Effect of nasal continuous positive airway pressure on neuropsychological function in sleep apnea-hypopnea syndrome. A randomized, placebo-controlled trial.

A placebo-controlled, partial cross-over, double-blind, randomized study was performed with 46 adults with sleep apnea-hypopnea syndrome (SAHS) to determine the effect of therapeutic and subtherapeutic (0-1 cm H(2)O) nasal continuous positive airway pressure (CPAP) treatment on polysomnographic and neuropsychological testing. The following neuropsychological tests were administered: Geriatric Depression Scale, Trail Making A and B, Digit Span Test Forward and Backward, Epworth Sleepiness Scale, SteerClear, Digit Symbol, Controlled Oral Word Association, and Complex Figure Recall. Compared with results without CPAP, subtherapeutic CPAP did not affect any measured polysomnographic parameter. Comparison of neuropsychological test results obtained between the initial periods of effective treatment (Group 1, 16.1 d; Group 2, 19.6 d; p = NS) in all subjects showed significant improvements in Digit Symbol, Digit Span Backward, and Complex Figure tests. However, there were no group differences in changes in test results during the period when one group was on effective CPAP and the other on ineffective CPAP (Group 1, 16.1 d; Group 2, 13.9 d; p = NS). The results indicate the feasibility and importance of using ineffective CPAP as a placebo treatment and the importance of including a placebo control in studies evaluating the effect of treatment on neuropsychological function in SAHS.

An oral elastic mandibular advancement device for obstructive sleep apnea.

Oral mandibular advancement devices are becoming an increasingly important treatment alternative for obstructive sleep apnea (OSA). The first aim of the study was to determine whether a new oral elastic mandibular advancement device (EMA) prevents pharyngeal airway closure during sleep in patients with OSA. The second aim of the study was to determine if the polysomnographic response to the oral mandibular advancement device was dependent on the site of airway closure. Overnight polysomnograms were performed in 28 untreated OSA subjects with and without EMA. A third polysomnogram was performed in 12 of the subjects to determine the site of airway closure without the device. Site of airway closure above or below the oropharynx was determined by measuring the respective presence or absence of respiratory fluctuations in oropharyngeal pressure during induced occlusions in non-rapid eye movement (NREM) sleep. Mean apnea-hypopnea index (AHI) was 52.6 +/- 28.2 (SD) events/h without the device and 21.2 +/- 19.3 events/h with the device. Nineteen subjects (68%) had at least a 50% reduction in AHI with the device. The change in AHI with the device (AHI without device - AHI with device) was directly related to the AHI without the device. All three subjects with airway closure in the lower pharyngeal airway had a greater than 80% reduction in AHI with the device. Two of the nine subjects with airway closure in the velopharynx had a similar therapeutic response. The results show the effectiveness of EMA in the treatment of OSA. The results also indicate that polysomnographic severity of OSA and the site of airway closure should not be used to exclude patients from this oral device treatment.

Upper airway muscle activity and upper airway resistance in young adults during sleep.

To determine the relationship between upper airway muscle activity and upper airway resistance in nonsnoring and snoring young adults, 17 subjects were studied during sleep. Genioglossus and alae nasi electromyogram activity were recorded. Inspiratory and expiratory supraglottic resistance (Rinsp and Rexp, respectively) were measured at peak flow, and the coefficients of resistance (Kinsp and Kexp, respectively) were calculated. Data were recorded during control, with continuous positive airway pressure (CPAP), and on the breath immediately after termination of CPAP. Rinsp during control averaged 7 +/- 1 and 10 +/- 2 cmH2O.l-1.s and Kinsp averaged 26 +/- 5 and 80 +/- 27 cmH2O.l-1.s-2 in the nonsnorers and snorers, respectively (P = not significant). On the breath immediately after CPAP, Kinsp did not increase over control in snorers (80 +/- 27 for control vs. 46 +/- 6 cmH2O.l-1.s-2 for the breath after CPAP) or nonsnorers (26 +/- 5 vs. 29 +/- 6 cmH2O.l-1.s-2). These findings held true for Rinsp. Kexp did not increase in either group on the breath immediately after termination of CPAP. Therefore, 1) increases in upper airway resistance do not occur, despite reductions in electromyogram activity in young snorers and nonsnorers, and 2) increases in Rexp and expiratory flow limitation are not observed in young snorers.

