Effect of negative ionisation of inspired air on the response of asthmatic children to exercise and inhaled histamine

To evaluate the effect of negative ionisation of inspired air on bronchial reactivity, 11 asthmatic children were challenged twice by exercise and 10 were challenged twice by histamine inhalation. The children breathed negatively ionised air (4 X 10(5) - 10 X 10(5) ions/cm3) or control room air in random order in a double-blind fashion. All challenges were matched in terms of basal lung function and the exercise tests were matched in terms of ventilation and respiratory heat loss. Exercise-induced asthma was significantly attenuated by exposure to negatively ionised air, the mean postexercise fall in one-second forced expiratory volume (FEV1) being 29% (SE 5%) of the initial value after the control and 21% (3%) after the ionised air test (p less than 0.02). Ten of the 11 subjects developed less exercise-induced asthma while breathing ionised air. Although the median dose of histamine (cumulative breath units) which caused a constant fall in FEV1 for each individual was higher with the ionised air challenge than with the control challenge the difference was not significant. Five of the 10 subjects were less sensitive to histamine and the other five more sensitive when breathing ionised air. It is concluded that negative ionisation of inspired air can modulate the bronchial response to exercise but the effect on the response to histamine is much more variable.     

Absence of refractoriness in asthmatic subjects after exercise with warm, humid inspirate.

Twelve asthmatic adults each completed two six minute treadmill runs separated by an interval of 20 minutes. Running speed was constant for each subject, and inspired air temperature averaged 5.5 degrees C (SD 1.5 degree) for both tests. Total minute ventilation and total respiratory heat loss showed no significant difference between the two runs. Forced expiratory volume in one second (FEV1) was measured before exercise and at five minute intervals throughout the recovery periods, during which subjects breathed room air at an average temperature of 17.8 degrees C (1.8 degree). Reduction in FEV1 from pre-exercise readings averaged 39.3% (13.3%) for the first run and 11.5% (7.3%) for the second. On another day the subjects underwent an identical procedure except that the first exercise period was performed with the saturated inspirate at 37.3 degrees C (1.7 degree). This run produced a mean FEV1 reduction of only 3.1% (7.3%). The ensuing run, during which the inspiratory temperature averaged 6.0 degrees C (2.0 degrees), led to a mean fall in FEV1 of 37.3% (17.3%). This was not significantly different from the value recorded for the first of the paired runs with cool air. We therefore have been unable to confirm that exercise with warm humid inspirate may induce refractoriness to exercise induced asthma. Our data are compatible with the theory that refractoriness may be due to depletion of mediators during an initial exercise induced asthma attack.     

Effect of positive ionisation of inspired air on the response of asthmatic children to exercise.

To evaluate the effect of positive ionisation of inspired air on bronchial reactivity, 12 asthmatic children were twice challenged by exercise in random order. During one test positively ionised air (5-10 X 10(5) ions/cm) was breathed. All challenges were matched in terms of basal lung function and exercise tests were matched in terms of ventilation and respiratory heat loss. Exercise induced asthma was significantly aggravated by exposure to positively ionised air, the postexercise fall in FEV1 (delta FEV1) being 24.7% (SEM and 5.3%) and 35.3% (5%) after the control and ionised air tests respectively (p less than 0.04). It is concluded that positive ionisation aggravates the bronchial response to exercise.     

Comparison of airway reactivity induced by histamine, methacholine, and isocapnic hyperventilation in normal and asthmatic subjects

