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• W2079671805 abstract "We investigated the relation between inflammation and incident hypertension, independent of obesity, and tested the associations of cardiorespiratory fitness (fitness) and indexes of inflammation for the development of hypertension in 2,475 normotensive men. Inflammatory markers were C-reactive protein (CRP) and fibrinogen. Fitness was directly measured by peak oxygen uptake during sign/symptom-limited treadmill exercise testing to volitional fatigue; 266 men (10.7%) developed hypertension during an average of 4 years follow-up. After adjusting for potential confounding variables, the relative risk (RR) and 95% confidence interval (CI) for incident hypertension in those in the upper tertile versus lower tertile were 1.55 (95% CI 1.15 to 2.09) for CRP and 1.51 (95% CI 1.10 to 2.06) for fibrinogen. Although the association between fibrinogen and incident hypertension persisted after adjusting for body mass index (p = 0.049), the relation between CRP and incident hypertension was no longer statistically significant (p = 0.08). Fit men had a 27% decreased (RR 0.73, 95% CI 0.56 to 0.94) risk of incident hypertension compared with unfit men in a multivariable adjusted model. In the joint analysis, unfit men with upper CRP had 1.81 times (95% CI 1.21 to 2.70) and unfit men with upper fibrinogen had 2.03 times (95% CI 1.33 to 3.12) greater risks of incident hypertension compared with fit men with low CRP and fibrinogen, respectively. However, these risks did not significantly increase in fit men with upper CRP (RR 1.12, 95% CI 0.76 to 1.63) and fibrinogen (RR 1.26, 95% CI 0.86 to 1.85) groups. In conclusion, these results suggest that heightened levels of fibrinogen, but not CRP, are associated with incident hypertension, independent of body weight, and that high fitness attenuates the risk of incident hypertension across upper levels of inflammatory markers in men. We investigated the relation between inflammation and incident hypertension, independent of obesity, and tested the associations of cardiorespiratory fitness (fitness) and indexes of inflammation for the development of hypertension in 2,475 normotensive men. Inflammatory markers were C-reactive protein (CRP) and fibrinogen. Fitness was directly measured by peak oxygen uptake during sign/symptom-limited treadmill exercise testing to volitional fatigue; 266 men (10.7%) developed hypertension during an average of 4 years follow-up. After adjusting for potential confounding variables, the relative risk (RR) and 95% confidence interval (CI) for incident hypertension in those in the upper tertile versus lower tertile were 1.55 (95% CI 1.15 to 2.09) for CRP and 1.51 (95% CI 1.10 to 2.06) for fibrinogen. Although the association between fibrinogen and incident hypertension persisted after adjusting for body mass index (p = 0.049), the relation between CRP and incident hypertension was no longer statistically significant (p = 0.08). Fit men had a 27% decreased (RR 0.73, 95% CI 0.56 to 0.94) risk of incident hypertension compared with unfit men in a multivariable adjusted model. In the joint analysis, unfit men with upper CRP had 1.81 times (95% CI 1.21 to 2.70) and unfit men with upper fibrinogen had 2.03 times (95% CI 1.33 to 3.12) greater risks of incident hypertension compared with fit men with low CRP and fibrinogen, respectively. However, these risks did not significantly increase in fit men with upper CRP (RR 1.12, 95% CI 0.76 to 1.63) and fibrinogen (RR 1.26, 95% CI 0.86 to 1.85) groups. In conclusion, these results suggest that heightened levels of fibrinogen, but not CRP, are associated with incident hypertension, independent of body weight, and that high fitness attenuates the risk of incident hypertension across upper levels of inflammatory markers in men. Although the favorable effects of high fitness on the prevention of hypertension have previously been reported in normotensive populations1Carnethon M.R. Gidding S.S. Nehgme R. Sidney S. Jacobs Jr., D.R. Liu K. Cardiorespiratory fitness in young adulthood and the development of cardiovascular disease risk factors.JAMA. 2003; 290: 3092-3100Crossref PubMed Scopus (485) Google Scholar, 2Barlow C.E. LaMonte M.J. Fitzgerald S.J. Kampert J.B. Perrin J.L. Blair S.N. Cardiorespiratory fitness is an independent predictor of hypertension incidence among initially normotensive healthy women.Am J Epidemiol. 