Koehle, Michael S. | DOOR - DOuglas Open Repository

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Michael S. Koehle

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Performance of a compact end-tidal forcing system

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The purpose of the present study was to develop and validate a new compact, portable end-tidal forcing (ETF) system capable of reliably controlling end-tidal gases. The system consists of compressed gas sources (air, N 2 and CO 2) that are connected via three solenoid valves to a humidification chamber and an inspiratory reservoir bag from which the participant breathes. This computer-controlled system compares actual end-tidal gas partial pressures with target pressures and mixes the gases on a breath-by-breath basis. This leaves no unused exhaust gas and keeps gas requirements to a minimum. Eight participants underwent two different 30-min protocols that included each possible combination of end-tidal O 2 partial pressure ( PE T O 2 ) and end-tidal CO 2 partial pressure ( PE T C O 2 ) control at two different levels ( PE T O 2 at 55 and 75 mmHg; and PE T C O 2 at 4 and 7 mmHg above resting). The ETF system maintained the mean PE T C O 2 at 0.13 mmHg from the target values, with a pooled S.D. across conditions of ±0.91 mmHg and a 95% confidence interval (CI) of ±0.63 mmHg. The mean PE T O 2 was held at 0.49 mmHg from its target values, with a pooled S.D. across conditions of ±1.31 mmHg and a 95% CI of ±0.91 mmHg. To demonstrate suitability of this system for measuring chemosensitivity to hypoxia, hypoxic ventilatory response (HVR) tests were conducted in a subset of five participants. During a 20-min HVR test both PE T C O 2 and PE T O 2 were not significantly different from their target values. These data demonstrate the performance of a portable, compact, economical system that controls PE T C O 2 within 1 mmHg and PE T O 2 within 2 mmHg of their respective target values.

The effects of lower body positive and negative pressure on the hypoxic ventilatory decline

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Purpose Lower body negative pressure (LBNP) augments the acute hypoxic ventilatory response (AHVR) in humans, presumably through altered central integration of baro- and chemoreceptor afferents. This study investigated the effects of LBNP and lower body positive pressure (LBPP) on hypoxic ventilatory decline (HVD) in humans. Methods Nine individuals (4 females and 5 males) were tested in a supine position with the lower body supported inside a hypo/hyperbaric chamber. During each test the participant was exposed in a random order to LBNP at −37.5 mmHg, LBPP at +37.5 mmHg and to ambient pressure (LBAP) at 0 mmHg. Blood pressure, expired gases and haemoglobin O2 saturation were continuously recorded. Hypoxia was administered in a single step to a of 50 mmHg for 20 min. For all tests was maintained at the pre-hypoxic resting level. Results The peak ventilation was significantly greater during LBNP (36.0 ± 10.8 L min−1) than during ambient pressure (29.4 ± 8.1 L min−1; p = 0.032). However, peak ventilation was not significantly different between LBPP and ambient pressure. The HVD was not significantly different across the three conditions (p = 0.144). Both mean arterial pressure and pulse pressure were not affected by 37.5 mmHg of either LBPP (p = 0.941) or LBNP (p = 0.275). Baroreflex slope was decreased by both hypoxia and LBNP. Conclusion These data suggest that LBNP increases AHVR through an effect on the baroreflex, while LBPP has no effect on AHVR. Since LBNP increases AHVR without affecting HVD, these findings support that the mechanism accounting for the HVD includes afferent output originating from the peripheral rather than the central chemosensitive tissues.

The effect of pre-exercise diesel exhaust exposure on cycling performance and cardio-respiratory variables

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Purpose: To determine the effect of pre-exercise exposure to diesel exhaust (DE) on 20-km cycling performance, pulmonary function, and cardio-respiratory variables during exercise. Methods: Eight endurance-trained males participated in the study. Test days consisted of a 60-min exposure to either filtered air (FA) or DE, followed by a 20 km cycling time trial. Exposures to DE were at a concentration of 300 µg/m3 of PM2.5. Forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) were measured before and after exposure, and after exercise. Oxygen consumption (VO2) and carbon dioxide production (VCO2), minute ventilation (VE), tidal volume (VT), breathing frequency (FB), heart rate and oxyhemoglobin saturation (SpO2), were collected during the time trials. The effect of condition on time trial duration, an order effect, and mean cardio-respiratory variables were each analysed using paired T-tests. Repeated-measures ANOVA were used to assess the effect of DE exposure on pulmonary function. Results: There was a main effect of condition (FA vs. DE) on the change in FEV1 from baseline, and in exercise heart rate. Post hoc tests revealed that exercise-induced bronchodilation was significantly attenuated following DE compared to FA. There were no main effects of condition on 20 km cycling performance, or VO2, VCO2, VE, VT, FB and SpO2 during a 20 km time trial. Conclusion: A 60-min exposure to DE prior to exercise significantly attenuated exercise-induced bronchodilation and significantly increased heart rate during exercise. Pre-exercise exposure to diesel exhaust did not significantly impair 20 km cycling time trial performance.

