***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Context : Internal combustion engines are a major source of particulate matter ( PM ) which has been shown to result in vasoconstriction , yet no present study to our knowledge has investigated the effect of exhaust emissions on both exercise performance and the vasculature . Objective : To examine the effect of freshly generated whole exhaust on exercise performance , pulmonary arterial pressure ( PP ) , and flow-mediated vasodilation ( FMD ) of the brachial artery . Material s and Methods : Sixteen male , collegiate athletes ( age : 20.8 ± 1.28 years ) were r and omly assigned to submaximal exercise for 20 min followed by a 6 min maximal work accumulation exercise test in either high PM ( HPM ) or low PM ( LPM ) conditions on two consecutive days . After a 7-day washout period , subjects completed identical exercise trials in the alternate condition . HPM conditions were generated from a 4-cycle gasoline engine . The participants ’ PP and FMD were assessed before and after each exercise trial by tricuspid regurgitant velocity and brachial artery imaging , respectively . Results : Total work ( LPM : 108.0 ± 14.8 kJ ; HPM : 104.9 ± 15.2kJ , p = 0.019 ) and FMD ( LPM : 8.17 ± 6.41 % ; HPM : 6.59 ± 2.53 % ; p = 0.034 ) significantly decreased in HPM while PP was significantly increased ( LPM : 16.9 ± 1.13 mmHg ; HPM : 17.9 ± 1.70 mmHg ; p = 0.004 ) . A significant correlation was identified between the change in exercise performance and the change in FMD ( r = 0.494 ; p = 0.026 ) after the first HPM trial . Conclusion : Exercise performance declined in HPM conditions in part due to impaired vasodilation in the peripheral vasculature Exposure to diesel exhaust is an important cardiovascular risk factor and may promote atherothrombotic events . Some data suggest that polluted air exposure could affect haemostasis through platelet activation . The aim of the study was to investigate the effects of acute exposure to diesel exhaust on platelet activation and platelet function . We tested the hypothesis in a r and omised , crossover study in 25 healthy men exposed to ambient and polluted air ; 11 of the subjects also performed exercise during exposure sessions .  Platelet activation was evaluated by surface expression of CD62P ( P-selectin ) and CD63 ( dense granule glycoprotein ) using flow cytometry of labelled platelets . Platelet function was measured using the PFA-100 platelet function analyser and by Multiplate whole blood impedance platelet aggregometry . Acute diesel exhaust exposure had no effect on platelet activation at rest , but exercise in polluted air increased the collagen-induced expression of CD62P and CD63 ( both p < 0.05 ) . The increase in the expression of CD62P and CD63 was related to the total amount of PM2.5 inhaled during the exercise sessions ( r=+0.58 and + 0.60 , respectively , both p < 0.05 ) . Platelet aggregation was not impaired after polluted air exposure at rest or during exercise . In conclusion , in healthy subjects , diesel exhaust exposure induces platelet activation as illustrated by a dose-response increase in the release of CD62P and CD63 . This platelet priming effect could be a contributor to the triggering of atherothrombotic events related to air pollution exposure To investigate the acute effect of a hot , humid and ozone-polluted ( O3 ) environment on lung inflammation and oxidative tress of runners performing 8 km time trial run . Using a single-blinded r and omized design , 10 male athletes ( mean$$ \dot{V}{\text{O}}_{2\max } $ $ = 64.4 mlO2 kg−1 min−1 , SD = 4.4 ) took part in a time trial run in four different environmental conditions : 20 ° C + 50 % relative humidity ( rh ) ( Control ) ; 20 ° C + 50 % rh + 0.10 ppm O3 ( Control + O3 ) ; 31 ° C + 70 % rh ( Heat ) ; 31 ° C + 70 % rh + 0.10 ppm O3 ( Heat + O3 ) . Blood sample s and nasal lavage were collected post-exercise and analyzed for inflammatory , epithelial damage and oxidative stress markers . Data were analyzed using repeated measures ANOVA with Tukey ’s post hoc test . A significant increase in CC16 concentration ( P < 0.05 ) and GSH/protein concentration ( P < 0.05 ) in the upper respiratory airways