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Left ventricular (LV) structural remodeling following athletic training has been evidenced through training-specific changes in wall thickness and geometry. Whether the LV response to changes in hemodynamic load also adapts in a training-specific manner is unknown. Using echocardiography, we examined LV responses of endurance-trained (

What is the central question of this study? Carotid artery peak circumferential strain (PCS) and strain rate attenuate with age, but appear to be modulated by cardiorespiratory fitness status in young males. However, the relationship between habitual endurance exercise (running) and these parameters has not been studied in young and middle-aged men. What is the main finding and its importance? Young and middle-aged runners exhibited elevated PCS and systolic strain rate (S-SR) compared with non-runners, but habitual running did not influence diastolic strain rate (D-SR). Habitual exercise is associated with comparable improvements in carotid strain parameters in young and middle-aged men, but the age-related decline in PCS and S-SR might be more amenable to habitual endurance exercise than D-SR.Central arterial stiffness is an independent predictor of cardiovascular risk that can be modified by exercise training. However, conventional local measures of carotid artery stiffness display conflicting responses to habitual endurance exercise in young and older adults. Two-dimensional (2D)-Strain imaging of the common carotid artery (CCA) quantifies circumferential deformation (strain) of the arterial wall across the cardiac cycle, which is more sensitive at detecting age-related alterations in CCA stiffness than conventional methods. Therefore, the study was designed to examine the relationship between habitual endurance exercise (running) and CCA 2D-Strain parameters in young and middle-aged men. Short-axis ultrasound images of the CCA were obtained from 13 young non-runners [23 years of age (95% confidence interval: 21, 26 years of age)], 19 young runners [24 (22, 26) years of age], 13 middle-aged non-runners [54 (52, 56) years of age] and 19 middle-aged runners [56 (54, 58) years of age]. Images were analysed for peak circumferential strain (PCS; magnitude of deformation) and systolic and diastolic strain rates (S-SR and D-SR; deformation velocity), and group differences were examined via two-way ANOVA. PCS, S-SR and D-SR were attenuated in middle-aged men compared with young men (all P ≤ 0.001). PCS and S-SR were elevated in young and middle-aged runners when compared with non-runners (P = 0.002 and P = 0.009, respectively), but no age × training status interaction was observed. In contrast, there was no influence of habitual running on D-SR. Habitual exercise is associated with comparable improvements in CCA 2D-Strain parameters in young and middle-aged men, but the age-related decline in PCS and S-SR might be more amenable to habitual endurance exercise than D-SR.

There is increasing interest in using neuro-stimulation devices to achieve an ergogenic effect in elite athletes. Although the World Anti-Doping Authority (WADA) does not currently prohibit neuro-stimulation techniques, a number of researchers have called on WADA to consider its position on this issue. Focusing on trans-cranial direct current stimulation (tDCS) as a case study of an imminent so-called ‘neuro-doping’ intervention, we argue that the emerging evidence suggests that tDCS may meet WADA’s own criteria (pertaining to safety, performance-enhancing effect, and incompatibility with the ‘spirit of sport’) for a method’s inclusion on its list of prohibited substances and methods. We begin by surveying WADA’s general approach to doping, and highlight important limitations to the current evidence base regarding the performance-enhancing effect of pharmacological doping substances. We then review the current evidence base for the safety and efficacy of tDCS, and argue that despite significant shortcomings, there may be sufficient evidence for WADA to consider prohibiting tDCS, in light of the comparable flaws in the evidence base for pharmacological doping substances. In the second half of the paper, we argue that the question of whether WADA ought to ban tDCS turns significantly on the question of whether it is compatible with the ‘spirit of sport’ criterion. We critique some of the previously published positions on this, and advocate our own sport-specific and application-specific approach. Despite these arguments, we finally conclude by suggesting that tDCS ought to be monitored rather than prohibited due to compelling non-ideal considerations.

NEW FINDINGS What is the central question of this study? Endurance athletes demonstrate altered regional right ventricular (RV) wall mechanics, characterized by lower basal deformation, in comparison to non-athletic control subjects at rest. We hypothesized that regional adaptations at the RV base reflect an enhanced functional reserve capacity in response to haemodynamic volume loading. What is the main finding and its importance? Free wall RV longitudinal strain is elevated in response to acute volume loading in both endurance athletes and control subjects. However, the RV basal segment longitudinal strain response to acute volume infusion is greater in endurance athletes. Our findings suggest that training-induced cardiac remodelling might involve region-specific adaptation in the RV functional response to volume manipulation. ABSTRACT Eccentric remodelling of the right ventricle (RV) in response to increased blood volume and repetitive haemodynamic load during endurance exercise is well established. Structural remodelling is accompanied by decreased deformation at the base of the RV free wall, which might reflect an enhanced functional reserve capacity in response to haemodynamic perturbation. Therefore, in this study we examined the impact of acute blood volume expansion on RV wall mechanics in 16 young endurance-trained men (aged 24 ± 3 years) and 13 non-athletic male control subjects (aged 27 ± 5 years). Conventional echocardiographic parameters and the longitudinal strain and strain rate were quantified at the basal and apical levels of the RV free wall. Measurements were obtained at rest and after 7 ml/kg i.v. Gelofusine infusion, with and without a passive leg raise. After infusion, blood volume increased by 12 ± 4 and 14 ± 5% in endurance-trained individuals versus control subjects, respectively (P = 0.264). Both endurance-trained individuals (8 ± 10%) and control subjects (7 ± 9%) experienced an increase in free wall strain from baseline, which was also similar following leg raise (7 ± 10 and 6 ± 10%, respectively; P = 0.464). However, infusion evoked a greater increase in basal longitudinal strain in endurance-trained versus control subjects (16 ± 14 vs. 6 ± 11%; P = 0.048), which persisted after leg raise (16 ± 18 vs. 3 ± 11%; P = 0.032). Apical longitudinal strain and RV free wall strain rates were not different between groups and remained unchanged after infusion across all segments. Endurance training results in a greater contribution of longitudinal myocardial deformation at the base of the RV in response to a haemodynamic volume challenge, which might reflect a greater region-specific functional reserve capacity.