Benefits of nocturnal nasal CPAP in patients with cystic fibrosis.

Patients with cystic fibrosis (CF) often hypoventilate during sleep with marked falls in oxygen saturation (SaO2%). This occurs most commonly during REM sleep, when there is a reduction in rib cage excursion and a fall in end-expiratory lung volume (EELV). The aim of this study was to examine the effect of nocturnal nasal continuous positive airway pressure (nCPAP) on SaO2 and the respiratory disturbance index (RDI) during sleep in patients with CF and severe lung disease. Seven patients (FEV1% pred, 23 +/- 5; range, 14 to 28%) were evaluated during sleep on two nights, control and nCPAP (11 +/- 2 cm H2O; range, 8 to 16 cm H2O), with four patients breathing room air and three patients breathing supplemental oxygen on both nights. Mean awake SaO2 was 91 +/- 1% (range, 89 to 93%). All patients showed significant oxyhemoglobin desaturation and respiratory disturbance in the control study. The maximal falls in SaO2 (15 +/- 10%) were most often associated with phasic eye movements, and a decline in rib cage excursion and the sum signal (Respitrace) during REM sleep. Nasal CPAP resulted in a significant improvement in the mean minimum oxygen saturation (MMOS) during both NREM (nCPAP 91 +/- 3% vs control 88 +/- 2%, p < 0.05) and REM sleep (nCPAP 89 +/- 6% vs control 83 +/- 6%, p < 0.05). Transcutaneous CO2 measurements were not significantly different between the control and the nCPAP studies. The RDI was also significantly reduced with nCPAP especially during REM sleep (9 +/- 7 events per hour vs control 25 +/- 11 events per hour, p < 0.05). Nasal CPAP caused no change in total sleep time or sleep efficiency yet significantly reduced the RDI and improved baseline SaO2 during both NREM and REM sleep.

Sleep apnea and vigilance performance in a community-dwelling older sample.

Impaired vigilance performance has been reported in older subjects with sleep apnea syndrome (SAS). The current study is an attempt to extend these findings and to investigate additional factors that might have implications for vigilance in the older adult. Fifty-nine older adults [age: 62 +/- 5 (mean +/- SD), range 54-75 years; respiratory disturbance index (RDI): 8.8 +/- 14.4 (mean +/- SD), range 0-67.5] were categorized as SAS or NotSAS, based on various classification criteria [i.e. apnea index (AI) > or = 5, and 10, RDI > or = 5, 10 and 15], and were compared on their vigilance performance as assessed by the computer program "Steer Clear". Vigilance performance did not discriminate the groups, independent of how they were formed. Groups were then formed based on vigilance performance (HiVig vs. LowVig) and compared on assorted sleep variables, periodic leg movements, and self-reported hypersomnolence and depression. Only age discriminated vigilance performance (an inverse relationship), accounting for 31% of the observed variance. Our findings suggest that subject selection may unintentionally bias findings regarding the neuropsychological functioning of individuals with SAS, that vigilance may be impaired only in relatively more "severe" SAS, and that severity of SAS in older adults may not be well characterized by current classification standards. Age clearly impacted vigilance performance, despite the constricted age range sampled, and should be taken into account in future research.

Benefits of continuous positive airway pressure during exercise in cystic fibrosis and relationship to disease severity.