2006; 163: 142-150Crossref PubMed Scopus (142) Google Scholar and in subjects who are at high risk of developing hypertension,3Shook R.P. Lee D.C. Sui X. Prasad V. Hooker S.P. Church T.S. Blair S.N. Cardiorespiratory fitness reduces the risk of incident hypertension associated with a parental history of hypertension.Hypertension. 2012; 59: 1220-1224Crossref PubMed Scopus (31) Google Scholar, 4Faselis C. Doumas M. Kokkinos J.P. Panagiotakos D. Kheirbek R. Sheriff H.M. Hare K. Papademetriou V. Fletcher R. Kokkinos P. Exercise capacity and progression from prehypertension to hypertension.Hypertension. 2012; 60: 333-338Crossref PubMed Scopus (84) Google Scholar a key unanswered question is whether high fitness attenuates the likelihood of developing hypertension in subjects with elevated inflammatory markers. The purposes of the present study were (1) to investigate the association between low-grade inflammatory markers and incident hypertension, independent of obesity, and (2) to test the joint associations of fitness and inflammatory markers for the development of hypertension in men. We hypothesized that low-grade inflammatory markers would be associated with incident hypertension but that high fitness may attenuate this association. In this study, we recruited 5,616 men who participated in 2 general health examinations during 1998 to 2009 at Samsung Medical Center, Seoul, South Korea. Of these subjects, 3,620 healthy men without hypertension, cardiovascular disease, and type 2 diabetes at baseline examination were included. An additional 1,145 men whose inflammatory markers were not measured at baseline were excluded. Accordingly, 2,475 men (aged 20 to 76 years) free of hypertension, cardiovascular disease, and type 2 diabetes, who underwent peak or symptom-limited cardiopulmonary exercise testing and whose inflammatory markers were measured at baseline, were included in the analysis. Participants were followed from 1 to 11 years after the baseline examination, over an average follow-up of 4 years. Written informed consent was obtained from all participants before health screening, and the study was approved by the Medical Center Institutional Review Board. Cardiorespiratory fitness was directly measured by peak oxygen uptake (VO2peak, ml/kg/min) using expired gas analysis during peak or symptom-limited exercise testing. Treadmill exercise testing was conducted using a Bruce or modified Bruce protocol. Expired gases were collected breath-by-breath through a 1-way valve and analyzed using a metabolic measurement cart (Jaeger Oxycon Delta; Erich Jaeger, Hoechberg, Germany). Oxygen uptake data were measured in 20-second intervals. VO2peak was defined as the highest oxygen consumption recorded during peak exercise or immediate recovery. Exercise electrocardiograms were measured using 12-lead recordings (Q-4500; Quinton, Bothell, Washington). Exercise tests were stopped for any of the following reasons: a rating of perceived exertion (6 to 20 scale) >17 (very hard) and/or a respiratory exchange ratio >1.15; if the participant achieved >90% of age-predicted maximal heart rate; patient request because of volitional fatigue; attainment of a systolic blood pressure (BP) >250 mm Hg; increasing chest discomfort; threatening arrhythmias; or >1 mm of horizontal or downsloping ST-segment depression. Age-specific distributions of VO2peak were created by the following age groups: 20 to 39, 40 to 49, 50 to 59, and ≥60. All participants were classified into fit (middle and upper tertiles) and unfit (low tertile) categories based on age-specific VO2peak percentiles. Blood samples were collected in the morning after a 12-hour overnight fast and analyzed by the hospital clinical laboratory. Total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides were analyzed by enzymatic colorimetric and liquid selective detergent methods, respectively, using a Hitachi 7600 (Hitachi Co., Tokyo, Japan) analyzer. Fasting glucose levels were determined using the Hexokinase, UV method (Hitachi 7600; Hitachi Co.). High-sensitivity C-reactive protein (CRP) was measured using a CRP (II) Latax X2 turbidimetric method (Hitachi Corporation, Tokyo, Japan). Fibrinogen was measured by a clotting method using an STA coagulation analyzer (Diagnostica Stago, Asniere, France). Inter- and intra-assay coefficients of variation were <5% for all blood variables. CRP and fibrinogen were classified into tertile categories (low, middle, and upper). Heart rate in the supine position was obtained using the electrocardiogram at rest. Body mass index (BMI) was calculated as weight (kg) divided by height squared (m2). Smoking habits (never, past, and current), alcohol consumption (none, ≥3 d/wk), and related demographic/lifestyle information were evaluated through questionnaire. BP at rest was measured in the seated position after ≥5 minutes of quiet rest using an automated BP monitor (Dinamap PRO 100; GE Healthcare, Milwaukee, Wisconsin). The lowest reading of 2 measurements was used as the baseline value. Hypertension was defined as systolic and/or diastolic BP ≥140/90 mm Hg, diagnosed hypertension by a physician and/or the use of antihypertensive medications at baseline examination. Participants with hypertension by these criteria at baseline were excluded from the present study. The incidence of hypertension was assessed at follow-up health examinations as systolic and/or diastolic BP ≥140/90 mm Hg or diagnosed hypertension by a physician because we did not have information regarding prescribed antihypertensive medications at the follow-up examination. Data are presented as mean ± SD or median (interquartile range) for continuous variables and proportions for categorical variables. For group comparisons by incident hypertension at follow-up, independent t tests were used to test mean differences for continuous variables, and the chi-square tests were used to test frequency differences for categorical variables. Cox proportional hazards regression was used to examine the effect of inflammatory markers and fitness on the incidence of hypertension. Relative risks (RRs) and 95% confidence intervals (CIs) for incident hypertension were estimated with adjustment for potential confounding variables with specific reference to fitness, expressed as VO2peak and inflammatory markers (i.e., CRP and fibrinogen). We additionally investigated this association by including BMI from the earlier referenced model to determine whether inflammatory markers predict the incidence of hypertension, independent of obesity. The joint effects of inflammatory markers and fitness on the risk of incident hypertension were examined using combined groups. Participants were divided into 6 groups based on cross-classification of inflammation levels (low, middle, and upper) and fitness status (fit and unfit). Reference groups were fit-low CRP or fit-low fibrinogen cohorts. The interactions between inflammatory markers and fitness were tested. Inspection of empirical cumulative hazard plots (log-log [survival function] vs log [time]) across exposure categories indicated that the proportional hazards assumption was appropriate. Trends across fitness, CRP, and fibrinogen were tested by treating these exposure categories as an ordinal scale. Statistical significance was set at p <0.05. All data analyses were carried out using Statistical Package for the Social Sciences (IBM SPSS Statistics for Windows, version 21.0; IBM Corp., Armonk, New York). During an average 4-year follow-up, 266 men (10.7%) developed hypertension. Men who developed hypertension had greater mean BMI, heart rate at rest, systolic and/or diastolic BP at rest, total cholesterol, low-density lipoprotein cholesterol, fibrinogen, and CRP but lower VO2peak (all p <0.05) at baseline compared with men who remained normotensive (Table 1). Table 2 lists the RRs and 95% CIs of incidence of hypertension by fitness