Exercise can induce numerous health benefits that can reduce the risk of chronic diseases and all-cause mortality, yet a significant percentage of the population do not meet minimal physical activity guidelines. Several recent studies have shown that passive heating can induce numerous health benefits, many of which are comparable with exercise, such as improvements to cardiorespiratory fitness, vascular health, glycemic control, and chronic low-grade inflammation. As such, passive heating is emerging as a promising therapy for populations who cannot perform sustained exercise or display poor exercise adherence. There appears to be some overlap between the cellular signaling responses that are regulated by temperature and the mechanisms that underpin beneficial adaptations to exercise, but detailed comparisons have not yet been made. Therefore, the purpose of this mini review is to assess the similarities and distinctions between adaptations to passive heating and exercise. Understanding the potential shared mechanisms of action between passive heating and exercise may help to direct future studies to implement passive heating more effectively and identify differences between passive heating and exercise-induced adaptations.

We assessed the influence of barosensory vessel mechanics (magnitude and rate of unloading and time spent unloaded) as a surrogate for baroreceptor unloading. In young men, aortic unloading mechanics are important in regulating the operating point of the vascular sympathetic baroreflex, whereas in middle-aged men, these arterial mechanics do not influence this operating point. The age-related increase in resting muscle sympathetic nerve activity does not appear to be driven by altered baroreceptor input from stiffer barosensory vessels.

Introduction: The assessment of middle cerebral artery (MCA) haemodynamics is essential for the diagnosis and monitoring of cerebrovascular disease. However, conventional transcranial Doppler (TCD) may not capture the correct flow velocities because of sub-optimal angles of insonation. Conversely, 2-D ultrasound (2D-US) allows for the visualisation and angle-correction of MCA haemodynamics. Therefore, this study aimed to determine potential differences in MCA haemodynamics obtained with TCD and 2D-US. Methods: MCA haemodynamics were obtained in a blinded, randomised order with TCD and 2D-US (non-angle-corrected = 2D-US-NON and angle-corrected = 2D-US-ANGLE) from the temporal left posterior window in twenty-seven healthy participants. Recordings were analysed for peak-systolic velocity (PSV), end-diastolic velocity (ED), pulsatility index (PI) and resistance index (RI). Statistical agreements between TCD and 2D-US were determined using linear regression, independent samples t-test and Bland-Altman analysis. Results: MCA haemodynamics obtained with TCD explained less than 50% of the values obtained with 2D-US-NON & 2D-US-ANGLE, respectively (PSV r2 = 0.34 & 0.37; ED: r2 = 0.37 & 0.44; PI: r2 = 0.20 & 0.22; RI: r2 = 0.30 & 0.32). Compared with 2D-US-NON, TCD produced similar PSV (p = 0.65) but significantly higher ED (p < 0.0001), lower PI (p < 0.0001) and lower RI (p < 0.0001). 2D-US angle-correction resulted in a significantly higher PSV compared with TCD (p = 0.005) while all other differences remained. Bland-Altman analysis revealed a bias between the two methods ranging from 11–40%, with large individual variability. Conclusion: TCD and 2D ultrasound produce significantly different values for MCA haemodynamics, even when 2D-US is non-angle-corrected. This may have important implications when using indices of MCA haemodynamics in the evaluation of cerebrovascular disease.

This study focused on the influence of habitual endurance exercise training (i.e., committed runner or nonrunner) on the regulation of muscle sympathetic nerve activity (MSNA) and arterial pressure in middle-aged (50 to 63 yr, n = 23) and younger (19 to 30 yr; n = 23) normotensive men. Hemodynamic and neurophysiological assessments were performed at rest. Indices of vascular sympathetic baroreflex function were determined from the relationship between spontaneous changes in diastolic blood pressure (DBP) and MSNA. Large vessel arterial stiffness and left ventricular stroke volume also were measured. Paired comparisons were performed within each age category. Mean arterial pressure and basal MSNA bursts/min were not different between age-matched runners and nonrunners. However, MSNA bursts/100 heartbeats, an index of baroreflex regulation of MSNA (vascular sympathetic baroreflex operating point), was higher for middle-aged runners ( P = 0.006), whereas this was not different between young runners and nonrunners. The slope of the DBP-MSNA relationship (vascular sympathetic baroreflex gain) was not different between groups in either age category. Aortic pulse wave velocity was lower for runners of both age categories ( P < 0.03), although carotid β-stiffness was lower only for middle-aged runners ( P = 0.04). For runners of both age categories, stroke volume was larger, whereas heart rate was lower (both P < 0.01). In conclusion, we suggest that neural remodeling and upward setting of the vascular sympathetic baroreflex compensates for cardiovascular adaptations after many years committed to endurance exercise training, presumably to maintain arterial blood pressure stability. NEW & NOTEWORTHY Exercise training reduces muscle sympathetic burst activity in disease; this is often extrapolated to infer a similar effect in health. We demonstrate that burst frequency of middle-aged and younger men committed to endurance training is not different compared with age-matched casual exercisers. Notably, well-trained, middle-aged runners display similar arterial pressure but higher sympathetic burst occurrence than untrained peers. We suggest that homeostatic plasticity and upward setting of the vascular sympathetic baroreflex maintains arterial pressure stability following years of training.