The aim of this study was to determine the benefits of CPAP applied during exercise in patients with cystic fibrosis (CF). A total of 33 CF patients with a wide range of lung function were studied. Pulmonary function tests were measured at rest. Endurance tests (80% of previously determined Wpeak) were performed on a bicycle ergometer with and without CPAP (5 cm H2O). Oxygen saturation (SaO2) was monitored by oximetry. Transdiaphragmatic pressure (Pdi) was measured in 7 patients. We found significant correlations between indices of disease severity (NIH score, FEV1, % of predicted, and RV/TLC) and the effects of CPAP on VO2, Pdi, and dyspnea score. CPAP reduced isotime (defined as the last common minute of exercise) VO2 and dyspnea in those patients with more severe lung disease, but these values tended to increase slightly in the patients with only mild lung disease. The change in dyspnea score related to changes in endurance time and VO2. In many patients isotime SaO2 was improved with CPAP, with the largest changes observed in those patients with severe disease. The decreases in VO2, Pdi, and dyspnea score with CPAP in patients with severe lung disease suggest that CPAP can reduce the work of breathing and increase exercise tolerance in patients with CF. These beneficial effects of CPAP during exercise in CF patients are related to disease severity.

Effects of high-frequency oscillating pressures on upper airway muscles in humans.

We examined the effects of high-frequency- (30-Hz) low-pressure oscillations (< 1 cmH2O) applied to the upper airway, via a nose mask, on genioglossus (EMGgg), sternomastoid (EMGsm), and diaphragm electromyogram (EMGdia) activity in sleeping humans. Ten patients with sleep apnea and six normal subjects were studied. The pressure oscillations were applied through the mask for a single breath. The subjects were studied in non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. In the normal subjects, during NREM sleep, peak EMGgg, EMGsm, and EMGdia activity increased significantly in response to the oscillations in 63, 51, and 46%, respectively, of all trials. During REM sleep, significant increases occurred in 73, 88, and 13%, respectively, of all trials. Similar responses were observed in the patients with obstructive sleep apnea. Peak EMGgg, EMGsm, and EMGdia activity increased significantly in 74, 50, and 67%, respectively, of all NREM sleep trials and in 55, 81, and 76%, respectively, of all REM sleep trials. An important finding was that in 46% of the trials in the patients with sleep apnea the oscillation-induced increase in EMGgg activity was associated with a partial or complete reversal of the upper airway obstruction with an increase in tidal volume. This was observed in NREM and REM sleep. We conclude that there are upper airway receptors that respond to low-pressure-high-frequency oscillations applied to the upper airway that have input to the genioglossus and other muscles of respiration. These responses may be utilized in future treatment for sleep apnea.

Effects of high-frequency pressure waves applied to upper airway on respiration in central apnea.

We examined the effects of high-frequency (30-Hz) low-pressure oscillations on respiration in nine patients with central sleep apnea. All patients were studied during sleep and wore a nasal mask through which the oscillations were applied. All tests were performed during periods of repetitive central apneas. Respiratory efforts were monitored from the airflow and calibrated Respitrace signals. After several cycles of apnea were monitored, the oscillatory pressures were applied for brief periods (less than 5 s) at the midpoint of the central apneas. All trials in which arousal occurred were discarded, leaving a total of 106 trials in the nine patients. High-frequency oscillation of the upper airway stimulated respiratory effort(s) in 68% of all trials (72 of 106). Apnea length was significantly shortened in four of the nine patients. In one patient with a tracheostomy, the stimulus applied to his isolated upper airway evoked respiratory efforts during central apnea in 13 of 15 trials. We conclude that high-frequency oscillatory pressures applied to the upper airway can stimulate respiratory efforts during central apnea. This response may be mediated by upper airway receptors involved in nonrespiratory airway defense reflexes and may have implications in the treatment of patients with central sleep apnea.

Load compensation and respiratory muscle function during sleep.

