartilage destruction while inhibiting matrix synthesis. Investigations reveal that mechanical signals exploit nuclear factor-kappa B (NF-kB) for the activation of inflammation and cartilage destruction.
Mechanical strain of low magnitude inhibits NF-kB whereas mechanical strain of high magnitude activates NF-kB.
SUMMARY: The beneficial effects of exercise result from the inhibition of NF-kB.