The health effects of exercising in air pollution

Digital Document

The health benefits of exercise are well known. Many of the most accessible forms of exercise, such as walking, cycling, and running often occur outdoors. This means that exercising outdoors may increase exposure to urban air pollution. Regular exercise plays a key role in improving some of the physiologic mechanisms and health outcomes that air pollution exposure may exacerbate. This problem presents an interesting challenge of balancing the beneficial effects of exercise along with the detrimental effects of air pollution upon health. This article summarizes the pulmonary, cardiovascular, cognitive, and systemic health effects of exposure to particulate matter, ozone, and carbon monoxide during exercise. It also summarizes how air pollution exposure affects maximal oxygen consumption and exercise performance. This article highlights ways in which exercisers could mitigate the adverse health effects of air pollution exposure during exercise and draws attention to the potential importance of land use planning in selecting exercise facilities.

Physiological responses to diesel exhaust exposure are modified by cycling intensity

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Background Outdoor exercisers are frequently exposed to diesel exhaust (DE) that contains particulate matter (PM) air pollution. How the respiratory and metabolic responses to exercise are affected by DE exposure and how these responses change with exercise intensity are unknown. Purpose This study aimed to determine the respiratory and metabolic responses to low- and high-intensity cycling with DE exposure containing high levels of PM. Methods Eighteen males age 24.5 ± 6.2 yr performed 30-min trials of low-intensity (30% of power at V˙O2peak) and high-intensity (60% of power at V˙O2peak) cycling as well as rest. Each trial was performed once while breathing filtered air (FA) and once while breathing DE (300 μg·m−3 of PM2.5) for a total of six trials, each separated by 7 d. During the trials, minute ventilation (V˙E), oxygen consumption (V˙O2), CO2 production (V˙CO2), RER, and perceived exertion for lungs (RPELungs) and legs (RPELegs) were measured. Work of breathing, respiratory muscle V˙O2, ratio of O2 consumption to power output, and gross efficiency were estimated. Results The RER was significantly lower (0.02 lower, P = 0.008), and the RPELungs (0.9 greater, P = 0.001) and the RPELegs (0.6 greater, P = 0.017) were significantly greater, in DE compared with FA. During low-intensity exercise, V˙E (44.5 ± 8.9 vs 40.5 ± 8.0 L·min−1, P < 0.001), V˙O2 (27.9 ± 5.4 vs 24.9 ± 4.4 mL·kg−1·min−1, P = 0.001), and V˙CO2 (25.9 ± 5.3 vs 23.5 ± 4.5 mL·kg−1·min−1, P = 0.006) were significantly greater in DE. This pattern was not seen during high-intensity cycling. Conclusions Respiratory and metabolic responses to low-intensity, but not high-intensity, cycling in DE exceed FA. Practically, the greater responses during low-intensity exercise in DE could have implications for individuals with cardiopulmonary disease. Also, the elevated RPE during DE could impair performance in self-paced exercise.

The effect of low and high-intensity cycling in diesel exhaust on flow-mediated dilation, circulating NOx, endothelin-1 and blood pressure

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INTRODUCTION: Exposure to air pollution impairs aspects of endothelial function such as flow-mediated dilation (FMD). Outdoor exercisers are frequently exposed to air pollution, but how exercising in air pollution affects endothelial function and how these effects are modified by exercise intensity are poorly understood. OBJECTIVES: Therefore, the purpose of this study was to determine the effects of low-intensity and high-intensity cycling with diesel exhaust (DE) exposure on FMD, blood pressure, plasma nitrite and nitrate (NOx) and endothelin-1. METHODS: Eighteen males performed 30-minute trials of low or high-intensity cycling (30% and 60% of power at VO2peak) or a resting control condition. For each subject, each trial was performed once while breathing filtered air (FA) and once while breathing DE (300ug/m3 of PM2.5, six trials in total). Preceding exposure, immediately post-exposure, 1 hour and 2 hours post-exposure, FMD, blood pressure and plasma endothelin-1 and NOx concentrations were measured. Data were analyzed using repeated-measures ANOVA and linear mixed model. RESULTS: Following exercise in DE, plasma NOx significantly increased and was significantly greater than FA (p<0.05). Two hours following DE exposure, endothelin-1 was significantly less than FA (p = 0.037) but exercise intensity did not modify this response. DE exposure did not affect FMD or blood pressure. CONCLUSION: Our results suggest that exercising in DE did not adversely affect plasma NOX, endothelin-1, FMD and blood pressure. Therefore, recommendations for healthy individuals to moderate or avoid exercise during bouts of high pollution appear to have no acute protective effect.