The influence of cardiorespiratory fitness (CRF) on arterial stiffness in young adults remains equivocal. Beyond conventional measures of arterial stiffness, 2D strain imaging of the common carotid artery (CCA) provides novel information related to the intrinsic properties of the arterial wall. Therefore, this study aimed to assess the effect of CRF on both conventional indices of CCA stiffness and 2D strain parameters, at rest and following a bout of aerobic exercise in young healthy males. Short‐axis ultrasound images of the CCA were recorded in 34 healthy men [22 years (95%CI, 19–22)] before, and immediately after 5‐minutes of aerobic exercise (40% VO2max). Images were analysed for arterial diameter, peak circumferential strain (PCS), and peak systolic and diastolic strain rates (S‐SR, D‐SR). Heart rate (HR), systolic and diastolic blood pressure (SBP, DBP) were simultaneously assessed and Petersons' elastic modulus (Ep) and Beta stiffness (β1) were calculated. Participants were separated post hoc into moderate and high fitness groups [VO2max: 48.9 ml.kg‐1 min‐1 (95%CI, 44.7–53.2) vs. 65.6 ml.kg‐1 min‐1 (95%CI, 63.1–68.1); P < 0.001]. Ep and β1 were similar between groups at baseline (P > 0.13) but were elevated in the moderate‐fitness group post‐exercise (P < 0.04). PCS and S‐SR were elevated in the high‐fitness group at both time‐points [3.0% (95%CI = 1.2, 4.9); P = 0.002; 0.401/s (95%CI = 0.085, 0.72); P = 0.02, respectively]. No group differences were observed in diameter, HR, SBP, DBP or D‐SR throughout the protocol (P > 0.05). High‐fit individuals exhibit elevated CCA PCS and S‐SR, which may reflect training‐induced adaptations that help to buffer the rise in pulse‐pressure and stroke volume during exercise.

An abundance of data unequivocally demonstrates that exercise can be an effective tool in the fight against obesity and its associated comorbidities.1 Indeed, physical activity can be more effective than widely used pharmaceutical interventions. While metformin reduces the incidence of diabetes by 31% (as compared with a placebo) in both men and women across different racial and ethnic groups, lifestyle intervention (including exercise) reduces the incidence by 58%.2 In this context, it is notable that a group of prominent medics and exercise scientists recently sent a well-publicised letter to the General Medical Council (GMC) and Medical Schools Council calling for the introduction of evidence-based lifestyle education into all medical curricula.3 The letter warns that there is a lack of understanding of the impact that exercise and nutrition can have on physical health among doctors. In the absence of an educational overhaul, the signatories warn that the government is likely to fail to reach its goal of preventing tens of thousands of premature deaths from heart disease and cancer by 2020. While we agree with the need to address this apparent lack of understanding, the ethical justification of doing so is not limited to this broadly beneficence-based justification. There is also a justification grounded in the duty of non-maleficence, that is, the duty to avoid unreasonable harm to patients. Despite the well-established long-term beneficial effects of exercise, the risk of an acute cardiovascular event may be transiently elevated during and just after vigorous physical exertion for susceptible individuals. This is the so-called ‘paradox of exercise’.4 This paradox does not mean doctors should refrain from prescribing exercise; the …

Nonalcoholic fatty liver disease (NAFLD) is an independent risk factor for cardiovascular disease (CVD). Endothelial dysfunction is an early manifestation of atherosclerosis and an important prognostic marker for future cardiovascular events. The aim of this study was twofold: to examine 1) the association between liver fat, visceral adipose tissue (VAT), and endothelial dysfunction in obese NAFLD patients and 2) the impact of supervised exercise training on this vascular defect. Brachial artery endothelial function was assessed by flow-mediated dilatation (FMD) in 34 obese NAFLD patients and 20 obese controls of similar age and cardiorespiratory fitness [peak oxygen uptake (V̇o2 peak)] (48 ± 2 vs. 47 ± 2 yr; 27 ± 1 vs. 26 ± 2 ml·kg−1·min−1−1). Magnetic resonance imaging and spectroscopy quantified abdominal and liver fat, respectively. Twenty-one NAFLD patients completed either 16 wk of supervised moderate-intensity exercise training ( n = 13) or conventional care ( n = 8). Differences between NAFLD and controls were compared using independent t-tests and effects of interventions by analysis of covariance. NAFLD patients had higher liver fat [11.6% (95% CI = 7.4, 18.1), P < 0.0005] and VAT [1.6 liters (95% CI = 1.2, 2.0), P < 0.0001] than controls and exhibited impaired FMD compared with controls [−3.6% (95% CI = −4.9, −2.2), P < 0.0001]. FMD was inversely correlated with VAT ( r = −0.54, P = 0.001) in NAFLD, although the impairment in FMD remained following covariate adjustment for VAT [3.1% (95% CI = 1.8, 4.5), P < 0.001]. Exercise training, but not conventional care, significantly improved V̇o2 peak [9.1 ml·kg−1·min−1 (95% CI = 4.1, 14.1); P = 0.001] and FMD [3.6% (95% CI = 1.6, 5.7), P = 0.002]. Endothelial dysfunction in NAFLD cannot be fully explained by excess VAT but can be reversed with exercise training; this has potential implications for the primary prevention of CVD in NAFLD.

