Ozone inhalation effects consequent to continuous exercise in females: comparison to males

Exposure to ozone (O3) at ambient photochemical smog alert levels has been shown to cause alteration in pulmonary function and exercise response in humans, but there is a paucity of data on females. The initial purpose of the present investigation was to study the effects of O3 inhalation on pulmonary function and selected exercise respiratory metabolism and breathing pattern responses in young adult females. Six female subjects exercised continuously on a bicycle ergometer for 1 h on 10 occasions at one of three intensities, while exposed to 0.0, 0.20, 0.30, or 0.40 ppm O3. Forced expiratory volume and flow rates and residual volume (RV) were measured before and immediately following each protocol. During exercise, expired minute ventilation (VE), respiratory frequency (fR), tidal volume, O2 uptake (VO2), and heart rate (HR) were measured every 10 min. O3 dose-dependent decrements were observed for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1.0), and forced expiratory flow rate during the middle half of FVC, coupled with an increase in RV and altered exercise ventilatory pattern. There was also an increased VE but no significant O3 effect on VO2 or HR. Comparison of the females' responses to those of a group of young adult males (previously studied) at the same total O3 effective dose (i.e., expressed as the simple product of O3 concentration, VE, and exposure time) revealed significantly greater effects on FVC, FEV1.0, and fR for the females. With VE reduced for females as a function of exercise intensity at the same percent of maximum VO2, these differences were considerably attenuated, although not negated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ozone inhalation effects in females varying widely in lung size: comparison with males

It has been suggested that lung size accounts for observed gender differences in responsiveness to the same total inhaled dose of O3. To test the hypothesis that lung size is a determinant of magnitude of response within a gender, two groups of 14 healthy young adult females differing significantly in forced vital capacity [FVC; i.e., small-lung group mean = 3.74 liters (range 3.2-4.0) and large-lung group mean = 5.11 liters (range 4.5-6.2] were exposed for 1 h to filtered air (FA) and to 0.18 and 0.30 ppm O3. On each occasion, subjects exercised continuously on a cycle ergometer at a work rate that elicited a mean minute ventilation of approximately 47 l/min. For the small-lung group [mean total lung capacity (TLC) = 4.52 liters] exercise O2 uptake was 67% of maximal O2 uptake (VO2max), and that for the large-lung group (TLC 6.37 liters) was 61% of VO2max. Statistical analysis revealed significant decrements for both groups in FVC, forced expiratory volume in 1 s (FEV1.0), and forced expiratory flow rate in the middle half of FVC on exposure to 0.18 and 0.30 ppm O3. Exercise respiratory frequency increased, and tidal volume decreased significantly in both groups in response to 0.18 and 0.30 ppm O3 exposure. On exposure to 0.30 ppm O3, the number of individual subjective symptoms reported and their severity were significantly greater for both groups than those reported for the FA and 0.18 ppm O3 exposures. Both groups evidenced similar percent changes in pulmonary function and exercise ventilation response, and in subjective symptom response.(ABSTRACT TRUNCATED AT 250 WORDS)     

O.35 ppm O3 exposure induces hyperresponsiveness on 24-h reexposure to 0.20 ppm O3

Pulmonary function hyperresponsiveness, defined as enhanced response on reexposure to O3, compared with initial O3 exposure, has been previously noted in consecutive day exposures to high ambient O3 concentrations (i.e., 0.32-0.42 ppm). Effects of consecutive-day exposure to lower O3 concentrations (0.20-0.25 ppm) have yielded equivocal results. To examine the occurrence of hyperresponsiveness at two levels of O3 exposure, 15 aerobically trained males completed seven 1-h exposures of continuous exercise at work rates eliciting a mean minute ventilation of 60 1/min. Three sets of consecutive-day exposures, involving day 1/day 2 exposures to 0.20/0.20 ppm O3, 0.35/0.20 ppm O3, and 0.35/0.35 ppm O3, were randomly delivered via an obligatory mouthpiece inhalation system. A filtered-air exposure was randomly placed 24 h before one of the three sets. Treatment effects were assessed by standard pulmonary function tests, exercise ventilatory pattern (i.e., respiratory frequency, f; and tidal volume, VT) changes and subjective symptom (SS) response. Initial O3 exposures to 0.35 and 0.20 ppm had a statistically significant effect, compared with filtered air, on all measurements. On reexposure to 0.35 ppm O3 24 h after an initial 0.35 ppm O3 exposure, significant hyperresponsiveness was demonstrated for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), f, VT, and total SS score. Exposure to 0.20 ppm O3 24 h after 0.35 ppm O3 exposure, however, resulted in significantly enhanced responses (compared with initial 0.20 ppm O3 exposure) only for FEV1, f, and VT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulmonary response to threshold levels of sulfur dioxide (1.0 ppm) and ozone (0.3 ppm)

