Maximal exercise response of paraplegic wheelchair road racers.

The maximal metabolic responses of 11 paraplegic wheelchair road racers were evaluated with 2 wheelchair exercise protocols: increasing speed and increasing resistance. The maximal heart rates, minute ventilations and oxygen uptakes were similar for the 2 tests, indicating that either protocol is suitable for maximal wheelchair dynamometer exercise tests for groups. The resulting data were then compared to published data on maximal arm exercise by athletic and non athletic paraplegics and ambulatory males of the same age group. The combined mean values for both exercise tests of maximal oxygen consumption rate (VO2max = 37.4 ml/kg/min), minute ventilation (VE = 109.4 l/min), respiratory exchange quotient (RQmax = 1.18) and heart rate (187 beats/min) are in the mid range of reported data on wheelchair athletes. The mean RQ and heart rate values were similar to those achieved by ambulatory individuals performing maximal exercise tests. The mean VO2max of 37.4 ml/kg/min in our subjects is comparable to that achieved by sedentary ambulatory males of this age group. The data and the comparison to published data suggest several conclusions: in some parameters elite male paraplegic road racers have maximal values similar to those of ambulatory males, and in others they have maximal values substantially lower than might be expected; there is considerable variability among paraplegics in the metabolic responses to maximal exercise, most likely related to differences in cardiovascular fitness; and paraplegics can improve their cardiovascular fitness by training.

Heat, cold, noise, and vibration.

Exposure to a cold environment induces a number of physiological alterations, the most serious being hypothermia. This state can occur in all individuals, but the very young and the elderly are more susceptible. Environmental and industrially generated high ambient temperature can place further stress on aged individuals and workers, resulting in a complex symptom picture. Morbidity and death may result from such exposures. Causative factors have been identified. Noise exposure induces hearing losses above those secondary to the aging process. Psychophysiological effects during noise exposure are considered to result from the sympathetic activity secondary to a general stress reaction. Vibration from the use of power tools results in Raynaud's phenomenon. However, modification of power tools has reduced the symptoms associated with vibration exposure. Termination of exposure to vibration appears eventually to reduce symptoms related to white-finger spasms. Interaction between these stressors has not been clarified because of the complex effects of each. The need for additional information about the response to these stressors is evident.

The "effective dose" concept in older adults exposed to ozone.

Previous research on young adults has indicated that the magnitude of pulmonary function decrements induced by exposure to ambient ozone (O3) is related to the effective dose of O3 inhaled. The effective dose is defined as the product of O3 concentration (in ppm), mean minute ventilation (VE) and duration of exposure (min). The relative contributions of the three components of effective dose to the development of pulmonary function decrements in older adults are unknown. Twelve healthy, nonsmoking men and women (60-79 years) participated in each of four experiments: (1) a 1-h continuous exercise protocol, and (2) a 2-h intermittent exercise protocol, each performed while exposed to filtered air (FA), and to 0.45 ppm O3, resulting in different effective doses of O3. Pulmonary function (forced vital capacity, FVC, functional residual capacity, FRC, and associated calculated parameters) was measured pre- and postexposure. Ozone exposure induced significant decrements in forced expiratory volume in 0.5, 1.0 and 3.0 seconds (FEV0.5, 1.0, 3.0), regardless of the exercise protocol. There were no changes in FVC with any exposure protocol. There were significant decrements in forced expiratory flow rate at 25% and 50% of FVC (FEF25%, FEF50%) and in forced expiratory flow rate between 25% and 75% of FVC (FEF25-75%) with all four exposures, suggesting a fatigue effect. There were no differences between the decrements induced in FEV1.0 by O3 exposure under the two exercise protocols. The mean exercise VE was 25.3 l/min for the continuous exercise protocol, and was 25.2 l/min for the three exercise periods of the intermittent exercise protocol.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhalation route effects on exposure to 2.0 parts per million sulfur dioxide in normal subjects.