The aim of this study was to examine the contribution of arterial shear to changes in flow-mediated dilation (FMD) during sympathetic nervous system (SNS) activation in healthy humans. Ten healthy men reported to our laboratory four times. Bilateral FMD, shear rate (SR), and catecholamines were examined before/after 10-min of −35-mmHg lower body negative pressure (LBNP10). On day 1, localized forearm heating (LBNP10+heat) was applied in one limb to abolish the increase in retrograde SR associated with LBNP. Day 2 involved unilateral cuff inflation to 75 mmHg around one limb to exaggerate the LBNP-induced increase retrograde SR (LBNP10+cuff). Tests were repeated on days 3 and 4, using 30-min interventions (i.e., LBNP30+heat and LBNP30+cuff). LBNP10 significantly increased epinephrine levels and retrograde SR and decreased FMD (all P < 0.05). LBNP10+heat prevented the increase in retrograde SR, whereas LBNP10+cuff further increased retrograde SR ( P < 0.05). Heating prevented the decrease in percent FMD (FMD%) after LBNP10 (interaction effect, P < 0.05), whereas cuffing did not significantly exaggerate the decrease in FMD% (interaction effect, P > 0.05). Prolongation of the LBNP stimulus for 30-min normalized retrograde SR, catecholamine levels, and FMD (all P > 0.05). Attenuation of retrograde SR during 30 min (LBNP30+heat) was associated with increased FMD% (interaction effects, P < 0.05), whereas increased retrograde SR (LBNP30+cuff) diminished FMD% (interaction effects, P < 0.05). These data suggest that LBNP-induced SNS stimulation decreases FMD, at least in part due to the impact of LBNP on arterial shear stress. Prolonged LBNP stimulation was not associated with changes in SR or FMD%. Our data support a role for changes in SR to the impact of SNS stimulation on FMD.

SPRUNG, V. S., D. J. CUTHBERTSON, C. J. A. PUGH, N. AZIZ, G. J. KEMP, C. DAOUSI, D. J. GREEN, N. T. CABLE, and H. JONES. Exercise Training in Polycystic Ovarian Syndrome Enhances Flow-Mediated Dilation in the Absence of Changes in Fatness. Med. Sci. Sports Exerc., Vol. 45, No. 12, pp. 2234–2242, 2013. Introduction: Polycystic ovarian syndrome (PCOS) is associated with an adverse cardiovascular disease (CVD) profile. A surrogate marker for CVD risk is endothelial dysfunction. Limited studies exist examining the cardiovascular and metabolic effects of exercise in PCOS and specifically its impact on endothelial function. Therefore, the aim of the current study was to investigate the impact of exercise on endothelial function, in parallel with body composition, insulin resistance, and cardiopulmonary fitness in PCOS. Methods: Ten women with PCOS (27 yr, 95% confidence interval [CI] = 23–32; 31 kgIm j2 , 95% CI = 28–34) completed a 16-wk exercise (EX) program, and seven women with PCOS (29 yr, 95% CI = 24–35; 35 kgIm j2 , 95% CI = 31–40) undertook conventional care (CC) following lifestyle advice. Brachial artery endothelial function was assessed pre- and postintervention using flow-mediated dilation adjusted for variability in baseline diameter. Visceral and abdominal subcutaneous adipose tissue was assessed using whole-body magnetic resonance imaging and 1 H magnetic resonance spectroscopy quantified liver fat. Cardiorespiratory fitness, glycemic control, hormone, and lipid profiles were also assessed. Data were analyzed using covariate-controlled generalized estimating equations. Results: At follow-up, EX improved flow-mediated dilation by 3.6% (95% CI = 0.5–6.7, P = 0.03) more than CC. There was a parallel improvement in cardiorespiratory fitness of 4.7 mLIkg j1 Imin j1 (95% CI = 1.4–7.9, P G 0.001) with EX versus CC. These changes were not explained by changes in visceral adipose tissue, subcutaneous adipose tissue, liver fat or insulin resistance. Conclusions: Supervised exercise in women with PCOS improves endothelial function, an adaptation associated with reduced CVD risk. This change occurs independent of changes in body weight or composition. The success of public health interventions in this

PCOS (polycystic ovary syndrome) is associated with IR (insulin resistance), increased visceral fat and NAFLD (non-alcoholic fatty liver disease) all of which may contribute to endothelial dysfunction, an early marker of CVD (cardiovascular disease) risk. Our objective was to examine the relationships between endothelial dysfunction in PCOS, the volume of AT (adipose tissue) compartments and the size of intracellular TAG (triacylglycerol) pools in liver and skeletal muscle. A total of 19 women with PCOS (means±S.D.; 26±6 years, 36±5 kg/m2) and 16 control women (31±8 years, 30±6 kg/m2) were recruited. Endothelial function was assessed in the brachial artery using FMD (flow-mediated dilation). VAT (visceral AT) and abdominal SAT (subcutaneous AT) volume were determined by whole body MRI, and liver and skeletal muscle TAG by 1H-MRS (proton magnetic resonance spectroscopy). Cardiorespiratory fitness and HOMA-IR (homoeostasis model assessment of IR) were also determined. Differences between groups were analysed using independent Student's t tests and ANCOVA (analysis of co-variance). FMD was impaired in PCOS by 4.6% [95% CI (confidence interval), 3.0–7.7; P

Glucagon-like peptide-1 receptor agonists (GLP-1 RA) are used for treatment in type 2 diabetes mellitus (T2DM). Little is known about their cardiovascular (CV) impact. We sought to determine the effects of chronic treatment on vascular function in T2DM. Brachial artery endothelial-dependent flow-mediated dilation (FMD) and endothelial-independent glyceryl trinitrate (GTN) function and carotid intima-medial thickness (cIMT) were assessed in 11 severely obese T2DMs (4 females, 7 males: 55 ± 8 years, diabetes duration 8.3 ± 4.7 years mean ± s.d.) before and after 6 months GLP-1 RA. Body weight (5.3 ± 1.2 kg; p < 0.05) and magnetic resonance imaging determined total and subcutaneous fat, but not visceral fat, decreased. Glycaemic control improved. There were no significant changes in FMD, GTN and cIMT (-1.1 ± 0.4%, 0.3 ± 3.0% and 0.00 ± 0.04 mm, respectively). Despite significant improvements in body composition and glycaemic control, 6 months GLP-1 RA treatment did not modulate vascular function. Alternative strategies may therefore be needed to reduce the burden of CV risk in severely obese patients with long-standing T2DM.

