1. We have validated a method for the continuous display and ‘on-line’ measurement of total pulmonary resistance in man, using a hybrid digital/analog computer. 2. The basic variables, which are measured by standard techniques, are flow rate of the mouth (V̇) and oesophageal pressure ( P oes ), and these are the only analog inputs necessary to the computer. 3. Resistance ( R L, cont ) is calculated continuously as: R L, cont = ( P oes - V/C )/V̇ where V is tidal volume and C is the dynamic compliance. R L, cont is continuously displayed as an analog signal on an oscilloscope. 4. Changes in resistance, measured by this method over a wide range of values in three subjects, showed an almost exact correlation with those measured by a standard method (Mead-Whittenberger).

1. The effect of adding low-level (2.7 cmH 2 O 1 −1 s) external respiratory resistive loads on exercise-induced breathlessness has been examined in naive normal subjects; the intensity of this loading was chosen to simulate that confronting an asthmatic subject during exercise. 2. Each of 18 subjects performed two separate tests in which workload was oscillated while the respiratory loading was changed every minute between no loading, inspiratory loading only, and inspiratory plus expiratory loading. Each loading condition was given three times, and both these changes and those in workload were unpredictable as far as the subject was concerned. 3. The purpose was to ‘confuse’ subjects and obtain subjective estimates of their intensity of breathlessness independent of any expectation associated solely with the readily perceptible changes in external resistances to breathing. The study design was balanced for the group as a whole, both in terms of workload and respiratory loading condition. 4. The addition of these respiratory resistive loads during exercise did not result in a significant increase in the intensity of breathlessness. 5. Estimates of the rate of work of breathing revealed that this increased more with respiratory loading than it did as ventilation rose throughout the test; on the other hand, the intensity of breathlessness increased by a greater extent with continued exercise compared with the changes accompanying the addition of respiratory loads. 6. It is concluded that the intensity of the sensation of breathlessness experienced by normal subjects during exercise is not simply a reflection of an increased rate of work of breathing being performed by the respiratory muscles. 7. It is further suggested that similar studies in which internal resistances are increased experimentally are indicated in order to analyse the factors underlying the breathlessness of asthma.

1. Nine normal subjects performed 6 min, constant-workload, exercise tests on a bicycle ergometer at either a ‘high workload’ or at a ‘low workload’. During the first ‘high workload’ test their spontaneous breathing pattern was recorded on to magnetic tape. During one subsequent ‘high workload’ test and one ‘low workload’ test they voluntarily copied their recorded breathing pattern. During a second ‘low workload’ test they breathed spontaneously. Isocapnia was maintained by the operator throughout both the copying tests. During the exercise tests ventilation was recorded and subjects indicated the level of their sensation of breathlessness every 30 s. 2. Subjects felt markedly less breathless when a proportion of their ventilation was produced by voluntary effort than when the same total level of ventilation was produced entirely by the stimulus of exercise. Furthermore, voluntary isocapnic hyperventilation during exercise did not increase breathlessness above that normally associated with that level of exercise. 3. These results suggest that it is reflexly driven ventilation, and not simply the level of ventilation itself, which relates to the level of breathlessness during exercise.

1. Six patients with chronic airflow limitation rebreathed CO 2 . Subsequently they voluntarily copied their stimulated breathing pattern while normocapnia was maintained. On a separate occasion four of these patients performed progressively increasing exercise and later copied these breathing patterns. 2. During all experiments flow, ventilation and pleural pressures were recorded. In addition, breathlessness was measured on a visual analogue scale every 30 s. 3. In these patients voluntary copying of either form of stimulated breathing resulted in diminished breathlessness and in some cases in complete abolition of the sensation, despite similar levels and patterns of ventilation in the two situations. 4. No systematic or consistent differences in the mechanics of breathing between stimulated and voluntarily copied breathing were found. 5. There was no correlation found between breathlessness score and any mechanical variable measured. 6. These results show that despite similarity in mechanics between stimulated and voluntary hyperventilation, the sensation of breathlessness is much diminished during the latter in these patients. This suggests that the sensation of breathlessness is more dependent upon the awareness of central processing than upon input from peripheral mechanoreceptors.

1. Nine patients with chronic obstructive airways disease performed a 6 min self-paced walk (breathing air) on a treadmill and then identical (but operator-controlled) treadmill walks breathing either air or supplemental oxygen sufficient to just prevent arterial oxygen desaturation during the exercise. 2. During the exercises, ventilation was recorded and patients recorded their sensation of breathlessness on a visual analogue scale (VAS) every 30 s. 3. Breathing supplemental oxygen produced a small fall in mean exercise ventilation and a large and consistent reduction in mean exercise breathlessness. In seven patients the VAS scores were higher on air than with supplemental oxygen, at similar levels of ventilation. An analysis of co-variance, to control for reduction in ventilation, showed a decrease in mean breathlessness when breathing supplemental oxygen, significant at the 8% level. 4. The reduction in breathlessness produced by preventing exercise desaturation cannot be explained by the decrease in ventilation. This suggests that hypoxia may be a stimulus for breathlessness. The mechanism is unknown.

1. Normal subjects show wide variability in their sensory scaling of breathlessness for equivalent degrees of ventilatory stimulation and behave ‘characteristically’ irrespective of stimulus type. 2. Observed differences are not explained by physical characteristics, ventilatory sensitivity or pattern of breathing although there is a weak association with the degree of physical fitness. 3. Differences are seen when scaling is performed with reference to both rigidly defined extremes of breathlessness (visual analogue scaling) and a subject's own relative changes in the intensity of this sensation (magnitude estimation). 4. These findings may explain the common observation, in patients with respiratory disease, of dyspnoea out of proportion to the pathophysiological state.

1. This study investigates the mechanisms underlying the perception of breathlessness induced by hypoxia and hypercapnia in both naive normal subjects and patients with respiratory mechanical problems. 2. In normal subjects separately receiving both oscillating hypercapnic and hypoxic ventilatory stimulation, equivalent peak stimulus intensities in end-tidal gas were associated with a ‘damped’ ventilatory response when the frequency of stimulation was increased. A concomitant fall in peak breathlessness levels on a visual analogue scale was recorded in each case. 3. In normal subjects and patients, the voluntary copying of a ventilatory pattern recorded during oscillating hypercapnic stimulation was associated with a marked diminution or complete absence of breathlessness despite equivalent levels of peak ventilations achieved. 4. Voluntary copying of hypercapnic stimulated ventilation was not associated with any demonstrable change in the distribution of muscle movements between the chest wall and abdomen. 5. These results suggest that the intensity of breathlessness depends on the level of effective reflex stimulation of the respiratory-related neurones in the medulla. They cannot be explained solely in terms of perception of afferent neural information arising from either chemoreceptors or respiratory mechanoreceptors.

1. The intensity of breathlessness induced by ventilatory stimulation resulting from hypercapnia, hypoxia or exercise has been quantified in normals by using the two different sensory scaling techniques of linear visual analogue scaling and ratio magnitude estimation. 2. In naive individuals both techniques show good face validity. 3. When related to ventilation, quantification of breathlessness is moderately reproducible with both methods, even when subjects are kept in ignorance of the pattern of ventilatory stimulation. 4. There is a small within- and large between-subject variability with both scaling techniques; possible factors responsible are discussed. 5. The reproducibility of visual analogue scaling when related to ventilation is independent of the nature of the ventilatory stimulus and is maintained over intervals as long as 1 week when memory for the score given is unlikely to be an important factor. 6. The difficulties of interpreting subjective estimates of perceived breathlessness are discussed, together with the relative merits of the two scaling techniques.