Search

To assess the influence of changes in cardiorespiratory fitness (CRF) after exercise training on mortality risk in a cohort of self-referred, apparently healthy adults.A total of 683 participants (404 men, 279 women; mean age: 42.7±11.0 y) underwent two maximal cardiopulmonary exercise tests (CPX) between March 20, 1970, and December 11, 2012, to assess CRF at baseline (CPX1) and post-exercise training (CPX2). Participants were followed for an average of 29.8±10.7 years after their CPX2. Cox proportional hazards models were performed to determine the relationship of CRF change with mortality, with change in CRF as a continuous variable, as well as a categorical variable. A Wald chi-square test was used to compare the coefficients estimating the relationship of peak oxygen consumption (VODuring the follow-up period there were 180 deaths. When assessed independently, there were 20% (95% CI, 10-49%) and 38% (95% CI, 7-66%) lower mortality risks per 1 metabolic equivalent improvement in CRF (P.01) in men and women, respectively, after multivariable adjustment. Those that remained unfit had ∼2-fold higher risk for all-cause mortality compared with those that remained fit and CRF at CPX2 was a stronger predictor of all-cause mortality than at CPX1 (P=.02).Improving CRF through exercise training lowers mortality risk. Clinicians should encourage individuals to participate in exercise training to improve CRF to lower risk of mortality.

Background The relationship between cardiorespiratory fitness (CRF) and mortality risk has typically been assessed using a single measurement, though some evidence suggests the change in CRF over time influences risk. This evidence is predominantly based on studies using estimated CRF (CRFe). The strength of this relationship using change in directly measured CRF over time in apparently healthy men and women is not well understood. Purpose To examine the association of change in CRF over time, measured using cardiopulmonary exercise testing (CPX), with all-cause and disease-specific mortality and to compare baseline and subsequent CRF measurements as predictors of all-cause mortality. Methods Participants included 833 apparently healthy men and women (42.9 ± 10.8 years) who underwent two maximal CPXs, the second CPX being ≥1 year following the baseline assessment (mean 8.6 years, range 1.0 to 40.3 years). Participants were followed for up to 17.7 (SD 11.8) years for all-cause-, cardiovascular disease- (CVD), and cancer mortality. Cox-proportional hazard models were performed to determine the association between the change in CRF, computed as visit 1 (CPX1) peak oxygen consumption (VO2peak [mL·kg−1·min−1]) – visit 2 (CPX2) VO2peak, and mortality outcomes. A Wald-Chi square test of equality was used to compare the strength of CPX1 to CPX2 VO2peak in predicting mortality. Results During follow-up, 172 participants died. Overall, the change in CPX-CRF was inversely related to all-cause, CVD, and cancer mortality (p Conclusion The change in CRF over time was inversely related to mortality outcomes, and mortality was better predicted by CRF measured at subsequent test than CPX1 CRF. These findings emphasize the importance of adopting lifestyle behaviors that promote CRF, as well as support the need for routine assessment of CRF in clinical practice to better assess risk.

Cardiovascular diseases (CVD) are the leading cause of mortality in modernized societies. Arterial stiffening with aging and disease is a key pathological event leading to increased CVD morbidity and mortality. Perivascular adipose tissue (PVAT) is a fat depot not widely studied yet has direct and profound effects on arterial stiffening. Identifying PVAT as a novel therapeutic target to lower arterial stiffness and thereby CVD risk has potentially important clinical ramifications. Thus, herein, we will overview the current preclinical evidence and the associated mechanisms for PVAT to promote arterial stiffness with aging and other disease conditions. We will also discuss viable translational lifestyle and pharmacological interventions for altering PVAT function that may de-stiffen arteries. Last, the translational potential for PVAT as a therapeutic target to lower arterial stiffness and CVD risk for clinical populations will be discussed.

Objective Obesity is a risk factor for cardiovascular disease that increases aortic stiffness, which predicts future cardiovascular events. Additionally, obesity is associated with overconsumption, which contributes to aortic stiffening. Recent work has highlighted the role of various foods and nutrients on aortic stiffness among the general population. The objective of the present study was to explore the influence of dietary factors on obesity-associated aortic stiffness, as food choices might be a potential explanation for accelerated aortic stiffening in obesity rather than overconsumption alone. Methods Data collected in our laboratory were evaluated in aggregate considering obese men with available measures of aortic stiffness and habitual dietary intake (n = 22). Aortic stiffness was assessed with the gold standard carotid-femoral pulse wave velocity, and habitual dietary intake was determined with the National Institutes of Health's Dietary History Questionnaire-II. Results Whole grain consumption predicted obesity-associated aortic stiffness in regression analyses (R 2 = 0.29, P = 0.010). This correlation remained significant after adjusting for traditional risk factors (age, body mass index, blood pressure) (R 2 = 0.27, P = 0.027). Overconsumption determined by daily caloric intake was not predictive of aortic stiffness (R 2 = 0.09, P = 0.17) nor was total fiber content (R 2 = 0.06, P = 0.29). Conclusions These findings suggest a potential role of whole grains to protect against aortic stiffness even when dietary overconsumption is present. Fiber content has been proposed as a major beneficial component in whole grains, but it did not correlate with obesity-related aortic stiffness, suggesting whole grains may have a unique and potentially synergistic role in the protection of obesity-associated aortic health.

