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Higher fine particulate matter and temperature levels impair exercise capacity in cardiac patients
Abstract
Fine particulate matter (PM2.5) air pollution and variations in ambient temperature have been linked to increased cardiovascular morbidity and mortality. However, no large-scale study has assessed their effects on directly measured aerobic functional capacity among high-risk patients.
Using a cross-sectional observational design, we evaluated the effects of ambient PM2.5 and temperature levels over 7 days on cardiopulmonary exercise test results performed among 2078 patients enrolling into a cardiac rehabilitation programme at the University of Michigan (from January 2003 to August 2011) using multiple linear regression analyses (controlling for age, sex, body mass index).
Peak exercise oxygen consumption was significantly decreased by approximately 14.9% per 10 μg/m(3) increase in ambient PM2.5 levels (median 10.7 μg/m(3), IQR 10.1 μg/m(3)) (lag days 6-7). Elevations in PM2.5 were also related to decreases in ventilatory threshold (lag days 5-7) and peak heart rate (lag days 2-3) and increases in peak systolic blood pressure (lag days 4-5). A 10°C increase in temperature (median 10.5°C, IQR 17.5°C) was associated with reductions in peak exercise oxygen consumption (20.6-27.3%) and ventilatory threshold (22.9-29.2%) during all 7 lag days. In models including both factors, the outcome associations with PM2.5 were attenuated whereas the effects of temperature remained significant.
Short-term elevations in ambient PM2.5, even at low concentrations within current air quality standards, and/or higher temperatures were associated with detrimental changes in aerobic exercise capacity, which can be linked to a worse quality of life and cardiovascular prognosis among cardiac rehabilitation patients.
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... Some previous studies have shown that acute exposure to air pollution during exercise may override its benefits, 8,9 or enhance exerciseinduced increases in blood pressure. 10 Unlike acute exposure, the associations between long-term exposure and health may not be reversible and may result in a much larger disease burden. However, whether longterm exposure to air pollution affects the efficacy of habitual PA remains inconclusive. ...
... 35,36 A few studies have even shown that acute exposure to air pollution during exercise may override the benefits of PA, 8,9 or enhance the exercise-induced increase in blood pressure. 10 However, the development of hypertension is a chronic process. It takes time for a person to develop (or prevent) hypertension via the effects of PM 2.5 or PA. ...
Background
We investigated the joint associations of habitual physical activity (PA) and long-term exposure to fine particulate matter (PM 2.5 ) with the development of hypertension in a longitudinal cohort in Taiwan.
Methods
We selected 140 072 adults (≥18 years of age) without hypertension who joined a standard medical screening program with 360 905 medical examinations between 2001 and 2016. PM 2.5 exposure was estimated at each participant’s address using a satellite data-based spatiotemporal model with 1 km ² resolution. Information on habitual PA and a wide range of covariates was collected using a standard self-administered questionnaire. We used the Cox regression model with time-dependent covariates to examine the joint associations.
Results
The mean age of all observations was 41.7 years, and 48.8% were male. The mean value for systolic and diastolic blood pressure was 112.5 and 68.7mm Hg, respectively. Approximately 34.2% of all observations were inactive (0 metabolic equivalence values-hours), 29.8% had moderate-PA (median [interquartile range]; 3.75 [3.38 to 4.38] metabolic equivalence values-hours), and 36.0% had high-PA (15.7 [10.3 to 24.8] metabolic equivalence values-hours). The mean±SD of PM 2.5 was 26.1±7.3 μg/m ³ . The prevalence of cardiovascular disease, diabetes mellitus, and cancer was 2.1%, 2.9%, and 1.5%, respectively. After adjusting for a wide range of covariates (including a mutual adjustment for PA or PM 2.5 ), a higher PA level was associated with a lower risk of hypertension (hazard ratio [HR] for the moderate- and high-PA was 0.93 [95% CI, 0.89–0.97] and 0.92 [95% CI, 0.88–0.96], respectively, as compared with the inactive-PA), whereas a higher level of PM 2.5 was associated with a higher risk of hypertension (HR for the moderate- and high-PM 2.5 was 1.37 [95% CI, 1.32–1.43] and 1.92 [95% CI, 1.81–2.04], respectively, as compared with the low-PM 2.5 group]. No significant interaction was observed between PA and PM 2.5 (HR 1.01 [95% CI, 1.00–1.02]).
Conclusions
A high-PA and low PM 2.5 exposure were associated with a lower risk of hypertension. The negative association between PA and hypertension remained stable in people exposed to various levels of PM 2.5 , and the positive association between PM 2.5 and hypertension was not modified by PA. Our results indicated that PA is a suitable hypertension prevention strategy for people residing in relatively polluted regions.
... The increase in air pollution reduces aerobic performance and maximal oxygen uptake in soccer players, especially in the evening and winter seasons [46]. Short-term elevations of fine particulate matter of 10 μg/m 3 well within current air quality standards are associated with detrimental changes (−15%) in peak oxygen consumption among cardiac rehabilitation patients [47]. Patients with chronic coronary syndromes showed a peculiar sensitivity of coronary flow velocity reserve [48] and especially B-lines [49] to same-day increase in NOx and fine particulate matter. ...
There is increasing awareness of the impact of climate change and air pollution on public health. The environmental impact of medical imaging can vary 100-fold between one test and the other. One echocardiogram produces 2 kg, and a 3 Tesla magnetic resonance imaging produces 200 to 300 kg of carbon dioxide equivalent. In 2016, carbon dioxide emissions from magnetic resonance imaging and computed tomography calculated in 120 countries accounted for 0.77% of global emissions. Climate change worsens air pollution. Air pollution is a chronic risk factor for cardiovascular disease and an acute trigger of acute coronary syndromes, heart failure, cardiac arrhythmias, sudden death, inducible myocardial ischemia, and pulmonary congestion. The prescription of medical imaging may incorporate carbon dioxide emissions in the decision-making. Industry research will target the progressive decarbonization of testing. Clinical practice should recognize air pollution as a chronic risk factor, an acute modulator of cardiovascular test results, and an actionable therapeutic target. Climate-neutral imaging is recommended whenever possible.
... Exercise may increase the frequency and volume of inhalation of air pollutants, which would hypothetically increase the adverse health effects of air pollution. Previous studies have found that the acute hazard caused by extra intake of air pollution during exercise might surpass the beneficial effects of PA (Giorgini et al., 2015;Kubesch et al., 2015;Sinharay et al., 2018). However, previous studies on the interaction between PM 2.5 and PA were mostly conducted on cardiopulmonary diseases, and it is unclear whether such interactions are present for cataract. ...
The aim of this study was to examine the associations of fine particulate matter (PM2.5) and physical activity (PA) with age-related cataract and its subtypes, and to explore potential interactions between PM2.5 and PA. A total of 291,627 participants enrolled in the UK Biobank cohort during 2006–2010 was included. The annual mean concentration of PM2.5 at each participant's residential address was estimated using Land Use Regression models. PA was measured using the International Physical Activity Questionnaire. Cox proportional hazards model was used to examine the associations of PM2.5 and PA with incident age-related cataract, and to assess their interactions on additive and multiplicative scales. We identified 12,826 incident cases of age-related cataract, including 7686 cases of nuclear cataract and 5140 cases of non-nuclear cataract. Higher PM2.5 exposure was associated with a higher risk of age-related cataract [HR = 1.140; 95% CI: 1.105, 1.177; per 1 μg/m³ increase], and the association was stronger for non-nuclear cataract than for nuclear cataract. There was a negative association between PA and cataract [HR = 0.925; 95% CI: 0.879, 0.974; comparing high to low level]. No clear evidence of the interactions between PM2.5 and PA was found. Our findings indicated that high PM2.5 exposure and low levels of PA were independently associated with increased risks of incident age-related cataract.
... Therefore, there is possibly a risk-benefit tradeoff of ambient PM 2.5 exposure and physical activity on the risk of conjunctivitis. Limited studies have investigated the interaction effects between air pollution exposure and PA on cardiopulmonary diseases (Giorgini et al., 2015;Guo et al., 2020;Kubesch et al., 2015;Ran et al., 2021;Sinharay et al., 2018), whereas their combined effects on conjunctivitis have not yet been investigated. ...
Background
Currently, there is no evidence of fine particulate matter pollution (PM2.5) altering the relationship between physical activity (PA) and the risk of conjunctivitis.
Methods
Based on the UK Biobank study, we included 308,507 participants aged 40–69 years at baseline (2006 to 2010) and prospectively followed up for conjunctivitis diagnosis till 2020. Annual concentrations of PM2.5 in 2010 were estimated for each participant using Land Use Regression models. PA levels during work and leisure time were reported via the International Physical Activity Questionnaire at baseline. We used Cox proportional hazards models to examine the associations of PM2.5 and PA with incident conjunctivitis, as well as their interaction at both multiplicative and additive scales.
Results
During the 11.6 years of follow up, we identified 4002 incident conjunctivitis cases. High-PA (≥3000 metabolic equivalent of task [MET]-mins/week) was associated with lower risk of conjunctivitis (hazard ratio [HR]: 0.79, 95 % confidence interval [CI]: 0.73–0.86) compared to low-PA (0 to <600 MET-mins/week), while every 1 μg/m³ increment in PM2.5 was associated with a 16 % higher risk of conjunctivitis (HR = 1.16, 95 % CI: 1.09–1.23). We did not observe statistically significant interactions between PM2.5 and PA on their associations with conjunctivitis.
Conclusion
Habitual PA and PM2.5 exposure were oppositely related to incident conjunctivitis. The benefits of PA remain in people irrespective of exposure to air pollution.