status and tertiles of inflammatory markers. Fit men had 31% lower risk of developing hypertension compared with unfit men after adjusting for potential confounding variables (model 1). The association remained unchanged after further adjustment for BMI (model 2). Men in the highest tertile of CRP had 1.55 times (95% CI 1.15, 2.09) the risk of incident hypertension than did men in the lowest tertile of CRP (model 1). Similarly, men in the highest tertile of fibrinogen had 1.51 times (95% CI 1.10, 2.06) the risk of incident hypertension compared with men in the lowest tertile of fibrinogen (model 1). The positive associations between fibrinogen and incident hypertension persisted after additional adjustment for BMI (p = 0.049) in model 2. Although further adjustment for BMI had only a modest effect on the strength of associations between CRP and incident hypertension, this association was no longer statistically significant (p = 0.08).Table 1Baseline characteristics of men with and without incident hypertension during follow-up (n = 2475)VariableNo Hypertension(n=2209)Hypertension (n=266)P valuesAge (years)48.3 (5.9)48.6 (6.6)0.333Body mass index (kg/m2)24.4 (2.4)25.2 (2.3)<0.001Current smoker39.2 %43.2 %0.057Alcohol intake ( ≥ 3 day/week)8.1 %7.5 %0.702Resting heart rate (bpm)62.5 (8.7)64.1 (9.0)0.006Systolic blood pressure (mmHg)116.1 (11.9)123.3 (10.4)<0.001Diastolic blood pressure (mmHg)73.7 (8.6)78.6 (7.1)<0.001Total cholesterol (mg/dl)201.4 (32.6)206.7 (35.9)0.014High-density lipoprotein cholesterol (mg/dl)48.7 (11.2)48.9 (11.9)0.866Low-density lipoprotein cholesterol (mg/dl)130.7 (29.3)135.1 (32.3)0.020Triglycerides (mg/dl)143.2 (76.3)144.0 (71.1)0.871Glucose (mg/dl)94.5 (9.7)95.5 (10.1)0.117Fibrinogen (mg/dl)278.2 (54.6)290.4 (54.3)0.001C-reactive protein (mg/dl)∗Median and interquartile ranges.0.07 (0.04-0.12)0.09 (0.05-0.15)<0.001VO2peak (ml/kg/min)34.6 (5.0)33.8 (4.8)0.027Data are presented as mean (SD) or percentage.∗ Median and interquartile ranges. Open table in a new tab Table 2Relative risks and 95% CI of incidence of hypertension by cardiorespiratory fitness and inflammatory markersVariablesNNo. of Incidentn (%)UnadjustedRR (95% CI)Model 1RR (95% CI)Model 2RR (95% CI)VO2peak (ml/kg/min)Per 1 METs increment0.87 (0.80-0.95)0.89 (0.81-0.97)0.91 (0.83-0.99)Unfit (29.8, 27.7-31.3)826104 (12.6)1 (ref)1 (ref)1 (ref)Fit (36.4, 34.4-39.2)1649162 (9.8)0.67 (0.53-0.86)0.69 (0.53-0.89)0.73 (0.56-0.94)P-value0.0020.0040.015C-reactive protein (mg/dl)Per 1 SD increment1.06 (0.97-1.17)1.03 (0.94-1.13)1.01 (0.92-1.11)Low (<0.05)94977 (8.1)1 (ref)1 (ref)1 (ref)Middle (0.06-0.10)73879 (10.7)1.22 (0.90-1.68)1.19 (0.86-1.63)1.12 (0.81-1.54)Upper (>0.11)788110 (14.0)1.60 (1.19-2.14)1.55 (1.15-2.09)1.41 (1.03-1.93)P-value0.0060.0140.08Fibrinogen (mg/dl)∗(n = 2471).Per 1 SD increment1.17 (1.05-1.31)1.21 (1.07-1.36)1.19 (1.06-1.34)Low (<253)85771 (8.3)1 (ref)1 (ref)1 (ref)Middle (254-294)77586 (11.1)1.29 (0.94-1.77)1.27 (0.93-1.75)1.27 (0.92-1.74)Upper (>295)839107 (12.8)1.46 (1.08-1.98)1.51 (1.10-2.06)1.48 (1.08-2.02)P-value0.0450.0370.049Model 1: Adjusted for age, systolic blood pressure, total cholesterol, high density lipoprotein cholesterol, triglycerides, glucose, resting heart rate, smoking, alcohol consumption, C-reactive protein, and fibrinogen when cardiorespiratory fitness is exposure or VO2peak when C-reactive protein and fibrinogen are exposures. Model 2: Adjusted for model 1 plus body mass index. VO2peak (ml/kg/min) present median (interquartile ranges).SD = standard deviation.