The nasal response to exercise in patients with cystic fibrosis.

This study has evaluated the nasal response to exercise in patients with cystic fibrosis (CF), a genetic disease in which factors such as chronic lung disease and/or nasal polyposis might be anticipated to modify nasal function responses. Measurements of nasal resistance (NAR) by posterior rhinomanometry and specific airway resistance (sRAW) were made before and 1, 5, 10, and 30 min after a 4-min period of exhausting legwork exercise (50% predicted maximal) in 19 CF patients (aged 11-29 years) and 10 healthy subjects (aged 11-31 years). One minute after exercise, healthy subjects showed a 54 +/- 5% (mean +/- SEM; standard error of the mean) relative fall from baseline in NAR and CF patients showed a 31 +/- 8% relative fall from baseline (p < 0.05). There were no significant differences in the magnitude or pattern of recovery in NAR after exercise (1 to 30 min) between the groups, largely because of the variability in NAR responses in CF patients. Exercise did not result in significant changes in sRAW in either group. We also found that a history or presence of nasal polyposis does not significantly affect functional nasal responses to exercise. Our conclusion is that the CF genotype and its airway sequelae do not substantively affect the control of the nasal response to exercise.

Nasal flow-resistive responses to challenge with cold dry air.

Recent studies have suggested that the inhalation of cold air through the nose is associated with the subsequent release of mediators of immediate hypersensitivity. To determine if mucosal surface heat and water loss influence the nasal functional response to cold air, we measured nasal resistance by posterior rhinomanometry before and 1, 5, and 10 min after a 4-min period of isocapnic hyperventilation (30 l/min) through the nose in nine healthy subjects (5 males, 4 females; aged 25-39 yr) while they inhaled air at 0 degrees C. During the challenge period, the subjects breathed either in and out of the nose or in through the nose and out through the mouth. No changes in nasal resistance developed when subjects breathed exclusively through the nose; however, when subjects breathed in through the nose and out through the mouth, nasal resistance was increased 200% at 1 min (P less than 0.01) after the challenge and returned to baseline values by 10 min after cessation of the challenge. These data indicate that nasal functional responses to cold dry air are dependent on the pattern of the ventilatory challenge. If the heat given up from the nasal mucosa to the incoming air is not recovered during expiration (as is the case with inspiration through the nose and expiration through the mouth), nasal obstruction will occur. Hyperpnea of cold air, per se, does not influence nasal resistance.

Assessing the characteristic between length of hypoxic exposure and serum erythropoietin levels.

We examined the relationship between the duration of hypoxic exposure and serum erythropoietin (EPO) production. Adult male Long-Evans rats were exposed to hypobaric hypoxia (HH = 0.5 atm) for a period of 15 min to 20 days. Serum for EPO by radioimmunoassay was collected immediately, 1 or 2 h after HH exposure. A significant rise in EPO levels occurred 1 h after a 30-min HH exposure that was not sustained 2 h after termination. One hour of HH exposure resulted in increased EPO levels 1 h after termination of exposure and further increased levels 2 h after termination of exposure. With prolonged exposure, serum levels remained elevated at 6 and 20 days, despite the development of polycythemia. We concluded that the hypoxic stimulus for elevation of serum EPO could be as short as 30 min and that EPO levels remained elevated after chronic HH. The experimental data were consistent with a mathematical model in which stimulated EPO production was proportional to the time of HH stimulus.

Agreement between noninvasive oximetric values for oxygen saturation.

We made an assessment of five pulse oximeters in regard to their ability to replace the HP ear oximeter as a noninvasive measurement of SaO2. Trials were performed during isocapnic progressive hypoxia (SaO2 range, 99 to 70 percent) in 22 white and six black subjects. Comparisons between values of SaO2 by oximetry were analyzed by comparing the difference of values by the two methods against their mean. The difference between pulse oximeters and the HP was 2.6 +/- 10.3 percent in all subjects. Results in whites were 1.9 +/- 10.2 percent and in blacks were 5.1 +/- 9.2 percent. The distribution of differences between pulse oximeters and the HP were larger below 80 percent than above 85 percent. We conclude that pulse oximeters give higher values than the HP, a tendency which is more pronounced in black than in white subjects. While the limits of agreement are better at saturations above 85 percent, the 95 percent confidence limits of agreement between pulse oximeters and the HP are rather large (+/- 10 percent) and unacceptable for assuming that pulse oximeters will provide the same values as found in clinical studies using the HP.

Ambulatory monitoring of arterial oxygen saturation.

We have developed a method of recording oxygen saturation over time using ambulatory equipment. A pulse oximeter was modified to be powered by battery, and values for oxygen saturation were recorded by an analog recorder. The unit is compact and functions for 30 hours between battery changes. The mean difference between oxygen saturation reported by the pulse oximeter and an IL 282 CO-oximeter was -1.12 percent, with a range of difference +/- 2.75 percent, indicating 95 percent confidence limits 5.5 percent either side of the mean. Continuous ambulatory recordings were obtained in 16 male subjects; six were healthy nonsnorers, five were healthy snorers, and five had sleep apnea. Of the average recording time, 19 +/- 5 hours, records contained 89 +/- 7 percent usable data. We conclude that ambulatory pulse oximetry is a feasible means of unsupervised long-term monitoring of oxygenation during daily activities.

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.