... Hypertension is also a potential mechanism because it is a key risk factor for AF (Huxley et al. 2011;Perez et al. 2013). Short-and long-term air pollution exposures have been associated with hypertension in numerous studies (Brook et al. 2009(Brook et al. , 2011Chan et al. 2015;Coogan et al. 2012Coogan et al. , 2015Dai et al. 2016;Delfino et al. 2010;Dong et al. 2013;Dvonch et al. 2009;Giorgini et al. 2015Giorgini et al. , 2016Liang et al. 2014;Zanobetti et al. 2004), and higher levels of long-term traffic exposure have been associated with higher left and right ventricular mass (Leary et al. 2014;Van Hee et al. 2009. The available evidence also suggests that short-term air pollution exposure is associated with higher heart rate, reductions in most indices of heart rate variability, and changes in electrophysiology, particularly among older or susceptible individuals, such as those with obesity (Brook et al. 2010;Ishida et al. 2010;Koide et al. 2008;Link and Dockery 2010;Magnani et al. 2011;Schnabel et al. 2009). ...
Background:
Atrial fibrillation (AF) is associated with substantial morbidity and mortality. Short-term exposures to air pollution have been associated with AF triggering; less is known regarding associations between long-term air pollution exposures and AF incidence.
Objectives:
Our objective was to assess the association between long-term exposures to air pollution and distance to road on incidence of AF in a cohort of U.S. women.
Methods:
We assessed the association of high resolution spatiotemporal model predictions of long-term exposures to particulate matter (PM10 and PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), and distance to major roads with incidence of AF diagnosis, identified through Medicare linkage, among 83,117 women in the prospective Women's Health Initiative cohort, followed from enrollment in Medicare through December 2012, incidence of AF, or death. Using time-varying Cox proportional hazards models adjusted for age, race/ethnicity, study component, body mass index, physical activity, menopausal hormone therapy, smoking, diet quality, alcohol consumption, educational attainment, and neighborhood socioeconomic status, we estimated the relative risk of incident AF in association with each pollutant.
Results:
A total of 16,348 incident AF cases were observed over 660,236 person-years of follow-up. Most exposure-response associations were nonlinear. NO2 was associated with risk of AF in multivariable adjusted models [Hazard Ratio (HR)=1.18; 95% confidence interval (CI): 1.13, 1.24, comparing the top to bottom quartile, p-for-trend=<0.0001]. Women living closer to roadways were at higher risk of AF (e.g., HR=1.07; 95% CI: 1.01, 1.13 for living within 50m of A3 roads, compared with ≥1,000 m, p-for-trend=0.02), but we did not observe adverse associations with exposures to PM10, PM2.5, or SO2. There were adverse associations with PM10 (top quartile HR=1.10; 95% CI: 1.05, 1.16, p-for-trend=<0.0001) and PM2.5 (top quartile HR=1.09; 95% CI: 1.03, 1.14, p-for-trend=0.002) in sensitivity models adjusting for census region.
Discussion:
In this study of postmenopausal women, NO2 and distance to road were consistently associated with higher risk of AF. https://doi.org/10.1289/EHP7683.
... Moreover, the internal distribution of pollutants can also be accelerated during exercises by enhancing blood follow. Studies reported that the benefits of habitual PA would be diminished by concurrent air pollution exposure during exercises, especially benefits to blood pressure control, cardiac rehabilitation, and lung function recovery for patients with COPD or asthma (Giorgini et al., 2015;Kubesch et al., 2015;McCreanor et al., 2007;Sinharay et al., 2018). A few other studies, nevertheless, found that exposure to high levels of air pollution might not modify associations, which indicated benefits of habitual PA to the lung and cardiac functions might not be influenced by the amplified air pollutants (Cole-Hunter et al., 2018;Fisher et al., 2016;Guo et al., 2020b;Kubesch et al., 2018;Sun et al., 2019). ...
Objective
The evidence for the beneficial effects of physical activity (PA) and potentially detrimental effects of long-term exposure to fine particulate matter (PM2.5) on neurodegeneration diseases is accumulating. However, their joint effects remain unclear. We evaluated joint associations of habitual PA and PM2.5 exposure with incident dementia in a longitudinal elderly cohort in Hong Kong.
Methods
A total of 57,775 elderly participants (≥65 years) without dementia were enrolled during 1998–2001 and followed up till 2011. Their information on PA and other relevant covariates were collected at baseline (1998–2001) by a standard self-administered questionnaire, including PA volumes (high, moderate, low, and inactive) and types (aerobic exercise, traditional Chinese exercise, stretching exercise, walking slowly, and no exercise). Their annual mean PM2.5 exposures at the residential address were estimated using a satellite-based spatiotemporal model. We then adopted the Cox proportional hazards model to examine the joint associations with the incidence of all-cause dementia, Alzheimer’s diseases, and vascular dementia on additive and multiplicative scales.
Results
During the follow-up period, we identified 1,157 incident cases of dementia, including 642 cases of Alzheimer’s disease and 324 cases of vascular dementia. A higher PA level was associated with a lower risk of incident all-cause dementia (hazard ratio (HR) for the high-PA volume was 0.59 (95% CI, 0.47, 0.75), as compared with the inactive-PA), whereas a high level of PM2.5 was related to the higher risk with an HR of 1.15 (95%CI: 1.00, 1.33) compared with the low-level of PM2.5. No clear evidence was observed of interaction between habitual PA (volume and type) and PM2.5 inhalation to incident dementia on either additive or multiplicative scale.
Conclusion
Habitual PA and long-term PM2.5 exposure were oppositely related to incident dementia in the Hong Kong aged population. The benefits of PA remain in people irrespective of exposure to air pollution.
... In a cross-over study among 28 healthy adults assigned to settings with high-and low-traffic exposures and rest or intermittent exercise, the association between traffic-related air pollution (TRAP) and heart rate variability was modified by physical activity in high-traffic but not low-traffic exposure settings (Cole-Hunter et al. 2016). Among 2,078 patients enrolled in a cardiac rehabilitation program, short-term elevation in PM 2:5 exposure was associated with decreased cardiopulmonary responses measured during cardiopulmonary exercise tests conducted between 2003 and 2011 (Giorgini et al. 2015). In a study of 122 adults across three European cities, physical activity was measured using a wearable activity tracker over the course of 3 separate weeks spread across 3 seasons. ...
Background:
Increased respiration during physical activity may increase air pollution dose, which may attenuate the benefits of physical activity on cardiovascular disease (CVD) risk and overall mortality.
Objectives:
We aimed to examine the multiplicative interaction between long-term ambient residential exposure to fine particulate matter <2.5 microns (PM2.5) and physical activity in the association with CVD risk and overall mortality.
Methods:
We followed 104,990 female participants of the U.S.-based prospective Nurses' Health Study from 1988 to 2008. We used Cox proportional hazards models to assess the independent associations of 24-months moving average residential PM2.5 exposure and physical activity updated every 4 y and the multiplicative interaction of the two on CVD (myocardial infarction and stroke) risk and overall mortality, after adjusting for demographics and CVD risk factors.
Results:
During 20 years of follow-up, we documented 6,074 incident CVD cases and 9,827 deaths. In fully adjusted models, PM2.5 exposure was associated with modest increased risks of CVD [hazard ratio (HR) for fifth quintile ≥16.5 μg/m3 compared to first quintile <10.7 μg/m3: 1.09, 95% confidence interval (CI): 0.99, 1.20; ptrend=0.05] and overall mortality (HR fifth compared to first quintile: 1.10, 95% CI: 1.02, 1.19; ptrend=0.07). Higher overall physical activity was associated with substantially lower risk of CVD [HR fourth quartile, which was ≥24.4 metabolic equivalent of task (MET)-h/wk, compared to first quartile (<3.7MET-h/wk): 0.61, 95% CI: 0.57, 0.66; ptrend<0.0001] and overall mortality (HR fourth compared to first quartile: 0.40, 95% CI: 0.37, 0.42; ptrend<0.0001). We observed no statistically significant interactions between PM2.5 exposure and physical activity (overall, walking, vigorous activity) in association with CVD risk and overall mortality.
Discussion:
In this study of U.S. women, we observed no multiplicative interaction between long-term PM2.5 exposure and physical activity; higher physical activity was strongly associated with lower CVD risk and overall mortality at all levels of PM2.5 exposure. https://doi.org/10.1289/EHP7402.
... For example, decreases in peak oxygen consumption of 15% per 10 micrograms$m -3 increase in ambient PM 2.5 have been reported for patients undergoing cardiac rehabilitation. 15 This decrement was observed even at low PM 2.5 concentrations within the standards for acceptable air quality. ...
Introduction:
Wintertime thermal inversions can lead to the accumulation of small particulate matter (PM2.5). Despite an association between respiratory hospital admissions and elevated PM2.5 levels, many people continue to exercise outdoors during inversions. This study compared pulmonary function and exercise performance during periods of low and high ambient PM2.5 concentrations.
Methods:
Forced vital capacity and forced expiratory volume in 1 s were measured outdoors before and after two 3200 m running time trials: one with low ambient PM2.5 (0.6-14.7 microgram·m-3), and the other during high PM2.5 (19.1-42.5 micrograms·m-3). A 10 cm visual analog scale (VAS) administered postexercise quantified subjective ratings of respiratory discomfort.
Results:
The PM2.5 differential between trials was ≥18 micrograms·m-3 for 10 healthy runners. Despite feeling more respiratory discomfort (P=0.044) during the bad air trial (VAS: 4.6±1.8 cm) compared with the good air trial (VAS: 2.9±1.8 cm), the 3200 m run time (low PM2.5: 13:54±1:34 min:s; high PM2.5: 14:07±1:44 min:s) was not different (P=0.261) between trials. Postexercise forced vital capacity was not significantly different (P=0.846) between the low (4.86±1.00 L) and high (4.84±0.95 L) PM2.5 conditions. Similarly, the difference in postexercise forced expiratory volume in 1 s was not significant (P=0.750) between trials (4.22±0.89 L vs 4.23±0.85 L).