In an investigation of a rapid screening test for airway reactivity using isocapnic hyperventilation with room air and cold air the results of this test were compared with the airway response to histamine and methacholine challenge. Twelve non-atopic, non-smoking normal subjects and 11 subjects with stable asthma who had an FEV1 above 74% of the predicted value were studied. In the normal subjects isocapnic hyperventilation with room air (75 l/min; 22 degrees C (SEM 0.2 degrees); 10 mg H2O/l air) and isocapnic hyperventilation with cold air (77 l/min; -10 degrees C (0.9 degrees); 2.4 mg H2O/l air) produced no significant change in FEV1. In the asthmatic subjects, hyperventilation with room air (71 l/min; 22 degrees C (0.8 degrees); 10 mg H2O/l air) caused a mean fall in FEV1 of 11.7%; cold air hyperventilation (70 l/min; -10 degrees C (0.9 degrees); 2.4 mg H2O/l air) caused a mean fall in FEV1 of 20.4%. Cold air hyperventilation produced greater separation between normal and asthmatic subjects than room air. The provocative concentration of histamine required to reduce the FEV1 by 20% (PC20) correlated closely with the PC20 for methacholine (r = 0.95; p less than 0.001). Both tests separated normal from asthmatic subjects. PC20 for both histamine and methacholine correlated with the fall in FEV1 after cold air hyperventilation (r = 0.93, p less than 0.001; r = 0.87, p less than 0.001 respectively). We conclude that the results of a rapid screening test based on hyperventilation with cold air correlate well with a standard pharmacological challenge.     

Respiratory heat loss in exercise-induced asthma. Measurement and clinical application

The theoretical considerations of conditioning inspired air and the application of the respiratory heat loss (RHL) formula are discussed. An on-line method for measuring RHL is described together with the apparatus for generating frigid dry and warm humid air. Exercise-induced asthma (EIA) was studied using these methods. Thirteen asthmatic and 6 normal children and adolescents participated in the study. Each subject undertook two submaximal exercise tests consisting of 6 minutes' ergometric cycling against a fixed load. One test was done while breathing cold dry air (mean temperature -22 degrees C and 0% relative humidity) and the other while breathing warm humid air (mean temperature 36 degrees C and 100% relative humidity). All the other exercise parameters (e.g. heart rate, minute ventilation, oxygen uptake) were carefully matched between the two tests. In the cold dry air tests with a mean RHL of 1,43 kcal/min, all asthmatic subjects developed EIA with a mean fall in forced expiratory volume in the 1st second (FEV1) of 48% from baseline. In the warm humid air tests with negligible RHL (0,02 kcal/min) none of the asthmatics developed EIA (mean fall in FEV1 5%). The difference between the two tests was highly significant (P less than 0,001). Neither air condition caused bronchospasm in the normal subjects. A dose-response relationship was obtained between the degree of RHL and corresponding fall in FEV1.     

Role of cooling and drying in hyperventilation induced asthma.

Respiratory heat loss has been proposed as a mechanism of exercise induced asthma. Whether the predominant stimulus is airway drying or cooling remains unclear. We have measured changes in FEV1 after isocapnic cold air hyperventilation (CAH) (-23.4 degrees (SD 0.43 degrees) C) and dry ambient air hyperventilation (AAH) (18.7 degrees (0.52 degrees)C) in seven asthmatic patients (mean age 31 (SD 9) years and baseline FEV1 3.2(0.9)1) and in seven normal subjects (age 28(6) years and FEV1 3.6(0.7)1). The inspired water content in both cases was 0.3 mg/l air. The rate of respiratory heat exchange per breath was calculated in watts (W) with microcomputer based equipment. Cold air hyperventilation caused a fall in FEV1 almost twice that of ambient air hyperventilation at each level of ventilation: CAH v AAH (% fall) 8.0 (5.1) v 3.9 (4.0) at 15 l/min, 11.6 (7.8) v 7.0 (4.4) at 30 l/min, and 20.7 (10.9) v 12.4 (6.3) at 60 l/min. Identical latent heat loss (evaporative drying) was imposed on the airway during the two challenges. Sensible heat loss (convective cooling) in cold air hyperventilation was 41 W at 15 l/min, 63 W at 30 l/min, and 114 W at 60 l/min; whereas in ambient air hyperventilation the loss was 6, 13, and 23 W respectively. It is concluded that the rate of cooling of the upper airway is the predominant stimulus in hyperventilation induced asthma.     

Effectiveness of a heat and moisture exchanger in preventing hyperpnoea induced bronchoconstriction in subjects with asthma.