The sleeping state places unique demands on the ventilatory control system. The sleep-induced increase in airway resistance, the loss of consciousness, and the need to maintain the sleeping state without frequent arousals require the presence of complex compensatory mechanisms. The increase in upper airway resistance during sleep represents the major effect of sleep on ventilatory control. This occurs because of a loss of muscle activity, which narrows the airway and also makes it more susceptible to collapse in response to the intraluminal pressure generated by other inspiratory muscles. The magnitude and timing of the drive to upper airway vs. other inspiratory pump muscles determine the level of resistance and can lead to inspiratory flow limitation and complete upper airway occlusion. The fall in ventilation with this mechanical load is not prevented, as it is in the awake state, because of the absence of immediate compensatory responses during sleep. However, during sleep, compensatory mechanisms are activated that tend to return ventilation toward control levels if the load is maintained. Upper airway protective reflexes, intrinsic properties of the chest wall, muscle length-compensating reflexes, and most importantly chemoresponsiveness of both upper airway and inspiratory pump muscles are all present during sleep to minimize the adverse effect of loading on ventilation. In non-rapid-eye-movement sleep, the high mechanical impedance combined with incomplete load compensation causes an increase in arterial PCO2 and augmented respiratory muscle activity. Phasic rapid-eye-movement sleep, however, interferes further with effective load compensation, primarily by its selective inhibitory effects on the phasic activation of postural muscles of the chest wall. The level and pattern of ventilation during sleep in health and disease states represent a compromise toward the ideal goal, which is to achieve maximum load compensation and meet the demand for chemical homeostasis while maintaining sleep state.

Changes in end-expiratory lung volume during exercise in cystic fibrosis relate to severity of lung disease.

Changes in end-expiratory lung volume (EELV) during exercise in normal subjects and in patients with severe chronic obstructive lung disease have previously been examined. To date there are no studies that have examined the changes in EELV in patients with mild to moderate lung disease. We studied the changes in EELV during exercise in patients with cystic fibrosis (CF) with a wide range of pulmonary impairment to determine if changes in EELV were related to the severity of lung disease. Twenty-two patients with CF were studied (FEV1 17 to 112% of predicted) during progressive bicycle exercise, and changes in EELV were determined by repeat measures of inspiratory capacity. Changes in EELV at end exercise ranged from an increase of 0.67 L to a decrease of 0.61 L, and significant relationships were found between the changes in EELV and resting lung function (FEV1 percent predicted r = 0.79 and VR/TLC r = 0.58), indices of maximal expiratory flow (FEF50 r = -0.72 and FEF25-75 r = -0.71), and maximal work capacity (W-Max r = -0.76 and W-Max percent predicted r = -0.69). For subsequent analysis, patients were divided into two subgroups. Patients who were able to decrease EELV during exercise (Subgroup A) had significantly better resting lung function and SaO2 and significantly higher W-Max, peak oxygen consumption, and SaO2 at W-Max. Patients in Subgroup A also had a near normal ventilatory pattern during exercise. In contrast, the patients who increased EELV during exercise (Subgroup B) had severe lung disease (mean FEV1 29 +/- 4 percent predicted), limited work capacity, and desaturated during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of sleep-induced increases in upper airway resistance on respiratory muscle activity.

To investigate the response of inspiratory and expiratory muscles to naturally occurring inspiratory resistive loads in the absence of conscious control, five male "snorers" were studied during non-rapid-eye-movement (NREM) sleep with and without continuous positive airway pressure (CPAP). Diaphragm (EMGdi) and scalene (EMGsc) electromyographic activity were monitored with surface electrodes and abdominal EMG activity (EMGab) with wire electrodes. Subjects were studied in the following conditions: 1) awake, 2) stage 2 sleep, 3) stage 3/4 sleep, 4) CPAP during stage 3/4 sleep, 5) CPAP plus end-tidal CO2 pressure (PETCO2) isocapnic to stage 2 sleep, and 6) CPAP plus PETCO2 isocapnic to stage 3/4 sleep. Inspired pulmonary resistance (RL) at peak flow rate and PETCO2 increased in all stages of sleep. Activity of EMGdi, EMGsc, and EMGab increased significantly in stage 3/4 sleep. CPAP reduced RL at peak flow, increased tidal volume and expired ventilation, and reduced PETCO2. EMGdi and EMGsc were reduced, and EMGab was silenced. During CPAP, with CO2 added to make PETCO2 isocapnic to stage 3/4 sleep, EMGsc and EMGab increased, but EMGdi was augmented in only one-half of the trials. EMG activity in this condition, however, was only 75% (EMGsc) and 43% (EMGab) of the activity observed during eupneic breathing in stage 3/4 sleep when PETCO2 was equal but RL was much higher. We conclude that during NREM sleep 1) inspiratory and expiratory muscles respond to internal inspiratory resistive loads and the associated dynamic airway narrowing and turbulent flow developed throughout inspiration, 2) some of the augmentation of respiratory muscle activity is also due to the hypercapnia that accompanies loading, and 3) the abdominal muscles are the most sensitive to load and CO2 and the diaphragm is the least sensitive.