Conclusions:
Neither run time nor pulmonary function of healthy adults were adversely affected by an acute bout of exercise in elevated ambient PM2.5, equivalent to yellow or orange on the air quality index.
... In the context of high temperatures, the mechanisms responsible for BP reduction induced by high temperature levels will be shortterm thermoregulation and a physiological adaptation that included arteriolar vasodilatation and the reduction of peripheral resistance. More specifically, in patients with cardiac rehabilitation have seen that elevating short-term effects of air pollutants with high temperatures can lead to harmful changes in the ability to exercise aerobic, which can be related to a worse quality of life and a poor cardiovascular prognosis in these high-risk patients [27]. ...
Introduction:
Air in urban areas is usually contaminated with particle matter. High concentrations lead to a rise in the risk of cardiovascular and respiratory diseases. Some studies have reported that ultrafine particles (UFP) play a greater role in cardiovascular diseases than other particle matter, particularly regarding hypertensive crises and DBP, although in the latter such effects were described concerning clinical blood pressure (BP). In this study, we evaluate the relationship between 24-h ambulatory BP monitoring (ABPM) and atmospheric UFP concentrations in Barcelona.
Methods:
An observational study of individual patients' temporal and geographical characteristics attended in Primary Care Centres and Hypertensive Units during 2009-2014 was performed.
Results:
The participants were 521 hypertensive patients, mean age 56.8 years (SD 14.5), 52.4% were women. Mean BMI was 28.0 kg/m and the most prominent cardiovascular risk factors were diabetes (N = 66, 12.7%) and smoking (N = 79, 15.2%). We describe UFP effects at short-term and up to 1 week (from lag 0 to 7). For every 10 000 particle/cm UFP increase measured at an urban background site, a corresponding statistically significant increase of 2.7 mmHg [95% confidence interval = (0.5-4.8)] in 24-h DBP with ABPM for the following day was observed (lag 1).
Conclusion:
We have observed that a rise in UFP concentrations during the day prior to ABPM is significantly associated with an increase in 24 h and diurnal DBP. It has been increasingly demonstrated that UFP play a key role in cardiovascular risk factors and, as we have demonstrated, in good BP control.
... For physical activity, a study in Japan showed that the daily step count peaks at the ambient temperature of 17°C, while physical activity decreased at higher or lower temperatures [42]. In contrast, Giorgini et al., reported that a higher temperature was associated with a decrease in aerobic exercise capacity, leading to a worse QoL in patients undergoing cardiac rehabilitation [43]. The result in Niigata from the present study was consistent with this report, suggesting that higher ambient temperature is associated with a detrimental change in the 'overall health' , and 'QoL' even in healthy subjects. ...
Background:
There has been growing global concern about air pollution due to its great risk to public health. In Japan, although industrial- and traffic-related air pollution has been decreasing, concerns about particulate matter air pollution has been growing in recent years. In this study, we examined the effects of air pollution on symptoms and the health status of healthy subjects in Japan.
Methods:
Participants (n = 2887) who visited healthcare centers in Kumamoto or Niigata prefectures in February from 2010 to 2015 were asked to fill out a questionnaire, which was a self-completed booklet containing questions on the characteristics of participants, their respiratory symptoms, and questionnaires on their health status in February, May, and July. Generalized estimating equation analyses were performed to predict the factors associated with the symptoms and health status using two-week averages of air quality parameters obtained from 49 monitoring stations as independent variables.
Results:
Only allergy was associated with air quality in both areas. Prevalence of the other respiratory symptoms were correlated with air quality only in Kumamoto. The health statuses including the 'physical fitness', 'daily activities', and 'social activities' domains were related only to time spent outdoors. The 'overall health' was associated with time spent outdoors and concentrations of nitrogen dioxide and suspended particulate matters (SPM) in Kumamoto, and with temperatures and SPM in Niigata. The 'pain' score was correlated with temperature and carbon monoxide concentration only in Kumamoto. In Kumamoto, the 'quality of life (QoL)' was worse in those who spent shorter hours outdoors, were exposed to lower humidity, higher concentrations of oxidants, SPM, and PM2.5, and who experienced more Asian sand dust (ASD) events. In Niigata, a worsened 'QoL' was associated with time spent outdoors, temperature, and SPM.
Conclusions:
The associations between air quality and the health status was found mainly in the comprehensive domain of the health status such as 'overall health' and 'QoL'. The effect of short-term exposure to larger particles, such as SPM, on health status was observed when compared to smaller particles such as PM2.5 and gaseous pollutants.
... Epidemiologic studies have linked short-and longterm air pollution exposure to increased risk for subclinical CVD [7][8][9][10][11][12][13][14], major cardiovascular events [15][16][17][18][19][20][21][22][23][24][25][26][27], and cardiovascular mortality . The proposed mechanisms include through the promotion of CVD risk factors [48][49][50][51][52][53][54][55][56][57][58][59][60][61][62][63][64][65][66][67], as well as through increased systemic inflammation and coagulation [9••]. For example, Bell et al. recently reported a 1.68 mg/dL lower high-density lipoprotein (HDL)-cholesterol level for each 0.7 × 10 −6 m −1 higher 3-month cumulative exposures to BC and a 0.64 μmol/L lower HDL particle number for each 5 μg/m 3 higher 3-month cumulative exposures to PM 2.5 among a multi-ethnic cohort from six major US cities [59•]. ...
Purpose of Review
Certain subgroups defined by sociodemographics (race/ethnicity, age, sex, and socioeconomic status [SES]), geographic location (rural vs. urban), comorbid conditions, and country economic conditions (developed vs. developing) may disproportionately suffer the adverse cardiovascular effects of exposure to ambient air pollution. Yet, previous reviews have had a broad focus on the general population without consideration of these potentially vulnerable populations.
Recent Findings
Over the past decade, a wealth of epidemiologic studies have linked air pollutants including particulate matter, oxides of nitrogen, and carbon monoxide to cardiovascular disease (CVD) risk factors, subclinical CVD, clinical cardiovascular outcomes, and cardiovascular mortality in certain susceptible populations. Highest risk for poor CVD outcomes from air pollution exists in racial/ethnic minorities, especially in blacks compared to whites in the US, those at low SES, elderly populations, women, those with certain comorbid conditions, and developing countries compared to developed countries. However, findings are less consistent for urban compared to rural populations.
Summary
Vulnerable subgroups including racial/ethnic minorities, women, the elderly, smokers, diabetics, and those with prior heart disease had higher risk for adverse cardiovascular outcomes from exposure to air pollution. There is limited data from developing countries where concentrations of air pollutants are more extreme and cardiovascular event rates are higher than that of developed countries. Further epidemiologic studies are needed to understand and address the marked disparities in CVD risk conferred by air pollution globally, particularly among these vulnerable subgroups.
... The majority of articles cited in a review of particulate matter and exercise 11 involved participants with cardiopulmonary disease. In contrast to our study, peak oxygen consumption of cardiac rehabilitation patients decreased by 14.9% per 10 mg/m 3 increase in ambient PM 2.5 , even within acceptable AQI standards, 21 but we are unaware of any similar studies conducted with mild pollution that have been done on healthy participants. ...
Background/objective:
Wintertime thermal inversions in narrow mountain valleys create a ceiling effect, increasing concentration of small particulate matter (PM2.5). Despite potential health risks, many people continue to exercise outdoors in thermal inversions. This study measured the effects of ambient PM2.5 exposure associated with a typical thermal inversion on exercise performance, pulmonary function, and biological markers of inflammation.
Methods:
Healthy, active adults (5 males, 11 females) performed two cycle ergometer time trials outdoors in a counterbalanced design: 1) low ambient PM2.5 concentrations (<12 μg/m3), and 2) an air quality index (AQI) ranking of "yellow." Variables of interest were exercise performance, exhaled nitric oxide (eNO), c-reactive protein (CRP), forced vital capacity (FVC), and forced expiratory volume in 1 s (FEV1).
Results:
Despite a significant difference in mean PM2.5 concentration of 9.3 ± 3.0 μg/m3 between trials (p < .001), there was no significant difference (p = .424) in the distance covered during low PM2.5 conditions (9.9 ± 1.7 km) compared to high PM2.5 conditions (10.1 ± 1.5 km). There were no clinically significant differences across time or between trials for eNO, CRP, FVC, or FEV1. Additionally, there were no dose-response relationships (p > .05) for PM2.5 concentration and the measured variables.
Conclusion:
An acute bout of vigorous exercise during an AQI of "yellow" did not diminish exercise performance in healthy adults, nor did it have a negative effect on pulmonary function or biological health markers. These variables might not be sensitive to small changes from acute, mild PM2.5 exposure.
... Epidemiologic studies document associations between both acute and chronic exposures to fine particulate matter (particulate matter (PM) having an aerodynamic diameter of 2.5 μm or less (PM 2.5 )) and morbidity and mortality from cardiovascular disease (CVD) (1)(2)(3)(4)(5) and respiratory disease (RD) (2,(5)(6)(7). Acute effects are evident in "natural experiments." ...