The effect of a heat and moisture exchanger, a device with hygroscopic material for conditioning inspired air, on hyperpnoea induced bronchoconstriction was studied in nine non-smoking volunteers with asthma, aged 19-32 years. Each had previously shown an increase of at least 100% in specific airways resistance (sRaw) to isocapnic hyperpnoea with dry air. On two separate days the subject performed isocapnic hyperpnoea with dry air at 60-70 l min-1 for five minutes. Before, immediately after, and five minutes after completion of a test sRaw measurements were made. Heat and moisture exchangers were placed in the breathing circuit on one of the two days. All subjects had an increase in sRaw of 100% or more without the heat and moisture exchangers (average increase 300%) but were protected from bronchoconstriction with the devices in place (average increase 7%) (p less than 0.005). The exchanger's resistance to airflow was less than 1 cm H2O for flow rates of 100 l min-1. A heat and moisture exchanger designed as a facemask or mouthpiece may allow a person with asthma to exercise without the need for prophylactic drugs.     

Demonstration of a problem in estimating sensible heat loss from the respiratory tract by thermometry

We have investigated sensible respiratory loss, which is usually taken as the product of expired volume and the temperature difference between inspired and expired air (VE X delta T). Air temperature was measured with a 0.122 mm copper-constantan thermocouple mounted in the mouthpiece of a T-piece breathing system, and expired volume with a pneumotachograph. Changing air temperature (delta T) at the mouth and expired air volume (VE) were recorded simultaneously while the subject voluntarily breathed at different tidal volumes and rates. Inspired temperatures were controlled at 12.05 degrees C, 21.80 degrees C and 25.74 degrees C at a low dewpoint temperature of 4-5 degrees C. Temperature volume "loops" were constructed using an x-y plotter. The areas of each "loop" and enclosing rectangle (VE X delta T) were measured. The difference was divided by the weight of the rectangle to give the percentage of overestimation of sensible heat loss, which ranged from 5.5 to 17.2 per cent. The error increased significantly with decreasing tidal volume and increasing respiratory rate.     

Effect of nifedipine on bronchoconstriction induced by inhalation of cold air

The effect of nifedipine (20 mg sublingually) on the bronchial response to cold air was studied in eight asthmatic patients and eight normal subjects. Eucapnic hyperventilation with dry subfreezing air was performed for three minutes by each subject, with a minute volume of 30 X FEV1 for normal subjects and half that for the asthmatics. In the normal subjects there was no difference in the falls in the one-second forced expiratory volume (FEV1) and specific airways conductance (sGaw) produced by cold air inhalation on the days when they were pretreated with placebo and with nifedipine. In asthmatic patients, however, significant protection with nifedipine was demonstrated. The maximum recorded fall in FEV1 was reduced from 13% +/- 2% (SE) to 4% +/- 2% (p less than 0.005) and the maximum fall in sGaw from 35% +/- 5% to 17% +/- 4% (p less than 0.002). The possible causes of this difference are discussed. It is suggested that these results present further evidence for a different mechanism of response to cold air in asthmatic and normal subjects.     

Attenuation of exercise induced asthma by local hyperthermia.

BACKGROUND: Prior treatment with local hyperthermia has been shown to prevent mast cell degranulation and leucocyte histamine release, and to reduce mortality and cellular infiltrates in a model of acute lung injury. Local hyperthermia is effective in reducing the symptoms of the common cold and perennial and seasonal allergic rhinitis, nasal patency also being improved in rhinitis. It is possible that these effects are mediated by common anti-inflammatory mechanisms, and that this treatment may be effective in the treatment of asthma. The effect of prior local hyperthermia on the response to exercise challenge and histamine bronchoprovocation was therefore examined. METHODS: In a randomised, double blind, placebo controlled, crossover study, 10 asthmatic subjects with exercise induced asthma used machines delivering 40 1/minute of fully humidified air at either 42 degrees C (active treatment) or 31 degrees C (placebo treatment) for 30 minutes' tidal breathing. For each pretreatment, at two week intervals they underwent exercise challenges starting one and 24 hours after starting the inhalations. After a further two weeks the protocol was repeated with histamine substituted for the exercise challenges. RESULTS: The mean (SE) maximum percentage fall in forced expiratory volume in one second (FEV1) was significantly lower one hour after treatment with air at 42 degrees C (30.8% (3.1%)) than after treatment with air at 31 degrees C (22.3% (2.9%)). There was no significant effect on exercise challenge at 24 hours, or on histamine challenge at either time point, though there were nonsignificant trends towards protection with exercise at 24 hours and with histamine at one hour. CONCLUSION: In asthmatic subjects the response to exercise challenge is significantly attenuated one hour after treatment with local hyperthermia. This treatment warrants further investigation in the treatment of clinical asthma and other inflammatory disorders.     

