Pulmonary Impacts of Exercise in Polluted Environments

       Air pollution arises from multiple sources that are increasing in frequency, including industrial processes, traffic exhaust and climatic events such as wildfires. Therefore, it is a major issue that can cause severe health problems for multitudes of people. This is particularly the case for elite athletes, who perform intensive activities in conditions that often include high air pollution when training or competing in the outdoors. Previous studies confirm that exposure to key air pollutants, including particulate matter (PM), diesel exhaust particles (DEP), and ozone (O₃) are capable of triggering pulmonary Group 2 Innate Lymphoid Cells (ILC2) to produce high levels of immune system markers: Interleukin (IL)-5 and IL-13 [1].

       Quiet breathing in healthy adult humans is typically in the range of 12 breaths/min at a tidal volume of 0.5L/breath. During exercise, ventilation increases up to 150 L/min and, for elite athletes, up to 200 L/min is possible for short periods of time [2]. This increase in respiratory rate results in inhalation of a much higher level of potential harmful air pollutants in a given time period [2]. The combination of air pollution and exercise is already associated with an increase in risk for cardiopulmonary problems and immune alternations [3]; however, it is not known if air pollution inhibits or enhances the pro- and/or anti-inflammatory effects of intensive exercise.

       Dr. Vanoirbeek [4] and his team recently investigate this question via development of a sub-maximal 3-week running model in mice. This study provides important details in the combined effect of intensive exercise and DEP exposure on airway inflammation, hyperresponsiveness, airway integrity and airway immune responses.

       A Double Chamber Plethysmography setup enables measurement of respiratory parameters including peak inspiratory flow (PIF), peak expiratory flow (PEF), inspiratory time (Ti), expiratory time (Te) etc.. The results exhibit an acute change of the breathing pattern of mice after intensive exercise, by an increase in inspiratory and expiratory times and decreases in both peak inspiratory and expiratory flows. Assessment of lung function parameters using the flexiVent® in combination with methacholine airway hyperresponsiveness challenges, confirm lower airway hyperreactivity in exercising mice than controls. The high ventilation in the exercise mice is hypothesized to aid in eliminating accumulated DEP from the lungs of exposed subjects.

       These results suggest that exercising outdoors, particularly when done at high intensity and in high-pollution areas, could cause molecular alterations that could contribute to respiratory issues.

Figure 1: Breathing pattern of mice based on the breathing parameters measured pre and post exposure and running. Ti: inspiratory time, Te: expiratory time, PIF: peak inspiratory flow, PEF: peak expiratory flow, TV: tidal volume, EV: expiratory volume.