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Context:Compression socks have become increasingly popular with athletes due to perceived enhancement of exercise performance and recovery. However, research examining the efficacy of compression socks to reduce exercise-associated muscle damage has been equivocal, with few direct measurements of markers of muscle damage.Objective:To examine the influence of compression socks worn during a marathon on creatine kinase (CK) levels.Design:A randomized controlled trial.Setting:2013 Hartford Marathon, Hartford, CT.Participants:Adults (n = 20) randomized to control (CONTROL; n = 10) or compression sock (SOCK; n = 10) groups.Main Outcome Measures:Blood samples were collected 24 hours before, immediately after, and 24 hours following the marathon for the analysis of CK, a marker of muscle damage.Results:Baseline CK levels did not differ between CONTROL (89.3 [41.2] U/L) and SOCK (100.0 [56.2] U/L) (P = .63). Immediately following the marathon (≤1 h), CK increased 273% from baseline (P P = .60 for time × group). The day following the marathon (≤24 h), CK further increased 1094% from baseline (P P = .53 for time × group). These similar trends persisted despite controlling for potential covariates such as age, body mass index, and race finishing time (Ps > .29).Conclusions:Compression socks worn during a marathon do not appear to mitigate objectively measured markers of muscle damage immediately following and 24 hours after a marathon.

Postprandial hyperglycemia (PPH) impairs vascular endothelial function (VEF). A single bout of aerobic exercise (AE) attenuates PPH-induced decreases in brachial artery flow-mediated dilation (FMD), a non-invasive measure of VEF, in healthy adults for up to 17 h post-exercise. Studies examining the effects of resistance exercise (RE) on postprandial FMD responses are lacking. We hypothesized that a single bout of exercise performed the prior evening would attenuate PPH-induced decreases in FMD, independent of exercise modality. In a randomized, cross-over design, overweight/obese adults [n = 11 (8 women); 22 ± 4 years; 32.3 ± 5.8 kg m−2] completed 3 separate trials: control (seated rest), AE (30 min at ~ 60% VO2max), or whole-body RE (30 min, 6 exercises, 3 × 10-repetition maximum). Each trial occurred 14–17 h prior to an oral glucose tolerance test (OGTT). Brachial artery FMD and plasma glucose and insulin were measured prior to and at 30-min intervals for 2 h following the OGTT. Repeated-measures ANOVA and Bonferroni post hoc tests were used to evaluate differences within and between trials. Trials occurred 15.3 ± 1.0 h prior to the OGTT. Relative to baseline, FMD transiently decreased (P

Reduced flow-mediated dilation (FMD) and elevated plasma endothelin-1 (ET-1) levels may contribute to the higher incidence of adverse cardiovascular events observed in the morning hours. A single bout of intermittent exercise abolishes the diurnal variation in FMD. Studies examining the effects of exercise on vascular and plasma ET-1 responses at different times of day are lacking. We determined the effects of time of day and intermittent aerobic exercise on brachial artery FMD and plasma ET-1 levels in healthy adults. We hypothesized that lower brachial artery FMD in the morning (compared to the afternoon) will be accompanied by higher plasma ET-1 levels. Additionally, we hypothesized that the diurnal variation in brachial artery FMD and plasma ET-1 will be abolished by performing a single bout of intermittent aerobic exercise. Utilizing a randomized, cross-over design, healthy adults [n = 12; 22 ± 4 y; 25.2 ± 2.7 kg/m

This study determined if varying physical activity (PA) the day prior to an oral glucose tolerance test (OGTT) differentially influenced postprandial glucose and insulin kinetics. Fifteen healthy, young adults participated in three OGTT trials the morning after performing 50% (LOW), 100% (HABITUAL), or 150% (HIGH) of their habitual PA (determined by 7-day pedometry). Trials were randomized and separated by at least 1-wk. For each OGTT trial, blood glucose and insulin were measured after an overnight fast and at 30-min intervals for 2 h following ingestion of the glucose beverage. Between-trial differences were analyzed using a general linear model with repeated measures. Subjects successfully achieved the desired percentage of habitual steps prior to each trial: LOW: 51±5%, HABITUAL: 99±6%, and HIGH: 149±9%. Fasting blood glucose and glucose total area under the curve (AUC) did not differ between trials. Serum insulin AUC was lower (p

Serum creatine kinase (CK) levels are higher after eccentric, muscle-damaging exercise in statin-treated patients. This could contribute to the increased statin-associated muscle symptoms reported in physically active individuals.We tested the hypothesis in this pilot study that creatine (Cr) monohydrate supplementation would reduce the CK response to eccentric exercise in patients using statins to determine if Cr supplementation could be a strategy to mitigate statin-associated muscle symptoms in physically active individuals.Healthy, nonsmoking men (n = 5) and women (n = 14) were randomized to Cr monohydrate = atorvastatin 80 mg + 10 g Cr monohydrate (n = 10, age = 60 ± 7 years) or to placebo (PL) = atorvastatin 80 mg + PL (n = 9, age = 52 ± 6 years). After 4 weeks of treatment, subjects performed 45 minutes of eccentric exercise (downhill walking at a -15% grade). Serum CK levels, muscle soreness (visual analog scale after two squats), and muscle pain severity and interference (using the brief pain inventory) were measured before and after 4 weeks of treatment, and then for 4 consecutive days after downhill walking. Vitamin D, or serum 25(OH)D, was also measured at baseline.The PL group was younger (P = .01) but not otherwise different in blood lipids, vitamin D, CK, muscle visual analog scale, and pain scores before (all P .21) or after (all P .12) treatment. CK increased in all subjects after downhill walking (P .01), but neither the relative peak change (expressed as group mean difference with 95% confidence intervals: 43.52% [-196.41, 283.45]) nor the absolute peak change (67.38 U/L [-121.55, 256.31]) relative to baseline was different between groups (P = .46 and .71, respectively). A similar lack of treatment effect was observed for muscle soreness (11.03 mm [-9.49, 31.55]), pain severity (0.77 pts [-0.95, 2.50]), and pain interference (1.02 pts [-1.25, 3.29]) with P-values for group comparisons = 0.27, 0.36, and 0.35, respectively. However, subjects with "insufficient" Vitamin D 30 ng/mL (n = 10) had an ∼2-fold greater CK increase with eccentric exercise (nominal P-value = .04) than subjects with higher vitamin D levels.Cr monohydrate did not reduce CK increases after exercise in statin-treated subjects. We did observe that low vitamin D levels are associated with a greater CK response to eccentric exercise in statin-treated subjects.