Inhibition by sodium cromoglycate of bronchoconstriction stimulated by respiratory heat loss: comparison of pressurised aerosol and powder

The protective effect was examined of three doses (2, 10, and 20 mg) of sodium cromoglycate inhaled from a pressurised metered dose inhaler on the response to isocapnic hyperventilation of cold dry air in 10 asthmatic subjects. This was compared with the effect of cromoglycate powder (20 mg) inhaled from a Spincap and with placebo given on two occasions. The medications were inhaled on separate days, in random order and with the use of a double blind double dummy technique, 20 minutes before isocapnic hyperventilation of two fold increasing volumes of air (-15 degrees C, 0% humidity) to produce a 20% fall in the post-treatment FEV1. The response was expressed as the provocative dose of respiratory heat loss required to cause a fall in FEV1 of 15% (PD15, kcal/min). The mean baseline spirometric indices exceeded 85% of predicted normal values on each test day; both placebo treatments reduced the baseline FEV1 by comparison with all active treatments (p less than 0.0001). Comparison of the PD15 on the two placebo days confirmed excellent reproducibility. All doses of cromoglycate shifted the respiratory heat loss dose-response curve to the right of the placebo curve; PD15 after all active treatments exceeded PD15 after placebo (p less than 0.0001). There was no cromoglycate dose-response relationship between the three doses of aerosol (p greater than 0.05), or between any dose of aerosol and powder (p greater than 0.05). It is concluded that cromoglycate aerosol inhaled from a pressurised inhaler in a dose of 2 mg gives the same magnitude of protection against bronchoconstriction stimulated by airway cooling as 20 mg of pressurised aerosol or powder from a Spincap.     

The nasal response to exercise and exercise induced bronchoconstriction in normal and asthmatic subjects.

Two studies were carried out to test the hypothesis that the fall and recovery of nasal resistance after exercise in asthmatic and non-asthmatic subjects are related to the development of bronchoconstriction after exercise. In study 1 nasal resistance (posterior rhinomanometry) and specific airway resistance (sRaw) were measured before challenge and one, five, 10 and 30 minutes after four minutes of exhausting legwork exercise in nine asthmatic subjects and nine age matched healthy subjects. One minute after exercise there was a reduction in nasal resistance of 49% (SD 15%) from baseline in the healthy subjects and of 66% (17%) in the asthmatic subjects. This response and the subsequent return of nasal resistance to baseline values did not differ significantly between the two groups despite a substantial difference in the change in sRaw, an increase of 74% (45%) in the asthmatic subjects 10 minutes after exercise, and no change in the non-asthmatic subjects. In study 2, nasal and specific airway resistances were monitored according to the same measurement protocol in six subjects with increased airway reactivity. Subjects exercised on two occasions, wearing a noseclip, once while breathing cold, dry air and once while breathing warm, humid air. The fall in nasal resistance was similar under both conditions (to 47% and 39% of baseline), through sRaw rose only after cold air inhalation (to 172% of baseline). The results indicate that the nasal response to exercise is not related to bronchial obstruction in asthmatic subjects after exercise or to the temperature or humidity of the air inspired through the mouth during exercise.     

Effect of apparatus on functional residual capacity

As the route of breathing and use of airway apparatus such as mask, mouthpiece and noseclip can alter breathing pattern, this study has used the helium dilution method to estimate the effects of mouthpiece and mask breathing on functional residual capacity (FRC) in the supine position, and the change in FRC that occurs between the sitting and supine positions while breathing by mouthpiece. In 13 normal subjects, breathing by mouthpiece, FRC was smaller, by a median of 1.07 litre (interquartile values 0.73-1.43 litre) in the supine compared with the sitting position (P < 0.01), but residual volume (RV) did not change significantly. FRC measured in the supine position was significantly greater when breathing by mask than by mouthpiece (0.25, 0.04-0.38 litre) and RV was greater by similar amounts (0.20, -0.02 to 0.49 litre). This difference may result from increased inspiratory activity while breathing via the mask.      