We exposed 22 healthy adult nonsmoking male subjects for 2 h to filtered air, 1.0 ppm sulfur dioxide (SO2), 0.3 ppm ozone (O3), or the combination of 1.0 ppm SO2 + 0.3 ppm O3. We hypothesized that exposure to near-threshold concentrations of these pollutants would allow us to observe any interaction between the two pollutants that might have been masked by the more obvious response to the higher concentrations of O3 used in previous studies. Each subject alternated 30-min treadmill exercise with 10-min rest periods for the 2 h. The average exercise ventilation measured during the last 5 min of exercise was 38 1/min (BTPS). Forced expiratory maneuvers were performed before exposure and 5 min after each of the three exercise periods. Maximum voluntary ventilation, He dilution functional residual capacity, thoracic gas volume, and airway resistance were measured before and after the exposure. After O3 exposure alone, forced expiratory measurements (FVC, FEV1.0, and FEF25-75%) were significantly decreased. The combined exposure to SO2 + O3 produced similar but smaller decreases in these measures. There were small but significant differences between the O3 and the O3 + SO2 exposure for FVC, FEV1.0, FEV2.0, FEV3.0, and FEF25-75% at the end of the 2-h exposure. We conclude that, with these pollutant concentrations, there is no additive or synergistic effect of the two pollutants on pulmonary function.     

Effects of NO2 alone and in combination with O3 on young men and women

Previous studies of 2 h of exposure to NO2 at high urban atmospheric levels (i.e., 0.50-1.0 ppm), utilizing light-to-moderate exercise for up to 1 h have failed to demonstrate significant pulmonary dysfunction in healthy humans. To test the hypothesis that heavy sustained exercise would elicit pulmonary dysfunction on exposure to 0.60 ppm NO2 and/or enhance the effects of exposure to 0.30 ppm O3, 40 aerobically trained young adults (20 males and 20 females) completed 1 h of continuous exercise at work rates eliciting a mean minute ventilation of 70 and 50 l/min for the males and females, respectively. Exposures to filtered air, 0.60 ppm NO2, 0.30 ppm O3, and 0.60 ppm NO2 plus 0.30 ppm O3 were randomly delivered via an obligatory mouthpiece inhalation system. Treatment effects were assessed by standard pulmonary function tests and exercise ventilatory and subjective symptoms response. Two-way analysis of variance with repeated measures and post hoc analyses revealed a statistically significant (P less than 0.05) effect of O3 on forced expiratory parameters, specific airway resistance, exercise ventilatory response, and reported subjective symptoms of respiratory discomfort. In contrast, no significant effect of NO2 was observed nor was there any significant interaction of NO2 and O3 in combination. There were no significant differences between male and female responses to gas mixture treatments. It was concluded that inhalation of 0.60 ppm NO2 for 1 h while engaged in heavy sustained exercise does not elicit effects evidenced by measurement techniques used in this study nor evoke additive effects beyond those induced by 0.30 ppm O3 in healthy young adults.     

Dynamic BTPS correction factors for spirometric data

Because it is often difficult to completely control ambient temperature, a study was conducted to investigate dynamic body temperature pressure saturated (BTPS) correction factors for spirometric data. A forced expiratory simulator system was heated to 37 degrees C and loaded with air saturated with water vapor. This air was then forced from the simulator into a dry rolling-seal spirometer maintained at various ambient temperatures from 3 to 32 degrees C. Errors in forced expiratory volume in 1 s (FEV1) and peak flow from assuming a constant BTPS correction ranged from 7.7 and 14.1% at 3 degrees C to 2.1 and 4.6% at 23 degrees C. Differences between errors observed when saturated and dry air were forced into the spirometer indicate that water vapor condensation introduces an added heat load to the spirometer, adding approximately one percent to the error in FEV1 at lower temperatures. By use of a model to estimate the dynamic BTPS correction factor, errors in FEV1 at all temperatures between 3 and 32 degrees C were reduced to less than 1.5%.     