Although higher intakes of dairy milk are associated with a lower risk of metabolic syndrome (MetS), the underlying protective mechanism remains unclear. This study investigated the dynamic metabolic profile shift following the ingestion of low-fat milk or an isocaloric volume of rice milk in obese individuals with metabolic syndrome (MetS). In a randomized, double-blind, crossover study, postprandial plasma samples ( n = 266) were collected from 19 MetS participants. Plasma samples were analyzed by a targeted metabolomics platform which specifically detects 117 metabolites from 25 metabolic pathways. The comprehensive time-course metabolic profiling in MetS participants indicated that the postprandial metabolic profiles distinguish low-fat milk and rice milk consumption in a time-dependent manner. Metabolic biomarkers, such as orotate, leucine/isoleucine and adenine, showed significantly different trends in the two test beverages. Bayesian statistics identified 12 metabolites associated with clinical characteristics of postprandial vascular endothelial function, such as flow-mediated dilation (FMD), postprandial plasma markers of oxidative stress and NO status. Furthermore, metabolic pathway analysis based on these metabolite data indicated the potential utility of metabolomics to provide mechanistic insights of dietary interventions to regulate postprandial metabolic excursions.

Eggs attenuate postprandial hyperglycaemia (PPH), which transiently impairs vascular endothelial function (VEF). We hypothesised that co-ingestion of a glucose challenge with egg-based meals would protect against glucose-induced impairments in VEF by attenuating PPH and oxidative stress. A randomised, cross-over study was conducted in prediabetic men (n20) who ingested isoenegertic meals (1674 kJ (400 kcal)) containing 100 g glucose (GLU), or 75 g glucose with 1·5 whole eggs (EGG), seven egg whites (WHITE) or two egg yolks (YOLK). At 30 min intervals for 3 h, brachial artery flow-mediated dilation (FMD), plasma glucose, insulin, cholecystokinin (CCK), lipids (total, LDL- and HDL-cholesterol; TAG), F2-isoprostanes normalised to arachidonic acid (F2-IsoPs/AA), and methylglyoxal were assessed. In GLU, FMD decreased at 30–60 min and returned to baseline levels by 90 min. GLU-mediated decreases in FMD were attenuated at 30–60 min in EGG and WHITE. Compared with GLU, FMDAUCwas higher in EGG and WHITE only. Relative to baseline, glucose increased at 30–120 min in GLU and YOLK but only at 30–90 min in EGG and WHITE. GlucoseAUCand insulinAUCwere also lower in EGG and WHITE only. However, CCKAUCwas higher in EGG and WHITE compared with GLU. Compared with GLU, F2-IsoPs/AAAUCwas lower in EGG and WHITE but unaffected by YOLK. Postprandial lipids and methylglyoxal did not differ between treatments. Thus, replacing a portion of a glucose challenge with whole eggs or egg whites, but not yolks, limits postprandial impairments in VEF by attenuating increases in glycaemia and lipid peroxidation.

Background: Endogenous antioxidants are critical to limiting cellular oxidative damage. Methods: The authors determined if habitual physical activity (PA) and cardiorespiratory fitness were associated with skeletal muscle expression of endogenous antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) and circulating oxidative stress markers (serum 8-hydroxy-2′-deoxyguanosine [8-OHdG]; oxidized low-density lipoprotein [LDL]) in older adults. Moderate to vigorous PA (MVPA) was estimated using a validated PA questionnaire in 26 older adults (mean [SD]; M/F = 9/17, age = 68 [4] y, body mass index = 26 [3] kg·m−2). Maximal oxygen consumption was estimated using the YMCA submaximal cycle test. Skeletal muscle endogenous antioxidants and serum 8-OHdG and oxidized LDL were measured. Bivariate and partial correlations (controlling for body mass index) were utilized to determine associations among variables. Results: MVPA (1640 [1176] kcal·wk−1) was correlated with superoxide dismutase 2 (r = .55), catalase (r = .55), glutathione peroxidase 1 (r = .48), and 8-OHdG (r = −.41) (all Ps r = −.29). Estimated maximal oxygen consumption was correlated with glutathione peroxidase 1 (r = .48; P Conclusions: These data show that skeletal muscle endogenous antioxidant expression and circulating oxidative damage are associated with habitual MVPA in older adults. Thus, MVPA in older adults may be protective against reactive oxygen species damage due to higher expression of endogenous antioxidants.