Polycystic ovary syndrome (PCOS) is associated with cardiovascular disease. The contribution of the nitric oxide (NO) dilator system to cutaneous endothelial dysfunction is currently unknown in PCOS. Our aim was to examine whether women with PCOS demonstrate impaired cutaneous microvascular NO function and whether exercise training can ameliorate any impairment. Eleven women with PCOS (age, 29 ± 7 years; body mass index, 34 ± 6 kg m(-2)) were compared with six healthy obese control women (age, 29 ± 7 years; body mass index, 34 ± 5 kg m(-2)). Six women with PCOS (30 ± 7 years; 31 ± 6 kg m(-2)) then completed 16 weeks of exercise training. Laser Doppler flowmetry, combined with intradermal microdialysis of l-N(G)-monomethyl-l-arginine, a nitric oxide antagonist, in response to incremental local heating of the forearm was assessed in women with PCOS and control women, and again in women with PCOS following exercise training. Cardiorespiratory fitness, homeostasis model assessment for insulin resistance, hormone and lipid profiles were also assessed. Differences between women with PCOS and control women and changes with exercise were analysed using Student's unpaired t tests. Differences in the contribution of NO to cutaneous blood flow [expressed as a percentage of maximal cutaneous vasodilatation (CVCmax)] were analysed using general linear models. At 42°C heating, cutaneous NO-mediated vasodilatation was attenuated by 17.5%CVCmax (95% confidence interval, 33.3, 1.7; P = 0.03) in women with PCOS vs. control women. Exercise training improved cardiorespiratory fitness by 5.0 ml kg(-1) min(-1) (95% confidence interval, 0.9, 9.2; P = 0.03) and NO-mediated cutaneous vasodilatation at 42°C heating by 19.6% CVCmax (95% confidence interval, 4.3, 34.9; P = 0.02). Cutaneous microvascular NO function is impaired in women with PCOS compared with obese matched control women but can be improved with exercise training.

AIMS: Supervised exercise reduces liver fat and improves endothelial function, a surrogate of cardiovascular disease risk, in non-alcoholic fatty liver disease (NAFLD). We hypothesised that after a 16-week supervised exercise program, patients would maintain longer-term improvements in cardiorespiratory fitness, liver fat and endothelial function. MATHERIALS AND METHODS: Ten NAFLD patients [5/5 males/females, age 51±13years, BMI 31±3 kg.m(2) (mean±s.d.)] underwent a 16-week supervised moderate-intensity exercise intervention. Biochemical markers, cardiorespiratory fitness (VO2peak), subcutaneous, visceral and liver fat (measured by magnetic resonance imaging and spectroscopy respectively) and brachial artery flow-mediated dilation (FMD) were assessed at baseline, after 16 weeks supervised training and 12-months after ending supervision. RESULTS: Despite no significant change in body weight, there were significant improvements in VO2peak [6.5 ml.kg(-1).min(-1) (95% CI 2.8, 10.1); P=0.003], FMD [2.9% (1.5, 4.2); P=0.001], liver transaminases (P0.05) and liver fat [1.4% (-13.0, 15.9); P=0.83] were not significantly different from baseline. CONCLUSIONS: Twelve months following cessation of supervision, exercise-mediated improvements in liver fat and other cardiometabolic variables had reversed with cardiorespiratory fitness at baseline levels. Maintenance of high cardiorespiratory fitness and stability of body weight are critical public health considerations for the treatment of NAFLD.International Journal of Obesity accepted article preview online, 21 July 2016. doi:10.1038/ijo.2016.123.

Non-alcoholic fatty liver disease (NAFLD) is associated with multi-organ (hepatic, skeletal muscle, adipose tissue) insulin resistance (IR). Exercise is an effective treatment for lowering liver fat but its effect on IR in NAFLD is unknown. We aimed to determine whether supervised exercise in NAFLD would reduce liver fat and improve hepatic and peripheral (skeletal muscle and adipose tissue) insulin sensitivity. Sixty nine NAFLD patients were randomized to 16 weeks exercise supervision (n=38) or counselling (n=31) without dietary modification. All participants underwent MRI/spectroscopy to assess changes in body fat and in liver and skeletal muscle triglyceride, before and following exercise/counselling. To quantify changes in hepatic and peripheral insulin sensitivity, a pre-determined subset (n=12 per group) underwent a two-stage hyperinsulinaemic euglycaemic clamp pre- and post-intervention. Results are shown as mean [95% confidence interval (CI)]. Fifty participants (30 exercise, 20 counselling), 51 years (IQR 40, 56), body mass index (BMI) 31 kg/m2 (IQR 29, 35) with baseline liver fat/water % of 18.8% (IQR 10.7, 34.6) completed the study (12/12 exercise and 7/12 counselling completed the clamp studies). Supervised exercise mediated a greater reduction in liver fat/water percentage than counselling [Δ mean change 4.7% (0.01, 9.4); P

