Project at a Glance
Project Status: complete
Title: Ozone toxicity effects consequent to prolonged, high intensity exercise in trained endurance athletes.
Principal Investigator / Author(s): Adams, William C.
Contractor: Human Performance Laboratory, Physical Education Department, UC Davis
Contract Number: A0-078-32
Research Program Area: Health & Exposure
Topic Areas: Health Effects of Air Pollution
The purpose of the present investigation was: (1) to investigate the effects of ozone (O₃) exposure combined with high ventilation volumes incurred during training and competitive simulation protocols and (2) to study selected ventilatory and respiratory metabolism parameters and subjective symptomatology which could suggest mechanisms involved in previously observed decrements in maximal aerobic performance following O₃ exposure. Ten well trained distance runners, age 21-31 years, with normal pulmonary function, served as subjects. Each subject was exposed on six occasions for one hour to either filtered air or to O₃ concentrations of 0.20 or 0.35 parts per million (ppm), while riding on a bicycle ergometer at workloads simulating either, a one-hour steady-state training bout, or a 30 minutes warm-up followed immediately by a 30 minutes competitive bout. Workloads were set such that the mean ventilation (VE) for 1 h was approximately 80 L⋅min⁻¹. Standard pulmonary function (PF) tests and periodic observations of exercise respiratory metabolism, heart rate (HR), and VE were obtained. Following each protocol subjects completed a subjective symptom form. Statistical analyses revealed no significant difference between the training and competitive simulations on PF, but a significant effect across 0₃ concentration for FVC, FEV1.0 and FEF25-75 for all comparisons between FA, 0.20 ppm 0₃ and 0.35 ppm 0₃, was observed. Significant effects across 0₃ concentration for the training protocols for all comparisons of respiratory frequency (FR) and comparisons between FA and 0.35 and 0.20 and 0.35 ppm 0₃ for tidal volume (VT), were observed. No significant 0₃ effect was observed for exercise VO₂, HR, VE or VA, responses, suggesting no alteration in pulmonary gas exchange or O₂ transport or delivery. Subjective symptoms increased as a function of O₃ concentration, and following the competitive protocols, four subjects consequent to the 0.20 ppm O₃ and nine at the 0.35 ppm O₃ exposures, respectively, indicated that they could not have performed maximally. Three subjects were unable to complete both the training and competitive simulation rides at 0.35 ppm O₃, while a fourth failed to complete the competitive ride, only at this concentration. These observations indicate that high mean VE(~80 L⋅min⁻¹ ) incurred during training and competition simulation resulted in an increased susceptibility of endurance athletes to the toxic effects of O₃ exposure. Further, these findings suggest that the O₃ concentrations utilized did not result in any decrement in pulmonary gas exchange and / or oxygen delivery, and that observed performance decrements were the result of physiologically induced subjective limitations of respiratory discomfort.
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