Obesity results in greater aortic stiffness assessed by carotid-femoral Pulse Wave Velocity (cfPWV), which is an independent predictor of cardiovascular (CV) events. We hypothesized that a novel curcumin formulation with enhanced bioavailability, CurQfen®, would reduce cfPWV and inflammation in young, obese men. In the present placebo-controlled pilot study, 22 obese subjects (BMI ⩾ 30.0 kg/m2) were randomized into placebo (n = 11, BMI = 33.18 ± 3.38 kg/m2) and curcumin (n = 11, BMI = 33.29 ± 3.69 kg/m2) supplemented groups. When CurQfen® was supplemented at 500 mg/day for 12 weeks, it was found that individuals who did respond to the treatment (n = 6) entered the study with higher baseline cfPWV versus those who did not respond (n = 5) (6.81 ± 0.83 m/s v. 5.84 ± 0.41 m/s, p = 0.045, group by time interaction). The curcumin responders also had increased plasma IL-13 concentrations (p = 0.018, 12 weeks v. baseline). These findings suggest CurQfen curcumin has potential to de-stiffen arteries in young, obese men with greater aortic stiffness.

Carbohydrates are the primary source of energy for human body. Carbohydrates increase resting muscle glycogen levels and help in delaying muscle fatigue. But, higher intake of high glycemic carbohydrates may lead to complications, if not balanced by physical activities. Our earlier studies have indicated that a proprietary powder preparation of coconut inflorescence sap (COCOZEN™, abbreviated as ‘CSP’ meaning ‘coconut sap powder’) contains relatively higher levels of micronutrients and possess antioxidant, anti-inflammatory, nephroprotective, hepatoprotective, gastroprotective and ergogenic activities. Thus, the present study was aimed to investigate the safety and efficacy of CSP (15 g/day for 90 days) on healthy and nonathletic subjects (n = 20). The study was performed in two phases. In the first phase, glycemic index (GI) was measured using glucose as a reference standard. In the second phase, CSP was supplemented at (15g × 1)/day dosage for 90 days and monitored the anthropometric parameters, adverse events, blood sugar levels (fasting and postprandial), blood pressure, and other routine hematological and biochemical parameters. It was observed that CSP possess a GI of 52.47 and is safe with an acceptable sensory attribute. It did not contribute any side effects or deviations in blood sugar or other hematological and biochemical parameters, except in Hb and lipid profile which showed significant (p

We tested the hypothesis that curcumin supplementation would reverse arterial dysfunction and vascular oxidative stress with aging. Young (Y, 4–6 mo) and old (O, 26–28 mo) male C57BL6/N mice were given normal or curcumin supplemented (0.2%) chow for 4 weeks (n = 5–10/group/measure). Large elastic artery stiffness, assessed by aortic pulse wave velocity (aPWV), was greater in O (448 ± 15 vs. 349 ± 15 cm/s) and associated with greater collagen I and advanced glycation end-products and less elastin (all P < 0.05). In O, curcumin restored aPWV (386 ± 15 cm/s), collagen I and AGEs to levels not different vs. Y. Ex vivo carotid artery acetylcholine (ACh)-induced endothelial-dependent dilation (EDD, 79 ± 3 vs. 94 ± 2%), nitric oxide (NO) bioavailability and protein expression of endothelial NO synthase (eNOS) were lower in O (all P < 0.05). In O, curcumin restored NO-mediated EDD (92 ± 2%) to levels of Y. Acute ex vivo administration of the superoxide dismutase (SOD) mimetic TEMPOL normalized EDD in O control mice (93 ± 3%), but had no effect in Y control or O curcumin treated animals. O had greater arterial nitrotyrosine abundance, superoxide production and NADPH oxidase p67 subunit expression, and lower manganese SOD (all P < 0.05), all of which were reversed with curcumin. Curcumin had no effects on Y. Curcumin supplementation ameliorates age-associated large elastic artery stiffening, NO-mediated vascular endothelial dysfunction, oxidative stress and increases in collagen and AGEs in mice. Curcumin may be a novel therapy for treating arterial aging in humans.

We tested the hypothesis that sodium nitrite treatment reverses large elastic artery stiffening in old mice via reductions in collagen I, increases in elastin and/or decreases in advanced glycation endproducts (AGEs) mediated by reduced oxidative stress. Aortic pulse wave velocity (aPWV), a measure of large elastic artery stiffness, was greater in old (26–28 mo) compared with young (4–6 mo) control animals (520 ± 9 vs. 405 ± 6 cm/s, p