Research Projects

The purpose of the present investigation was: (1) to investigate the effects of ozone (03) 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 03 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 03 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-l. 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, FEVT o 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 03for tidal volume (VT), were observed. No significant 03 effect was observed for exercise 002, HR, V or 0, responses, suggesting no alteration in pulmonary gas exchange or 02 transport or delivery. Subjective symptoms increased as a function of 03 concentration, and following the competitive protocols, four subjects consequent to the 0.20 ppm 03 and nine at the 0.35 ppm 03 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 03, 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 03 exposure. Further, these findings suggest that the 03 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.