Bronchial reactivity of healthy subjects: 18-20 h postexposure to ozone.

Exposure of humans to ambient levels of ozone (O(3)) causes inflammatory changes within lung tissues. These changes have been reported for the "initial" (1- to 3-h) and "late" (18- to 20-h) postexposure periods. We hypothesized that at the late period, when protein and cellular markers of inflammation at the airway surface remain abnormal and the integrity of the epithelial barrier is compromised, bronchial reactivity would be increased. To test this, we measured airway responsiveness to cumulative doses of methacholine (MCh) aerosol in healthy subjects 19+/-1 h after a single exposure to O(3) (130 min at ambient levels between 120 and 240 parts/billion and alternate periods of rest and moderate exercise) or filtered air. Exposures were conducted at two temperatures: mild (22 degrees C) and moderate (30 degrees C). At the late period, bronchial reactivity to MCh increased, i.e., interpolated dose of MCh leading to a 50% fall in specific airway conductance (PC(50)) was less after O(3) than after filtered air. PC(50) for O(3) at 22 degrees C was 27 mg/ml (20% less than the PC(50) after filtered air), and for O(3) at 30 degrees C it was 19 mg/ml (70% less than the PC(50) after filtered air). The forced expiratory volume in 1 s (FEV(1)) at the late time point after O(3) was slightly but significantly reduced (2.3%) from the preexposure level. There was no relationship found between the functional changes observed early after exposure to O(3) and subsequent changes in bronchial reactivity or FEV(1) at the late time point. These results suggest that bronchial reactivity is significantly altered approximately 1 day after O(3); this injury may contribute to the respiratory morbidity that is observed 1-2 days after an episode of ambient air pollution.     

Ozone-induced changes in pulmonary function and bronchial responsiveness in asthmatics

To compare the responses of asthmatic and normal subjects to high effective doses of ozone, nine asthmatic and nine normal subjects underwent two randomly assigned 2-h exposures to filtered, purified air and 0.4 ppm ozone with alternating 15-min periods of rest and exercise on a cycle ergometer (minute ventilation = 30 l.min-1.m-2). Before and after each exposure, pulmonary function and bronchial responsiveness to methacholine were measured and symptoms were recorded. Ozone exposure was associated with a statistically significant decrease in forced vital capacity (FVC), forced expired volume in 1 s (FEV1), percent FEV1 (FEV1%), and forced expired flow at 25-75% FVC (FEF25-75) in both normal and asthmatic subjects. However, comparing the response of asthmatic and normal subjects to ozone revealed a significantly greater percent decrease in FEV1, FEV1%, and FEF25-75 in the asthmatic subjects. The effect of ozone on FVC and symptom scores did not differ between the two groups. In both normal and asthmatic subjects, exposure to ozone was accompanied by a significant increase in bronchial responsiveness. We conclude that exposure to a high effective ozone dose produces 1) increased bronchial responsiveness in both normal and asthmatic subjects, 2) greater airways obstruction in asthmatic than in normal subjects, and 3) similar symptoms and changes in lung volumes in the two groups.     

Pulmonary function in normal subjects following exercise at cold ambient temperatures

We measured pulmonary function in 12 healthy volunteers before and at 5-min intervals for 30 min following treadmill exercise of 30 min duration performed under control (20 degrees C) and cold (-11 degrees C) ambient temperatures. Post-run changes in forced vital capacity (FVC), residual volume (RV) and peak expiratory flow rate were similar between the two temperature conditions. FVC decreased slightly but significantly 5 min post-run (-0.25 +/- 0.20 l and -0.21 +/- 0.20 l, for control and cold conditions respectively) and returned to baseline by 30 min. RV increased significantly post-exercise (+0.07 +/- 0.09 l and +0.14 +/- 0.1 l, control and cold respectively) and remained elevated for 30 min. Forced expired volume in 1 s was not significantly different following either run. Post-exercise, maximum mid-expiratory flow rate and flows at 50% and 25% of vital capacity were not significantly different between warm and cold conditions. These data suggest that changes in lung volumes following exercise under cold ambient conditions are similar to changes seen following warm exercise of similar duration. In non-asthmatics, moderate exertion under cold ambient conditions does not appear to cause clinically significant decreases in expiratory flow rates as compared to similar exertion under warm conditions.     

