The case against inspiratory muscle training in COPD

Abstract

Despite maximal medical therapy, many chronic obstructive pulmonary disease (COPD) patients remain breathless and this has led to persistent and commendable efforts to reduce symptoms and improve exercise performance using nonpharmacological approaches; some of these, for example pulmonary rehabilitation (PR) 1, comprising general exercise and fitness training, are of proven benefit, while others remain controversial. Inspiratory muscle training (IMT), being cheap and free of side-effects, is intuitively attractive, since improving the capacity of the inspiratory muscles should “make breathing easier” and so improve exercise performance. Enthusiasts do not allow the superficial attractiveness of this proposition to be clouded by aspects of the data. These are that the diaphragm is already working hard and well trained in emphysema, with a shift towards fatigue resistant type I fibres 2, that at a single fibre level it is energetically more efficient 3, that (allowing for hyperinflation) it is not actually weak 4, 5 and that diaphragm fatigue cannot be elicited in patients in vivo 6, 7, even when patients are sufficiently ill to require mechanical ventilation 8. The question of whether the respiratory muscles are weak in COPD seems particularly important in the context of IMT. In the current issue of the European Respiratory Journal , Gosselink et al. 9 cite our paper 5 as evidence that the diaphragm is weak; in fact, we concluded that the major reason for the reduced transdiaphragmatic pressures observed in COPD was hyperinflation, which of course would not be expected to improve with IMT. They also state that inspiratory …