Efficacy of Preoxygenation with Tidal Volume Breathing: Comparison of Breathing Systems

Background: Preoxygenation before tracheal intubation is intended to increase oxygen reserves and delay the onset of hypoxemia during apnea. Various systems are used for preoxygenation. Designed specifically for preoxygenation, the NasOral system uses a small nasal mask for inspiration and a mouthpiece for exhalation. One-way valves in the nasal mask and the mouthpiece ensure unidirectional flow. This investigation compares the efficacy of preoxygenation using the standard circle system with the NasOral system and five different resuscitation bags.

Methods: Twenty consenting, healthy volunteers were studied in the supine position for 5-min periods of tidal volume breathing using the circle absorber system, the NasOral system, and five resuscitation bags in a randomized order. Data were collected during room air breathing and at 30-s intervals during 5 min of oxygen administration. Inspired oxygen, end-tidal oxygen, and end-tidal nitrogen were measured by mass spectrometry.

Results: At 2.5 min of oxygenation, end-tidal oxygen plateaued at 88.1 +/- 4.8 and 89.3 +/- 6.4% (mean +/- SD) for the circle absorber and NasOral systems, respectively. This was associated with inverse decreases in end-tidal nitrogen. At no time did these end-tidal oxygen or nitrogen values differ from each other. Three of the resuscitation bags (one disk type and two duck-bill type with one-way exhalation valves) delivered inspired oxygen more than 90%, and the end-tidal oxygen plateaued between 77 and 89% at 2 min of tidal volume breathing. The other two resuscitation bags (both duck-bill bags without exhalation valves) delivered inspired oxygen less than 40%, and the end-tidal oxygen values ranged between 21.8 +/- 5.0 and 31.9 +/- 8.7%.     

Effect of nebulised salbutamol on maximal exercise performance in men with mild asthma.

The effect of 5 mg nebulised salbutamol on the cardiorespiratory responses to a progressive maximal exercise test was investigated in eight asthmatic (mean forced expiratory volume in one second (FEV1) 3.48 (1.0) litres) and eight non-asthmatic men. Exercise tests were performed on a bicycle ergometer after administration of nebulised salbutamol or matched saline placebo. In the asthmatic subjects salbutamol increased the resting FEV1 by 11%. The mean (SD) percentage fall in FEV1 after exercise did not change significantly (salbutamol 9.4 (12.8); placebo 15.0 (8.0], but because the FEV1 before exercise was increased the lowest FEV1 after exercise was also significantly higher after salbutamol than placebo (3.60 (1.13) v 2.85 (0.80) litres). Despite the improvement in FEV1 before exercise there was no significant difference in maximal workload, oxygen uptake, heart rate, or ventilation during exercise after salbutamol compared with placebo in the asthmatic patients. Tidal volume was higher at maximal exercise after salbutamol but there was no change in perception of breathlessness or exertion in the asthmatic subjects. During submaximal progressive exercise the perceived rate of exertion was reduced in the asthmatic patients and oxygen pulse was reduced in both groups owing to a small and non-significant increase in heart rate. The FEV1 and cardiorespiratory response to the progressive maximal exercise test in the non-asthmatic subjects were otherwise unchanged after salbutamol. The results suggest that 5 mg nebulised salbutamol has little effect on the cardiorespiratory responses to progressive maximal exercise in patients with mild asthma and in non-asthmatic subjects. Salbutamol in this dose may reduce the severity of exercise induced asthma, but no ergogenic effect on maximal exercise performance was shown.     

Airway response of asthmatic subjects to inhaled allergen after exposure to pollutants.