Item does not contain fulltext INTRODUCTION: Regular exercise induces recurrent increases in cerebrovascular perfusion. In peripheral arteries, such episodic increases in perfusion are responsible for improvement in arterial function and health. We examined the hypothesis that exercise during immersion augments cerebral blood flow velocity compared with intensity-matched land-based exercise. METHODS: Fifteen normotensive participants were recruited (26 +/- 4 yr, 24.3 +/- 1.9 kg.m). We continuously assessed mean arterial blood pressure, HR, stroke volume, oxygen consumption, and blood flow velocities through the middle and posterior cerebral arteries before, during, and after 20-min bouts of water- and land-based stepping exercise of matched intensity. The order in which the exercise conditions were performed was randomized between subjects. Water-based exercise was performed in 30 degrees C water to the level of the right atrium. RESULTS: The water- and land-based exercise bouts were closely matched for oxygen consumption (13.3 mL.kg.min (95% confidence interval (CI), 12.2-14.6) vs 13.5 mL.kg.min (95% CI, 12.1-14.8), P = 0.89) and HR (95 bpm (95% CI, 90-101) vs 96 bpm (95% CI, 91-102), P = 0.65). Compared with land-based exercise, water-based exercise induced an increase in middle cerebral artery blood flow velocity (74 cm.s (95% CI, 66-81) vs 67 cm.s (95% CI, 60-74) P < 0.001), posterior cerebral artery blood flow velocity (47 cm.s (95% CI, 40-53) vs 43 cm.s (95% CI, 37-49), P < 0.001), mean arterial blood pressure (106 mm Hg (95% CI, 100-111) vs 101 mm Hg (95% CI, 95-106), P < 0.001), and partial pressure of expired CO2 (P

Contains fulltext : 137986.pdf (Publisher’s version ) (Closed access) The objectives of our study were to examine 1) the proportion of responders and nonresponders to exercise training in terms of vascular function; 2) a priori factors related to exercise training-induced changes in conduit artery function, and 3) the contribution of traditional cardiovascular risk factors to exercise-induced changes in artery function. We pooled data from our laboratories involving 182 subjects who underwent supervised, large-muscle group, endurance-type exercise training interventions with pre-/posttraining measures of flow-mediated dilation (FMD%) to assess artery function. All studies adopted an identical FMD protocol (5-min ischemia, distal cuff inflation), contemporary echo-Doppler methodology, and observer-independent automated analysis. Linear regression analysis was used to identify factors contributing to changes in FMD%. We found that cardiopulmonary fitness improved, and weight, body mass index (BMI), cholesterol, and mean arterial pressure (MAP) decreased after training, while FMD% increased in 76% of subjects (P < 0.001). Training-induced increase in FMD% was predicted by lower body weight (beta = -0.212), lower baseline FMD% (beta = -0.469), lower training frequency (beta = -0.256), and longer training duration (beta = 0.367) (combined: P < 0.001, r = 0.63). With the exception of a modest correlation with total cholesterol (r = -0.243, P < 0.01), changes in traditional cardiovascular risk factors were not significantly related to changes in FMD% (P > 0.05). In conclusion, we found that, while some subjects do not demonstrate increases following exercise training, improvement in FMD% is present in those with lower pretraining body weight and endothelial function. Moreover, exercise training-induced change in FMD% did not correlate with changes in traditional cardiovascular risk factors, indicating that some cardioprotective effects of exercise training are independent of improvement in risk factors.

Episodic increases in cerebrovascular perfusion and shear stress may have beneficial impacts on endothelial function that improve brain health. We hypothesized that water immersion to the level of the right atrium in humans would increase cerebral perfusion. We continuously measured, in 9 young (means ± SD, 24.6 ± 2.0 yr) healthy men, systemic hemodynamic variables along with blood flows in the common carotid and middle and posterior cerebral arteries during controlled filling and emptying of a water tank to the level of the right atrium. Mean arterial pressure (80 ± 9 vs. 91 ± 12 mmHg, P < 0.05), cardiac output (4.8 ± 0.7 vs. 5.1 ± 0.6 l/min, P < 0.05) and end-tidal carbon dioxide (PetCO2, 39.5 ± 2.0 vs. 44.4 ± 3.5 mmHg, P < 0.05) increased with water immersion, along with middle (59 ± 6 vs. 64 ± 6 cm/s, P < 0.05) and posterior cerebral artery blood flow velocities (41 ± 9 vs. 44 ± 10 cm/s, P < 0.05). These changes were reversed when the tank was emptied. Water immersion is associated with hemodynamic and PetCO2 changes, which increase cerebral blood velocities in humans. This study provides an evidence base for future studies to examine the potential additive effect of exercise in water on improving cerebrovascular health.

Shear stress is a known stimulus to vascular adaptation in humans. However, it is not known whether thermoregulatory reflex increases in blood flow and shear can induce conduit artery adaptation. Ten healthy young volunteers therefore underwent 8 weeks of 3 × weekly bouts of 30 min lower limb heating (40 °C) during which the upper body was not directly heated. Throughout each leg heating session, a pneumatic cuff was placed on one forearm and inflated to unilaterally restrict reflex-mediated blood flow responses. Each bout of leg heating significantly increased brachial artery shear rate in the uncuffed arm (96 ± 97 vs 401 ± 96 l/s, P