Both obesity and the metabolic syndrome are risk factors for type 2 diabetes and cardiovascular disease. Identification of novel biomarkers are needed to distinguish metabolic syndrome from equally obese individuals in order to direct them to early interventions that reduce their risk of developing further health problems. We utilized mass spectrometry-based targeted metabolic profiling of 221 metabolites to evaluate the associations between metabolite profiles and established metabolic syndrome criteria (i.e. elevated waist circumference, hypertension, elevated fasting glucose, elevated triglycerides, and low high-density lipoprotein cholesterol) in plasma samples from obese men ( n = 29; BMI = 35.5 ± 5.2 kg/m2) and women ( n = 40; 34.9 ± 6.7 kg/m2), of which 26 met the criteria for metabolic syndrome (17 men and 9 women). Compared to obese individuals without metabolic syndrome, univariate statistical analysis and partial least squares discriminant analysis showed that a specific group of metabolites from multiple metabolic pathways (i.e. purine metabolism, valine, leucine and isoleucine degradation, and tryptophan metabolism) were associated with the presence of metabolic syndrome. Receiver operating characteristic curves generated based on the PLS–DA models showed excellent areas under the curve (0.85 and 0.96, for metabolites only model and enhanced metabolites model, respectively), high specificities (0.86 and 0.93), and good sensitivities (0.71 and 0.91). Moreover, principal component analysis revealed that metabolic profiles can be used to further differentiate metabolic syndrome with 3 versus 4–5 metabolic syndrome criteria. Collectively, these findings support targeted metabolomics approaches to distinguish metabolic syndrome from obesity alone, and to stratify metabolic syndrome status based on the number of criteria met. Impact statement We utilized mass spectrometry-based targeted metabolic profiling of 221 metabolites to evaluate the associations between metabolite profiles and established MetS criteria. To our best knowledge, the findings of this study provide the first evidence that metabolic profiles can be used to differentiate participants with MetS from similarly obese individuals who do not meet established criteria of MetS. Furthermore, the study demonstrated that within MetS participants, their unique metabolic profiles correlated to the number of criteria used for MetS determination. Taken together, this metabolic profiling approach can potentially serve as a novel tool for MetS detection and monitoring, and provide useful metabolic information for future interventions targeting obesity and MetS.

Aerobic exercise reduces blood pressure (BP) on average 5-7 mmHg among those with hypertension; limited evidence suggests similar or even greater BP benefits may result from isometric handgrip (IHG) resistance exercise.We conducted a randomized controlled trial investigating the antihypertensive effects of an acute bout of aerobic compared with IHG exercise in the same individuals. Middle-aged adults (n = 27) with prehypertension and obesity randomly completed three experiments: aerobic (60% peak oxygen uptake, 30 min); IHG (30% maximum voluntary contraction, 4 × 2 min bilateral); and nonexercise control. Study participants were assessed for carotid-femoral pulse wave velocity pre and post exercise, and left the laboratory wearing an ambulatory BP monitor.SBP and DBP were lower after aerobic versus IHG (4.8 ± 1.8/3.1 ± 1.3 mmHg, P = 0.01/0.04) and control (5.6 ± 1.8/3.6 ± 1.3 mmHg, P = 0.02/0.04) over the awake hours, with no difference between IHG versus control (P = 0.80/0.83). Pulse wave velocity changes following acute exercise did not differ by modality (aerobic increased 0.01 ± 0.21 ms, IHG decreased 0.06 ± 0.15 ms, control increased 0.25 ± 0.17 ms, P 0.05). A subset of participants then completed either 8 weeks of aerobic or IHG training. Awake SBP was lower after versus before aerobic training (7.6 ± 3.1 mmHg, P = 0.02), whereas sleep DBP was higher after IHG training (7.7 ± 2.3 mmHg, P = 0.02).Our findings did not support IHG as antihypertensive therapy but that aerobic exercise should continue to be recommended as the primary exercise modality for its immediate and sustained BP benefits.

BackgroundCardiovascular disease (CVD) is a leading cause of death among adults with type 2 diabetes mellitus (T2D). We recently reported that glycemic control in patients with T2D can be significantly improved through a continuous care intervention (CCI) including nutritional ketosis. The purpose of this study was to examine CVD risk factors in this cohort.MethodsWe investigated CVD risk factors in patients with T2D who participated in a one year open label, non-randomized, controlled study. The CCI group (n = 262) received treatment from a health coach and medical provider. A usual care (UC) group (n = 87) was independently recruited to track customary T2D progression. Circulating biomarkers of cholesterol metabolism and inflammation, blood pressure (BP), carotid intima media thickness (cIMT), multi-factorial risk scores and medication use were examined.ResultsThe CCI group consisted of 262 patients (baseline mean(SD): age 54(8) y, BMI 40.4(8.8) kg/m2). Intention-to-treat analysis (% change) revealed the following at 1-year with P values < 0.0019 indicating statistical significance after adjustment for multiple comparisons: total LDL-particles (LDL-P) (−4.9%, P=0.02), small LDL-P (−20.8%, P=1.2×10−12), LDL-P size (+1.1%, P=6.0×10−10), ApoB (−1.6%, P=0.37), ApoA1 (+9.8%, P−16), ApoB/ApoA1 ratio (−9.5%, P=1.9×10−7), triglyceride/HDL-C ratio (−29.1%, P−16), large VLDL-P (−38.9%, P=4.2×10−15), and LDL-C (+9.9%, P=4.9×10−5). Additional effects were reductions in blood pressure, high sensitivity C-reactive protein, and white blood cell count (all P−7) while cIMT was unchanged. The 10-year atherosclerotic cardiovascular disease (ASCVD) risk score decreased −11.9% (P=4.9×10−5). Antihypertensive medication use was discontinued in 11.4 % of CCI participants (P=5.3×10−5). The UC group of 87 patients (baseline mean(SD): age 52(10)y, BMI 36.7(7.2) kg/m2) showed no significant changes. After adjusting for baseline differences when comparing CCI and UC groups, significant improvements for the CCI group included small LDL-P, ApoA1, triglyceride/HDL-C ratio, HDL-C, hs-CRP, and ASCVD score. The CCI group showed a greater rise in LDL-C.ConclusionsA continuous care treatment including nutritional ketosis in patients with T2D improved most biomarkers of CVD risk after one year. The increase in LDL-cholesterol appeared limited to the large LDL subfraction. LDL particle size increased, total LDL-P and ApoB were unchanged, and inflammation and blood pressure decreased.Trial registrationClinicaltrials.gov:NCT02519309. Registered 10 August 2015

