Abstract 268: Vascular Dysfunction in High BMI Black College Football Players

Background: Former football players (FP) who competed with BMI > 30 have high rates of atherosclerosis and early mortality (28% by age 50). FP are disproportionately black, a group predisposed to hypertension and atherosclerosis. Hypothesis: Positive energy balance and oxidative stress lead to vascular dysfunction in black FP. Methods: High BMI college FP (n=33) underwent metabolic and vascular testing at the Vanderbilt Medical Center during the offseason training program. Endothelial function was tested using flow-mediated dilation (FMD) of the brachial artery. Arterial elasticity and vascular resistance were tested using a calibrated tonometer. Regression was performed using least squares on Stat, version 12. Results: Elevated blood pressure (EBP) (SBP > 130) was common in both black (n = 14) and white (n = 19) athletes (78% vs 63%, p = .34). Black players had significantly higher systemic vascular resistance and lower arterial elasticity. However, they had significantly better lipid profiles and body composition, and comparable insulin resistance assessed by HOMA. In black FP, EBP was associated with positive energy balance (4.3 kg gained during six weeks from enrollment to clinic visit vs. 0.7 kg, p = .05). Daily caloric intake predicted endothelial function as measured by flow mediated vasodilation (FMD) (r=.76, p=.001). Caloric intake and oxidative stress (F2-isoprostanes) trended to inversely correlate with larger artery elasticity (r=.40, p=.09 and r=.41, p=.09, respectively). HOMA did not predict FMD (r < .01, p = .56). Respiratory quotient (RQ) correlated with f2-isoprostanes (r=.53, p=.02), suggesting a link between mitochondrial dysfunction and oxidative stress. Conclusion: High BMI black FP suffer from vascular dysfunction, possibly due to oxidative stress from overfeeding. This correlates with studies of non-athlete adult population, but differs notably in being independent of insulin resistance. A larger, longitudinal study is needed to establish a link between overfeeding, vascular dysfunction and early cardiovascular morbidity and mortality in high BMI black athletes. The role of oxidative stress and selective use of nitric oxide donor drugs in black athletes should be explored.

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Abstract 17720: Unique Features of Metabolic Syndrome in High BMI College Football Players

Circulation ◽

10.1161/circ.132.suppl_3.17720 ◽

2015 ◽

Vol 132 (suppl_3) ◽

Author(s):

Edward M Powers ◽

Heidi J Silver ◽

Lynn A Seabolt ◽

Abbie L Warren ◽

Hakmook Kang ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Energy Balance ◽

Medical Center ◽

College Football ◽

Positive Energy ◽

Football Players ◽

The Metabolic Syndrome ◽

Positive Energy Balance ◽

High Bmi

Background: Metabolic syndrome in football players is a common, yet poorly understood phenomenon. With 88,000 college football players and one million high school football players, there is a large, at-risk population. Hypothesis: We hypothesized that metabolic syndrome in football players is driven by oxidative stress and positive energy balance. Methods: A single site, cross-sectional study was performed at Vanderbilt University Medical Center of high BMI college football players (n=33). Prevalence of metabolic syndrome was determined. Data related to diet composition, oxidative stress, inflammation, body composition, glucose disposition, lipoprotein metabolism, and endothelial function were assessed to identify drivers of the metabolic syndrome in this cohort. Results: Prevalence of clinical metabolic syndrome was 33% (11/33) despite high cardiorespiratory fitness in all players (Table 1). Elevated waist circumference, HDL, and elevated blood pressure were present together in 73% of cases. Cases had increased oxidative stress (F2-isoprostanes) and inflammation (CRP). Insulin resistance was not worse by HOMA. Visceral fat predicted HDL and CRP. Respiratory quotient was identical between groups but metabolomics revealed decreased TCA cycle intermediates in cases. There were no differences in caloric intake but cases had gained more weight (4.2 vs 2.0 kg, p=.06). Conclusion: High BMI collegiate football players have metabolic syndrome at unexpectedly high rates with a unique set of risk factors and unusual pathophysiology. They have low HDL despite normal triglyceride levels and no defects in glucose metabolism. These data suggest deleterious effects of positive energy balance and oxidative stress irrespective of exercise quantity. These results provide strong rationale to conduct larger, longitudinal studies.