The leading causes of mortality in nonalcoholic fatty liver disease (NAFLD) relate to cardiovascular disease (CVD). The contribution of nitric oxide (NO) to endothelial function, a surrogate of CVD risk, is currently unknown in NAFLD. We hypothesize that NO-mediated cutaneous microvessel function would be impaired in NAFLD compared with controls and that exercise would enhance microvessel function compared with conventional care. Thirteen NAFLD patients (aged 50 ± 3 yr, BMI 31 ± 1 kg/m2) and seven controls (48 ± 4 yr, 30 ± 2 kg/m2) were studied. NAFLD patients were randomized to either 16 wk of exercise or conventional care. Cutaneous microvessel function was examined using laser Doppler flowmetry combined with intradermal microdialysis of NG-monomethyl-l-arginine to assay the NO dilator response to local forearm heating. Magnetic resonance imaging and spectroscopy quantified abdominal and liver fat, respectively, and cardiorespiratory fitness was assessed. Differences in NO contribution to cutaneous blood flow between NAFLD and control individuals and between interventions were analyzed using general linear modeling. NO contribution to cutaneous blood flow was similar between NAFLD and controls ( P = 0.47). Cardiorespiratory fitness was greater following exercise training compared with conventional care. NO contribution to cutaneous blood flow in response to heating at 42°C was 20.4% CVCmax (95% CI = 4.4, 36.4) greater following exercise training compared with conventional care ( P = 0.02). Exercise training improves cutaneous microvascular NO function in NAFLD patients. The benefit of exercise training compared with conventional care strongly supports a role for exercise in the prevention of CVD in NAFLD.

Arterial wall mechanics likely play an integral role in arterial responses to acute physiological stress. Therefore, this study aimed to determine the impact of low and moderate intensity double‐leg press exercise on common carotid artery (CCA) wall mechanics using 2D vascular strain imaging. Short‐axis CCA ultrasound images were collected in 15 healthy men (age: 21 ± 3 years; stature: 176.5 ± 6.2 cm; body mass; 80.6 ± 15.3 kg) before, during, and immediately after short‐duration isometric double‐leg press exercise at 30% and 60% of participants' one‐repetition maximum (1RM: 317 ± 72 kg). Images were analyzed for peak circumferential strain (PCS), peak systolic and diastolic strain rate (S‐SR and D‐SR), and arterial diameter. Heart rate (HR), systolic and diastolic blood pressure (SBP and DBP) were simultaneously assessed and arterial stiffness indices were calculated post hoc. A two‐way repeated measures ANOVA revealed that during isometric contraction, PCS and S‐SR decreased significantly (P

Objectives To assess whether exergaming can induce measurable changes in heart rate (HR), energy expenditure (EE), and flow-mediated dilation (FMD) arterial function in healthy children. Studydesign Fifteenchildren(8males,10.10.7years,bodymassindex17.92.4kg.m 2 )undertookagraded exercise test and 2 15 minute exergaming sessions (Xbox 360‐Kinect); high intensity exergaming (HiE, Kinect Sports‐200 m Hurdles) and low intensity exergaming (LoE, Kinect Sports‐Ten Pin Bowling). Brachial artery FMD, a measure of endothelial function and arterial health, was measured before and immediately after each exergaming intervention. Actihearts were used to measure EE and HR during game play and a physical activity enjoyment scale assessed enjoyment. Results Average HR during HiE (146 11 beats per minute) was greater than during LoE (104 11 beats per minute, P < .05), a pattern reinforced by EE data (HiE 294.6 75.2 J.min 1 .kg 1 , LoE 73.7 44.0 J.min 1 .kg 1 , P < .05). FMD decreased after HiE (P < .05), whereas no change was observed following LoE. Subjects reported no differences in enjoyment between LoE and HiE. Conclusion HiE, but not LoE, induced large HR and EE responses that were associated with effects on vascular function. This study suggests that an acute bout of HiE exergaming may provide a substrate for beneficial arterial adaptations in children. (J Pediatr 2013;163:806-10).

Nonalcoholic fatty liver disease may be evident in women with polycystic ovary syndrome (PCOS), both conditions being associated with obesity and insulin resistance. However, few studies have accounted for the high prevalence of obesity in PCOS.The aim of this study was to determine whether PCOS is independently associated with hepatic steatosis, compared with healthy controls of similar age and body mass index (BMI), and whether steatosis is associated with hyperandrogenemia.We conducted a cross-sectional, case-control study at two tertiary referral centers.Twenty-nine women with PCOS diagnosed by the Rotterdam criteria [aged 28 yr; 95% confidence interval (CI), 26-31; BMI, 33 kg/m2; 95% CI, 31-36] and 22 healthy controls (aged 29 yr; 95% CI, 28-31; BMI, 30 kg/m2; 95% CI, 28-33) were studied.Proton-magnetic resonance spectroscopy quantified hepatic and skeletal muscle fat; whole body magnetic resonance imaging quantified internal, visceral, and sc adipose tissue volumes. Differences were assessed between PCOS and controls using t tests, and between hyperandrogenic (HA) PCOS, PCOS with normal androgens (NA), and controls using analysis of covariance.After statistical adjustment for BMI, HA-PCOS had significantly higher liver fat vs. NA-PCOS (3.7%; 95% CI, 0.6-13.1) and vs. controls (2.1%; 95% CI, 0.3-6.6). Similarly, after adjustment for homeostasis model assessment for insulin resistance, internal and visceral adipose tissue volumes, liver fat remained significantly greater in HA-PCOS compared to NA-PCOS and controls.These data suggest that HA-PCOS is associated with hepatic steatosis, independent of obesity and insulin resistance.

