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I read with great interest the article by Stevenson and Calverley and related editorial.1,2 An important and unexplained finding was the fact that instrumented patients using a mouthpiece and noseclip took significantly longer to recover from breathlessness after exercise than those who wore only a facemask (non-instrumented), irrespective of oxygen or air delivery. The mean (SE) difference was 3.94 (1.77) minutes in a total exercise recovery period of 11.38 (1.49) minutes for fully instrumented patients. Various theories to explain this exceptional difference have been offered both by the authors and reviewer. These have mainly centred on the theme of inhibition of ventilation from the persistence of primitive diving reflexes.3 However, the precise mode of ventilation of these patients in the recovery phase via the mouth or nose needs consideration.
We have recently reported that normal subjects have both quantitative and qualitative differences in ventilation and ventilatory patterns when adopting nasal compared with oral routes for ventilation.4,5 Minute ventilation and its components (tidal volume and breathing frequency) were reduced by a mean of 33% and followed a shift of thoracoabdominal respiration to favour “diaphragmatic” breathing during nasal ventilation and “upper thoracic cage” during mouth breathing. The clinical implications of this have been explored by using a specifically designed questionnaire to discover breathing preferences (mouth/nose) in patients with chronic respiratory diseases including COPD. The findings revealed a high prevalence of symptoms of dysfunctional ventilation and, for the first time, strongly linked them to a preference for mouth breathing.6,7
Evidence now suggests that proprioceptive input from a number of sources (including pulmonary and chest wall) forms the final common pathway for the perception of breathlessness.8 Thus, it seems that mouth breathing per se may predispose to the perception of breathlessness by dynamically changing chest wall mechanics by a resultant increase in ventilation and subtle shift in thoracoabdominal respiration.
Fully instrumented patients in the study are, by definition, obligate mouth breathers and, for the reasons offered, this may provide the sole explanation for the findings of the persistent breathlessness. The relevance of the time honoured practice of measuring ventilation with a mouthpiece and noseclip needs to be carefully reviewed in the future.
We are grateful for Dr Williams’ positive comments about our study which was primarily designed to evaluate the relationship between the physiological effects of supplementary oxygen in normoxaemic COPD patients and the intensity of their dyspnoea when oxygen was administered after a standardised exercise stimulus.1 The difference between the instrumented and non-instrumented patients was not a primary outcome and should therefore be interpreted with some caution, at least from the statistical point of view. Nonetheless, we agree that stimulation of upper airway receptors can be an important mechanism for modifying respiratory sensation, as we suggested several years ago when we found that administering cold air during exercise reduced the intensity of exercise induced dyspnoea.2 We can confirm that breathing with a noseclip and mouthpiece modifies the pattern of regional chest wall ventilation in COPD patients compared with non-instrumented breathing when assessed by opto-electronic plethysmography. These changes at rest did not modify the pattern of chest wall movement during exercise that we recently described,3 and this would argue against Dr Williams’ suggestion that the breathing route is a major contributory factor to dyspnoea intensity. It is possible that the switch to mouth breathing reflects a need to reduce inspiratory resistance and is thus an adaptive response in these patients. Further work in this interesting area will be needed to resolve these important issues.