∗ (n = 2471). Open table in a new tab Data are presented as mean (SD) or percentage. Model 1: Adjusted for age, systolic blood pressure, total cholesterol, high density lipoprotein cholesterol, triglycerides, glucose, resting heart rate, smoking, alcohol consumption, C-reactive protein, and fibrinogen when cardiorespiratory fitness is exposure or VO2peak when C-reactive protein and fibrinogen are exposures. Model 2: Adjusted for model 1 plus body mass index. VO2peak (ml/kg/min) present median (interquartile ranges). SD = standard deviation. Figure 1 shows the joint associations of inflammatory markers with fitness on the risk of incident hypertension. There were no significant interactions between inflammatory markers and fitness on incident hypertension (p for interactions = 0.38 for CRP and 0.90 for fibrinogen). After adjustment for risk factors, unfit men in the highest tertile of CRP had 1.81 times (95% CI 1.21, 2.70) the risk of incident hypertension than did fit men in the lowest tertile of CRP (Figure 1). Unfit men in the highest tertile of fibrinogen had twice the risk of hypertension (2.03, 95% CI 1.33, 3.12) compared with fit men in the lowest tertile of fibrinogen after adjustment for risk factors (Figure 1). However, these risks did not significantly increase in fit men with upper CRP and fibrinogen values. We found that upper levels of fibrinogen were associated with the incidence of hypertension, independent of BMI and other potential confounding variables. In addition, we found a positive association between CRP and incident hypertension independent of other confounders, but this finding was nullified after adjusting for BMI. Therefore, the association between elevated levels of CRP and the incidence of hypertension may be largely explained by obesity. Furthermore, the novel finding from the present study is that unfit men with upper inflammatory markers were at a greater risk of incident hypertension, but fit men with upper inflammatory markers had a similar risk of incident hypertension than did fit men with low inflammatory markers. These findings suggest that high fitness may attenuate the risk of developing hypertension in subjects with elevated inflammatory markers. There is evidence that inflammation independently predicts cardiovascular disease risks,5Ridker P.M. Buring J.E. Cook N.R. Rifai N. C-reactive protein, the metabolic syndrome, and risk of incident cardiovascular events: an 8-year follow-up of 14 719 initially healthy American women.Circulation. 2003; 107: 391-397Crossref PubMed Scopus (2024) Google Scholar but whether inflammation predicts the incidence of hypertension, independent of obesity and other factors, is controversial. In the Coronary Artery Risk Development in Young Adults study, CRP did not predict incident hypertension after adjusting for BMI.6Lakoski S.G. Herrington D.M. Siscovick D.M. Hulley S.B. C-reactive protein concentration and incident hypertension in young adults: the CARDIA study.Arch Intern Med. 2006; 166: 345-349Crossref PubMed Scopus (76) Google Scholar Although CRP and fibrinogen were associated with the risk of future hypertension in the Multi-Ethnic Study of Atherosclerosis,7Lakoski S.G. Cushman M. Siscovick D.S. Blumenthal R.S. Palmas W. Burke G. Herrington D.M. The relationship between inflammation, obesity and risk for hypertension in the Multi-Ethnic Study of Atherosclerosis (MESA).J Hum Hypertens. 2011; 25: 73-79Crossref PubMed Scopus (75) Google Scholar these associations were attenuated after adjusting for BMI. The investigators suggested that the relation between inflammation and incident hypertension may be largely explained by obesity and related risk factors.8Engstrom G. Inflammation, obesity and risk of hypertension: shared pathways or independent risk factors?.J Hum Hypertens. 2011; 25: 71-72Crossref PubMed Scopus (4) Google Scholar Our results are consistent with these studies, suggesting that the role of CRP in association with future hypertension is attributed, at least in part, to obesity and other risk factors. Because obesity is a major cause of elevated pro-inflammatory cytokines and is associated with increased CRP levels, it is plausible that it may be a mediator between CRP and incident hypertension. In contrast, CRP levels at baseline were independently associated with incident hypertension in the Framingham Offspring Study.9Wang T.J. Gona P. Larson M.G. Levy D. Benjamin E.J. Tofler G.H. Jacques P.F. Meigs J.B. Rifai N. Selhub J. Robins S.J. Newton-Cheh C. Vasan R.S. Multiple biomarkers and the risk of incident hypertension.Hypertension. 