Air pollution may increase cardiovascular and respiratory risk through inflammatory pathways, but evidence for acute effects has been weak and indirect. We enrolled 36 healthy nonsmoking college students for a panel study in Shanghai, China, a city with highly variable levels of air pollution, between December 2014 and July 2015. We measured personal exposure to fine particulate matter (PM2.5) continuously for 72-hour preceding each of four clinical visits that included phlebotomy. We measured four inflammation proteins and DNA methylation at nearby regulatory CpG loci. We applied linear mixed-effect models to examine associations over various lag times. When results suggested mediation, we evaluated methylation as mediator. Increased PM2.5 was positively associated with all four inflammation proteins, and negatively associated with DNA methylation at regulatory loci for tumor necrosis factor alpha (TNFα) and soluble intercellular adhesion molecule-1. A 10 μg/m3 increase in average PM2.5 during the 24 hours preceding blood draw corresponded to a 4.4% increase in TNFα and a statistically significant decrease in methylation at one of the two studied candidate CpG loci for TNFα. Epigenetics may play an important role in mediating effects of PM2.5 on inflammatory pathways.
... b 0 is a constant, while b 1 , b 2 , and b 3 are the coefficients of the independent effects of T, R, and W (subject to per unit change) on glyoxal/methylglyoxal concentration. For further information about the regression model, the reader is referred to Giorgini et al. (2015) and Ocak and Turalioglu (2008). All the data were analyzed using IBM SPSS statistics 21.0 (IBM ®, New York, NY) or using GraphPad Prism software (Version 5 for Windows). ...
Gaseous glyoxal and methylglyoxal concentrations were characterized in nine cities of China during 2010–2011. The average summer (winter) glyoxal and methylglyoxal concentrations were 36.4–178.4 (12.3–241.4) and 67.8–359.4 (28.4–530.0) ng/m³, respectively. In summer, the highest average glyoxal concentration was in Guangzhou (GZ), while the lowest was in Shanghai (SH). In winter, Xiamen (XM) showed the highest average methylglyoxal concentration and Yantai (YT) reported the lowest. Both di-carbonyls showed distinct seasonal variations. The maximum average methylglyoxal concentration was approximately twice as much as glyoxal, which is consistent with the results of other studies. Glyoxal-to-methylglyoxal ratios showed that there was a consistent direct source of emissions in remote areas such as Qinghai Lake and Lhasa in both seasons (r ≥ 0.9). Pearson's correlation analysis suggested possible similar sources formation (R ≥ 0.7) for the two di-carbonyls in winter. Multiple linear regression analyses demonstrated that every 1 °C temperature increase could lead to a > 2% increase in the concentration of the di-carbonyls in both seasons. There was a greater percentage gain for glyoxal in winter than in summer for the same temperature increase. The northeast monsoon occurs in winter, and for every 1 ms− 1 increase in wind speed, > 20% of the di-carbonyls can be transferred out of China. This study is useful to understand about the secondary organic aerosol formation in the areas, the statistical analysis can provide information about the relationships between these carbonyls in atmosphere.
Background-- Most metabolic and bariatric surgery (MBS) patients perform too little moderate-to-vigorous intensity physical activity (MVPA) and too much sedentary time (ST). Identifying factors that influence MVPA and ST in MBS patients is necessary to inform the development of interventions to target these behaviors. Research has focused on individual-level factors and neglected those related to the physical environment (e.g., weather and pollution). These factors may be especially important considering rapid climate change and emerging data that suggest adverse effects of weather and pollution on physical activity are more severe in people with obesity.
Objectives--To examine the associations of weather (maximal, average and Wet Bulb Globe Temperatures), and air pollution indices (air quality index [AQI]) with daily physical activity (PA) of both light (LPA) and MVPA and ST before and after MBS.
Methods--Participants (n=77) wore an accelerometer at pre- and 3, 6, and 12-months post-MBS to assess LPA/MVPA/ST (min/d). These data were combined with participants local (Boston, MA or Providence, RI, USA) daily weather and AQI data (extracted from federal weather and environmental websites).
Results--Multilevel generalized additive models showed inverted U-shaped associations between weather indices and MVPA (R2≥.63, p<.001), with a marked reduction in MVPA for daily maximal temperatures ≥20C. Sensitivity analysis showed a less marked decrease of MVPA (min/d) during higher temperatures after versus before MBS. Both MVPA before and after MBS (R2=0.64, p<.001) and ST before MBS (R2=0.395; p<.05) were negatively impacted by higher AQI levels.
Discussion--This study is the first to show that weather and air pollution indices are related to variability in activity behaviors, particularly MVPA, during pre- and post-MBS. Weather/environmental conditions should be considered in MVPA prescription/strategies for MBS patients, especially in the context of climate change.
Objectives:
To explore whether lower outdoor temperature increases cardio-cerebrovascular disease risk through regulating blood pressure and whether indoor heating in winter is beneficial to prevent cardio-cerebrovascular disease in cold areas.
Methods:
We analyzed the data of 38 589 participants in Harbin from the China Kadoorie Biobank (CKB) during 2004-2008, with an average of 7.14-year follow-up. Linear regression analysis was performed to estimate the relationship between outdoor temperature and blood pressure. Cox regression analysis and logistic regression analysis were used to analyze the association of blood pressure with cardio-cerebrovascular event risk. Mediation analysis was performed to explore the role of blood pressure in the association between outdoor temperature and cardio-cerebrovascular events risk.
Results:
There was an increase of 6.7 mmHg in SBP and 2.1 mmHg in DBP for each 10 °C decrease in outdoor temperature when outdoor temperature was higher than 5 °C. There was an inverse association between outdoor temperature and cardio-cerebrovascular event morbidity. The increases in blood pressure and cardio-cerebrovascular event morbidity were attenuated in months when central heating was fully provided. Participants with hypertension have higher risks of cardio-cerebrovascular disease (hazard ratio 1.347; 95% CI 1.281--1.415), CVD (hazard ratio 1.347; 95% CI 1.282--1.416), MACE (hazard ratio 1.670; 95% CI 1.560--1.788) and stroke (hazard ratio 1.683; 95% CI 1.571--1.803). Mediation analysis demonstrated that the association between outdoor temperature and cardio-cerebrovascular events risk was potentially mediated by blood pressure.
Conclusion:
Temperature-driven blood pressure potentially mediates the association between outdoor temperature and cardio-cerebrovascular events risk. Indoor heating in winter is probably beneficial to cardio-cerebrovascular disease prevention by inhibition of blood pressure increase.
Nonparametric regression has received considerable attention in biomedical research because it allows for data-driven dependence of the response variable on covariates. In the presence of missing data, doubly robust estimators have been proposed for nonparametric regression, which allow one model for the missingness mechanism and one model for the outcome regression. We propose multiply robust kernel estimating equations (MRKEEs) for nonparametric regression that can accommodate multiple working models for either the missingness mechanism or the outcome regression, or both. The resulting estimator is consistent if any one of those models is correctly specified. When including correctly specified models for both the missingness mechanism and the outcome regression, the proposed estimator achieves the optimal efficiency within the class of augmented inverse propensity weighted (AIPW) kernel estimators. We conduct simulation studies to evaluate the finite sample performance of the proposed method and further demonstrate it through a real-data example.
The objective of the present study was to determine the impact of acute short-term exposure to air pollution on the cardiorespiratory performance of military fireman living and working in the city of Guarujá, São Paulo, Brazil. Twenty-five healthy non-smoking firemen aged 24 to 45 years had about 1 h of exposure to low and high levels of air pollution. The tests consisted of two phases: phase A, in Bertioga, a town with low levels of air pollution, and phase B, in Cubatão, a polluted town, with a 7-day interval between phases. The volunteers remained in the cities (Bertioga/Cubatão) only for the time required to perform the tests. Cumulative load 10 ± 2 min-long exertion tests were performed on a treadmill, consisting of a 2-min stage at a load of 7 km/h, followed by increasing exertion of 1 km h-1 min-1 until the maximum individual limit. There were statistically significant differences (P
Background
Endurance exercise capacity diminishes under hot environmental conditions. Time to exhaustion can be increased by lowering body temperature prior to exercise (pre-cooling). This systematic literature review synthesizes the current findings of the effects of pre-cooling on endurance exercise performance, providing guidance for clinical practice and further research.
Methods
The MEDLINE, EMBASE, CINAHL, Web of Science and SPORTDiscus databases were searched in May 2012 for studies evaluating the effectiveness of pre-cooling to enhance endurance exercise performance in hot environmental conditions (≥ 28°C). Studies involving participants with increased susceptibility to heat strain, cooling during or between bouts of exercise, and protocols where aerobic endurance was not the principle performance outcome were excluded. Potential publications were assessed by two independent reviewers for inclusion and quality. Means and standard deviations of exercise performance variables were extracted or sought from original authors to enable effect size calculations.
Results
In all, 13 studies were identified. The majority of studies contained low participant numbers and/or absence of sample size calculations. Six studies used cold water immersion, four crushed ice ingestion and three cooling garments. The remaining study utilized mixed methods. Large heterogeneity in methodological design and exercise protocols was identified. Effect size calculations indicated moderate evidence that cold water immersion effectively improved endurance performance, and limited evidence that ice slurry ingestion improved performance. Cooling garments were ineffective. Most studies failed to document or report adverse events. Low participant numbers in each study limited the statistical power of certain reported trends and lack of blinding could potentially have introduced either participant or researcher bias in some studies.
Conclusions
Current evidence indicates cold water immersion may be the most effective method of pre-cooling to improve endurance performance in hot conditions, although practicality must be considered. Ice slurry ingestion appears to be the most promising practical alternative. Interestingly, cooling garments appear of limited efficacy, despite their frequent use. Mechanisms behind effective pre-cooling remain uncertain, and optimal protocols have yet to be established. Future research should focus on standardizing exercise performance protocols, recruiting larger participant numbers to enable direct comparisons of effectiveness and practicality for each method, and ensuring potential adverse events are evaluated.
The objectives of this study were to describe the distribution of all runners' performances in the largest marathons worldwide and to determine which environmental parameters have the maximal impact.
