Adult athletes have a higher prevalence (11%-50%) of exercise-induced bronchoconstriction (EIB) and airways hyperresponsiveness (AHR) than the population at large (7%-11%): reports describing EIB/AHR in adolescent athletes are scant. Hypotheses: 1) a minimum AHR prevalence of 20% would be revealed in a group of high school athletes; 2) demographic data would predict AHR; 3) AHR-positive athletes would preferentially choose low ventilation sports. Eucapnic voluntary hyperpnea (EVH) was used to test for AHR in 23% of all athletes (79 of 343) of a midwestern high school. The AHR was defined by at least a 10%, 20%, or 25% decline in FEV1, FEF25-75, or PEFR at 1, 5, 10, or 15-min post-EVH, respectively. Results: 30 of 79 (38%) tested positive for AHR; demographic data tended to predict AHR, as correlations between the total number of years exercised with the greatest decline in FEV1 and the total number of days exercised with the greatest decline in FEV1 following the EVH challenge tended to be significant (r=0.354; p=0.055 and r=0.314; p=0.091, respectively); and 69% of AHR-positive students played only low ventilation sports. Conclusion: AHR prevalence was 38% in athletes of a midwestern high school; demographic data tended to predict AHR; those with AHR preferentially play low ventilation sports.

Athletes have a high prevalence (11-50%) of exercise-induced asthma, which may be caused by the hyperventilation accompanying repetitive bouts of strenuous exercise. We hypothesized that recreational exercisers would display a similar trend. Eucapnic voluntary hyperventilation (EVH) bronchoprovocation (breathing 21% O2, 5% CO2, and 74% N2 at 60% of MVV for 5 minutes) was performed to determine the prevalence of airways hyperresponsiveness (AHR) in adults (n=212, 146 males, mean +/- standard deviation, age 32 +/- 10 years) who exercised regularly (10 +/- 10 years, 31 +/- 28% of their lives): none had a previous diagnosis of asthma. AHR was defined by at least a 10%, 20%, or 25% decline in FEV1, FEF(25-75), or PEFR, respectively, by spirometry at 1, 5, 10, and 15 minutes post-EVH. Forty-one of 212 (19%) tested positive for AHR: 20 of 41 (49%) were positive by FEV1, 28 of 41 (68%) by FEF(25-75), and 27 of 41 (66%) by PEFR. Comparing responders with nonresponders: pre-EVH lung function was equivalent, except for FEV1, which was reduced (p<0.05) in responders (96 +/- 13 vs. 102 +/- 12% predicted). Mean maximal negative deflections for responders were: for FEV1, -17 +/- 7%; FEF(25-75), -31 +/- 10%; PEFR, -38 +/- 11%. Ranges of decline for responders were: FEV1, -10 to -33%; FEF(25-75), -20 to -59%; PEFR, -25- to -70%. We conclude that in these regular exercisers, the prevalence of AHR is high and comparable with some athletic populations.

OBJECTIVES Studies documenting the increased incidence of exercise-induced bronchospasm (EIB) in figure skaters have employed a method that incorporates on-ice exercise with rink-side spirometry. The literature suggests that bronchial provocation challenge testing is better than exercise testing for identifying EIB. To test this hypothesis in figure skaters, a unique athletic population that trains and competes in cold air, we compared these two methods in the same individuals. PATIENTS/METHODS Two challenge tests were performed on a group of competitive figure skaters (n = 29, 26 female subjects; mean+/-SD age = 12.3+/-3.5 years): (1) rink-side (temperature = 14 degrees C, humidity = 60%) spirometry before and 1, 5, 10, and 15 min after 5 min of intense skating; and (2) eucapnic voluntary hyperventilation (EVH), breathing 5% CO2, 21% O2, balance N2 at a rate of 60% of maximum voluntary ventilation (not to exceed 70 L/min) for 5 min (temperature = 18 degrees C, humidity = 50%), with an identical pretest and posttest spirometry schedule. EIB was defined as at least one of the following: a > or =10% decline in Fev1; a > or = 20% decline in maximum midexpiratory flow rate; or a > or = 25% decline in peak expiratory flow rate. RESULTS Sixteen of 29 skaters (55%) developed EIB: 9 were positive by on-ice testing; 12 were positive by EVH testing; 5 were positive on both tests; on-ice testing missed 7 skaters with EIB; EVH testing missed 4 with EIB. CONCLUSION In the group of figure skaters studied, EVH challenge testing was better at identifying EIB than on-ice exercise testing. However, these data suggest that evaluation for EIB in athletes who train and compete in the cold should include exercise testing in cold air along with a challenge test such as EVH to increase the yield of positive responders.