Effects of sleep-induced increases in upper airway resistance on ventilation.

To determine the effects of the sleep-induced increases in upper airway resistance on ventilatory output, we studied five subjects who were habitual snorers but otherwise normal while awake (AW) and during non-rapid-eye-movement (NREM) sleep under the following conditions: 1) stage 2, low-resistance sleep (LRS); 2) stage 3-4, high-resistance sleep (HRS) (snoring); 3) with continuous positive airway pressure (CPAP); 4) CPAP + end-tidal CO2 partial pressure (PETCO2) mode isocapnic to LRS; and 5) CPAP + PETCO2 isocapnic to HRS. We measured ventilatory output via pneumotachograph in the nasal mask, PETCO2, esophageal pressure, inspiratory and expiratory resistance (RL,I and RL,E). Changes in PETCO2 were confirmed with PCO2 measurements in arterialized venous blood in all conditions in one subject. During wakefulness, pulmonary resistance (RL) remained constant throughout inspiration, whereas in stage 2 and especially in stage 3-4 NREM sleep, RL rose markedly throughout inspiration. Expired minute ventilation (VE) decreased by 12% in HRS, and PETCO2 increased in LRS (3.3 Torr) and HRS (4.9 Torr). CPAP decreased RL,I to AW levels and increased end-expiratory lung volume 0.25-0.93 liter. Tidal volume (VT) and mean inspiratory flow rate (VT/TI) increased significantly with CPAP. Inspiratory time (TI) shortened, and PETCO2 decreased 3.6 Torr but remained 1.3 Torr above AW. During CPAP (RL,I equal to AW), with PETCO2 returned to the level of LRS, VT/TI and VE were 83 and 52% higher than during LRS alone. Also on CPAP, with PETCO2 made equal to HRS, VT, VT/TI, and VE were 67, 112, and 67% higher than during HRS alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition of inspiratory muscle activity during sleep. Chemical and nonchemical influences.

The purpose of this study was twofold, namely, to determine (1) if phasic respiratory muscle activity can be inhibited during nocturnal mechanical ventilation, and (2) the mechanism by which this inhibition occurs. Twelve normal subjects were studied during non-rapid eye movement (NREM) sleep (Stages 2 to 4) while receiving negative (NPV, 8 subjects) or positive (PPV, 4 subjects) pressure ventilation and during spontaneous breathing. EMGdia (surface), end-tidal CO2 pressure (PETCO2), esophageal pressure (Pe), and ventilation were measured with a flow-through hood (NPV) or a mask (PPV). The following results were obtained during steady-state (3 to 22 min) mechanical ventilation. (1) A decrease in PETCO2 of 2 to 6 mm Hg resulted in elimination of phasic EMGdia in all subjects. Inhibition of respiratory muscle EMG (and a positive shift in Pe) occurred coincident with the breath-by-breath reduction in PETCO2, so that EMGdia was usually eliminated after the initial 4 to 6 breaths while using the ventilator. (2) Returning PETCO2 to the spontaneous sleeping level by adding CO2 to the inspired air (isocapnic mechanical ventilation) caused significant increases in EMGdia. During this isocapnic mechanical ventilation, however, EMGdia usually remained less than during eucapnic control. (3) Stopping the ventilator during hypocapnic ventilation caused a prolongation of expiratory time (TE) that was proportional to the degree of hypocapnia during the mechanical ventilation (100 to 1,200% increase over control). During isocapnic ventilation, cessation of mechanical ventilation caused no change in TE.(ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of end-expiratory lung volume during exercise.