We analysed the results of six European (Paris, London, Berlin) and American (Boston, Chicago, New York) marathon races from 2001 to 2010 through 1,791,972 participants' performances (all finishers per year and race). Four environmental factors were gathered for each of the 60 races: temperature (°C), humidity (%), dew point (°C), and the atmospheric pressure at sea level (hPA); as well as the concentrations of four atmospheric pollutants: NO(2)-SO(2)-O(3) and PM(10) (μg x m(-3)).
All performances per year and race are normally distributed with distribution parameters (mean and standard deviation) that differ according to environmental factors. Air temperature and performance are significantly correlated through a quadratic model. The optimal temperatures for maximal mean speed of all runners vary depending on the performance level. When temperature increases above these optima, running speed decreases and withdrawal rates increase. Ozone also impacts performance but its effect might be linked to temperature. The other environmental parameters do not have any significant impact.
The large amount of data analyzed and the model developed in this study highlight the major influence of air temperature above all other climatic parameter on human running capacity and adaptation to race conditions.
Background: Mechanisms underlying previously reported air pollution and cardiovascular (CV) morbidity associations remain poorly understood.
Objectives: We examined associations between markers of pathways thought to underlie these air pollution and CV associations and ambient particle concentrations in postinfarction patients.
Methods: We studied 76 patients, from June 2006 to November 2009, who participated in a 10-week cardiac rehabilitation program following a recent (within 3 months) myocardial infarction or unstable angina. Ambient ultrafine particle (UFP; 10–100 nm), accumulation mode particle (AMP; 100–500 nm), and fine particle concentrations (PM2.5; ≤ 2.5 μm in aerodynamic diameter) were monitored continuously. Continuous Holter electrocardiogram (ECG) recordings were made before and during supervised, graded, twice weekly, exercise sessions. A venous blood sample was collected and blood pressure was measured before sessions.
Results: Using mixed effects models, we observed adverse changes in rMSSD [square root of the mean of the sum of the squared differences between adjacent normal-to-normal (NN) intervals], SDNN (standard deviation of all NN beat intervals), TpTe (time from peak to end of T-wave), heart rate turbulence, systolic and diastolic blood pressures, C-reactive protein, and fibrinogen associated with interquartile range increases in UFP, AMP, and PM2.5 at 1 or more lag times within the previous 5 days. Exposures were not associated with MeanNN, heart-rate–corrected QT interval duration (QTc), deceleration capacity, and white blood cell count was not associated with UFP, AMP, and PM2.5 at any lag time.
Conclusions: In cardiac rehabilitation patients, particles were associated with subclinical decreases in parasympathetic modulation, prolongation of late repolarization duration, increased blood pressure, and systemic inflammation. It is possible that such changes could increase the risk of CV events in this susceptible population.
In this paper, we review the epidemiological evidence on the relationship between ambient temperature and morbidity. We assessed the methodological issues in previous studies and proposed future research directions. DATA SOURCES AND DATA EXTRACTION: We searched the PubMed database for epidemiological studies on ambient temperature and morbidity of noncommunicable diseases published in refereed English journals before 30 June 2010. Forty relevant studies were identified. Of these, 24 examined the relationship between ambient temperature and morbidity, 15 investigated the short-term effects of heat wave on morbidity, and 1 assessed both temperature and heat wave effects.
Descriptive and time-series studies were the two main research designs used to investigate the temperature-morbidity relationship. Measurements of temperature exposure and health outcomes used in these studies differed widely. The majority of studies reported a significant relationship between ambient temperature and total or cause-specific morbidities. However, there were some inconsistencies in the direction and magnitude of nonlinear lag effects. The lag effect of hot temperature on morbidity was shorter (several days) compared with that of cold temperature (up to a few weeks). The temperature-morbidity relationship may be confounded or modified by sociodemographic factors and air pollution.
There is a significant short-term effect of ambient temperature on total and cause-specific morbidities. However, further research is needed to determine an appropriate temperature measure, consider a diverse range of morbidities, and to use consistent methodology to make different studies more comparable.
Environmental heat stress can challenge the limits of human cardiovascular and temperature regulation, body fluid balance, and thus aerobic performance. This minireview proposes that the cardiovascular adjustments accompanying high skin temperatures (T(sk)), alone or in combination with high core body temperatures (T(c)), provide a primary explanation for impaired aerobic exercise performance in warm-hot environments. The independent (T(sk)) and combined (T(sk) + T(c)) effects of hyperthermia reduce maximal oxygen uptake (Vo(2max)), which leads to higher relative exercise intensity and an exponential decline in aerobic performance at any given exercise workload. Greater relative exercise intensity increases cardiovascular strain, which is a prominent mediator of rated perceived exertion. As a consequence, incremental or constant-rate exercise is more difficult to sustain (earlier fatigue) or requires a slowing of self-paced exercise to achieve a similar sensation of effort. It is proposed that high T(sk) and T(c) impair aerobic performance in tandem primarily through elevated cardiovascular strain, rather than a deterioration in central nervous system (CNS) function or skeletal muscle metabolism. Evaporative sweating is the principal means of heat loss in warm-hot environments where sweat losses frequently exceed fluid intakes. When dehydration exceeds 3% of total body water (2% of body mass) then aerobic performance is consistently impaired independent and additive to heat stress. Dehydration augments hyperthermia and plasma volume reductions, which combine to accentuate cardiovascular strain and reduce Vo(2max). Importantly, the negative performance consequences of dehydration worsen as T(sk) increases.
We sought to clarify the prognostic importance of an "exaggerated" or "hypertensive" systolic blood pressure response to exercise during an exercise test. Studies evaluating the prognosis for cardiovascular events and cardiovascular mortality in those with hypertension during exercise testing were systematically reviewed. Fourteen studies were identified. Six studies were of healthy volunteers or hypertensives. Eight studies were in subjects with known or suspected heart disease. Without established heart disease, exercise hypertension predicted cardiovascular events and cardiovascular death. However, two of the six studies included a multivariate analysis; both demonstrated no independent association. Studies in subjects with known or suspected heart disease demonstrated that exercise hypertension predicted fewer cardiac events and lesser mortality or, after multivariate adjustment, no associated risk. In a healthy population, a higher exercise blood pressure may indicate hypertension or prehypertension, instead of normal vascular function, and an associated long-term adverse prognosis. In a population with a high burden of heart disease, the highest risk subjects with the most extensive cardiac disease may not be capable of generating pressure or workload to allow the manifestation of exercise systolic hypertension. By comparison, therefore, those with exercise hypertension have a better prognosis.
While the effects of weather and, in particular, ambient temperature on overall mortality are well documented, the strength of the evidence base for the effects on acute myocardial infarction (MI) are less clear.
To systematically review studies specifically focusing on the effects of temperature on MI.
Medline, Embase, and GeoBase publication databases, as well as reference lists, and the websites of a number of relevant public organisations.
Studies of original data in which ambient temperature was an exposure of interest and MI a specific outcome were selected.
The reported effects of ambient temperature on the risk of MI, including effect sizes and confidence intervals, where possible, were recorded. Methodological details were also extracted, including study population, location and setting, ascertainment of MI events, adjustment for potential confounders and consideration of lagged effects.
19 studies were identified, of which 14 considered the short-term effects of temperature on a daily timescale, the remainder looking at longer-term effects. Overall, 8 of the 12 studies which included relevant data from the winter season reported a statistically significant short-term increased risk of MI at lower temperatures, while increases in risk at higher temperatures were reported in 7 of the 13 studies with relevant data. A number of differences were identified between studies in the population included demographics, location, local climate, study design and statistical methodology.
A number of studies, including some that were large and relatively well controlled, suggested that both hot and cold weather had detrimental effects on the short-term risk of MI. However, further research with consistent methodology is needed to clarify the magnitude of these effects and to show which populations and individuals are vulnerable.
Epidemiological studies have indicated an inverse association between cardiorespiratory fitness (CRF) and coronary heart disease (CHD) or all-cause mortality in healthy participants.
To define quantitative relationships between CRF and CHD events, cardiovascular disease (CVD) events, or all-cause mortality in healthy men and women.
A systematic literature search was conducted for observational cohort studies using MEDLINE (1966 to December 31, 2008) and EMBASE (1980 to December 31, 2008). The Medical Subject Headings search terms used included exercise tolerance, exercise test, exercise/physiology, physical fitness, oxygen consumption, cardiovascular diseases, myocardial ischemia, mortality, mortalities, death, fatality, fatal, incidence, or morbidity. Studies reporting associations of baseline CRF with CHD events, CVD events, or all-cause mortality in healthy participants were included.
Two authors independently extracted relevant data. CRF was estimated as maximal aerobic capacity (MAC) expressed in metabolic equivalent (MET) units. Participants were categorized as low CRF (< 7.9 METs), intermediate CRF (7.9-10.8 METs), or high CRF (> or = 10.9 METs). CHD and CVD were combined into 1 outcome (CHD/CVD). Risk ratios (RRs) for a 1-MET higher level of MAC and for participants with lower vs higher CRF were calculated with a random-effects model.
Data were obtained from 33 eligible studies (all-cause mortality, 102 980 participants and 6910 cases; CHD/CVD, 84 323 participants and 4485 cases). Pooled RRs of all-cause mortality and CHD/CVD events per 1-MET higher level of MAC (corresponding to 1-km/h higher running/jogging speed) were 0.87 (95% confidence interval [CI], 0.84-0.90) and 0.85 (95% CI, 0.82-0.88), respectively. Compared with participants with high CRF, those with low CRF had an RR for all-cause mortality of 1.70 (95% CI, 1.51-1.92; P < .001) and for CHD/CVD events of 1.56 (95% CI, 1.39-1.75; P < .001), adjusting for heterogeneity of study design. Compared with participants with intermediate CRF, those with low CRF had an RR for all-cause mortality of 1.40 (95% CI, 1.32-1.48; P < .001) and for CHD/CVD events of 1.47 (95% CI, 1.35-1.61; P < .001), adjusting for heterogeneity of study design.