A number of investigations have attributed the control of the nasal to oral/nasal ventilation transition to nasal resistance. To investigate possible changes in nasal resistance due to sulfur dioxide (SO2) exposure, 14 subjects (7 men and 7 women), healthy non-smokers, between the ages of 20 and 46 years, were exposed for 30 minutes to filtered air while free breathing and to 2.0 ppm SO2 with either free breathing, forced oral or forced nasal breathing with continuous exercise at a workload 300 kg.m/min below the workload which initiated cross-over from nasal to oral/nasal breathing in a preliminary incremental workload test. An incremental work test under the ambient conditions was performed immediately following the 30-minute exercise to ascertain any change in the cross-over ventilation. Pre- and post-measures of pulmonary functions were obtained to ascertain any changes in these parameters due to the exposure. There was a significant difference in the workload at which cross-over occurred following forced oral breathing in 2.0 ppm sulfur dioxide. The nasal ventilation prior to cross-over and the nasal component of ventilation were significantly smaller for this exposure condition, indicating a possible change in nasal dynamics following the 30 minutes of forced oral breathing in 2.0 ppm SO2. Lack of concomitant changes in pulmonary function tests including airway resistance suggests that breathing 2.0 ppm SO2 does not affect normal subjects whether administration is by free, forced oral or forced nasal breathing.

Alteration in carboxyhemoglobin concentrations during exposure to 9 ppm carbon monoxide for 8 hours at sea level and 2134 m altitude in a hypobaric chamber.

Seventeen non-smoking young men served as subjects to determine the alteration in carboxyhemoglobin (COHb) concentrations during exposure to 0 or 9 ppm carbon monoxide for 8 hours (CO) at sea level or an altitude of 2134 meters (7000 feet) in a hypobaric chamber. Nine subjects rested during the exposure and 8 exercised for 10 minutes of each exposure hour at a mean ventilation of 25 L (BTPS). All subjects performed a maximal aerobic capacity test at the completion of their respective exposures. Carboxyhemoglobin concentrations fell in all subjects during their exposures to 0 ppm CO at sea level or 2134 m. During the 8-h exposures to 9 ppm CO, COHb rose linearly from approximately 0.2 percent to 0.7 percent. No significant differences in uptake were found whether the subjects were resting or intermittently exercising during their 8-h exposures. COHb levels attained were similar at both sea level and 2134 m. Maximal aerobic capacity was reduced approximately 7-10 percent consequent to altitude exposure during 0 ppm CO exposures. These values were not altered following exposure for 8 h to 9 ppm CO in either the resting or exercising subjects.

Pulmonary function responses of young and older adults to mixtures of O3, NO2 and PAN.

The pulmonary function of 32 nonsmokers (eight men and eight women, 18-26 years of age; eight men and eight women, 51-76 years of age) was measured before and after two-hour exposures to (1) filtered air (FA), (2) 0.45 ppm ozone (O3), (3) 0.13 ppm peroxyacetyl nitrate + 0.45 ppm O3 (PAN/O3), (4) 0.60 ppm nitrogen dioxide + 0.45 ppm O3 (NO2/O3), and (5) 0.13 ppm PAN + 0.60 ppm NO2 + 0.45 ppm O3 (PAN/NO2/O3). Subjects alternated 20-minute periods of rest and exercise (ventilation = 25 L/min). Forced vital capacity (FVC) was measured pre-exposure and five-minutes after each exercise period. Forced expiratory volume in one sec (FEV1.0) and forced expiratory flow between 25 and 75 percent of FVC (FEF25-75%) were calculated from the FVC tests. Data were analyzed by 4-factor analysis of variance (sex, age, time period, exposure). The responses of men and women were similar. FA exposure induced no effects. The young subjects' decrements in FVC, FEV1.0 and FEF25-75% became significant (P less than 0.01) after the second exercise period of the O3, NO2/O3 and PAN/NO2/O3 exposures, while the PAN/O3 decrements were significant (P less than 0.01) after the first exercise period. Although PAN/O3 induced significant decrements earlier than the other conditions including O3, the mean pre- to post-exposure decrements for the four conditions including O3 were similar. In contrast, the older subjects had smaller and fewer significant decrements in pulmonary functions. They had significant mean decrements in FVC following the third exercise period of the NO2/O3 and PAN/NO2/O3 exposures, in FEV1.0 after the third exercise period of the PAN/O3 and NO2/O3 exposures, and in FEF 25-75% beginning after the second exercise period of the NO2/O3 exposure. The results suggest that older men and women are less responsive to O3 and mixtures of O3, NO2 and PAN than young men and women, and that O3 is responsible for the decrements observed in pulmonary function.

Adaptation by older individuals repeatedly exposed to 0.45 parts per million ozone for two hours.