BackgroundCardiovascular disease (CVD) is a leading cause of death among adults with type 2 diabetes mellitus (T2D). We recently reported that glycemic control in patients with T2D can be significantly improved through a continuous care intervention (CCI) including nutritional ketosis. The purpose of this study was to examine CVD risk factors in this cohort.MethodsWe investigated CVD risk factors in patients with T2D who participated in a 1 year open label, non-randomized, controlled study. The CCI group (n = 262) received treatment from a health coach and medical provider. A usual care (UC) group (n = 87) was independently recruited to track customary T2D progression. Circulating biomarkers of cholesterol metabolism and inflammation, blood pressure (BP), carotid intima media thickness (cIMT), multi-factorial risk scores and medication use were examined. A significance level of P ResultsThe CCI group consisted of 262 participants (baseline mean (SD): age 54 (8) year, BMI 40.4 (8.8) kg m−2). Intention-to-treat analysis (% change) revealed the following at 1-year: total LDL-particles (LDL-P) (− 4.9%, P = 0.02), small LDL-P (− 20.8%, P = 1.2 × 10−12), LDL-P size (+ 1.1%, P = 6.0 × 10−10), ApoB (− 1.6%, P = 0.37), ApoA1 (+ 9.8%, P −16), ApoB/ApoA1 ratio (− 9.5%, P = 1.9 × 10−7), triglyceride/HDL-C ratio (− 29.1%, P −16), large VLDL-P (− 38.9%, P = 4.2 × 10−15), and LDL-C (+ 9.9%, P = 4.9 × 10−5). Additional effects were reductions in blood pressure, high sensitivity C-reactive protein, and white blood cell count (all P −7) while cIMT was unchanged. The 10-year atherosclerotic cardiovascular disease (ASCVD) risk score decreased − 11.9% (P = 4.9 × 10−5). Antihypertensive medication use was discontinued in 11.4% of CCI participants (P = 5.3 × 10−5). The UC group of 87 participants [baseline mean (SD): age 52 (10) year, BMI 36.7 (7.2) kg m−2] showed no significant changes. After adjusting for baseline differences when comparing CCI and UC groups, significant improvements for the CCI group included small LDL-P, ApoA1, triglyceride/HDL-C ratio, HDL-C, hsCRP, and LP-IR score in addition to other biomarkers that were previously reported. The CCI group showed a greater rise in LDL-C.ConclusionsA continuous care treatment including nutritional ketosis in patients with T2D improved most biomarkers of CVD risk after 1 year. The increase in LDL-cholesterol appeared limited to the large LDL subfraction. LDL particle size increased, total LDL-P and ApoB were unchanged, and inflammation and blood pressure decreased.Trial registrationClinicaltrials.gov: NCT02519309. Registered 10 August 2015

OBJECTIVE To investigate the effect of oral contraceptive (OC) use and compression socks on hemostatic activation in women flying cross-country to and from a marathon. DESIGN Prospective study. SETTING 2015 Boston Marathon. PARTICIPANTS Women were divided into non-OC using (CONTROL; n = 12), OC-using (OC; n = 15), and OC-using plus compression sock (OC + SOCK; n = 14) groups. INTERVENTION Women in OC + SOCK wore compression socks during flights to and from the marathon. MAIN OUTCOME MEASURES Venous blood samples were collected within 24 hours of arriving in Boston (EXPO), immediately after the marathon (RUN), and within 24 hours after a return flight home (Post-Flight) for analysis of thrombin-antithrombin complex (TAT), d-dimer, and tissue plasminogen activator (t-PA). RESULTS TAT did not increase with exercise (P = 0.48) and was not affected by group (P = 0.08) or the interaction between these 2 factors (P = 0.80). Group, time, and their interaction were significant for d-dimer (all P < 0.05) such that d-dimer increased with acute exercise to a greater extent (Δ d-dimer from expo to postrace = 909.5 ± 1021.9 ng/mL) in the OC + SOCK group relative to OC (Δ d-dimer = 240.0 ± 178.5 ng/mL; P = 0.02) and CONTROL (Δ d-dimer = 230.3 ± 120.3 ng/mL; P = 0.02). There was a significant effect of time, group, and the interaction on t-PA (all P < 0.01) such that t-PA increased with acute exercise to a greater extent (Δ t-PA from expo to postrace = 19.6 ± 10.0 ng/mL) in the CONTROL group relative to OC (Δ t-PA = 4.0 ± 1.8 ng/mL; P < 0.01) and OC + SOCK (Δ t-PA = 3.3 ± 1.2 ng/mL; P < 0.01). CONCLUSIONS Female runners using OCs did not exhibit disproportionately increased coagulation. The use of compression socks in women on OCs, surprisingly, resulted in a greater increase in d-dimer after exercise.

