A Systematic Review with Meta-Analysis of Randomized Controlled Trials

Objective Epidemiological evidence has linked consumption of black tea, produced from Camellia sinensis, with a reduced risk of cardiovascular diseases. However, intervention studies on the effects of tea consumption on blood pressure (BP) have reported inconsistent results. Our objective was to conduct a systematic literature review with meta-analysis of controlled human intervention studies examining the effect of tea consumption on BP. Methods We systematically searched Medline, Biosis, Chemical Abstracts and EMBASE databases through July 2013. For inclusion, studies had to meet the following pre-defined criteria: 1) placebo controlled design in human adults, 2) minimum of 1 week black tea consumption as the sole intervention, 3) reported effects on systolic BP (SBP) or diastolic BP (DBP) or both. A random effects model was used to calculate the pooled overall effect of black tea on BP. Results Eleven studies (12 intervention arms, 378 subjects, dose of 4–5 cups of tea) met our inclusion criteria. The pooled mean effect of regular tea ingestion was −1.8 mmHg (95% CI: −2.8, −0.7; P = 0.0013) for SBP and −1.3 mmHg (95% CI: −1.8, −0.8; P<0.0001) for DBP. In covariate analyses, we found that the method of tea preparation (tea extract powders versus leaf tea), baseline SBP and DBP, and the quality score of the study affected the effect size of the tea intervention (all P<0.05). No evidence of publication bias could be detected. Conclusions Our meta-analysis indicates that regular consumption of black tea can reduce BP. Although the effect is small, such effects could be important for cardiovascular health at population level

Vascular Function and Structure in Veteran Athletes after Myocardial Infarction.

PURPOSE: Although athletes demonstrate lower cardiovascular risk and superior vascular function compared with sedentary peers, they are not exempted from cardiac events (i.e., myocardial infarction [MI]). The presence of an MI is associated with increased cardiovascular risk and impaired vascular function. We tested the hypothesis that lifelong exercise training in post-MI athletes, similar as in healthy controls, is associated with a superior peripheral vascular function and structure compared with a sedentary lifestyle in post-MI individuals. METHODS: We included 18 veteran athletes (ATH) (>20 yr) and 18 sedentary controls (SED). To understand the effect of lifelong exercise training after MI, we included 20 veteran post-MI athletes (ATH + MI) and 19 sedentary post-MI controls (SED + MI). Participants underwent comprehensive assessment using vascular ultrasound (vascular stiffness, intima-media thickness, and endothelium (in)dependent mediated dilatation). Lifetime risk score was calculated for a 30-yr risk prediction of cardiovascular disease mortality of the participants. RESULTS: ATH demonstrated a lower vascular stiffness and smaller femoral intima-media thickness compared with SED. Vascular function and structure did not differ between ATH + MI and SED + MI. ATH (4.0% ± 5.1%) and ATH + MI (6.1% ± 3.7%) had a significantly better lifetime risk score compared with their sedentary peers (SED: 6.9% ± 3.7% and SED + MI: 9.3% ± 4.8%). ATH + MI had no secondary events versus two recurrent MI and six elective percutaneous coronary interventions within SED + MI (P < 0.05). CONCLUSION: Although veteran post-MI athletes did not have a superior peripheral vascular function and structure compared with their sedentary post-MI peers, benefits of lifelong exercise training in veteran post-MI athletes relate to a better cardiovascular risk profile and lower occurrence of secondary events