Ozone and high ventilation effects on pulmonary function and endurance performance

Ozone (O3) toxicity is potentiated by exercise-induced expired minute ventilation (VE) for a given exposure, which may also impair endurance performance. Ten healthy, well-trained long-distance runners were exposed on six occasions for 1 h to O3 concentrations of 0, 0.20, or 0.35 parts per million (ppm), during exercise simulating either training or competition, with mean VE = 77.5 1 X min -1. Standard pulmonary function tests, subjective symptoms, and periodic observations of exercise ventilatory response and respiratory metabolism were obtained. Statistical analyses revealed no significant exercise mode effect for pulmonary function, but a significant O3 effect for forced vital capacity and expiratory volume at 1 s was observed. Altered exercise ventilatory pattern response was noted, but there was no significant O3 effect on exercise oxygen uptake, heart rate, VE, or alveolar ventilation. Subjective symptoms increased with O3 concentration. Statistically significant pulmonary function impairment observed at 0.20 ppm O3 suggests that endurance athletes may be more susceptible to the effects of a given O3 concentration than normal young adult males as a result of sustained high mean VE incurred during training and competition. Three subjects were unable to complete both the training and competitive simulations at 0.35 ppm O3. Performance decrements appeared to be the result of physiologically induced respiratory discomfort rather than decrements in pulmonary gas exchange and/or oxygen transport and delivery.     

Exercise-induced bronchoconstriction alters airway nitric oxide exchange in a pattern distinct from spirometry

Exhaled nitric oxide (NO) is altered in asthmatic subjects with exercise-induced bronchoconstriction (EIB). However, the physiological interpretation of exhaled NO is limited because of its dependence on exhalation flow and the inability to distinguish completely proximal (large airway) from peripheral (small airway and alveolar) contributions. We estimated flow-independent NO exchange parameters that partition exhaled NO into proximal and peripheral contributions at baseline, postexercise challenge, and postbronchodilator administration in steroid-naive mild-intermittent asthmatic subjects with EIB (24-43 yr old, n = 9) and healthy controls (20-31 yr old, n = 9). The mean +/- SD maximum airway wall flux and airway diffusing capacity were elevated and forced expiratory flow, midexpiratory phase (FEF(25-75)), forced expiratory volume in 1 s (FEV(1)), and FEV(1)/forced vital capacity (FVC) were reduced at baseline in subjects with EIB compared with healthy controls, whereas the steady-state alveolar concentration of NO and FVC were not different. Compared with the response of healthy controls, exercise challenge significantly reduced FEV(1) (-23 +/- 15%), FEF(25-75) (-37 +/- 18%), FVC (-12 +/- 12%), FEV(1)/FVC (-13 +/- 8%), and maximum airway wall flux (-35 +/- 11%) relative to baseline in subjects with EIB, whereas bronchodilator administration only increased FEV(1) (+20 +/- 21%), FEF(25-75) (+56 +/- 41%), and FEV(1)/FVC (+13 +/- 9%). We conclude that mild-intermittent steroid-naive asthmatic subjects with EIB have altered airway NO exchange dynamics at baseline and after exercise challenge but that these changes occur by distinct mechanisms and are not correlated with alterations in spirometry.     

Effect of mild-to-moderate airflow limitation on exercise capacity

To determine the effect of mild-to-moderate airflow limitation on exercise tolerance and end-expiratory lung volume (EELV), we studied 9 control subjects with normal pulmonary function [forced expired volume in 1 s (FEV1) 105% pred; % of forced vital capacity expired in 1 s (FEV1/FVC%) 81] and 12 patients with mild-to-moderate airflow limitation (FEV1 72% pred; FEV1/FVC % 58) during progressive cycle ergometry. Maximal exercise capacity was reduced in patients [69% of pred maximal O2 uptake (VO2max)] compared with controls (104% pred VO2max, P less than 0.01); however, maximal expired minute ventilation-to-maximum voluntary ventilation ratio and maximal heart rate were not significantly different between controls and patients. Overall, there was a close relationship between VO2max and FEV1 (r2 = 0.62). Resting EELV was similar between controls and patients [53% of total lung capacity (TLC)], but at maximal exercise the controls decreased EELV to 45% of TLC (P less than 0.01), whereas the patients increased EELV to 58% of TLC (P less than 0.05). Overall, EELV was significantly correlated to both VO2max (r = -0.71, P less than 0.001) and FEV1 (r = -0.68, P less than 0.001). This relationship suggests a ventilatory influence on exercise capacity; however, the increased EELV and associated pleural pressures could influence cardiovascular function during exercise. We suggest that the increase in EELV should be considered a response reflective of the effect of airflow limitation on the ventilatory response to exercise.     