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Tetrahydrocurcumin in combination with deferiprone attenuates hypertension, vascular dysfunction, baroreflex dysfunction, and oxidative stress in iron-overloaded mice

Vascular Pharmacology ◽

10.1016/j.vph.2016.10.001 ◽

2016 ◽

Vol 87 ◽

pp. 199-208 ◽

Cited By ~ 15

Author(s):

Weerapon Sangartit ◽

Poungrat Pakdeechote ◽

Veerapol Kukongviriyapan ◽

Wanida Donpunha ◽

Shigeki Shibahara ◽

...

Keyword(s):

Oxidative Stress ◽

Vascular Dysfunction ◽

And Oxidative Stress

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Dietary rapamycin supplementation reverses age-related vascular dysfunction and oxidative stress, while modulating nutrient-sensing, cell cycle, and senescence pathways

Aging Cell ◽

10.1111/acel.12524 ◽

2016 ◽

Vol 16 (1) ◽

pp. 17-26 ◽

Cited By ~ 61

Author(s):

Lisa A. Lesniewski ◽

Douglas R. Seals ◽

Ashley E. Walker ◽

Grant D. Henson ◽

Mark W. Blimline ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Cycle ◽

Vascular Dysfunction ◽

Nutrient Sensing ◽

Age Related ◽

And Oxidative Stress

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Dietary fish oil prevents vascular dysfunction and oxidative stress in hyperinsulinemic rats

American Journal of Hypertension ◽

10.1016/j.amjhyper.2004.08.030 ◽

2005 ◽

Vol 18 (2) ◽

pp. 213-219 ◽

Cited By ~ 37

Author(s):

M NYBY ◽

K MATSUMOTO ◽

K YAMAMOTO ◽

K ABEDI ◽

P ESLAMI ◽

...

Keyword(s):

Oxidative Stress ◽

Fish Oil ◽

Vascular Dysfunction ◽

Dietary Fish ◽

And Oxidative Stress

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Calorie Restriction and Aging

Blood ◽

10.1182/blood.v116.21.sci-2.sci-2 ◽

2010 ◽

Vol 116 (21) ◽

pp. SCI-2-SCI-2

Author(s):

Rafael de Cabo

Keyword(s):

Oxidative Stress ◽

Life Span ◽

Calorie Restriction ◽

Stress Proteins ◽

Conflicts Of Interest ◽

Caloric Intake ◽

Tissue Growth ◽

Age Related ◽

Underlying Mechanisms ◽

And Oxidative Stress

Abstract Abstract SCI-2 A prominent manifestation of aging is a reduced ability to respond to environmental stressors, including heat and oxidative stress. Reduced stress tolerance and decreased ability to maintain homeostasis are at least partially responsible for the increased morbidity and mortality that occurs with advancing age. The age-related attenuation of stress pathways and increased expression of stress-response genes with aging are examples of the growing body of evidence linking reduced stress responsiveness to aging. In 1935, McCay and colleagues first reported that reducing the caloric intake of rodents could significantly lengthen their mean and maximal life span, slowing down basic aging processes. The effect of calorie restriction (CR) on delaying aging has been replicated in many animal species including nonhuman primates, although in these, potential life span alterations cannot be ascertained for several more years due to their longevity CR causes a reduction in body weight, tissue growth, blood glucose, insulin levels and body temperature. In addition, CR prevents the age-related decline in tolerance to different stressors such as oxidative and heat, and the age-related reduction in expression of protective heat shock and oxidative stress proteins. While CR is the only intervention that has consistently been shown to increase maximum life span and prevent or delay the onset of age-associated pathophysiological changes in laboratory rodents, the underlying mechanisms remain elusive. Using calorie restriction (CR) as their benchmark research tool, gerontologists are making progress in identifying dietary and pharmacologic interventions that may be applicable to retarding aging processes in humans. Disclosures: No relevant conflicts of interest to declare.