We determined the effects of exercise on active expiration and end-expiratory lung volume (EELV) during steady-state exercise in 13 healthy subjects. We also addressed the questions of what affects active expiration during exercise. Exercise effects on EELV were determined by a He-dilution technique and verified by changes in end-expiratory esophageal pressure. We also used abdominal pressure-volume loops to determine active expiration. EELV was reduced with increasing exercise intensity. EELV was reduced significantly during even mild steady-state exercise and during heavy exercise decreased an average of 0.71 +/- 0.3 liter. Dynamic lung compliance was reduced 30-50%; EELV remained greater than closing volume. Changing the resistance to airflow (via SF6-O2 or He-O2 breathing) during steady-state exercise changed the peak gastric and esophageal pressure generation during expiration but did not alter EELV; breathing through the mouthpiece produced similar effects during exercise. EELV was significantly reduced in the supine position. With supine exercise active expiration was not elicited, and EELV remained the same as in supine rest. With CO2-driven hyperpnea (7-70 l/min), EELV remained unchanged from resting levels, whereas during exercise, at similar minute ventilation (VE) values EELV was consistently decreased. At the same VE, treadmill running caused an increase in tonic gastric pressure and greater reductions in EELV than either walking or cycling. We conclude that both the exercise stimulus and the resultant hyperpnea stimulate active expiration and a reduced FRC. This new EELV is preserved in the face of moderate changes in mechanical time constants of the lung. This reduced EELV during exercise aids inspiration by optimizing diaphragmatic length and permitting elastic recoil of the chest wall.

Exercise-induced changes in functional residual capacity.

We used a helium-rebreathe technique in nine healthy subjects to determine the effects of exercise intensity and duration on end-expiratory lung volume (EELV). The rebreathe functional residual capacity (FRC) technique was shown: (a) to be similar to that measured in the body plethysmograph, at rest; (b) to agree closely with volitionally induced changes in EELV as determined by inductance plethysmography, at rest; (c) to be reproducible within subjects between trials conducted at rest or exercise on different days (r = 0.96, coefficient of variation +/- 3%); (d) to correlate significantly with coincident changes in end-expiratory esophageal pressure from rest to exercise, with increasing exercise intensity and over time at a constant exercise load. Exercise-induced reductions in EELV occurred in all subjects, averaging 0.3 L (-0.1 to -0.7 L) in light exercise and 0.79 L (-0.5 to -1.2 L) in heavy or maximum exercise. This reduction in EELV accounted for slightly more than one-half of the increase in VT during light exercise and slightly less than one-half of the increased VT in heavy exercise. In heavy prolonged exercise lasting 8-15 min, EELV fell in the initial 2 min and was either sustained at this reduced level or fell further with exercise duration to exhaustion. We found that FRC was reduced even in very light exercise when changes in TE and VE from rest were minimal; further reductions in EELV occurred as end-inspiratory lung volume increased and expiratory time shortened with increasing exercise intensity and duration. Based on these types of changes we speculate that active expiration during exercise in humans may be controlled by a combination of locomotor-related feed-forward and lung volume related feed-back mechanisms.

Variability of airway responsiveness to histamine aerosol in normal subjects. Role of deposition.