Respiratory mechanics in men following a deep air dive

The mechanical properties of the lungs were measured in 10 men before and after a simulated air dive to 285 ft of seawater (87 m). The objective was to determine whether a dive likely to produce pulmonary bubble emboli would alter lung mechanics. Lung function was measured predive and at 1, 2, 3, 6, 7, and 23 h postdive. Measurements of lung function were also made at identical times on a control day when no dive was made. Each set of measurements included precordial Doppler signals, pulmonary resistance, quasistatic lung compliance, forced vital capacity (FVC), forced expired volume after 1.0 s (FEV 1.0), the ratio of FEV 1.0 to FVC (FEV 1.0/FVC%), and maximal airflow after 50 and 75% of the vital capacity had been expired (Vmax50 and Vmax75, respectively). Base-line measurements of pulmonary resistance and quasistatic compliance were normal in all subjects. FVC and FEV 1.0 were greater than predicted for most subjects and were increased proportionately so that the FEV 1.0/FVC% was normal. Following the dive, bubble signals were heard in four subjects, and two subjects had mild symptoms of decompression sickness. No subject demonstrated any alteration in lung function that could be attributed to the dive. We concluded that stressful decompressions capable of producing "silent" pulmonary bubble emboli do not alter lung mechanics.     

Role of the parasympathetic nervous system in acute lung response to ozone

We conducted an ozone (O3) exposure study using atropine, a muscarinic receptor blocker, to determine the role of the parasympathetic nervous system in the acute response to O3. Eight normal subjects with predetermined O3 responsiveness were randomly assigned an order for four experimental exposures. For each exposure a subject inhaled either buffered saline or atropine aerosol followed by exposure either to clean air or 0.4 ppm O3. Measurements of lung mechanics, ventilatory response to exercise, and symptoms were obtained before and after exposure. O3 exposure alone resulted in significant changes in specific airway resistance, forced vital capacity (FVC), forced expiratory flow rates, tidal volume (VT), and respiratory rate (f). Atropine pretreatment prevented the significant increase in airway resistance with O3 exposure and partially blocked the decrease in forced expiratory flow rates but did not prevent a significant fall in FVC, changes in f and VT, or the frequency of reported respiratory symptoms after O3. These results suggest that the increase in pulmonary resistance during O3 exposure is mediated by a parasympathetic mechanism and that changes in other measured variables are mediated, at least partially, by mechanisms not dependent on muscarinic cholinergic receptors of the parasympathetic nervous system.     

Thermoregulatory and aerobic changes after endurance training in a hypobaric hypoxic and warm environment.

Plasma volume (PV) expansion by endurance training and/or heat acclimatization is known to increase aerobic and thermoregulatory capacities in humans. Also, higher erythrocyte volume (EV) fractions in blood are known to improve these capacities. We tested the hypothesis that training in a hypobaric hypoxic and warm environment would increase peak aerobic power (VO(2)(peak)) and forearm skin vascular conductance (FVC) response to increased esophageal temperature (T(es)) more than training in either environment alone, by increasing both PV and EV. Twenty men were divided into four training regimens (n = 5 each): low-altitude cool (610-m altitude, 20 degrees C ambient temperature, 50% relative humidity), high-altitude cool (2,000 m, 20 degrees C), low-altitude warm (610 m, 30 degrees C), and high-altitude warm (HW; 2,000 m, 30 degrees C). They exercised on a cycle ergometer at 60% VO(2)(peak) for 1 h/day for 10 days in a climate chamber. After training, PV increased in all trials, but EV increased in only high-altitude trials (both P < 0.05). VO(2)(peak) increased in all trials (P < 0.05) but without any significant differences among trials. FVC response to increased T(es) was measured during exercise at 60% of the pretraining VO(2)(peak) at 610 m and 30 degrees C. After the training, T(es) threshold for increasing FVC decreased in warm trials (P < 0.05) but not in cool trials and was significantly lower in HW than in cool trials (P < 0.05). The slope of FVC increase/T(es) increase increased in all trials (P < 0.05) except for high-altitude cool (P > 0.4) and was significantly higher in HW than in cool trials (P < 0.05). Thus, against our hypothesis, the VO(2)(peak) for HW did not increase more than in other trials. Moreover, slope of FVC increase/T(es) increase in HW increased most, despite the similar increase in blood volume, suggesting that factors other than blood volume were involved in the highest FVC response in HW.     