BACKGROUND AND OBJECTIVES Thirty to 50% of all COPD patients experience tissue wasting that may be caused by hypermetabolism, but the cause of the perturbed metabolic state is unclear. We hypothesized that the elevated O2 cost of ventilation (O2 COV) may be a contributing factor. All of the data are presented as means (+/-SEM). Ten hypoxemic (a PaO2 of 54+/-3 mm Hg) stable COPD patients (an FEV1/FVC ratio of 42+/-4%) and five healthy control subjects were studied. The patients were divided into two groups based on nutritional status. Group 1 (n = 6) was malnourished (a body mass index [BMI] of 17.6+/-0.7 kg/m2), and group 2 (n = 4) was normally nourished (a BMI of 26.0+/-3 kg/m2). The O2 COV was determined by measuring the change in the oxygen consumption (VO2) and the minute ventilation (VE) caused by CO2-induced hyperventilation. RESULTS AND CONCLUSIONS Group 1 had an elevated O2 COV when compared to group 2 and the control group, respectively: 16.4+/-1.0 vs 9.7+/-1.0 and 2.4+/-0.2 mL O2/L of VE (p < 0.05). The VO2 at rest was higher for group 1 than for group 2 and the control group, respectively: 4.5+/-0.3 vs 3.1+/-0.5 and 3.4+/-0.2 mL/kg/min (p < 0.05). The resting energy expenditure (REE) % predicted for group 1 was also higher than group 2 and the control group, respectively: 125+/-3% vs 87+/-7% and 97+/-2% (p < 0.05). Significant correlations were observed that implicate the increased O2 COV as a cause of tissue wasting: O2 COV vs BMI (r = -0.79; p = 0.007), O2 COV vs REE % predicted (r = 0.66; p = 0.039), and REE % predicted vs BMI (r = -0.83; p = 0.003). The O2 COV was also correlated with lung function: FEV1/FVC vs O2 COV (r = -0.84; p = 0.002). We conclude that in these COPD patients the O2 COV is associated with an increased metabolic rate which, in turn adversely affects the nutritional status.

BACKGROUND:Cardiopulmonary exercise testing (CPET) is a well recognized tool for the functional assessment of patients with cardiovascular and pulmonary disorders. The exercise response of asthmatics has been well characterized but the exercise response of patients with occupational asthma is less well understood. In this report we describe the clinical utility of CPET by characterizing the cardiovascular and pulmonary responses to exercise in patients with occupational asthma (OA) and a closely related entity, reactive airways dysfunction syndrome (RADS). METHODS:We evaluated clinical and cardiopulmonary exercise data (mean +/- SD) from patients with OA (n = 22, age = 40.1 +/- 8.9 years, 14 males) and RADS (n = 23, age = 37.7 +/- 9.7 years, 18 males) who exhibited comparable pulmonary function. Oxygen uptake, CO2 output, ventilatory parameters, cardiac hemodynamics, O2 delivery, 12 lead EKG, systemic BP, and O2 saturation were monitored at rest and during cycle ergometer exercise. RESULTS:Compared with the RADS group, OA patients demonstrated higher resting dead-space ventilation (41 +/- 8 vs 35 +/- 9%, p = 0.04), reduced exercise capacity (94 +/- 32 vs 122 +/- 47 W, p = 0.01), higher respiratory quotients at 50 W (0.98 +/- 0.14 vs 0.91 +/- 0.08, p = 0.04), decreased power output past attainment of the anaerobic threshold (28.1 +/- 17.1 vs 44.7 +/- 15.1 W, p = 0.002) and a strong tendency for lower anaerobic thresholds (53 +/- 9 vs 60 +/- 14% pred VO2max, p = 0.06). CONCLUSION:In the 2 groups with occupational bronchial hyperreactivity, each with mild disease severity, OA patients exhibited greater decrements in cardiovascular conditioning when compared with the RADS group, perhaps because of the more prolonged, chronic respiratory insult experienced by the OA group. These data indicate that CPET in patients with work-related bronchial hyperreactivity is of significant utility in the impairment evaluation process.

Ethylene oxide (EO) is commonly used to sterilize heat-sensitive products used by hospital patients and personnel. Ethylene chlorohydrin (EC), a by-product, is considered highly toxic. We report a cluster of 12 operating-room nurses and technicians who developed symptoms after a 5-month exposure to high levels of EO and EC in disposable surgical gowns. All patients reported a rash on the wrist where contact was made with the gowns, headaches, and hand numbness with weakness. Ten of 12 patients complained of memory loss. Neurologic evaluation revealed neuropathy on examination in nine of the 12 patients, elevated vibration threshold in four of nine, abnormal pressure threshold in 10 of 11, atrophy on head MRI in three of 10, and neuropathy on conduction studies in four of 10. Neuropsychological testing demonstrated mild cognitive impairment in four of six patients. Sural nerve biopsy in the most severely affected patient showed findings of axonal injury. Several patients in this group display signs of peripheral and CNS dysfunction following exposure to EO. Possible mechanisms of neurotoxicity include direct exposure of peripheral nerves through cutaneous absorption and central involvement through inhalation and vascular dissemination. The frequency of central and peripheral nervous system symptoms, supported by objective testing in these EO-exposed patients, suggests other healthcare personnel may be at similar risk.