Effects of low-intensity and high-intensity cycling with diesel exhaust exposure on soluble P-selectin, E-selectin, I-CAM-1, VCAM-1 and complete blood count

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Background: Exposure to particulate matter 2.5 μm or less (PM2.5) that contains transition metals may play a role in systemic oxidative stress and inflammation. Exposure to diesel exhaust (DE) can increase adhesion molecules, which are important in the inflammatory response; however, it is unclear how exercising in DE affects adhesion molecules and how exercise intensity modulates this response. Aim: To determine how DE exposure during exercise of varying intensities affects adhesion molecules and markers of systemic inflammation. Methods: Eighteen males performed 30 min cycling bouts at low intensity and high intensity (30% and 60% of power at VO2peak (peak oxygen consumption) and a control condition (rest)). Each trial was performed once breathing filtered air (FA) and once breathing DE (300 μg/m3 of PM2.5, six trials in total). Prior to, immediately post, 1 and 2 hours post exposure, blood was drawn to measure parameters of a complete blood count and soluble (s) platelet-Selectin, endothelin-Selectin, intracellular cell adhesion molecule (sICAM)-1 and vascular cell adhesion molecule (sVCAM)-1. Data were analysed using repeated-measures analysis of variance. Results: Two hours following high-intensity exercise, sICAM-1 was significantly less in DE compared with FA (p=0.008). Immediately following rest (p=0.013) and high-intensity exercise (p=0.042) in DE, sICAM-1 was significantly greater than immediately following low-intensity exercise in DE. There were no significant differences in other markers between DE and FA. Conclusions: Based on this study, healthy individuals may not experience an acute increase in adhesion molecules and systemic inflammatory markers from exercising in DE compared with FA, and higher exercise intensities do not appear to increase the likelihood that DE will affect adhesion molecules and systemic inflammatory markers.

The pulmonary and autonomic effects of high-intensity and low-intensity exercise in diesel exhaust

Digital Document

Background Exposure to air pollution impairs aspects of pulmonary and autonomic function and causes pulmonary inflammation. However, how exercising in air pollution affects these indices is poorly understood. Therefore, the purpose of this study was to determine the effects of low-intensity and high-intensity cycling with diesel exhaust (DE) exposure on pulmonary function, heart rate variability (HRV), fraction of exhaled nitric oxide (FeNO), norepinephrine and symptoms. Methods Eighteen males performed 30-min trials of low-intensity or high-intensity cycling (30 and 60% of power at VO2peak) or a resting control condition. For each subject, each trial was performed once breathing filtered air (FA) and once breathing DE (300μg/m3 of PM2.5, six trials in total). Pulmonary function, FeNO, HRV, norepinephrine and symptoms were measured prior to, immediately post, 1 h and 2 h post-exposure. Data were analyzed using repeated-measures ANOVA. Results Throat and chest symptoms were significantly greater immediately following DE exposure than following FA (p < 0.05). FeNO significantly increased 1 h following high-intensity exercise in DE (21.9 (2.4) vs. 19.3 (2.2) ppb) and FA (22.7 (1.7) vs. 19.9 (1.4)); however, there were no differences between the exposure conditions. All HRV indices significantly decreased following high-intensity exercise (p < 0.05) in DE and FA. The exception to this pattern was LF (nu) and LF/HF ratio, which significantly increased following high-intensity exercise (p < 0.05). Plasma norepinephrine (NE) significantly increased following high-intensity exercise in DE and FA, and this increase was greater than following rest and low-intensity exercise (p < 0.05). DE exposure did not modify any effects of exercise intensity on HRV or norepinephrine. Conclusions Healthy individuals may not experience greater acute pulmonary and autonomic effects from exercising in DE compared to FA; therefore, it is unclear if such individuals will benefit from reducing vigorous activity on days with high concentrations on particulate matter.

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