was observed following the 8 km run in the Heat + O3 trial compared with the control trial . There were no differences in the neutrophil counts between trials . No differences were observed for the other antioxidants analyzed . A hot , humid and ozone-polluted environment ( 0.1 ppm ) elicits an early epithelial damage and antioxidant protection process in the upper respiratory airways of athletes immediately after performing 8 km time trial run Background Traffic-related air pollution may contribute to cardiovascular morbidity . In urban areas , exposures during physical activity are of interest owing to increased breathing rates and close proximity to vehicle emissions . Methods We conducted a cross-over study among 53 healthy non-smoking women in Montreal , Canada during the summer of 2013 . Women were exposed to traffic pollutants for 2-hours on three separate occasions during cycling on high and low-traffic routes as well as indoors . Personal air pollution exposures ( PM2.5 , ultrafine particles ( UFP ) , black carbon , NO2 , and O3 ) were evaluated along each route and linear mixed-effects models with r and om subject intercepts were used to estimate the impact of air pollutants on acute changes in blood pressure , heart rate variability , and micro-vascular function in the hours immediately following exposure . Single and multi-pollutant models were examined and potential effect modification by mean regional air pollution concentrations ( PM2.5 , NO2 , and O3 ) was explored for the 24-hour and 5-day periods preceding exposure . Results In total , 143 exposure routes were completed . Each interquartile increase ( 10,850/cm3 ) in UFP exposure was associated with a 4.91 % ( 95 % CI : -9.31 , -0.512 ) decrease in reactive hyperemia index ( a measure of micro-vascular function ) and each 24 ppb increase in O3 exposure corresponded to a 2.49 % ( 95 % CI : 0.141 , 4.84 ) increase in systolic blood pressure and a 3.26 % ( 95 % CI : 0.0117 , 6.51 ) increase in diastolic blood pressure 3-hours after exposure . Personal exposure to PM2.5 was associated with decreases in HRV measures reflecting parasympathetic modulation of the heart and regional PM2.5 concentrations modified these relationships ( p < 0.05 ) . In particular , stronger inverse associations were observed when regional PM2.5 was higher on the days prior to the study period . Regional PM2.5 also modified the impact of personal O3 on the st and ard deviation of normal to normal intervals ( SDNN ) ( p < 0.05 ) : a significant inverse relationship was observed when regional PM2.5 was low prior to study periods and a significant positive relationship was observed when regional PM2.5 was high . Conclusion Exposure to traffic pollution may contribute to acute changes in blood pressure , autonomic and micro-vascular function in women . Regional air pollution concentrations may modify the impact of these exposures on autonomic function Background Traffic emissions including diesel engine exhaust are associated with increased respiratory and cardiovascular morbidity and mortality . Controlled human exposure studies have demonstrated impaired vascular function after inhalation of exhaust generated by a diesel engine under idling conditions . Objectives To assess the vascular and fibrinolytic effects of exposure to diesel exhaust generated during urban-cycle running conditions that mimic ambient ' real-world ' exposures . Methods In a r and omised double-blind crossover study , eighteen healthy male volunteers were exposed to  diesel exhaust ( approximately 250 μg/m3 ) or filtered air for one hour during intermittent exercise . Diesel exhaust was generated during the urban part of the st and ardized European Transient Cycle . Six hours post-exposure , vascular vasomotor and fibrinolytic function was assessed during venous occlusion plethysmography with intra-arterial agonist infusions . Measurements and Main Results Forearm blood flow increased in a dose-dependent manner with both endothelial-dependent ( acetylcholine and bradykinin ) and endothelial-independent ( sodium nitroprusside and verapamil ) vasodilators . Diesel exhaust exposure attenuated the vasodilatation to acetylcholine ( P < 0.001 ) , bradykinin ( P < 0.05 ) , sodium nitroprusside ( P < 0.05 ) and verapamil ( P < 0.001 ) . In addition , the net release of tissue plasminogen activator during bradykinin infusion was impaired following diesel exhaust exposure ( P < 0.05 ) . Conclusion Exposure to diesel exhaust generated under transient running conditions , as a relevant model of urban air pollution , impairs vasomotor function and endogenous fibrinolysis in a similar way as exposure to diesel exhaust generated at idling . This indicates that adverse vascular effects of diesel exhaust inhalation occur over different running conditions with varying exhaust composition and concentrations as well as physicochemical particle properties . Importantly , exposure to diesel exhaust under ETC conditions was also associated with a novel finding of impaired of calcium channel-dependent vasomotor function . This implies that certain cardiovascular endpoints seem to be related to general diesel exhaust properties , whereas the novel calcium flux-related effect may be associated with exhaust properties more specific for the ETC condition , for example a higher content of diesel soot particles along with their adsorbed organic compounds Exposure to alumina dust has been recently associated with impaired lung mechanics and inflammation . We aim ed at evaluating if moderate exercise training prevents these outcomes . Twenty-three female BALB/c mice ( 25 - 30 g ) were r and omly divided in two main groups : control ( C ) and exercise ( E ) , which were su bmi tted , or not , to 15min of swimming , 5 days/week during 4 weeks . Then , the animals were exposed for 1h to either saline solution ( CS or ES ) or to a suspension of 8mg/m(3 ) of alumina dust ( CA or EA ) . Twenty-four hours later pulmonary mechanics was determined by the end-inflation occlusion method . Left lungs were prepared for histology and right lungs for TGF-β determination . Static elastance increased after alumina dust exposure independently of swimming . In CA group the viscoelastic component of elastance , the viscoelastic/inhomogeneous pressure , the polymorphonuclear amount , the fraction area of alveolar collapse and TGF-β increased . Thus , exercise training may mitigate the pro-inflammatory response to inhaled aluminum refinery dust Large urbanized areas , where sports events take place , have a polluted environment and can also reach high temperatures and humidity levels . The aim of this study was to investigate the impact of a hot , humid and ozone-polluted ( O3 ) environment on ( 1 ) performance of an 8 km time trial run , ( 2 ) pulmonary function , and ( 3 ) subjective respiratory symptoms in endurance-trained runners . Using crossover r and omized design , 10 male participants ( mean$$ \mathop V\limits^{. } { \text{O}}_{2\max } = 64.4 $ $ mlO2 kg−1 min−1 , SD = 4.4 ) took part in a time trial run under four different conditions : 20 ° C + 50 % relative humidity ( rh ) ( Control ) , 20 ° C + 50 % rh + 0.10 ppm O3 ( Control + O3 ) , 31 ° C + 70 % rh ( Heat ) , 31 ° C + 70 % rh + 0.10 ppm O3 ( Heat + O3 ) . Heart rate , ratings of perceived exertion and minute ventilation were collected during the run . Lung function was measured pre and post-exercise . The runners completed a respiratory symptoms question naire after each trial . The completion time of both the Heat ( 32 min 35 s ) and Heat + O3 ( 33 min 09 s ) trials were significantly higher ( P < 0.0001 ) when compared to the Control + O3 ( 30 min 27 s ) and Control ( 30 min 15 s ) trials . There were no significant changes between pre/post lung function measures or between trials . The effective dose of ozone simulated in the present study did not affect the performance and therefore , ozone-pollution , at an environmentally relevant concentration , did not compound the impairment in performance beyond that induced by a hot , humid environment 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 aim ed 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˙O 
    Output:
    
The combination effect of air pollution and exercise was found to be associated with the increased risk of potential health problems of cardiopulmonary function , immune function , and exercise performance .