Effect of hypercapnia on thermoregulation at high ambient temperature

The reported investigations were carried out on rabbits exposed for three hours to ambient temperature of 25 degrees C or 35 degrees breathing athmospheric air (controls) or gas mixtures containing 4% or 7% of CO2. During the exposure to 35 degrees C in rabbits breathing the gas mixture with 7% of CO2 the rise of rectal temperature was significantly greater, heat elimination from the auricular surface was increased, whereas the oxygen uptake was increased insignificantly. In tracheostomized rabbits breathing the gas mixture with 7% of CO2 at 32 degrees C the respiratory rate decreased but the respiration volume increased as compared with the animals breathing atmospheric air. It seems that the hyperthermic effect of hypercapnia demonstrated in this work can be attributed to the impairment of heat elimination through the upper airways due to an inhibition of thermal panting.     

Temperature regulation in adult quail (Colinus virginianus) during acute thermal stress

1. Evaporative heat loss, O2 consumption, CO2 production, and internal body temperature were measured in unanesthetized, unrestrained bobwhite (Colinus virginianus) at specific ambient temperatures (Ta). 2. No significant change in body temperature occurred at any Ta tested, but metabolic heat production (H) increased from 42.17 W/m2 at Ta 35 degrees C to 102.89 W/m2 at Ta 10 degrees C. 3. Evaporative heat loss (E) increased approximately two-fold from Ta 10-35 degrees C, with E/H increasing exponentially over the same temperature range. 4. No significant change in thermal insulation occurred from Ta 10-30 degrees C. 5. Combined convective and radiative heat transfer for the bobwhite was 2.96 W/m2 X C from Ta 10-35 degrees C.     

Effects of exercise detraining and deacclimation to the heat on plasma volume dynamics

The effects of the discontinuation (DET) of an endurance training/heat acclimation (T/A) program on vascular volumes were studied in 16 adult males. Resting and exercise blood volume dynamics were examined prior to and during an exercise task performed after completion of T/A (CT1) and again at the end of DET (CT2). T/A consisted of cycling at 60% of peak VO2 for 90 min per day, 6 days per week, for 4 weeks. Ambient temperature was 20 degrees C for the first 3 weeks and 40 degrees C for the last week (rh = 30-35%). Subjects were randomly assigned to one of the following DET conditions: 1) cycling one day per week at 40 degrees C, 2) cycling one day per week at 20 degrees C, 3) resting one day per week at 40 degrees C, 4) control. The exercise tasks consisted of 60 min of continuous cycle ergometer exercise at 50% of peak VO2 (Ta = 30 degrees C, rh = 35%). Although significant differences were found between CT1 and CT2, there were no interactions between the various DET conditions. Resting red cell volume decreased 98 ml and plasma volume decreased 248 ml following DET. A reduction in plasma protein content accounted for 97% of the decrease in plasma volume. Hemoconcentration occurred during exercise in both CT1 and CT2, while there were slight increases in plasma [Na+] and [Cl-] and a rapid rise in [K+]. It appears that a single exercise and/or heat exposure per week was not different from complete cessation of endurance exercise in the heat with regard to maintenance of the various vascular volumes.     

Exercise responses following ozone exposure.

We have tested the response of 28 subjects to a three-stage ergometer test, with loads adjusted to 45, 60, and 75% of maximum aerobic power following ozone exposure. The subjects were exposed to one of 0.37, 0.50, or 0.75 ppm O3 for 2 h either at rest (R) or while exercising intermittently (IE) (15 min rest alternated with 15 min exercise at approximately 50 W. sufficient to increase VE by a factor of 2.5). Also, all subjects completed a mock exposure VE, respiratory frequency (fR), mixed expired PO2 and PCO2, and electrocardiogram were monitored continuously during the exercise test. Neither submaximal exercise oxygen consumption nor minute ventilation was significantly altered following any level of ozone exposure. The major response noted was an increase in respiratory frequency during exercise following ozone exposure. The increase in fR was closely correlated with the total dose of ozone (r = 0.98) and was accompanied by a decrease in tidal volume (r = 0.91) so that minute volume was unchanged. It is concluded that through its irritant properties, ozone modifies the normal ventilatory response to exercise, and that this effect is dose dependent.