BACKGROUND: Recent studies have suggested that air pollutants resulting from vehicle exhaust emissions and burning of fossil fuels, either in combination or individually, may enhance the airway response of asthmatic subjects to inhaled allergen. It was hypothesised that the airway response to inhaled allergen after exposure to a combination of 400 ppb nitrogen dioxide (NO2) and 200 ppb sulphur dioxide (SO2) is increased 24-48 hours after exposure. METHODS: Thirteen mild atopic asthmatic volunteers were exposed for six hours to a single exposure of air and three exposures of the combination of 400 ppb NO2 + 200 ppb SO2 in randomised order, and then challenged with increasing concentrations of Dermatophagoides pteronyssinus allergen either immediately after exposure to air, or immediately, 24 hours or 48 hours after exposure to the combination of the two pollutants, until a 20% fall in forced expiratory volume in one second (FEV1) was recorded. RESULTS: Exposure to 400 ppb NO2 + 200 ppb SO2 significantly decreased the dose of D pteronyssinus allergen required to produce a 20% fall in FEV1 (PD20FEV1) at all times after exposure when compared with air. The mean percentage changes in allergen PD20FEV1 immediately, 24 hours, and 48 hours after exposure to 400 ppb NO2 + 200 ppb SO2 were -37% (95% confidence intervals (CI) -50 to -23), -63% (CI -75 to -51), and -49% (CI -75 to -28.8), respectively, when compared with the PD20FEV1 after air exposure and were significant at all time points studied. The allergen PD20FEV1 at 24 hours after exposure to the combination of the two pollutants was also found to be significantly lower when compared with that immediately after exposure to the two pollutants. CONCLUSION: These results demonstrate that exposure to a combination of NO2 and SO2, at concentrations which can be encountered during episodes of increased outdoor and indoor air pollution, enhances the airway response to inhaled allergen in asthmatic subjects. This effect persists over a period of 24-48 hours and is maximal 24 hours after exposure to these air pollutants.     

Effect of terbutaline on mucociliary clearance in asthmatic and healthy subjects after inhalation from a pressurised inhaler and a dry powder inhaler.

BACKGROUND: beta Agonists have been shown to increase mucociliary clearance in some studies but not all. Whether the formulation of beta agonists affects mucociliary clearance is not known but may be important as the use of dry powder inhalers increases. METHODS: The effect of different methods of administration of inhaled terbutaline on mucociliary clearance and forced expiratory volume in one second (FEV1) was assessed in 10 patients with asthma and 10 healthy subjects. Terbutaline (1 mg) was administered through a metered dose inhaler with a spacer (Nebuhaler) or a dry powder inhaler (Turbuhaler), or both treatments were given, in a four way double blind, double dummy trial. Mucociliary clearance was measured by bronchoscintigraphy. RESULTS: Clearance of radioactivity from the lobar bronchi increased in the asthmatic patients by a median of 32% after terbutaline was given by metered dose inhaler and 55% after a combined dose of 2 mg from both inhalers (1 mg from each) compared with placebo but by only 9% after 1 mg of terbutaline was given by a dry powder inhaler. In the healthy subjects mucociliary clearance increased by 51% when terbutaline was given by a dry powder inhaler, by 66% when given by a metered dose inhaler, and by 66% when given by both inhalers combined. The effect of terbutaline on FEV1 was the same with each of the inhalers. CONCLUSION: Despite similar changes in FEV1 with the two formulations terbutaline increased mucociliary clearance significantly in asthmatic and healthy subjects when inhaled from a metered dose inhaler whereas when it was inhaled from a dry powder inhaler its effect was significant only in healthy subjects. The reason for the difference in asthmatic subjects is unclear, but may be associated with differences in the deposition of terbutaline.     

The oxygen delivery characteristics of the Hudson Oxy-one face mask

The inspired oxygen fraction (FIO2) delivered by the Hudson Oxy-one face mask was measured under changing conditions of ventilation, oxygen flow rate to mask, and mask fit. A single trained subject sat in a body plethysmograph to measure ventilation and breathed at a constant rate of 15 per minute at three different tidal volumes, of approximately 0.3, 0.6, and 1.2 litres, from the mouthpiece in the plethysmograph. The Oxy-one face mask was fitted to a plaster-of-Paris face model on the outside of the plethysmograph in a loose and then in a tight fashion. Oxygen concentration was continuously monitored from a point in the metal tube connecting the face model to the mouthpiece. The tightly fitting mask demonstrated an orderly reduction in FIO2 as ventilation increased and oxygen flow rate to the mask decreased. The mean FIO2 at a ventilation of 4.5 l.min-1 and 8 l.min-1 oxygen flow was 78% and this fell to 27% at a ventilation of 16 l.min-1 and oxygen flow of 2 l.min-1. The loosely fitting mask demonstrated larger SD of measurements and lower mean maximum FIO2 values of 46 to 49% and these fell in an irregular fashion to similar minimum values as ventilation increased and oxygen flow decreased. Although the precise definition of the FIO2 for each breath from the changing concentration during each inspiration was not possible, these results indicate that FIO2 changes in a predictable way as a function of ventilation and oxygen flow, if the mask is close fitting. This method could be conveniently used to study other oxygen delivery systems.     