Vascular adaptation to exercise in humans: Role of hemodynamic stimuli

On the 400th anniversary of Harvey’s Lumleian lectures, this review focuses on “hemodynamic” forces associated with the movement of blood through arteries in humans and the functional and structural adaptations that result from repeated episodic exposure to such stimuli. The late 20th century discovery that endothelial cells modify arterial tone via paracrine transduction provoked studies exploring the direct mechanical effects of blood flow and pressure on vascular function and adaptation in vivo. In this review, we address the impact of distinct hemodynamic signals that occur in response to exercise, the interrelationships between these signals, the nature of the adaptive responses that manifest under different physiological conditions, and the implications for human health. Exercise modifies blood flow, luminal shear stress, arterial pressure, and tangential wall stress, all of which can transduce changes in arterial function, diameter, and wall thickness. There are important clinical implications of the adaptation that occurs as a consequence of repeated hemodynamic stimulation associated with exercise training in humans, including impacts on atherosclerotic risk in conduit arteries, the control of blood pressure in resistance vessels, oxygen delivery and diffusion, and microvascular health. Exercise training studies have demonstrated that direct hemodynamic impacts on the health of the artery wall contribute to the well-established decrease in cardiovascular risk attributed to physical activity. © 2017 the American Physiological Society

Combined aerobic and resistance exercise training decreases peripheral but not central artery wall thickness in subjects with type 2 diabetes

Objective Little is known about the impact of exercise training on conduit artery wall thickness in type 2 diabetes. We examined the local and systemic impact of exercise training on superficial femoral (SFA), brachial (BA), and carotid artery (CA) wall thickness in type 2 diabetes patients and controls. Methods Twenty patients with type 2 diabetes and 10 age- and sex-matched controls performed an 8-week training study involving lower limb-based combined aerobic and resistance exercise training. We examined the SFA to study the local effect of exercise, and also the systemic impact of lower limb-based exercise training on peripheral (i.e. BA) and central (i.e. CA) arteries. Wall thickness (WT), diameter and wall:lumen(W:L)-ratios were examined using automated edge detection of ultrasound images. Results Exercise training did not alter SFA or CA diameter in type 2 diabetes or controls (all P > 0.05). BA diameter was increased after training in type 2 diabetes, but not in controls. Exercise training decreased WT and W:L ratio in the SFA and BA, but not in CA in type 2 diabetes. Training did not alter WT or W:L ratio in controls (P > 0.05). Conclusion Lower limb-dominant exercise training causes remodelling of peripheral arteries, supplying active and inactive vascular beds, but not central arteries in type 2 diabetes

Impact of sympathetic nervous system activity on post-exercise flow-mediated dilatation in humans

Transient reduction in vascular function following systemic large muscle group exercise has previously been reported in humans. The mechanisms responsible are currently unknown. We hypothesised that sympathetic nervous system activation, induced by cycle ergometer exercise, would contribute to post-exercise reductions in flow-mediated dilatation (FMD). Ten healthy male subjects (28 ± 5 years) undertook two 30 min sessions of cycle exercise at 75% HRmax. Prior to exercise, individuals ingested either a placebo or an α1-adrenoreceptor blocker (prazosin; 0.05 mg kg−1). Central haemodynamics, brachial artery shear rate (SR) and blood flow profiles were assessed throughout each exercise bout and in response to brachial artery FMD, measured prior to, immediately after and 60 min after exercise. Cycle exercise increased both mean and antegrade SR (P < 0.001) with retrograde SR also elevated under both conditions (P < 0.001). Pre-exercise FMD was similar on both occasions, and was significantly reduced (27%) immediately following exercise in the placebo condition (t-test, P = 0.03). In contrast, FMD increased (37%) immediately following exercise in the prazosin condition (t-test, P = 0.004, interaction effect P = 0.01). Post-exercise FMD remained different between conditions after correction for baseline diameters preceding cuff deflation and also post-deflation SR. No differences in FMD or other variables were evident 60 min following recovery. Our results indicate that sympathetic vasoconstriction competes with endothelium-dependent dilator activity to determine post-exercise arterial function. These findings have implications for understanding the chronic impacts of interventions, such as exercise training, which affect both sympathetic activity and arterial shear stress

Randomized controlled trial using bosentan to enhance the impact of exercise training in subjects with type 2 diabetes mellitus