To test for an increased reaction to ozone (O3) in older individuals following an initial exposure, and to test for adaptation and its duration, we exposed 10 men and 6 women (60-89 years old) in an environmental chamber to filtered air and 3 consecutive days of O3 exposure (0.45 ppm), followed by a fourth O3 exposure day after a two day hiatus. Subjects alternated 20-min exercise (minute ventilation = 27 L) and rest periods for 2 hours during each exposure. Subjects rated from one to five, 16 possible respiratory/exercise symptoms prior to and following the exposure. Pulmonary function tests were performed before, and during each rest period and following the exposure. Metabolic measurements were obtained during each exercise period. No significant changes in any symptom question occurred, in spite of a threefold increase in the total number of reported symptoms during O3 exposure. Small but significant pre-to-post decrements on the first and second O3 days in forced vital capacity (FVC-111 and 104 mL), forced expiratory volume in 1 (FEV1-171 and 164 mL) and 3 seconds (FEV3-185 and 172 mL) occurred without concomitant changes in any flow parameter of the forced expiratory maneuver. No differences in the group mean response in FVC, FEV1 or FEV3 on the third or fourth day of O3 exposure and the filtered air exposure were found. The observed changes were due to significant physiological changes in eight of the subjects. Unlike young subjects, no evidence of an increased pulmonary function response to a second consecutive O3 exposure was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Maximal aerobic capacity at several ambient concentrations of carbon monoxide at several altitudes.

In order to assess the combined effects of altitude and acute carbon monoxide exposure, 11 male and 12 female subjects, nonsmokers in good health, were given incremental (two minutes at each workload) maximal aerobic capacity tests at four levels of ambient carbon monoxide (0, 50, 100, and 150 parts per million) at four altitudes (55, 1,524, 2,134, and 3,048 m). Five male and four female subjects completed all 16 experiments. The remaining subjects completed either eight or 12 experiments; at least eight male and eight female subjects were tested at each combination of carbon monoxide and altitude. Test conditions were double-blind. Subjects initially were screened with a medical history questionnaire, a 12-lead electrocardiogram, pulmonary function tests, anthropometric and body fat measurements, blood volume determinations, and a maximal aerobic capacity test. Each subject, after attaining the required altitude and ambient carbon monoxide level, performed the maximal aerobic capacity test (maximum VO2) meeting required conditions to assure that a maximal level was attained. Blood samples were drawn prior to the aerobic capacity test; at workloads of 50 watts, 100 watts, 150 watts, and maximum; at the fifth minute of recovery; and prior to repressurization to sea level. Blood was analyzed for hemoglobin, hematocrit, plasma proteins, lactates, and carboxyhemoglobin. Carbon-monoxide-carboxyhemoglobin uptake rates were derived from the submaximal workloads. Maximum VO2 was similar at 55 m and 1,524 m, and decreased from the 55-m value by 4 percent at 2,134 m and by 8 percent at 3,048 m. Despite increases in carboxyhemoglobin, no additional significant decreases in maximal aerobic capacity were observed. With increasing carbon monoxide, a decrease in maximum VO2 independent of altitude was observed. Carboxyhemoglobin concentrations at maximum VO2 were highest at 55 m and lowest at 3,048 m. Carboxyhemoglobin concentrations were lower in female subjects than in male subjects. Immediately prior to and at maximal workloads, carbon monoxide shifted into extravascular spaces and returned to the vascular space within five minutes after exercise stopped. We demonstrated that altitude hypoxia and carbon monoxide hypoxia act independently on the parameters of the maximal aerobic capacity test. We also demonstrated a decrease in the carbon monoxide concentration to carboxyhemoglobin as altitude increased, which can be attributed to the decrease in driving pressure of carbon monoxide at altitude.

Maximal aerobic capacity at several ambient concentrations of CO at several altitudes.