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Inhibition of Protein Kinase Cβ Does Not Improve Endothelial Function in Type 2 Diabetes

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2010-0286 ◽

2010 ◽

Vol 95 (8) ◽

pp. 3783-3787 ◽

Cited By ~ 16

Author(s):

Joshua A. Beckman ◽

Allison B. Goldfine ◽

Alison Goldin ◽

Adnan Prsic ◽

Sora Kim ◽

...

Keyword(s):

Oxidative Stress ◽

Type 2 Diabetes ◽

Healthy Subjects ◽

Vascular Dysfunction ◽

Endothelial Damage ◽

Markers Of Inflammation ◽

Resistance Vessels ◽

Healthy Control ◽

And Oxidative Stress

Context: Antagonism of protein kinase Cβ (PKCβ) restores endothelial function in experimental models of diabetes and prevents vascular dysfunction in response to hyperglycemia in healthy humans. Objective: We tested the hypothesis that PKCβ antagonism would improve vascular function in subjects with type 2 diabetes compared with healthy control subjects. Design: The effect of PKCβ was evaluated in a randomized, placebo-controlled, double-blinded crossover trial. Setting: The study was performed in the outpatient setting of a university medical center. Participants: Thirteen subjects with type 2 diabetes without evidence of cardiovascular disease and 15 healthy control subjects were recruited via newspaper advertisement. Intervention: Subjects underwent a randomized, double-blind, crossover, placebo-controlled trial of the selective PKCβ antagonist ruboxistaurin mesylate. Subjects received each treatment for 14 d. Main Outcome Measure: Endothelium-dependent and endothelium-independent vasodilation of forearm resistance vessels was measured with mercury-in-silastic, strain-gauge plethysmography during intraarterial administration of methacholine chloride and verapamil, respectively. Markers of inflammation, fibrinolysis, endothelial damage, and oxidative stress were measured after each treatment. Results: Endothelium-dependent vasodilation of forearm resistance vessels was attenuated in diabetic subjects when compared with healthy subjects (P = 0.001). Endothelium-independent vasodilation did not differ between groups (P value not significant). Ruboxistaurin did not significantly change endothelium-dependent or endothelium-independent vasodilation or blood-based markers of inflammation, fibrinolysis, endothelial damage, and oxidative stress in either diabetic or healthy subjects. Conclusion: Endothelial dysfunction of forearm resistance vessels was not improved by 2 wk of selective PKCβ inhibition in patients with diabetes. These results suggest that PKCβ does not contribute significantly to vascular dysfunction in otherwise healthy patients with type 2 diabetes.

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COPD and stroke: are systemic inflammation and oxidative stress the missing links?

Clinical Science ◽

10.1042/cs20160043 ◽

2016 ◽

Vol 130 (13) ◽

pp. 1039-1050 ◽

Cited By ~ 61

Author(s):

Victoria Austin ◽

Peter J. Crack ◽

Steven Bozinovski ◽

Alyson A. Miller ◽

Ross Vlahos

Keyword(s):

Oxidative Stress ◽

Risk Factors ◽

Systemic Inflammation ◽

Vascular Dysfunction ◽

Airflow Limitation ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Cardiovascular Comorbidities ◽

Shared Risk ◽

And Oxidative Stress

Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation and loss of lung function, and is currently the third largest cause of death in the world. It is now well established that cardiovascular-related comorbidities such as stroke contribute to morbidity and mortality in COPD. The mechanisms linking COPD and stroke remain to be fully defined but are likely to be interconnected. The association between COPD and stroke may be largely dependent on shared risk factors such as aging and smoking, or the association of COPD with traditional stroke risk factors. In addition, we propose that COPD-related systemic inflammation and oxidative stress may play important roles by promoting cerebral vascular dysfunction and platelet hyperactivity. In this review, we briefly discuss the pathogenesis of COPD, acute exacerbations of COPD (AECOPD) and cardiovascular comorbidities associated with COPD, in particular stroke. We also highlight and discuss the potential mechanisms underpinning the link between COPD and stroke, with a particular focus on the roles of systemic inflammation and oxidative stress.

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