In type 2 diabetes patients, endothelin (ET) receptor blockade may enhance blood flow responses to exercise training. The combination of exercise training and ET receptor blockade may represent a more potent stimulus than training alone to improve vascular function, physical fitness and glucose homeostasis. We assessed the effect of an 8 week exercise training programme combined with either ET blockade or placebo on vasculature, fitness and glucose homeostasis in people with type 2 diabetes. In a double-blind randomized controlled trial, brachial endothelium-dependent and -independent dilatation (using flow-mediated dilatation and glyceryl trinitrate, respectively), glucose homeostasis (using Homeostasis Model Assessment for Insulin Resistance (HOMA-IR)) and physical fitness (maximal cycling test) were assessed in 18 men with type 2 diabetes (60 ± 6 years old). Subjects underwent an 8 week exercise training programme, with half of the subjects receiving ET receptor blockade (bosentan) and the other half a placebo, followed by reassessment of the tests above. Exercise training improved physical fitness to a similar extent in both groups, but we did not detect changes in vascular function in either group. This study suggests that there is no adaptation in brachial and femoral artery endothelial function after 8 weeks of training in type 2 diabetes patients. Endothelin receptor blockade combined with exercise training does not additionally alter conduit artery endothelial function or physical fitness in type 2 diabetes

Impact of lifelong exercise training on endothelial ischemia-reperfusion and ischemic preconditioning in humans.

Reperfusion is essential for ischemic tissue survival, but causes additional damage to the endothelium (i.e. ischemia-reperfusion [IR] injury). Ischemic preconditioning (IPC) refers to short repetitive episodes of ischemia that can protect against IR. However, IPC efficacy attenuates with older age. Whether physical inactivity contributes to the attenuated efficacy of IPC to protect against IR injury in older humans is unclear. We tested the hypotheses that lifelong exercise training relates to 1) attenuated endothelial IR and 2) maintained IPC efficacy that protects veteran athletes against endothelial IR. In 18 sedentary male individuals (SED, 20 years, 63±7 years) and 20 veteran male athletes (ATH, >5 exercise hours/week for >20 years, 63±6 years), we measured brachial artery endothelial function with flow-mediated dilation (FMD) before and after IR. We induced IR by 20-minutes of ischemia followed by 20-minutes of reperfusion. Randomized over 2 days, participants underwent either 35-minute rest or IPC (3 cycles of 5-minutes cuff inflation to 220 mmHg with 5-minutes of rest) before IR. In SED, FMD decreased after IR (median [interquartile range]): (3.0% [2.0-4.7] to 2.1% [1.5-3.9], P=0.046) and IPC did not prevent this decline (4.1% [2.6-5.2] to 2.8% [2.2-3.6],P=0.012). In ATH, FMD was preserved after IR (3.0% [1.7-5.4] to 3.0% [1.9-4.1], P=0.82) and when IPC preceded IR (3.2% [1.9-4.2] to 2.8% [1.4-4.6],P=0.18). These findings indicate that lifelong exercise training is associated with increased tolerance against endothelial IR. These protective, preconditioning effects of lifelong exercise against endothelial ischemia-reperfusion may contribute to the cardio-protective effects of exercise training

Heart failure patients demonstrate impaired changes in brachial artery blood flow and shear rate pattern during moderate-intensity cycle exercise

New Findings What is the central question of this study? We explored whether heart failure (HF) patients demonstrate different exercise-induced brachial artery shear rate patterns compared with control subjects. What is the main finding and its importance? Moderate-intensity cycle exercise in HF patients is associated with an attenuated increase in brachial artery anterograde and mean shear rate and skin temperature. Differences between HF patients and control subjects cannot be explained fully by differences in workload. HF patients demonstrate a less favourable shear rate pattern during cycle exercise compared with control subjects. Repeated elevations in shear rate (SR) in conduit arteries, which occur during exercise, represent a key stimulus to improve vascular function. We explored whether heart failure (HF) patients demonstrate distinct changes in SR in response to moderate-intensity cycle exercise compared with healthy control subjects. We examined brachial artery SR during 40 min of cycle exercise at a work rate equivalent to 65% peak oxygen uptake in 14 HF patients (65 ± 7 years old, 13 men and one woman) and 14 control subjects (61 ± 5 years old, 12 men and two women). Brachial artery diameter, SR and oscillatory shear index (OSI) were assessed using ultrasound at baseline and during exercise. The HF patients demonstrated an attenuated increase in mean and anterograde brachial artery SR during exercise compared with control subjects (time × group interaction, P = 0.003 and P 0.05). In conclusion, HF patients demonstrate a less favourable SR pattern during cycle exercise than control subjects, characterized by an attenuated mean and anterograde SR and by increased OSI