2007; 49: 432-438Crossref PubMed Scopus (146) Google Scholar Although CRP was not an independent risk factor associated with incident hypertension in the present study, the association between fibrinogen and incident hypertension remained significant, even after adjusting for BMI and other risk factors in our Asian cohort. This finding is consistent with that observed in the Atherosclerosis Risk in Communities Study women10Folsom A.R. Peacock J.M. Nieto F.J. Rosamond W.D. Eigenbrodt M.L. Davis C.E. Wu K.K. Plasma fibrinogen and incident hypertension in the Atherosclerosis Risk in Communities (ARIC) Study.J Hypertens. 1998; 16: 1579-1583Crossref PubMed Scopus (34) Google Scholar and the Blue Mountains cohort of older Australian women11Shankar A. Wang J.J. Rochtchina E. Mitchell P. Positive association between plasma fibrinogen level and incident hypertension among men: population-based cohort study.Hypertension. 2006; 48: 1043-1049Crossref PubMed Scopus (25) Google Scholar demonstrating that fibrinogen was positively associated with incident hypertension in men but not women. Because our study participants were initially normotensive men, further studies are needed to clarify potential gender differences in these relations. Although the favorable effects of high fitness on the prevention of hypertension have previously been reported in initially normotensive subjects,1Carnethon M.R. Gidding S.S. Nehgme R. Sidney S. Jacobs Jr., D.R. Liu K. Cardiorespiratory fitness in young adulthood and the development of cardiovascular disease risk factors.JAMA. 2003; 290: 3092-3100Crossref PubMed Scopus (485) Google Scholar, 2Barlow C.E. LaMonte M.J. Fitzgerald S.J. Kampert J.B. Perrin J.L. Blair S.N. Cardiorespiratory fitness is an independent predictor of hypertension incidence among initially normotensive healthy women.Am J Epidemiol. 2006; 163: 142-150Crossref PubMed Scopus (142) Google Scholar the potential impact of fitness on the development of hypertension in high-risk subjects has remained unclear. There have been few prospective studies investigating the role of fitness on the incidence of hypertension in subjects at risk for its development. One study found an inverse association between fitness and incident hypertension in a population with a family history of hypertension.3Shook R.P. Lee D.C. Sui X. Prasad V. Hooker S.P. Church T.S. Blair S.N. Cardiorespiratory fitness reduces the risk of incident hypertension associated with a parental history of hypertension.Hypertension. 2012; 59: 1220-1224Crossref PubMed Scopus (31) Google Scholar Nevertheless, high fitness did not completely eliminate the increased risks of genetic predisposition to incident hypertension.3Shook R.P. Lee D.C. Sui X. Prasad V. Hooker S.P. Church T.S. Blair S.N. Cardiorespiratory fitness reduces the risk of incident hypertension associated with a parental history of hypertension.Hypertension. 2012; 59: 1220-1224Crossref PubMed Scopus (31) Google Scholar In addition, in subjects with prehypertension who are at high risk of developing hypertension, the RR for developing hypertension was lower in high-fit subjects.4Faselis C. Doumas M. Kokkinos J.P. Panagiotakos D. Kheirbek R. Sheriff H.M. Hare K. Papademetriou V. Fletcher R. Kokkinos P. Exercise capacity and progression from prehypertension to hypertension.Hypertension. 2012; 60: 333-338Crossref PubMed Scopus (84) Google Scholar Our findings are in tandem with other observational studies reporting that high fitness attenuates the risk of incident hypertension in varied ethnic populations at high risk for its development. Although our findings suggest that fit men with elevated inflammatory markers are less likely to develop hypertension, the underlying mechanisms remain unclear. High-fit subjects are characterized by enhanced autonomic function (decreased sympathetic tone and enhanced parasympathetic activity)12da Silva D.F. Bianchini J.A. Antonini V.D. Hermoso D.A. Lopera C.A. Pagan B.G. McNeil J. Nardo Junior N. Parasympathetic cardiac activity is associated with cardiorespiratory fitness in overweight and obese adolescents.Pediatr Cardiol. 