57 research outputs found

    Immersion Pulmonary Edema in Female Triathletes

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    Pulmonary edema has been reported in SCUBA divers, apnea divers, and long-distance swimmers however, no instances of pulmonary edema in triathletes exist in the scientific literature. Pulmonary edema may cause seizures and loss of consciousness which in a water environment may become life threatening. This paper describes pulmonary edema in three female triathletes. Signs and symptoms including cough, fatigue, dyspnea, haemoptysis, and rales may occur within minutes of immersion. Contributing factors include hemodynamic changes due to water immersion, cold exposure, and exertion which elevate cardiac output, causing pulmonary capillary stress failure, resulting in extravasation of fluid into the airspace of the lung. Previous history is a major risk factor. Treatment involves immediate removal from immersion and in more serious cases, hospitalization, and oxygen administration. Immersion pulmonary edema is a critical environmental illness of which triathletes, race organizers, and medical staff, should be made aware

    The Critical Power Model as a Potential Tool for Anti-Doping

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    Existing doping detection strategies rely on direct and indirect biochemical measurement methods focused on detecting banned substances, their metabolites, or biomarkers related to their use. However, the goal of doping is to improve performance, and yet evidence from performance data is not considered by these strategies. The emergence of portable sensors for measuring exercise intensities and of player tracking technologies may enable the widespread collection of performance data. How these data should be used for doping detection is an open question. Herein, we review the basis by which performance models could be used for doping detection, followed by critically reviewing the potential of the critical power (CP) model as a prototypical performance model that could be used in this regard. Performance models are mathematical representations of performance data specific to the athlete. Some models feature parameters with physiological interpretations, changes to which may provide clues regarding the specific doping method. The CP model is a simple model of the power-duration curve and features two physiologically interpretable parameters, CP and W0 . We argue that the CP model could be useful for doping detection mainly based on the predictable sensitivities of its parameters to ergogenic aids and other performance-enhancing interventions. However, our argument is counterbalanced by the existence of important limitations and unresolved questions that need to be addressed before the model is used for doping detection. We conclude by providing a simple worked example showing how it could be used and propose recommendations for its implementation

    Normative Data for the Balance Error Scoring System in Adults

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    Background. The balance error scoring system (BESS) is a brief, easily administered test of static balance. The purpose of this study is to develop normative data for this test. Study Design. Cross-sectional, descriptive, and cohort design. Methods. The sample was drawn from a population of clients taking part in a comprehensive preventive health screen at a multidisciplinary healthcare center. Community-dwelling adults aged 20–69 (N=1,236) were administered the BESS within the context of a fitness evaluation. They did not have significant medical, neurological, or lower extremity problems that might have an adverse effect on balance. Results. There was a significant positive correlation between BESS scores and age (r=.34). BESS performance was similar for participants between the ages of 20 and 49 and significantly declined between ages 50 and 69. Men performed slightly better than women on the BESS. Women who were overweight performed significantly more poorly on the test compared to women who were not overweight (P<.0001; Cohen's d=.62). The BESS normative data are stratified by age and sex. Conclusions. These normative data provide a frame of reference for interpreting BESS performance in adults who sustain traumatic brain injuries and adults with diverse neurological or vestibular problems

    The Critical Power Model as a Potential Tool for Anti-doping

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    Existing doping detection strategies rely on direct and indirect biochemical measurement methods focused on detecting banned substances, their metabolites, or biomarkers related to their use. However, the goal of doping is to improve performance, and yet evidence from performance data is not considered by these strategies. The emergence of portable sensors for measuring exercise intensities and of player tracking technologies may enable the widespread collection of performance data. How these data should be used for doping detection is an open question. Herein, we review the basis by which performance models could be used for doping detection, followed by critically reviewing the potential of the critical power (CP) model as a prototypical performance model that could be used in this regard. Performance models are mathematical representations of performance data specific to the athlete. Some models feature parameters with physiological interpretations, changes to which may provide clues regarding the specific doping method. The CP model is a simple model of the power-duration curve and features two physiologically interpretable parameters, CP and W′. We argue that the CP model could be useful for doping detection mainly based on the predictable sensitivities of its parameters to ergogenic aids and other performance-enhancing interventions. However, our argument is counterbalanced by the existence of important limitations and unresolved questions that need to be addressed before the model is used for doping detection. We conclude by providing a simple worked example showing how it could be used and propose recommendations for its implementation

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

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    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.Education, Faculty ofMedicine, Faculty ofOther UBCNon UBCKinesiology, School ofMedicine, Department ofPopulation and Public Health (SPPH), School ofReviewedFacult

    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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    BackgroundExposure 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.AimTo determine how DE exposure during exercise of varying intensities affects adhesion molecules and markers of systemic inflammation.MethodsEighteen 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.ResultsTwo 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.ConclusionsBased 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 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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    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.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.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.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.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
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