Expired pentane, an index of lipid peroxidation, and pulmonary function were measured as a function of exercise for 1 h with and without exposure to 0.3 ppm ozone. In experiment 1, 10 subjects who exercised on a bicycle ergometer at 50% of maximal oxygen consumption while being exposed to 0.3 ppm ozone had increased lung residual volume and decreased vital capacity, maximal midexpiratory flow rate, and forced expiratory volume in 1 s. In experiment 2, breath collected into a spirometer filled with hydrocarbon-scrubbed air showed increased pentane from the stress of exercise but no effect of ozone. During rest and exercise in experiment 3, two of six subjects had higher pentane levels than the other subjects. Following daily supplementation with 1,200 IU dl-alpha-tocopherol for 2 wk, the mean production of pentane during rest and exercise was significantly lowered, and there was no difference in pentane production among the subjects. It was concluded that lipid peroxidation occurs during exercise and that it is attenuated by vitamin E.

To assess the contribution of the autonomic nervous system to heart rate recovery following exertion, heart rate was observed after peak treadmill exercise in six men following parasympathetic blockade (PB) with atropine sulfate (0.03 mg/kg), sympathetic blockade (SB) with propranolol hydrochloride (0.20 mg/kg), double blockade (DB) with both drugs, and no drugs (ND). Least-squares analysis of each subject's heart rate (HR) as an exponential function of recovery time (t) was computed for each treatment giving an equation of the form HR = aebt. HRs at rest, peak exercise, and 10 min of recovery, the coefficients a and b, and the least-squares correlation coefficient (r) were compared among treatments by nonparametric analysis of variance and rank-sum multiple comparisons. HR recovered in an exponential manner after dynamic exercise in each subject with each of the treatment modes (P less than 0.01 for each r, mean across all treatments r = 0.94). Coefficients a and b differed the most between PB and SB. At the cessation of exercise the decreases in venous return and the systemic need for cardiac output are accompanied by an exponential HR decline. The exponential character of the cardiodeceleration seen after peak exercise appears to be an intrinsic property of the circulation because it occurred under each experimental condition.

The electrocardiographic and ventilatory responses of 15 denervated heart patients who had undergone cardiac transplantation and 14 age-matched, normally innervated men were compared to assess the pattern of response to graded treadmill exercise. A 5-minute postexercise venous lactate sample was also obtained. Respiratory exchange ratio and ventilation (Ve) were higher in denervated patients than in normals during submaximal exercise. Peak values (normals vs denervated) for heart rate (172 vs 159 beats/min), blood pressure (189 vs 167 mm Hg), oxygen uptake (37 vs 25 ml/kg/min), oxygen pulse (0.22 vs 0.16 ml/kg/beat) and work time (26.2 vs 18.0 minutes) were higher in normals than in cardiac transplant recipients. Peak ventilatory equivalent (2.14 vs 3.13 l/ml/kg) and lactate values were higher for transplants than for normal subjects, but there were no significant intergroup differences in peak Ve or in the respiratory exchange ratio. In cardiac transplant recipients, work time correlated inversely with a measure of rejection history (r = -0.59, p less than 0.01). The response of cardiac transplant recipients to treadmill work differs from that of normal men and reflects a diminished ability to meet the oxygen demands of the exercising periphery.

In evaluating O3 toxicity in humans, the effective dose, expressed as the simple product of concentration, exposure duration and ventilation volume (VE), has been applied only to resting or intermittent exercise (IE) exposures. In the present study, we examined the validity of effective dose in predicting pulmonary function impairment when effective dose was determined both as a simple product and as a weighted function via multiple regression. Eight trained male subjects (ages 22-46) completed 18 protocols, including exposures (via mouthpiece) to filtered air and three levels of O3 concentration (0.20, 0.30, and 0.40 ppm), while exercising continuously for durations ranging from 30 to 80 min. The O3 effective dose was significantly related to pulmonary function impairment and exercise ventilatory pattern alteration. Multiple regression analysis, however, substantiated the predominant importance of O3 concentration, with the threshold for O3 toxicity during exercise at a moderately heavy work load [approximately 65% maximum O2 uptake (VO2 max)] shown to be between 0.20 and 0.30 ppm. Although considerable individual variability in O3 toxicity response was noted, group mean responses in our continuous exercise mouthpiece exposures were similar to those previously observed with IE chamber exposures. Thus while the effective dose concept has notable deficiencies in predicting the individual degree of O3 toxicity, it remains a useful approach and warrants further investigation.

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