Distinct Effects of Blood Flow and Temperature on Cutaneous Microvascular Adaptation

Aims: We performed two experiments to determine whether cutaneous microvascular adaptations in response to repeated core temperature elevation are mediated by increases in skin temperature, and/or, skin blood flow. Methods: Healthy subjects participated for 8-weeks in thrice-weekly bouts of 30mins lower limb heating (40°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 skin blood flow and temperature responses. We assessed forearm skin blood flow responses to both lower limb (systemic reflex) heating, and to local heating of the forearm skin, pre and post intervention. Results: Acutely, lower limb heating increased core temperature (Study 1: +0.63±0.15°C, Study 2: +0.69±0.19°C, P<0.001) and forearm skin blood flow (Study 1: 10±3 vs 125±44, Study 2: 16±9 vs 136±41 PU, P<0.001), with skin responses significantly attenuated in the cuffed forearm (P<0.01). Skin blood flow responses to local heating decreased in Study 1 (clamped forearms, week 0vs8: 1.46±0.52 vs 0.99±0.44 CVC, P<0.05), whereas increases occurred in Study 2 (unclamped; week 0vs8: 1.89±0.57 vs 2.27±0.52 CVC, P<0.05). Cuff placement abolished local adaptations in both studies. Conclusion: Our results indicate that repeated increases in skin blood flow and skin temperature result in increased skin flux responses to local heating, whereas repeated increases in skin blood flow in the absence of change in skin temperature induced the opposite response. Repeated increases in core temperature induce intrinsic microvascular changes, the nature of which are dependent upon both skin blood flow and skin temperature

The impact of obesity on cardiac troponin levels after prolonged exercise in humans

Elevated cardiac troponin I (cTnI), a marker for cardiac damage, has been reported after high-intensity exercise in healthy subjects. Currently, little is known about the impact of prolonged moderate-intensity exercise on cTnI release, but also the impact of obesity on this response. 97 volunteers (55 men and 42 women), stratified for BMI, performed a single bout of walking exercise (30–50 km). We examined cTnI-levels before and immediately after the exercise bout in lean (BMI < 25 kg/m2, n = 30, 57 ± 19 years), overweight (25 ≤ BMI < 30 kg/m2, n = 29, 56 ± 11 years), and obese subjects (BMI ≥ 30 kg/m2, n = 28, 53 ± 9 years). Walking was performed at a self-selected pace. cTnI was assessed using a high-sensitive cTnI-assay (Centaur; clinical cut-off value ≥0.04 μg/L). We recorded subject characteristics (body weight, blood pressure, presence of cardiovascular risk) and examined exercise intensity by recording heart rate. Mean cTnI-levels increased significantly from 0.010 ± 0.006 to 0.024 ± 0.046 μg/L (P < 0.001). The exercise-induced increase in cTnI was not different between lean, overweight and obese subjects (two-way ANOVA interaction; P = 0.27). In 11 participants, cTnI was elevated above the clinical cut-off value for myocardial infarction. Logistic regression analysis identified exercise intensity (P < 0.001), but not BMI, body fat percentage or waist circumference to significantly relate to positive troponin tests. In conclusion, prolonged, moderate-intensity exercise results in a comparable increase in cTnI-levels in lean, overweight and obese subjects. Therefore, measures of obesity unlikely relate to the magnitude of the post-exercise elevation in cTnI