To assess the nature of the combined effect of the hypoxias of altitude (ALT) and CO exposure, 11 men and 12 women nonsmokers served as subjects in a double-blind experiment. The exposure conditions were four ambient CO levels (0, 50, 100, and 150 ppm) at each of four ALT (55, 1,524, 2,134, and 3,048 m). Each subject, after attaining the required ALT and ambient CO level, performed a maximal aerobic capacity test (VO2max). Blood samples were obtained before, at 50-W, 100-W, 150-W, and maximum work loads and at the 5th min of recovery. Blood were analyzed for hemoglobin, hematocrit, plasma proteins, lactates, and carboxyhemoglobin (HbCO). VO2max was similar at 55 and 1,524 m and decreased by 4 and 8% from the 55-m value at 2,134 and 3,048 m, respectively. On the basis of all statistical analyses, we concluded that VO2max values measured in men were only slightly diminished due to increased ambient CO. HbCO attained at maximum was highest at 55 m and lowest at 3,048 m. Women's HbCO concentrations were lower than men's. At maximal work loads CO shifted into extravascular spaces and returned to the vascular space within 5 min after exercise stopped. The independence of altitude and CO hypoxias on parameters of the maximum aerobic capacity test and a decrease in the CO to HbCO uptake with increasing altitude were demonstrated and attributed in part to the decrease in driving pressure of CO at altitude.

Enhancement of exercise performance with inhaled albuterol.

The use of bronchodilators in athletic competition has allowed asthmatics to participate successfully in competitive events. Little information exists regarding possible bronchodilator use by non-asthmatic competitive athletes. Fifteen non-asthmatic cyclists participated in a double-blind, randomized, cross-over protocol involving a simulated race, i.e., one-hour heavy continuous exercise (minute ventilation (VE) 81 L/min BTPS) followed by maximal effort workload to exhaustion, with/without prior inhalation of albuterol to see if their exercise performance would be acutely altered. Each study day metabolic parameters were obtained four times. Pulmonary function tests were performed prior to and after the inhalant (albuterol/placebo) and following exercise. There was a significant increase in forced expiratory flow parameters following albuterol. Although not significant, oxygen uptake (VO2) and VE were smaller during the one-hour submaximal test following albuterol and VO2max and VEmax were higher. There was an increased ride time (196 vs. 159 s; p less than 0.05). Albuterol may provide a competitive advantage for non-asthmatic athletes who might use it.

Inhaled albuterol does not protect against ozone toxicity in nonasthmatic athletes.

We evaluated the acute prophylactic efficacy of albuterol aerosol in protecting nonasthmatic athletes from the untoward effects of 0.21 ppm ozone (O3) on symptoms, pulmonary function, exercise performance, and post-exposure histamine bronchoprovocation. Fifteen trained competitive cyclists participated in a randomized crossover study consisting of double-blinded inhalations of albuterol (180 micrograms) and placebo approximately 30 min prior to heavy continuous exercise (minute ventilation, [VE] greater than or equal to 80 L/min) for 60 min, followed by a maximal sprint (peak VE greater than 140 L/min) until exhaustion. Each subject was exposed randomly to either 0.21 ppm O3 or filtered air (FA) during the four single-blinded exposure sessions. Albuterol pretreatment resulted in modest but significant bronchodilation as compared to placebo. However, albuterol did not prevent O3-induced respiratory symptoms, decrements in forced vital capacity (FVC), forced expired volume in one second (FEV1.0), and maximum midexpiratory flow rate (FEF25-75%), and positive histamine challenges as compared to that with placebo/O3. There were no statistically significant differences in the metabolic data or ride times across all drugs and exposures, although the peak VE was significantly lower with O3 than FA (142.3 vs. 150.7 L/min, respectively) regardless of drug. The results indicate that acute pretreatment with inhaled albuterol is unable to prevent or ameliorate O3-induced symptoms and alterations in pulmonary function and exercise performance. The contribution of beta-adrenergic mechanisms in the acute airway responses to O3 appears to be minimal.

Pulmonary function responses of older men and women to NO2.

The pulmonary function of eight men and eight women (51 to 76 years of age), all non-smokers, was measured before and after 2-hr exposures to filtered air (FA) and 0.60 ppm nitrogen dioxide (NO2). The subjects alternated 20-min periods of rest and 20-min periods of cycle ergometer exercise at a work load predetermined to elicit a ventilatory minute volume (VE) of approximately 25 liter/min. Functional residual capacity was determined pre- and postexposure. Forced vital capacity was determined preexposure and 5 min after each exercise period. VE was measured during the last 2 min of each exercise period, and heart rate was monitored throughout each exposure. The pulmonary function data were evaluated as the percentage change from pre- to postexposure to partially remove the effect of differences between men and women in absolute lung volume. There were no statistically significant (P greater than 0.05) differences between the responses of men and women to FA or NO2 exposure. There were no significant (P greater than 0.05) changes in any variable consequent to FA or NO2 exposure. Our older subjects had responses to NO2 exposure similar to those of young adults, suggesting that, at least for healthy people, exposure to 0.60 ppm NO2 has little effect.