Acute aerobic exercise prevents sitting-induced impairment of flow-mediated dilation (FMD). Further, evidence suggests that sitting-induced impairment of FMD occurs via an oxidative stress-dependent mechanism that disrupts endothelial function. We hypothesized that acute aerobic exercise would prevent impairment of femoral artery FMD by limiting oxidative stress responses that increase endothelin-1 (ET-1) levels and disrupt nitric oxide (NO) status. In a randomized, cross-over study, healthy men (n = 11; 21.2 ± 1.9 years) completed two 3 h sitting trials that were preceded by 45 min of either quiet rest (REST) or a single bout of continuous treadmill exercise (65% maximal oxygen consumption) (EX). Superficial femoral artery FMD, plasma glucose, malondialdehyde (MDA), ET-1, arginine (ARG) and its related metabolites [homoarginine (HA), asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA)] were assessed at baseline, 1 h following EX (or REST) (0 h), and at 1 h intervals during 3 h of uninterrupted sitting. Data were analyzed using repeated measures ANOVA. During REST, femoral artery FMD declined from baseline (2.6 ± 1.8%) at 1, 2, and 3 h of sitting and resting shear rate decreased at 3 h. In contrast, when sitting was preceded by EX, femoral artery FMD (2.7 ± 2.0%) and resting shear rate responses were unaffected. No between trial differences were detected for plasma glucose, MDA, ET-1, ARG, HA, ADMA, or SDMA. Prior aerobic exercise prevented the decline in femoral artery FMD that is otherwise induced by prolonged sitting independent of changes in oxidative stress, ET-1, and NO status.

Introduction. Both statins and regular physical activity (PA) reduce arterial stiffness. The present post hoc analysis examined if arterial stiffness was improved with high-dose atorvastatin treatment in healthy adults and whether PA levels magnified this response. We utilized data from a double-blind, random-assignment clinical trial investigating the effects of atorvastatin 80 mg/d for 6 mo on skeletal muscle symptoms. Methods. Central and peripheral arterial pulse wave velocity (PWV) were measured and PA levels assessed at baseline and 6 mo in subjects randomized to atorvastatin (n=21, 9 men) or placebo (n=29, 16 men). Results. Baseline participant characteristics, PWV, and PA levels were not different between treatments. Central (means ± SD; 8.7±2.6 to 9.0±2.5 m/sec) and peripheral PWV (9.9±1.3 to 9.8±1.6 m/sec) were unchanged from baseline following atorvastatin treatment (time × drug interaction: P≥0.13). Similarly, PA levels were unaffected by time or treatment. In sex and age adjusted models, baseline levels of PA were not related to changes in PWV with atorvastatin treatment. Conclusion. These data indicate that high-dose atorvastatin treatment for 6 mo does not influence arterial stiffness in healthy adults. Participation in habitual PA did not magnify the vascular effects of statin therapy. This study was registered with ClinicalTrials.gov NCT00609063.

Oxidative stress and inflammation persist years after smoking cessation thereby limiting the restoration of vascular endothelial function (VEF). Although short-term smoking cessation improves VEF, no studies have examined co-therapy of antioxidants in combination with smoking cessation to improve VEF. We hypothesized that improvements in γ-tocopherol (γ-T) status during smoking cessation would improve VEF beyond that from smoking cessation alone by decreasing oxidative stress and proinflammatory responses. A randomized, double-blind, placebo-controlled study was conducted in otherwise healthy smokers (22 ± 1 years; mean ± SEM) who quit smoking for 7 days with placebo (n=14) or γ-T-rich supplementation (n=16; 500 mg γ-T/day). Brachial artery flow-mediated dilation (FMD), cotinine, and biomarkers of antioxidant status, oxidative stress, and inflammation were measured before and after 7 days of smoking cessation. Smoking cessation regardless of supplementation similarly decreased plasma cotinine, whereas γ-T-rich supplementation increased plasma γ-T by seven times and its urinary metabolite γ-carboxyethyl hydroxychroman by nine times (P

Statins positively impact plasma low-density lipoprotein cholesterol, inflammation and vascular endothelial function (VEF). Carbohydrate restricted diets (CRD) improve atherogenic dyslipidemia, and similar to statins, have been shown to favorably affect markers of inflammation and VEF. No studies have examined whether a CRD provides additional benefit beyond that achieved by habitual statin use. We hypothesized that a CRD (

article i nfo Background: A sedentary lifestyle is a major risk factor for cardiovascular and thrombotic complications. While habitual endurance activity will reduce the risk of these adverse events, the influence of habitual resis- tance exercise is less clear. This study examined coagulation and fibrinolytic responses to an acute exhaustive resistance exercise test (AERET) in both resistance-trained (RT, min 2 yr, 5 men and 5 women) and untrained (UT, 5 men and 5 women) subjects. Methods: The AERET consisted of six sets of 10 repetitions of squats at 80% of 1-repetition maximum. Venous blood was collected pre-exercise, immediate post exercise (IP), and +15, +60, and +120 minutes post exercise. Results: Compared to UT, RT exhibited a lower capacity to form a clot as seen by activated partial Thrombo- plastin time (aPTT) integrated area under the curve over time (iAUC) levels, lower pre-exercise and 120 min post-exercise plasminogen activator inhibitor −1 (PAI-1) activity, and higher tissue plasminogen activator (tPA) activity immediately post-exercise. There were no significant differences between RT and UT for fibrin- ogen, prothrombin fragment 1 + 2 (PTF 1 + 2), and thrombin-antithrombin complexes (TAT). Conclusion: These results suggest that habitual resistance exercise training may provide an enhanced fibrino- lytic state.

Compared to soy, whey protein is higher in leucine, absorbed quicker and results in a more pronounced increase in muscle protein synthesis.To determine whether supplementation with whey promotes greater increases in muscle mass compared to soy or carbohydrate, we randomized non-resistance-trained men and women into groups who consumed daily isocaloric supplements containing carbohydrate (carb; n = 22), whey protein (whey; n = 19), or soy protein (soy; n = 22).All subjects completed a supervised, whole-body periodized resistance training program consisting of 96 workouts (~9 months). Body composition was determined at baseline and after 3, 6, and 9 months. Plasma amino acid responses to resistance exercise followed by supplement ingestion were determined at baseline and 9 months.Daily protein intake (including the supplement) for carb, whey, and soy was 1.1, 1.4, and 1.4 g·kg body mass⁻¹, respectively. Lean body mass gains were significantly (p0.05) greater in whey (3.3 ± 1.5 kg) than carb (2.3 ± 1.7 kg) and soy (1.8 ± 1.6 kg). Fat mass decreased slightly but there were no differences between groups. Fasting concentrations of leucine were significantly elevated (20%) and postexercise plasma leucine increased more than 2-fold in whey. Fasting leucine concentrations were positively correlated with lean body mass responses.Despite consuming similar calories and protein during resistance training, daily supplementation with whey was more effective than soy protein or isocaloric carbohydrate control treatment conditions in promoting gains in lean body mass. These results highlight the importance of protein quality as an important determinant of lean body mass responses to resistance training.