The purpose of this investigation was to determine if the variability of bronchial responsiveness to inhaled histamine in normal subjects is related to the total dose of histamine deposited in the airways. To test this possibility, we used a new method of histamine challenge that permits calculating the histamine mass deposited in the airways in an attempt to correlate it with the magnitude of the response. Using a standardized breath-holding maneuver, 10 healthy nonsmokers and 10 healthy smokers with normal spirometry inhaled an aerosol generated from a solution containing a fixed ratio of histamine and a small quantity of hematoporphyrin serving as a fluorescent tracer. The mass of histamine deposited was calculated from the measured fluorescence of the inspired and expired aerosol. Forced expiratory volume in one second (FEV1) was measured before and 10 min after inhalation challenge. There was a negative correlation between percent decrease in FEV1 (delta FEV1) and histamine mass deposited in the nonsmokers (r = -0.83, p less than 0.005) and smokers (r = -0.82, p less than 0.005) without a difference between the 2 slopes. The range of delta FEV1 was 7 to 33% and of histamine mass deposited, 0.02 to 0.18 mg in the nonsmokers. The respective values in the smokers were 2 to 30% and 0.02 to 0.17 mg. In 6 subjects in whom dose-response curves were obtained, the mean deposited histamine mass required to decrease the FEV1 by 10% was 0.11 mg.(ABSTRACT TRUNCATED AT 250 WORDS)

Heat acclimation in cystic fibrosis.

Cystic fibrosis (CF) patients may be at risk for heat illness because of their high sweat chloride and sodium concentrations ([Cl-], [Na+]), but it is not known if they can heat acclimate. We studied 10 CF patients and 10 normal controls on 8 consecutive days of cycle exercise in the heat (37 degrees C dry bulb, 24-29 degrees C wet bulb). Both groups acclimated. CF peak rectal temperature (Tre) was 38.2 +/- 0.3 degrees C on day 1 and 37.8 +/- 0.4 degrees C on day 8 (P less than .005), and peak heart rates (HR) were 151 +/- 24 beats/min on day 1 and 136 +/- 22 beats/min on day 8 (P less than 0.025). Control temperature (T) and HR were similar. Controls decreased sweat [Cl-] from 37.2 +/- 14.6 meq/l on day 1 and to 24.9 +/- 10.6 meq/l on day 8 (P less than 0.005). CF sweat [Cl-] was significantly higher and did not change with acclimation (day 1, 71.1 +/- 20.9 meq/l; day 8, 72.6 +/- 21.6 meq/l, NS). Before and after acclimation, exercise-heat sessions resulted in significant decreases in serum [Cl-] in CF patients (104.5 +/- 4.6 to 101.3 +/- 4.4 meq/l on day 1, P less than 0.05; 103.5 +/- 5.1 to 99.7 +/- 4.2 meq/l on day 8, P less than 0.025) but not in controls. Serum [Cl-] was significantly lower in CF than control subjects at every measurement. Both groups had significant renal Na+ conservation after exercise on both days.(ABSTRACT TRUNCATED AT 250 WORDS)

Oxygen saturation during exercise in cystic fibrosis.

Cystic fibrosis (CF) is often associated with low hemoglobin oxygen saturation and with limited exercise tolerance, yet published reports do not agree on the effect of exercise on oxygenation in CF. We studied oxygen saturation (SaO2) by ear oximetry in 91 patients with CF during progressive exercise to exhaustion. Only 13 of 91 patients changed SaO2 by 5% or more; of these, 4 patients increased SaO2 by 5% or more, whereas 9 decreased by 5% or more. Small changes in SaO2 did not relate to resting pulmonary function, but large decreases in SaO2 were much more likely to be found in patients with forced expiratory volume in one second (FEV1) less than 50% of VC than in those with better pulmonary function (desaturation of 5% or greater was found in only 1 of 62 patients with FEV1 greater than 50% of VC, but in 8 of 29 patients with FEV1 less than or equal to 50% VC). However, even in severely affected patients, modest increases or no change in saturation were more common than large decreases, and 17 of 29 patients with FEV1 less than 50% VC ended exercise with SaO2 greater than 90%, including 3 patients with initial SaO2 below 90%. No single resting pulmonary function test or combination of tests could predict oxygen changes with exercise. Most patients with CF tolerate even maximal exercise without significant desaturation, but patients with FEV1 less than 50% of VC should have supervised exercise testing with ear oximetry before undertaking an exercise program.