Inflammatory response to exercise in COPD

IL-6 in turn appears to be the primary driver for CRP and is involved with regulation of TNF alpha with the effect of lowering TNF alpha via the presence of IL-1ra.5 Furthermore relationships between CRP and IL-6 have been demonstrated.6 The role of IL-6 seems so important in exercise in healthy subjects it has been termed the exercise "work factor" and is considered by our group to be a "fatigueogen" due to its impact on fatigue.7 We propose, in COPD, that elevated IL-6 concentrations may contribute to the early onset of fatigue and or breathlessness experienced during physical exercise.6 There is much debate concerning the type of muscle work, eccentric or concentric, and exercise, maximal or sub-maximal that provokes the greatest production of IL-6 but it is apparent that IL-6 increases exponentially with duration and intensity of exercise.5 van Helvoort et al. assessed levels of muscle damage after exercise and found no evidence of such.