Whey protein intake reduces CVD risk, but little is known whether whey-derived bioactive peptides regulate vascular endothelial function (VEF). We determined the impact of a whey-derived extract (NOP-47) on VEF in individuals with an increased cardiovascular risk profile. Men and women with impaired brachial artery flow-mediated dilation (FMD) (n 21, age 55 (sem 1·3) years, BMI 27·8 (sem 0·6) kg/m2, FMD 3·7 (sem 0·4) %) completed a randomised, cross-over study to examine whether ingestion of NOP-47 (5 g) improves postprandial VEF. Brachial artery FMD, plasma amino acids, insulin, and endothelium-derived vasodilators and vasoconstrictors were measured for 2 h after ingestion of NOP-47 or placebo. Acute NOP-47 ingestion increased FMD at 30 min (4·6 (sem 0·5) %) and 120 min (5·1 (sem 0·5) %) post-ingestion (Psem 0·5) %). Plasma amino acids increased at 30 min following NOP-47 ingestion (PP∙ and prostacyclin metabolites or endothelin-1. Ingestion of a rapidly absorbed extract derived from whey protein improved endothelium-dependent dilation in older adults by a mechanism independent of changes in circulating vasoactive compounds. Future investigation is warranted in individuals at an increased CVD risk to further elucidate potential health benefits and the underlying mechanisms of extracts derived from whey.

We measured the serum levels of myoglobin, total creatine kinase (CK), and the CK myocardial (CK-MB), muscle (CK-MM), and brain (CK-BB) isoenzymes in 37 subjects treated with statins and 43 nonstatin-treated controls running the 2011 Boston Marathon. Venous blood samples were obtained the day before (PRE) and within 1 hour (FINISH) and 24 hours after (POST) the race. The hematocrit and hemoglobin values were used to adjust for changes in the plasma volume. The CK distribution was normalized using log transformation before analysis. The exercise-related increase in CK 24 hours after exercise, adjusted for changes in plasma volume, was greater in the statin users (PRE to POST 133 ± 15 to 1,104 ± 150 U/L) than in the controls (PRE to POST 125 ± 12 to 813 ± 137 U/L; p = 0.03 for comparison). The increase in CK-MB 24 hours after exercise was also greater in the statin users (PRE to POST 1.1 ± 3.9 to 8.9 ± 7.0 U/L) than in the controls (PRE to POST 0.0 ± 0.0 to 4.2 ± 5.0 U/L; p0.05 for comparison). However, the increases in muscle myoglobin did not differ at any point between the 2 groups. Increases in CK at both FINISH and POST race measurements were directly related to age in the statin users (r(2) = 0.13 and r(2) = 0.14, respectively; p0.05) but not in the controls (r(2) = 0.02 and r(2) = 0.00, respectively; p0.42), suggesting that susceptibility to exercise-induced muscle injury with statins increases with age. In conclusion, our results show that statins increase exercise-related muscle injury.

Quercetin is a naturally occurring flavonoid with anti-oxidant and anti-inflammatory properties. The effect of quercetin supplementation on maximal oxygen uptake (VO(2max)) is unknown. The purpose of this investigation was to test the effects of quercetin supplementation on VO(2max) in untrained, sedentary individuals. After baseline treadmill VO(2max) testing, 11 participants (5 males, 6 females) ingested either placebo or quercetin-supplemented (1000 mg x day(-1)) food bars in a randomized, double-blind, counterbalanced, crossover research design. The participants ingested food bars for six consecutive mornings (5 days). On the sixth morning, participants underwent repeat VO(2max) testing. After a 22 day wash-out, the participants repeated baseline VO(2max) testing, daily consumption of the opposite food bars, and post-supplementation VO(2max) testing. The condition x time interaction for VO(2max) was non-significant when expressed in absolute (litres x min(-1); P = 0.929) and relative (ml x kg(-1) x min(-1); P = 0.778) terms. These findings were similar when taking sex into account (P0.05). The mean difference in VO(2max) change from pre to post between groups (quercetin vs. placebo) was 0.139 ml x kg(-1) x min(-1) (P = 0.780). Other physiological measures also were similar between conditions (P0.05). In conclusion, 5 days of quercetin supplementation did not influence VO(2max) or related variables in sedentary men and women.

We previously reported that a carbohydrate-restricted diet (CRD) ameliorated many of the traditional markers associated with metabolic syndrome and cardiovascular risk compared with a low-fat diet (LFD). There remains concern how CRD affects vascular function because acute meals high in fat have been shown to impair endothelial function. Here, we extend our work and address these concerns by measuring fasting and postprandial vascular function in 40 overweight men and women with moderate hypertriacylglycerolemia who were randomly assigned to consume hypocaloric diets (approximately 1500 kcal) restricted in carbohydrate (percentage of carbohydrate-fat-protein = 12:59:28) or LFD (56:24:20). Flow-mediated dilation of the brachial artery was assessed before and after ingestion of a high-fat meal (908 kcal, 84% fat) at baseline and after 12 weeks. Compared with the LFD, the CRD resulted in a greater decrease in postprandial triacylglycerol (-47% vs -15%, P = .007), insulin (-51% vs -6%, P = .009), and lymphocyte (-12% vs -1%, P = .050) responses. Postprandial fatty acids were significantly increased by the CRD compared with the LFD (P = .033). Serum interleukin-6 increased significantly over the postprandial period; and the response was augmented in the CRD (46%) compared with the LFD (-13%) group (P = .038). After 12 weeks, peak flow-mediated dilation at 3 hours increased from 5.1% to 6.5% in the CRD group and decreased from 7.9% to 5.2% in the LFD group (P = .004). These findings show that a 12-week low-carbohydrate diet improves postprandial vascular function more than a LFD in individuals with atherogenic dyslipidemia.