Better CRF was associated with lower risk of all-cause mortality and CHD/CVD. Participants with a MAC of 7.9 METs or more had substantially lower rates of all-cause mortality and CHD/CVD events compared with those with a MAC of less 7.9 METs.
Seventeen male patients with angina pectoris, and a history of increased severity of angina in the cold, performed submaximal bicycle exercise tests in a normal (20°C) and a cold environment (-10°C, 2.2 m/s wind velocity) wearing standardised clothing. Observations were made during and after serial short-term exercise periods each starting at 50 W, with continuous load increase of 10 to 30 W per minute, separated by 30-minute rest intervals. In the group as a whole, maximal work load decreased by 7 per cent during exposure to cold. Heart rate, systolic blood pressure, and rate-pressure product were significantly higher during submaximal exercise in the cold, but at maximal work load there was no difference in heart rate, rate-pressure product, or magnitude of ST segment depression. The decrease in maximal work load exceeded 5 per cent (mean 11%) in 10 patients, who were described as cold-susceptible, while the decrease averaged 1 per cent in the seven non-susceptible patients. The cold-induced reduction in maximal work load showed a significant correlation with the increase in heart rate, blood pressure, and rate-pressure product during submaximal exercise. After exercise, heart rate was significantly lower and blood pressure and rate-pressure product significantly higher in the cold than at normal temperature in all patients. In cold-susceptible patients, blood pressure was significantly higher at two and four minutes after exercise, and rate-pressure product at two minutes after exercise, than in non-susceptible patients, but in spite of this angina disappeared more quickly in cold-susceptible patients. In conclusion, subjective cold intolerance was objectively demonstrated in 10 out of 17 patients with angina pectoris, by exercise in a room at -10°C. Susceptibility to cold was explained by a higher heart rate and blood pressure during exercise in the cold room, than during exercise in the room at normal temperature.
Previous reports have suggested that an attenuated exercise heart rate response may be associated with coronary heart disease risk and with mortality. These observations may parallel the association between reduced heart rate variability during normal activities and adverse outcome. This investigation was designed to look at the prognostic implications of exercise heart rate response in a population-based sample.
In this prospective cohort investigation, 1575 male participants (mean age, 43 years) in the Framingham Offspring Study who were free of coronary heart disease, who were not taking beta-blockers, and who underwent submaximal treadmill exercise testing (Bruce protocol) were studied. Heart rate response was assessed in three ways: (1) failure to achieve 85% of the age-predicted maximum heart rate, which has been the traditional definition of chronotropic incompetence; (2) the actual increase in heart rate from rest to peak exercise; and (3) the ratio of heart rate to metabolic reserve used by stage 2 of exercise ("chronotropic response index"). Proportional hazards analyses were used to evaluate the associations of heart rate responses with all-cause mortality and with coronary heart disease incidence during 7.7 years of follow-up. Failure to achieve target heart rate occurred in 327 (21%) subjects. During follow-up there were 55 deaths (14 caused by coronary heart disease) and 95 cases of incident coronary heart disease. Failure to achieve target heart rate, a smaller increase in heart rate with exercise, and the chronotropic response index were predictive of total mortality and incident coronary heart disease (P <.01). Failure to achieve target heart rate remained predictive of incident coronary heart disease even after adjusting for age, ST-segment response, physical activity, and traditional coronary disease risk factors (adjusted hazard ratio, 1.75; 95% confidence interval, 1.11 to 2.74; P=.02). After adjusting for the same factors, the increase in exercise heart rate remained inversely predictive of total mortality (P=.04) and coronary heart disease incidence (P=.0003). The chronotropic response index also was predictive of total mortality (P=.05) and incident coronary heart disease (P=.001) after adjusting for age and other risk factors.
An attenuated heart rate response to exercise, a manifestation of chronotropic incompetence, is predictive of increased mortality and coronary heart disease incidence.
The effects of whole-body exposure to ambient temperatures of −15°C and 23°C on selected performance-related physiological variables were investigated in elite nonasthmatic cross-country skiers. At an ambient temperature of −15°C we also studied the effects of the selective β2-adrenergic agonist Salbutamol (0.4 mg × 3) which was administered 10 min before the exercise test. Eight male cross-country skiers with known maximal oxygen uptakes (V˙O2max
) of more than 70 ml · kg−1 · min−1 participated in the study. Oxygen uptake (V˙O2), heart rate (f
c), blood lactate concentration ([La−]b) and time to exhaustion were measured during controlled submaximal and maximal running on a treadmill in a climatic chamber. Lung function measured as forced expiratory volume in 1 s (FEV1) was recorded immediately before the warm-up period and at the conclusion of the exercise protocol. Submaximal V˙O2 and [La−]b at the two highest submaximal exercise intensities were significantly higher at −15°C than at 23°C. Time to exhaustion was significantly shorter in the cold environment. However, no differences in V˙O2max
or f
c were observed. Our results would suggest that exercise stress is higher at submaximal exercise intensities in a cold environment and support the contention that aerobic capacity is not altered by cold exposure. Furthermore, we found that after Salbutamol inhalation FEV1 was significantly higher than after placebo administration. However, the inhaled β2-agonist Salbutamol did not influence submaximal and maximal V˙O2, f
c, [La−]b or time to exhaustion in the elite, nonasthmatic cross-country skiers we studied. Thus, these results did not demonstrate any ergogenic effect of the β2-agonist used.
Exercise capacity is known to be an important prognostic factor in patients with cardiovascular disease, but it is uncertain whether it predicts mortality equally well among healthy persons. There is also uncertainty regarding the predictive power of exercise capacity relative to other clinical and exercise-test variables.
We studied a total of 6213 consecutive men referred for treadmill exercise testing for clinical reasons during a mean (+/-SD) of 6.2+/-3.7 years of follow-up. Subjects were classified into two groups: 3679 had an abnormal exercise-test result or a history of cardiovascular disease, or both, and 2534 had a normal exercise-test result and no history of cardiovascular disease. Overall mortality was the end point.
There were a total of 1256 deaths during the follow-up period, resulting in an average annual mortality of 2.6 percent. Men who died were older than those who survived and had a lower maximal heart rate, lower maximal systolic and diastolic blood pressure, and lower exercise capacity. After adjustment for age, the peak exercise capacity measured in metabolic equivalents (MET) was the strongest predictor of the risk of death among both normal subjects and those with cardiovascular disease. Absolute peak exercise capacity was a stronger predictor of the risk of death than the percentage of the age-predicted value achieved, and there was no interaction between the use or nonuse of beta-blockade and the predictive power of exercise capacity. Each 1-MET increase in exercise capacity conferred a 12 percent improvement in survival.
Exercise capacity is a more powerful predictor of mortality among men than other established risk factors for cardiovascular disease.
We studied the association between air pollution and cardiopulmonary fitness among 821 schoolchildren aged 8 to 12 from two districts with different air quality in Hong Kong. Their parents completed a respiratory questionnaire, and the maximum oxygen uptake (VO2max) of the children was assessed using the multistage fitness test. After adjusting for potential confounding factors, children in the high pollution district had a significantly lower VO2max than those in the low pollution district (27.9 mL.kg(-1).min(-1) vs. 29.8 mL.kg(-1).min(-1)). Habitual physical exercise was associated with a higher VO2max in the low-pollution district but not in the high-pollution district. Air pollution adversely affected the VO2max in children, and physical exercise in a polluted environment might not have beneficial effect on cardiopulmonary fitness.
The objective of the present study was to determine the impact of acute short-term exposure to air pollution on the cardiorespiratory performance of military firemen living and working in the city of Guarujá, São Paulo, Brazil. Twenty-five healthy non-smoking firemen aged 24 to 45 years had about 1 h of exposure to low and high levels of air pollution. The tests consisted of two phases: phase A, in Bertioga, a town with low levels of air pollution, and phase B, in Cubatão, a polluted town, with a 7-day interval between phases. The volunteers remained in the cities (Bertioga/Cubatão) only for the time required to perform the tests. Cumulative load 10 +/- 2 min-long exertion tests were performed on a treadmill, consisting of a 2-min stage at a load of 7 km/h, followed by increasing exertion of 1 km h-1 min-1 until the maximum individual limit. There were statistically significant differences (P < 0.05) in anaerobic threshold (AT) between Cubatão (35.04 +/- 4.91 mL kg-1 min-1) and Bertioga (36.98 +/- 5.62 mL kg-1 min-1; P = 0.01), in the heart rate at AT (AT HR; Cubatão 152.08 +/- 14.86 bpm, Bertioga 157.44 +/- 13.64 bpm; P = 0.001), and in percent maximal oxygen consumption at AT (AT%VO2max; Cubatão 64.56 +/- 6.55%, Bertioga 67.40 +/- 5.35%; P = 0.03). However, there were no differences in VO2max, maximal heart rate or velocity at AT (ATvel) observed in firemen between towns. The acute exposure to pollutants in Cubatão, SP, caused a significant reduction in the performance at submaximal levels of physical exertion.
Exposure to air pollution from traffic is associated with adverse cardiovascular events. The mechanisms for this association are unknown. We conducted a controlled exposure to dilute diesel exhaust in patients with stable coronary heart disease to determine the direct effect of air pollution on myocardial, vascular, and fibrinolytic function.