Perception of breathlessness during bronchoconstriction induced by antigen, exercise, and histamine challenges.

Perception of breathlessness was studied in eight patients with mild, stable asthma after a histamine and exercise challenge performed before and 24 and 48 hours respectively after an antigen challenge. FEV1 and perception of breathlessness, evaluated by Borg's 10 point category scale, were measured after each administration of doubling antigen or histamine concentrations to achieve a greater than 20% fall in FEV1, and after six minutes of steady state exercise at 80% of maximal oxygen consumption (VO2max). The geometric mean provocative concentration of histamine causing a 20% fall in FEV1 (PC20) fell from 1.67 mg/ml before antigen challenge to 0.52 mg/ml 24 hours after the challenge. The median maximal % fall in FEV1 with exercise was 24.9% (range 10.5-40.5%) before and 30.6% (range 13.8-52.3%) 48 hours after antigen challenge. The median maximum % fall in FEV1 after antigen inhalation was 20.1% (range 13.3-35.2%) within the first hour; only two subjects had a late fall in FEV1 (23% and 58%). The median (range) of Borg scores obtained when FEV1 was reduced by 20% did not differ significantly for the three types of acute challenges: 1.25 (0.5-2.5) and 1.0 (0.5-3.0) after histamine tests, 1.0 (0.5-4.1) and 1.55 (0.5-2.0) after exercise, and 1.5 (0-3.0) after antigen challenge. In the two subjects who had a late response to antigen the Borg score was reduced for the same % fall in FEV1 as with the early response. It is concluded that the perception of breathlessness does not differ appreciably during the early response to histamine, antigen exposure, or exercise, but that it is reduced during the late asthmatic response. It was not influenced by previous antigen exposure, despite an increase in airway responsiveness.     

Response of the nose to exercise in healthy subjects and in patients with rhinitis and asthma.

BACKGROUND--Although the nose and the bronchi are both involved in the process of regulating respiratory heat exchange, thermal changes may precipitate airway obstruction during exercise but rarely cause nasal obstruction in patients with rhinitis. The cause of the different response of the nose and bronchial tree has hardly been investigated. This study was performed to assess the response of the nose during exercise in the presence of rhinitis, asthma, and in normal controls. METHODS--Ten healthy subjects (group 1), 15 patients with asthma and rhinitis (group 2), 10 with rhinitis only (group 3), and 11 with asthma only (group 4) were included in the study. Exercise was performed on a bicycle ergometer for six minutes, reaching a heart rate of 80% of predicted. Bronchial and nasal responses were measured by forced expiratory volume in one second (FEV1) and posterior rhinomanometry, respectively. A drop in the FEV1 of 20% or more was considered a positive exercise induced asthma challenge test. RESULTS--Heart rate and ventilation increased by a similar proportion in the four groups. The FEV1 significantly decreased in asthmatic patients (groups 2 and 4) but it did not change in healthy subjects (group 1) or in those with rhinitis (group 3). Thirteen asthmatic patients developed exercise induced asthma. Nasal patency increased with exercise by a similar proportion in all groups, and no differences were detected between those with rhinitis (groups 2 and 3) and those without (groups 1 and 4). Nasal patency had returned to basal values at 25 minutes after completion of exercise in the four groups. The nose of patients with exercise induced asthma, however, remained significantly more patent than in patients without exercise induced asthma between 10 and 30 minutes after exercise. CONCLUSIONS--These results suggest that the nose responds differently from the bronchi during exercise induced airway obstruction: whereas the bronchial tree responds by becoming narrowed, the nose becomes more patent. These findings suggest that the mechanisms regulating the response of the nose to exercise are different from those involved in the response of the bronchial tree.