Metabolic and vascular abnormalities have been found in individuals with type 2 diabetes mellitus (T2D). Family history is often associated with increased risk of the development of T2D. We sought to determine if young, sedentary, insulin-sensitive individuals with a family history of T2D (FH+) have a reduced resting energy expenditure (REE) and vascular endothelial function compared with individuals who have no family history of T2D (FH-). The REE was determined in 18 FH+ individuals and 15 FH- individuals using indirect open-circuit calorimetry. Vascular endothelial function was measured via flow-mediated dilation (FMD) of the brachial artery. C-reactive protein and interleukin-6 were also measured to look at vascular inflammation. Body composition was measured via bioelectrical impedance analysis to determine fat-free mass and fat mass for each individual. Insulin resistance was calculated using the homeostasis model assessment equation and fasting insulin and glucose concentrations. Subjects (n = 42) were approximately 26 years old and had normal fasting serum insulin or glucose concentrations. The REE normalized for body weight (kilocalories per day per kilogram body weight) was significantly reduced in the FH+ women compared with FH- women (P < .001) but not in the men. The FMD was significantly reduced (34.3%) in the FH+ group compared with the FH- in women (P = .002). However, no between-group difference in FMD was present in male subjects (P = .376). Young, healthy, insulin-sensitive women with a family history of T2D have reduced whole-body metabolic rate and vascular endothelial function compared with those with no family history of disease. These differences in whole-body metabolic rate and vascular endothelial function were not present in male subjects.

Physically active adults may be especially vulnerable to the adverse muscular side effects of statins. We determined if short-term cessation of statin therapy would improve aerobic exercise performance in middle-aged adults engaged in regular aerobic exercise training.Physically active middle-aged adults on statin therapy ≥6 mo (n = 16; 58 ± 10 y) or not taking lipid-lowering medications (controls) (n = 19; 51 ± 9 y) completed a peak oxygen consumption (VO2peak) and time to exhaustion test on a cycle ergometer 2-7 d apart. Tests were repeated following 1 mo of statin cessation or a 1 mo period for controls. Questionnaires were administered to assess exercise history and muscle complaints.Statin users reported little or no muscle complaints and participation in aerobic exercise was similar between groups (p≥0.13). The lower VO2peak (37.3 ± 9.0 vs. 43.1 ± 4.9 ml/kg/min; p = 0.02) and time to exhaustion (21.9 ± 4.4 vs. 26.0 ± 6.3 min; p = 0.04) in statin users versus controls did not persist after controlling for age (p≥0.08). Aerobic exercise performance did not change with 1 mo of statin cessation (p≥0.54). No changes were observed in controls when tests were repeated 1 mo later (p≥0.38).Short-term cessation of statin therapy does not alter maximal aerobic capacity or aerobic endurance in physically active middle-aged adults with few or no statin muscle complaints.

PUBLICATIONS Ballard, K.D., Olive, J.L. Metabolic Rate in Individuals with a Predisposition for Type 2 Diabetes. American College of Sports Medicine 53 Annual Meeting, May 2006, Denver, CO. Olive, J.L., Ballard, K.D., Robinson, J. Vascular Function in Individuals with a Predisposition for Type 2 Diabetes. American College of Sports Medicine 53 Annual Meeting, May 2006, Denver, CO. Moreillon, J., Burgard, M.A., Ballard, K.D., Mercer, S.L., Felker, J.M., Hare, J.L., Adams, K.J., FACSM (2005). Metabolic Costs of Two Types of Barbell Lunges. Medicine and Science in Sports and Exercise 37(5): S191. CONFERENCE PRESENTATIONS Milliner, B., Ballard, K., Robinson, J., and Olive, J.L. Metabolic Rate in Individuals with a Predisposition for Type 2 Diabetes. Poster Presentation, Research Louisville, November 2005, Louisville, KY. Ballard, K.D., Olive, J.L. Metabolic Rate in Individuals with a Predisposition for Type 2 Diabetes. Slide Presentation, University of Louisville College of Education and Human Development Spring Research Conference, April 2006, Louisville, KY. Ballard, K.D., Olive, J.L. Metabolic Rate in Individuals with a Predisposition for Type 2 Diabetes. Slide Presentation (pending), American College of Sports Medicine 53 Annual Meeting, May 2006, Denver, CO. Olive, J.L., Ballard, K.D., Robinson, J. Vascular Function in Individuals with a Predisposition for Type 2 Diabetes. Poster Presentation (pending), American College of Sports Medicine 53 Annual Meeting, May 2006, Denver, CO. AFFILIATIONS/ MEMBERSHIPS National Strength and Conditioning Association-Certified Personal Trainer, 2002-present UofL Health Sciences Club, Vice President, 2005-2006 American Heart Association CPR Certified, 2000-present American College of Sports Medicine, 2006-present COMPUTER SKILLS: Proficient in Microsoft Windows, Microsoft Office, SPSS, Eat Right Analysis Nutrition software, LabVIEW and EndNote software