Many highly trained athletes experience exercise-induced bronchospasm (EIB): studies describing EIB in figure skaters, who may be at increased risk of EIB due to rink temperatures (7 to 10 degrees C), have not been published. We studied professionally coached figure skaters (n=124) for EIB by spirometry at rinkside immediately before a simulated long program and at 0 to 1, 5, 10, and 15 min postexercise. Postexercise spirometry revealed the presence of EIB (a decrease from baseline in FEV(1) of at least 10%) in 43 skaters, while the remainder (n=81, control group) remained relatively stable. Pre-exercise FEV(1), FVC, and FEV(1)/FVC ratio were not different between groups. The EIB group had significantly lower FEV(1) vs baseline at each measurement following exercise: baseline, 3.08+/-0.13, 0 to 1 min postexercise, 2.81+/-0.13 (p<0.05); 5 min postexercise, 2.77+/-0.14 (p<0.05); 10 min postexercise 2.78+/-0.13 (p<0.05); 15 min postexercise, 2.78+/-0.13 (p<0.05). The EIB group also had lower FVC: baseline, 3.48+/-0.16; 0 to 1 min postexercise, 3.16+/-0.15 (p<0.05); 5 min postexercise, 3.19+/-0.15 (p<0.05); 10 min postexercise, 3.27+/-0.16 (p<0.05); 15 min postexercise, 3.26+/-0.16 (p<0.05). Control subjects, however, experienced no decline in these variables. In conclusion, the incidence of EIB in the figure skaters measured during this investigation (43 of 124=35%) is greater than that of the population at large and other highly trained athletes, signifying that screening for EIB and therapeutic follow-up are reasonable considerations for participants in this sport.

Inadequate O2 supply may impair intramuscular oxidative metabolism and O2 availability may modulate ATP production within exercising muscle. Therefore, we studied ATP flux from anaerobic glycolysis, the creatine kinase reaction, and oxidative phosphorylation using 31P-magnetic resonance spectroscopy kinetic data collected during exercise. We examined six chronic obstructive pulmonary disease (COPD) patients with severe hypoxemia (group 1), seven COPD patients with mild hypoxemia (group 2), and seven healthy control subjects. Exercise (90-s isometric contraction of the gastrocnemius-soleus muscle group, 40% of max) was performed on room air for all subjects; for COPD patients, it was repeated during supplemental O2 at identical power outputs, with 60-min rest between the two sets. In group 1 (air vs. O2), oxidative phosphorylation ATP production was lower (P < 0.05), anaerobic glycolysis ATP production was higher (P < 0.05), and anaerobic glycolysis plus creatine kinase ATP production tended to be higher (P = 0.06). In group 2, no differences were observed across conditions. Assuming that mitochondrial size, density, function, and redox state were not affected by acute changes in the inspired O2 fraction, reduced O2 availability is the remaining factor that could have limited oxidative ATP production during hypoxemia. In conclusion, in severely hypoxemic COPD patients, O2 availability apparently limits intramuscular oxidative metabolism because acute hypoxemia increases anaerobic and decreases aerobic ATP production.

We evaluated the effect of supplemental O2 on energy metabolism of hypoxemic humans by measuring O2 uptake (VO2) kinetics and other cardiorespiratory parameters in nine male chronic obstructive pulmonary disease (COPD) patients and seven age-matched control subjects (on air and on 30% O2) at rest and during moderate cycle ergometer exercise. Heart rate, ventilation, VO2, CO2 output, respiratory exchange ratio, O2 cost of work, and work efficiency were measured with a computerized metabolic cart; O2 deficit and VO2 time courses were calculated. In COPD patients, 30% O2 breathing resulted in 1) reduction of O2 deficit (from 488 +/- 34 ml in air to 398 +/- 27 ml in O2; P < 0.05) and phase 2 VO2 time constant (from 116 +/- 13 s in air to 74 +/- 12 s in O2; P < 0.05); 2) a smaller steady-state increment in CO2 output than in room air (315 +/- 17 ml/min in O2 vs. 358 +/- 27 ml/min in air; P < 0.02), which resulted in a lower exercise respiratory exchange ratio (0.75 +/- 0.02 in O2 vs. 0.80 +/- 0.02 in air; P < 0.02); and 3) reduced steady-state ventilation (22.6 +/- 1.0 l/min in O2 vs. 25.4 +/- 1.1 l/min in air; P < 0.05). In conclusion, 30% O2 breathing accelerated exercise VO2 kinetics in mildly hypoxemic COPD patients. The observed VO2 kinetics improvement with O2 supplementation is consistent with an enhancement of aerobic metabolism in skeletal muscles during moderate exercise.