2014; 35: 684-690Crossref PubMed Scopus (40) Google Scholar and decreased cardiometabolic risk factors, including body fat, insulin resistance,13Larsen F.J. Anderson M. Ekblom B. Nystrom T. Cardiorespiratory fitness predicts insulin action and secretion in healthy individuals.Metabolism. 2012; 61: 12-16Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar and selected lipoproteins,14Grundy S.M. Barlow C.E. Farrell S.W. Vega G.L. Haskell W.L. Cardiorespiratory fitness and metabolic risk.Am J Cardiol. 2012; 109: 988-993Abstract Full Text Full Text PDF PubMed Scopus (55) Google Scholar all of which are independently associated with high BP. High fitness may also be associated with less vascular endothelial oxidative stress15Pierce G.L. Donato A.J. LaRocca T.J. Eskurza I. Silver A.E. Seals D.R. Habitually exercising older men do not demonstrate age-associated vascular endothelial oxidative stress.Aging Cell. 2011; 10: 1032-1037Crossref PubMed Scopus (89) Google Scholar and preserved antioxidant enzyme efficiency16Pialoux V. Brown A.D. Leigh R. Friedenreich C.M. Poulin M.J. Effect of cardiorespiratory fitness on vascular regulation and oxidative stress in postmenopausal women.Hypertension. 2009; 54: 1014-1020Crossref PubMed Scopus (72) Google Scholar and decreased arterial stiffness,17Fujie S. Iemitsu M. Murakami H. Sanada K. Kawano H. Gando Y. Kawakami R. Miyachi M. Higher cardiorespiratory fitness attenuates arterial stiffening associated with the Ala54Thr polymorphism in FABP2.Physiol Genomics. 2013; 45: 237-242Crossref PubMed Scopus (9) Google Scholar both of which are predictors of future hypertension.18Mitchell G.F. Arterial stiffness and hypertension.Hypertension. 2014; 64: 13-18Crossref PubMed Scopus (134) Google Scholar Interestingly, 1 previous study showed that inflammation was associated with increased arterial stiffness, but these increases were attenuated in fit subjects compared with their unfit counterparts.19Jae S.Y. Yoon E.S. Jung S.J. Jung S.G. Park S.H. Kim B.S. Heffernan K.S. Fernhall B. Effect of cardiorespiratory fitness on acute inflammation induced increases in arterial stiffness in older adults.Eur J Appl Physiol. 2013; 113: 2159-2166Crossref PubMed Scopus (17) Google Scholar The investigators suggested that high fitness may provide vascular protection, even in subjects with elevated inflammatory markers. This study has several potential limitations. Because our participants included only men, we were unable to determine whether this association extends to women. Our database did not include information about family history of hypertension and dietary sodium intake, which may potentially confound the relation between cardiorespiratory fitness and the incidence of hypertension. Although we adjusted for potential confounders to predict an independent association between inflammation and the incidence of hypertension, it is possible that residual variables that were not measured may have influenced the observed difference in RRs. Moreover, we used a single measurement of inflammatory markers and a single assessment of BP at baseline to predict the risk of hypertension and did not correct for potential regression dilution bias. Finally, participants in the present study were healthy normotensive men without cardiovascular disease and diabetes. Thus, it is possible that elevated levels of CRP and/or fibrinogen in some participants were because of subclinical infections or connective tissue disorders. Despite these limitations, we directly measured VO2peak using metabolic gas analysis during peak or symptom-limited exercise testing, the gold standard measure of cardiorespiratory fitness, and related these findings to inflammatory markers and the development of hypertension in a large cohort of normotensive men over an extended follow-up. This work was supported by the 2014 sabbatical year research grant of the University of Seoul. The authors have no conflicts of interest to disclose." @default.
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• W2079671805 title "Relation of C-Reactive Protein, Fibrinogen, and Cardiorespiratory Fitness to Risk of Systemic Hypertension in Men" @default.
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