Marathon running evokes parallel increases in markers of coagulation and fibrinolysis (i.e. hemostatic activation) immediately following strenuous, endurance exercise such that hemostatic balance is maintained. However, other factors incident to marathon running (i.e. dehydration, travel) may disproportionately activate the coagulatory system, increasing blood clot risk after an endurance event in otherwise healthy individuals. We investigated the effect of compression socks on exercise-induced hemostatic activation and balance in endurance athletes running the 2013 Hartford Marathon.Adults (n = 20) were divided into compression sock (SOCK; n = 10) and control (CONTROL; n = 10) groups. Age, anthropometrics, vital signs, training mileage and finishing time were collected. Venous blood samples were collected 1 day before, immediately after and 1 day following the marathon for analysis of coagulatory (i.e. thrombin-antithrombin complex [TAT] and D-dimer) and fibrinolytic (i.e. tissue plasminogen activator [t-PA]) factors.Plasma D-dimer, TAT and t-PA did not differ between groups at baseline (p0.16). There were no significant group · time interactions (all p ≥ 0.17), however, average t-PA was lower in SOCK (8.9 ± 0.7 ng/mL) than CONTROL (11.2 ± 0.7 ng/mL) (p = 0.04). Average TAT also tended to be lower in SOCK (2.8 ± 0.2 µg/L) than CONTROL (3.4 ± 0.2 µg/L) (p = 0.07).Our results suggest that overall hemostatic activation (both coagulation and fibrinolysis) following a marathon tended to be lower with compression socks. Thus, compression socks do not adversely influence markers of hemostasis, appear safe for overall use in runners and may reduce exercise-associated hemostatic activation in individuals at risk for deep vein thrombosis.

Greater intakes of dairy are frequently associated with reduced risk of cardiovascular disease. These observational studies have served as the basis for controlled interventions aimed at defining the cardioprotective mechanisms of dairy. Understanding these relationships is of public health importance because most of the US population fails to meet dietary recommendations for dairy, suggesting that many individuals could lower their cardiovascular disease risk by relatively simple dietary modification. Clinical studies investigating the acute ingestion of dairy or its constituents, including short-term (≤2 week) supplementation studies or those assessing postprandial responses, have largely shown benefits on vascular function without concomitant improvements in blood pressure. Chronic interventions have been less conclusive, with some showing benefits and others indicating a lack of improvement in vascular function regardless of blood pressure changes. Vasoprotective activities of dairy are likely mediated through improvements in nitric oxide bioavailability, oxidative stress, inflammation, and insulin resistance. Future controlled studies are needed to determine if these health benefits are mediated directly by dairy or indirectly by displacing other dietary components that otherwise impair vascular health.

Some clinical trials experts are concerned that statinassociated muscle symptoms (SAMS) are given more attention than the life-saving ability of these drugs, and some experts doubt the existence of SAMS. We recently completed a six-month, randomized-assignment, double-blind study of the effects of atorvastatin (80mg daily) vs placebo on skeletal muscle performance, myalgia, and creatine kinase (CK) levels in 419 healthy adults. There were no differences in muscle strength or exercise performance between the patient groups. More patients in the statin group (9.4%) met the study definition of myalgia vs placebo (4.6%) (p1⁄4 0.054), and average CK increased 21U/l (p 2 baseline levels compared to 12 placebo subjects (p1⁄4 0.02). Greater increases in CK with atorvastatin did not deleteriously impact skeletal muscle performance or predict myalgia. The increase of CK in 65% of statin-treated subjects and the doubling of CK in 12% suggests that statins produce mild muscle injury in a large proportion of treated patients. The long-term consequences of this observation are unknown. Funding

Low-density lipoprotein cholesterol (LDL-C) apheresis is an effective therapy to reduce CVD risk in hypercholesterolemic patients who are refractory or intolerant to lipid-lowering therapy. We hypothesized that a single treatment of LDL-C apheresis would increase vascular endothelial function by decreasing oxidative stress responses that limit nitric oxide (NO) bioavailability. Patients (n=5; 52±11 y) were actively receiving bi-weekly LDL-C apheresis treatments (duration=54±41 mo). Brachial artery flow-mediated dilation (FMD), plasma lipids, vitamin E (α- and γ-tocopherol), markers of oxidative stress (nitro-γ-tocopherol, malondialdehyde (MDA)), and regulators of NO metabolism (arginine (ARG), asymmetric dimethylarginine (ADMA)) were assessed prior to (Pre) and immediately following LDL-C apheresis (Post) and at 1, 3, 7, and 14 d Post. Relative to Pre, total C (300±58 mg/dL) and LDL-C (239±46 mg/dL) at Post were 61% and 70% lower (P

Statins reduce arterial stiffness but are also associated with mild muscle complaints. It is unclear whether individuals with muscle symptoms experience the same vascular benefit or whether statins affect striated and smooth muscle cells differently. We examined the effect of simvastatin treatment on arterial stiffness in patients who did versus those who did not exhibit muscle symptoms. Patients with a history of statin-related muscle complaints (n=115) completed an 8 wk randomized, double-blind, cross-over trial of daily simvastatin 20 mg and placebo. Serum lipids and pulse wave velocity (PWV) were assessed before and after each treatment. Muscle symptoms with daily simvastatin treatment were reported by 38 patients (33%). Compared to baseline, central PWV decreased (P=0.01) following simvastatin treatment but not placebo (drug ∗ time interaction:P=0.047). Changes in central PWV with simvastatin treatment were not influenced by myalgia status or time on simvastatin (P≥0.15). Change in central PWV after simvastatin treatment was inversely correlated with age (r=-0.207,P=0.030), suggesting that advancing age is associated with enhanced statin-mediated arterial destiffening. In patients with a history of statin-related muscle complaints, the development of myalgia with short-term simvastatin treatment did not attenuate the improvement in arterial stiffness.