In a double-blind, randomized, crossover study, 20 men with prior myocardial infarction were exposed, in two separate sessions, to dilute diesel exhaust (300 mug per cubic meter) or filtered air for 1 hour during periods of rest and moderate exercise in a controlled-exposure facility. During the exposure, myocardial ischemia was quantified by ST-segment analysis using continuous 12-lead electrocardiography. Six hours after exposure, vasomotor and fibrinolytic function were assessed by means of intraarterial agonist infusions.
During both exposure sessions, the heart rate increased with exercise (P<0.001); the increase was similar during exposure to diesel exhaust and exposure to filtered air (P=0.67). Exercise-induced ST-segment depression was present in all patients, but there was a greater increase in the ischemic burden during exposure to diesel exhaust (-22+/-4 vs. -8+/-6 millivolt seconds, P<0.001). Exposure to diesel exhaust did not aggravate preexisting vasomotor dysfunction, but it did reduce the acute release of endothelial tissue plasminogen activator (P=0.009; 35% decrease in the area under the curve).
Brief exposure to dilute diesel exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease. Our findings point to ischemic and thrombotic mechanisms that may explain in part the observation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events. (ClinicalTrials.gov number, NCT00437138 [ClinicalTrials.gov].).
Plots, probability plots and regression tests tests using moments other tests for univariate normality goodness of fit tests testing for outliers in univariate samples power comparisons for univariate tests for normality testing for normalitywith censored data assessing multivariate normality testing for multivariate outliers testing for normal mixtures robust methods computational methods and issues. Appendices: data sets used in examples critical values for tests.
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.
Acute exposure to air pollution has been linked to myocardial infarction, but its effect on heart failure is uncertain. We did a systematic review and meta-analysis to assess the association between air pollution and acute decompensated heart failure including hospitalisation and heart failure mortality.
Five databases were searched for studies investigating the association between daily increases in gaseous (carbon monoxide, sulphur dioxide, nitrogen dioxide, ozone) and particulate (diameter <2·5 μm [PM2·5] or <10 μm [PM10]) air pollutants, and heart failure hospitalisations or heart failure mortality. We used a random-effects model to derive overall risk estimates per pollutant.
Of 1146 identified articles, 195 were reviewed in-depth with 35 satisfying inclusion criteria. Heart failure hospitalisation or death was associated with increases in carbon monoxide (3·52% per 1 part per million; 95% CI 2·52-4·54), sulphur dioxide (2·36% per 10 parts per billion; 1·35-3·38), and nitrogen dioxide (1·70% per 10 parts per billion; 1·25-2·16), but not ozone (0·46% per 10 parts per billion; -0·10 to 1·02) concentrations. Increases in particulate matter concentration were associated with heart failure hospitalisation or death (PM2·5 2·12% per 10 μg/m(3), 95% CI 1·42-2·82; PM10 1·63% per 10 μg/m(3), 95% CI 1·20-2·07). Strongest associations were seen on the day of exposure, with more persistent effects for PM2·5. In the USA, we estimate that a mean reduction in PM2·5 of 3·9 μg/m(3) would prevent 7978 heart failure hospitalisations and save a third of a billion US dollars a year.
Air pollution has a close temporal association with heart failure hospitalisation and heart failure mortality. Although more studies from developing nations are required, air pollution is a pervasive public health issue with major cardiovascular and health economic consequences, and it should remain a key target for global health policy.
British Heart Foundation.
Prior toxicological exposure reports demonstrated the decremental effect of several air pollutants on the metabolic equivalents achieved during exercise testing (METs). There are no prior large scale epidemiological reports about the effect of environmental air pollution exposure on those parameters. We analyzed a cohort of apparently healthy individuals attending a screening survey program held between 2003 and 2009. Participants were included if residing within an 11 km radius from the nearest air pollution monitoring station. Linear regression models were fitted for the metabolic equivalents and adjusted to short- and long-term air pollutant exposure (particulate matter under 10 micron, sulfur dioxide, nitrogen dioxide, carbon monoxide and ozone). The models were adjusted for possible confounders that affect air pollution and stress testing measurements. The study population comprised 6,612 individuals (4,201 males and 2,411 females). We found a statistically significant short- and long-term negative correlation between air pollutants, mainly CO and NO2 and between the metabolic equivalents achieved. A similar short-term effect was found for SO2. We conclude that exposure to combustion-derived air pollutants has a short- and long-term decremental effect on cardiorespiratory fitness as measured by exercise stress testing. Our epidemiological data support previous toxicological reports.
The objective of the study is to assess the role of cardiopulmonary exercise testing (CPX) variables, including peak oxygen consumption (VO(2)), which is the most recognized CPX variable, the minute ventilation/carbon dioxide production (VE/VCO(2)) slope, the oxygen uptake efficiency slope (OUES), and exercise oscillatory ventilation (EOV) in a current meta-analysis investigating the prognostic value of a broader list of CPX-derived variables for major adverse cardiovascular events in patients with HF. A search for relevant CPX articles was performed using standard meta-analysis methods. Of the initial 890 articles found, 30 met our inclusion criteria and were included in the final analysis. The total subject populations included were as follows: peak VO(2) (7,319), VE/VCO(2) slope (5,044), EOV (1,617), and OUES (584). Peak VO(2), the VE/VCO(2) slope and EOV were all highly significant prognostic markers (diagnostic odds ratios ≥ 4.10). The OUES also demonstrated promise as a prognostic marker (diagnostic odds ratio = 8.08) but only in a limited number of studies (n = 2). No other independent variables (including age, ejection fraction, and beta-blockade) had a significant effect on the meta-analysis results for peak VO(2) and the VE/VCO(2) slope. CPX is an important component in the prognostic assessment of patients with HF. The results of this meta-analysis strongly confirm this and support a multivariate approach to the application of CPX in this patient population.
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.
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.
Sixteen male, collegiate athletes (age: 20.8±1.28 years) were randomly 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.
Total work (LPM: 108.0±14.8 kJ; HPM: 104.9±15.2 kJ, 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.
Exercise performance declined in HPM conditions in part due to impaired vasodilation in the peripheral vasculature.
The purpose of this study was to assess the effects of exercise on the aerobic power, serum lactate level, and cell blood count among active individuals in the environments with similar climatic characteristics differing in their level of air pollution.
This trial comprised 20 volunteer students of Physical education in The University of Isfahan, Iran. Two places with the same climate (altitude, temperature, and humidity), but low and high level of air pollutants air were selected in Isfahan, Iran. Participants underwent a field Cooper test with a 12-minute run for fitness assessment. Then the aerobic power, serum lactate, and cell blood counts were measured and compared between the two areas.
The study participants had a mean (SD) age of 21.70 (2.10) years and body mass index (BMI) of 24.44 (2.32) Kg/m2. We found a significant decrease in mean Vo2 max, red blood cell count, hemoglobin, hematocrit, and mean corpuscular hemoglobin, as well as significant increase in mean lactate level, white blood cell count and mean corpuscular volume in the higher-polluted than in the lower-polluted area. No significant difference was documented for other parameters as platelet counts or maximum heart rate.
Exercise in high-polluted air resulted in a significant reduction in the performance at submaximal levels of physical exertion. Therefore, the acute exposure to polluted air may cause a significant reduction in the performance of active individuals. The clinical importance of these findings should be assessed in longitudinal studies.
In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM <2.5 microm in diameter (PM(2.5)) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM(2.5) exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM(2.5) exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.
Before the 2008 Olympic Games, there was concern that air pollution in Beijing would affect the performance of marathon runners. Air pollutant concentrations during marathon running and their effect on performance have not been reported. Evidence suggests that the lung function of females may be more susceptible than that of males to air pollution, but it is uncertain if this translates to decreased marathon performance.
The purposes of this study were to 1) describe ambient air pollutant concentrations present during major US marathons, 2) quantify performance decrements associated with air pollutants, and 3) examine potential sex difference in performance related to air pollutants.
Marathon race results, weather data, and air pollutant concentrations were obtained for seven marathons for 8-28 yr. The top three male and female finishing times were compared with the course record and contrasted with air pollutant levels and wet bulb globe temperature (WBGT). A WBGT-adjusted performance decrement was calculated, and regression analysis was used to quantify performance decrements associated with pollutants.
The air pollutant concentrations of carbon monoxide, ozone, particulate matter smaller than 10 microm (PM(10)), PM(2.5), nitrogen dioxide, and sulfur dioxide ranged from 0 to 5.9 ppm, from 0 to 0.07 ppm, from 4.5 to 41.0 microg x m(-3), from 2.8 to 42.0 microg x m(-3), from 0 to 0.06 ppm, and from 0 to 0.05 ppm, respectively. After adjusting for WBGT-associated performance decrements, only PM(10) was associated with decrements in performance of women. For every 10-microg x m(-3) increase in PM(10), performance can be expected to decrease by 1.4%.
The concentrations of air pollution present during marathons rarely exceed health-based national standards and levels known to affect lung function in laboratory situations. Regardless, PM(10) was significantly correlated with performance of women marathon runners.
In six male subjects the sweating thresholds, heart rate (fc), as well as the metabolic responses to exercise of different intensities [40%, 60% and 80% maximal oxygen uptake (VO2max)], were compared at ambient temperatures (Ta) of 5 degrees C (LT) and 24 degrees C (MT). Each period of exercise was preceded by a rest period at the same temperature. In LT experiments, the subjects rested until shivering occurred and in MT experiments the rest period was made to be of exactly equivalent length. Oxygen uptake (VO2) at the end of each rest period was higher in LT than MT (P less than 0.05). During 20-min exercise at 40% VO2max performed in the cold no sweating was recorded, while at higher exercise intensities sweating occurred at similar rectal temperatures (Tre) but at lower mean skin (Tsk) and mean body temperatures (Tb) in LT than MT experiments (P less than 0.001). The exercise induced VO2 increase was greater only at the end of the light (40% VO2max) exercise in the cold in comparison with MT (P less than 0.001). Both fc and blood lactate concentration [1a]b were lower at the end of LT than MT for moderate (60% VO2max) and heavy (80% VO2max) exercises. It was concluded that the sweating threshold during exercise in the cold environment had shifted towards lower Tb and Tsk. It was also found that subjects exposed to cold possessed a potentially greater ability to exercise at moderate and high intensities than those at 24 degrees C since the increases in Tre, fc and [1a]b were lower at the lower Ta.