Combined effect of ozone and sulfuric acid on pulmonary function in man.

A potential effect of the combination of ozone and sulfuric acid mist (H2SO4) on respiratory function has been postulated for humans simultaneously exposed to these two pollutants. Nine young men were exposed to 0.25 ppm ozone (O3), 1200-1600 micrograms/m3 sulfuric acid aerosol (H2SO4), and a combination of O3 and H2SO4. During the 2-hr exposures, the subjects exercised (ventilation = 30 L/min) three times for 20 min each. Air temperature was 35 degrees C and relative humidity 83%. Pulmonary function changes after exposure to ozone alone were not expected and were not demonstrated. If a reaction between the combination of O3 and H2SO4 and pulmonary function occurred, pulmonary function responses may have been anticipated following the combination exposure, but no significant changes were seen. It was concluded that the combination of ozone and sulfuric acid aerosol at levels in excess of Threshold Limit Values (TLV) levels do not cause pulmonary dysfunction.

Pulmonary function responses of older men and women to ozone exposure.

The pulmonary function of 8 men and 8 women (51 to 76 years of age), all nonsmokers, was measured before and after 2-h exposures to filtered air (FA) and 0.45 ppm ozone (O3). The subjects alternated 20-min periods of rest and 20-min periods of cycle ergometer exercise at a workload predetermined to elicit a ventilatory minute ventilation (VE) of approximately 25 L/min (BTPS). Functional residual capacity (FRC) was determined pre- and post-exposure. Forced vital capacity (FVC) was determined before and after exposure, and 5 min after each exercise period. Ventilatory minute volume (VE) was measured during the last 2 min of each exercise period, and heart rate was monitored throughout each exposure. The pulmonary function data were evaluated as the percentage change from pre- to post-exposure to partially remove the effect of differences between men and women in absolute lung volume. There were no statistically significant (p greater than 0.05) differences between the responses of men and women to FA or O3 exposure. There were no significant (p greater than 0.05) changes in any variable consequent to FA exposure. Exposure to O3 induced significant (p less than 0.01) decrements in FVC, FEV1.0, and FEV3.0 at post-exposure compared to pre-exposure. Ozone exposure induced no significant (p greater than 0.05) effect on FEF25-75% or FEF75%. Men had a significantly (p less than 0.05) higher mean exercise VE than women (27.9 +/- 0.29 L vs. 25.4 +/- 0.8 L; mean +/- SD). Since the men and women had similar decrements in pulmonary function, even though the women inhaled less O3, the data suggest that women may be somewhat more responsive to O3 than men. We also compared the responses of our older subjects with those of young men and women that we studied with the same protocol, and with published results of other investigators who have studied young men and women. This comparison suggests that older individuals may be less responsive to O3 than young individuals.

Duration of increased pulmonary function sensitivity to an initial ozone exposure.

The metabolic and pulmonary function effects were investigated in six non-smoking young adults who were exposed for 2 hours (22 degrees C WBGT) to: filtered air (FA) 0.45 ppm ozone (DAY1); and two days later to a second exposure to 0.45 ppm ozone (DAY2). The subjects alternated 20-minute periods of rest and 20-minute periods of bicycle ergometer exercise at a workload predetermined to elicit a ventilatory minute volume (VE) of 27 L/min (BTPS). Functional residual capacity (FRC) was determined pre- and post-exposure. Forced vital capacity (FVC) was determined before and after exposure, as well as 5 minutes after each exercise period. Heart rate was monitored throughout the exposure, and VE, oxygen uptake (VO2), respiratory rate (fR), and tidal volume (VT) were measured during the last 2 minutes of each exercise period. There were no changes in any variable consequent to FA exposure. Both ozone exposures induced significant (P less than 0.05) decrements in FVC; FEV1.0 (forced expiratory volume in 1 second); FEV3.0 (forced expiratory volume in 3 seconds); FEF25-75% (average flow rate between 25% and 75% of FVC); and total lung capacity (TLC). The decrements following the DAY2 ozone exposure were significantly greater than following DAY1, and averaged 7.2 percentage points greater than those following the DAY1 exposure.

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.