Objective Women with polycystic ovary syndrome (PCOS) demonstrate an increased prevalence of cardiovascular disease (CVD) risk factors. Previous researchers have compared flow-mediated dilation (FMD), an early marker of CVD, in women with and without PCOS. Evidence for a PCOS-mediated reduction in FMD remains equivocal, potentially because of study differences in cohort-matching and measurement approaches. The aims of this systematic review and meta-analysis were to examine to what extent FMD is impaired in PCOS and to explore the influence of potential moderators of FMD reduction, such as age and BMI. Design A systematic review and meta-analysis of published observational studies comparing FMD in PCOS with control women. Patients Twenty-one published studies were included (PCOS, n = 908; controls, n = 566). A subanalysis, using tighter inclusion criteria, involved seven studies (PCOS, n = 402; control, n = 251). Measurements Mean differences in FMD between PCOS and controls were synthesized. The subanalysis was delimited to the inclusion of age and BMI-matched controls. These factors were then explored as moderators using meta-regression. Results The pooled mean FMD was 3·4% (95% CI=1·9, 4·9) lower in PCOS compared with control women, with substantial heterogeneity between studies. In the subanalysis, the PCOS-mediated reduction in FMD was 4·1% (95% CI=2·7, 5·5). Heterogeneity remained substantial (I2=81%). Subsequent meta-regression indicated that the magnitude of FMD difference was not influenced by BMI (P = 0·17) nor age (P = 0·38). Conclusions This systematic research synthesis indicates that endothelial function is compromised in PCOS women, even if they are young and nonobese.

Item does not contain fulltext PURPOSE: We performed two experiments to determine whether cutaneous microvascular adaptations in response to repeated core temperature (Tc) elevation are mediated by increases in skin blood flow (SkBF) and/or skin temperature. METHODS: Healthy subjects participated for 8 wk in thrice-weekly bouts of 30-min lower limb heating (40 degrees C). In study 1, both forearms were "clamped" at basal skin temperature throughout each heating bout (n = 9). Study 2 involved identical lower limb heating, with the forearms under ambient conditions (unclamped, n = 10). In both studies, a cuff was inflated around one forearm during the heating bouts to assess the contribution of SkBF and temperature responses. We assessed forearm SkBF responses to both lower limb (systemic reflex) heating and to local heating of the forearm skin, pre- and postintervention. RESULTS: Acutely, lower limb heating increased Tc (study 1, 0.63 degrees C +/- 0.15 degrees C; study 2, 0.69 degrees C +/- 0.19 degrees C; P < 0.001) and forearm SkBF (study 1, 0.13 +/- 0.03 vs 1.52 +/- 0.51; study 2, 0.14 +/- 0.01 vs 1.17 +/- 0.38 cutaneous vascular conductance (CVC); P < 0.001), with skin responses significantly attenuated in the cuffed forearm (P < 0.01). SkBF responses to local heating decreased in study 1 (clamped forearms; week 0 vs week 8, 1.46 +/- 0.52 vs 0.99 +/- 0.44 CVC; P < 0.05), whereas increases occurred in study 2 (unclamped; week 0 vs week 8, 1.89 +/- 0.57 vs 2.27 +/- 0.52 CVC; P < 0.05). Cuff placement abolished local adaptations in both studies. CONCLUSIONS: Our results indicate that repeated increases in SkBF and skin temperature result in increased skin flux responses to local heating, whereas repeated increases in SkBF in the absence of change in skin temperature induced the opposite response. Repeated increases in Tc induce intrinsic microvascular changes, the nature of which are dependent upon both SkBF and skin temperature. 01 november 2014

Background and Aims. Simple clinical algorithms including the Fatty Liver Index (FLI) and Lipid Accumulation Product (LAP) have been developed as a surrogate marker for Non-Alcoholic Fatty Liver Disease (NAFLD). These algorithms have been constructed using ultrasonography, a semi-quantitative method. This study aimed to validate FLI and LAP as measures of hepatic steatosis, as measured quantitatively by proton magnetic resonance spectroscopy (1H-MRS). \ud Methods. Data were collected from 168 patients with NAFLD and 168 controls who had undergone clinical, biochemical and anthropometric assessment in the course of research studies. Values of FLI and LAP were determined, and assessed both as predictors of the presence of hepatic steatosis (liver fat >5.5 %) and of actual liver fat content, as measured by 1H MRS. The discriminative ability of FLI and LAP was estimated using the area under the Receiver Operator Characteristic curve (AUROC). Since FLI can also be interpreted as a predictive probability of hepatic steatosis, we assessed how well calibrated it was in our cohort. Linear regression with prediction intervals was used to assess the ability of FLI and LAP to predict liver fat content. \ud Results. FLI and LAP discriminated between patients with and without hepatic steatosis with an AUROC of 0.79 (IQR= 0.74, 0.84) and 0.78 (IQR= 0.72, 0.83), although quantitative prediction of liver fat content was unsuccessful. Additionally, the algorithms accurately matched the observed percentages of patients with hepatic steatosis in our cohort. \ud Conclusions. FLI and LAP may be used clinically, and for metabolic and epidemiological research, to identify patients with hepatic steatosis, but not as surrogates for liver fat content.

Arterial shear stress is a potent stimulus to vascular adaptation in humans. Typically, increases in retrograde shear have been found to acutely impair vascular function while increases in antegrade shear enhance function. We hypothesized that blood flow and shear stress through the brachial and carotid arteries would change in a similar manner in response to water immersion, an intervention which modifies hemodynamics. Nine healthy young male subjects were recruited to undergo controlled water immersion in a standing upright position to the level of the right atrium in 30°C water. Diameters were continuously and simultaneously recorded in the brachial and common carotid arteries along with mean arterial pressure (MAP), cardiac output (CO), and heart rate before, during, and after 10 min of immersion. MAP and CO increased during water immersion (baseline vs. 8–10 min; 80 ± 9 vs. 91 ± 12 mmHg; and 4.8 ± 0.7 vs. 5.1 ± 0.6 L/min, P