This study was designed to clarify the effects of cold air exposure on metabolic and hormonal responses during progressive incremental exercise. Eight healthy males volunteered for the study. Informed consent was obtained from every participant. The following protocol was administered to each subject on three occasions in a climatic chamber in which the temperature was 20°, 0° or −20°C with relative humidity at 60%±1%. Exercise tests were conducted on an electrically braked ergocycle, and consisted of a propressive incremental maximal exercise. Respiratory parameters were continuously monitored by an automated open-circuit sampling system Exercise blood lactate (LA), free fatty acids (FFA), glucose levels, bicarbonate concentration (HCO
3−), acidbase balance, plasma epinephrine (E) and norepinephrine (NE) were determined from venous blood samples obtained through an indwelling brachial catheter. Maximal oxygen uptake was significantly different between conditions: 72.0±5.4 ml kg−1 min−1 at 20°C; 68.9±5.1 ml kg−1 min−1 at 0°C and 68.5±4.6 ml kg−1 min−1 at −20°C. Workload, time to exhaustion, glucose levels and rectal Catecholamines and lactate values were not significantly altered by thermal conditions after maximal exercise but the catecholamines were decreased during rest. Bicarbonate, respiratory quotient, lactate and ventilatory thresholds increased significantly at −20°C. The data support the contention that metabolic and hormonal responses following progressive incremental exercise are altered by cold exposure and they indicate a marked decrease in maximal oxygen uptake, time to exhaustion and workload.
A new treadmill exercise protocol, modified from the standard Bruce method, was designed to improve ST segment/heart rate slope accuracy and applicability by reducing heart rate increments between exercise stages. In 150 patients exercised according to the new protocol and in 150 patients exercised according to the Bruce protocol, similar exercise tolerance and similar overall heart rate, systolic blood pressure and double product responses to exercise were observed. The mean increment in heart rate between exercise stages of the new protocol was ten beats/minute, which was significantly lower than the 27 beats/minute/stage found with the Bruce protocol. The accuracy of computer-measured ST segment depression was validated by comparison with physician measurement in a separate subgroup of patients with angina pectoris, and serial testing demonstrated stronger interest reproducibility for the ST segment/heart rate slope than for either measured ST segment depression, peak heart rate achieved or duration of exercise.
There is a great demand for perceptual effort ratings in order to better understand man at work. Such ratings are important complements to behavioral and physiological measurements of physical performance and work capacity. This is true for both theoretical analysis and application in medicine, human factors, and sports. Perceptual estimates, obtained by psychophysical ratio-scaling methods, are valid when describing general perceptual variation, but category methods are more useful in several applied situations when differences between individuals are described. A presentation is made of ratio-scaling methods, category methods, especially the Borg Scale for ratings of perceived exertion, and a new method that combines the category method with ratio properties. Some of the advantages and disadvantages of the different methods are discussed in both theoretical-psychophysical and psychophysiological frames of reference.
Patients with angina often report that symptoms are worse in cold weather. This study was designed to determine differences between cold-tolerant and cold-intolerant patients in the hemodynamic and ischemic response to exercise at cold temperatures and to assess the role of catecholamines and baroreceptor function.
Studies have suggested that the heart rate response may differ at cold temperatures, but the mechanism and role of this variation have not been examined.
Seven cold-intolerant and seven cold-tolerant patients with angina underwent exercise treadmill testing at 6 and 25 degrees C with measurement of catecholamines. Baroreceptor function was assessed by the decrease in systolic blood pressure after patients stood up from the supine position.
Norepinephrine levels increased by 139% in the cold environment, but there were no differences between cold-intolerant and cold-tolerant patients. Consequently, blood pressure was higher in the cold environment in all patients, but the heart rate response was similar. However, cold-intolerant patients had a steeper heart rate response in the cold and developed ischemia (mean [+/- SEM] 201 +/- 58 vs. 242 +/- 50 s, p = 0.05) and angina (348 +/- 87 vs. 449 +/- 60 s, p = 0.04) earlier in the cold environment, a difference not seen in the cold-tolerant patients. Baroreceptor function was impaired in cold-intolerant patients (decrease in systolic blood pressure after patients stood up from the supine position 19 +/- 7 vs. 0 +/- 4 mm Hg, p = 0.04).
Exposure to cold causes an increase in blood pressure with an associated increase in myocardial oxygen demand in all patients. In cold-tolerant patients, this increase may be offset by a reduction in heart rate if baroreceptor function is normal. If baroreceptor function is abnormal, heart rate may not decrease in response to a cold-induced increase in blood pressure. This mechanism may account for some of the variability in tolerance to cold exposure that affects patients with exertional angina.
Eight healthy males performed four rides to exhaustion at approximately 70% of their VO2max obtained in a neutral environment. Subjects cycled at ambient temperatures (Ta) of 3.6 +/- 0.3 (SD), 10.5 +/- 0.5, 20.6 +/- 0.2, and 30.5 +/- 0.2 degrees C with a relative humidity of 70 +/- 2% and an air velocity of approximately 0.7 m.s-1. Weighted mean skin temperature (Tsk), rectal temperature (Tre), and heart rate (HR) were recorded at rest, during exercise and at exhaustion. Venous samples were drawn before and during exercise and at exhaustion for determination of hemoglobin, hematocrit, blood metabolites, and serum electrolytes and osmolality. Expired air was collected for calculation of VO2 and R which were used to estimate rates of fuel oxidation. Ratings of perceived exertion (RPE) were also obtained. Time to exhaustion was significantly influenced by Ta (P = 0.001): exercise duration was shortest at 30.5 degrees C (51.6 +/- 3.7 min) and longest at 10.5 degrees C (93.5 +/- 6.2 min). Significant effects of Ta were also observed on VE, VO2, R, estimated fuel oxidation, HR, Tre, Tsk, sweat rate, and RPE. This study demonstrates that there is a clear effect of temperature on exercise capacity which appears to follow an inverted U relationship.
Patients with congestive heart failure (CHF) exhibit a decrease in maximal exercise capacity in response to a cold environment. The aim of this study was to further investigate the impact of cold exposure on submaximal exercise capacity, systemic adrenergic drive, and the effects of long-term beta-adrenergic blockade on these parameters. Thirty-three patients with CHF, with exercise limited by dyspnea and left ventricular ejection fraction of 26 +/- 4%, were randomized to receive metoprolol or carvedilol for 6 months. The observations were compared with 12 age-matched healthy volunteers. Maximal exercise performance with gas exchange analyses were assessed using a ramp protocol, and endurance capacity was measured using 2 constant-load exercise tests performed randomly at 20 degrees C and -8 degrees C. Healthy volunteers increased their submaximal exercise time by 20% (1,353 +/- 455 [20 degrees C] vs 1,635 +/- 475 seconds [-8 degrees C]; p <0.05), whereas patients with CHF exhibited a 21% decrease in exercise time (1,182 +/- 549 [20 degrees C] vs 931 +/- 524 seconds [-8 degrees C]; p <0.05) at -8 degrees C. Beta blockers increased submaximal exercise duration at 20 degrees C (+261 +/- 617 seconds; p <0.05) and -8 degrees C (+374 +/- 729 seconds; p <0.05). Norepinephrine increased to a greater extent at 4 minutes and at the time of exhaustion (at -8 degrees C) only in patients with CHF. Beta-adrenergic blockade caused no significant decrease in plasma norepinephrine levels. Patients with symptomatic CHF exhibited a significant decrease in submaximal exercise time in response to moderate cold exposure. Beta-blocker therapy with either metoprolol or carvedilol significantly increases submaximal exercise time and attenuates the impact of cold exposure on functional capacity.
Multiple studies have demonstrated a consistent association between ambient particulate air pollution and increased risk of hospital admissions and deaths for cardiovascular causes. We investigated the associations between fine particulate pollution (PM2.5) and blood pressure during 631 repeated visits for cardiac rehabilitation in 62 Boston residents with cardiovascular disease.
Blood pressure, cardiac risk factor, and exercise data were abstracted from records of rehabilitation visits between 1999 and 2001. We applied mixed-effect models, controlling for body mass index, age, gender, number of visits, hour of day, and weather variables. For an increase from the 10th to the 90th percentile in mean PM2.5 level during the 5 days before the visit (10.5 microg/m3), there was a 2.8-mm Hg (95% CI, 0.1 to 5.5) increase in resting systolic, a 2.7-mm Hg (95% CI, 1.2 to 4.3) increase in resting diastolic, and a 2.7-mm Hg (95% CI, 1.0 to 4.5) increase in resting mean arterial blood pressure. The mean PM2.5 level during the 2 preceding days (13.9 microg/m3) was associated with a 7.0-mm Hg (95% CI, 2.3 to 12.1) increase in diastolic and a 4.7-mm Hg (95% CI, 0.5 to 9.1) increase in mean arterial blood pressure during exercise in persons with resting heart rate > or =70 bpm, but it was not associated with an increase in blood pressure during exercise in persons with heart rate <70 bpm.
In patients with preexisting cardiac disease, particle pollution may contribute to increased risk of cardiac morbidity and mortality through short-term increases in systemic arterial vascular narrowing, as manifested by increased peripheral blood pressure.